THIS IS VITAL. STUDY THIS ALL QUARTER. DR. LEFEBVRE WILL/SHOULD POST QUESTIONS SIMILAR TO THIS.

BUT
THIS IS EVERYTHING WE NEED TO KNOW. I'VE BEEN TOLD THIS COURSE IS UN-CRAMMABLE. JUST FYI.

THINK THIS PACKET INCLUDES THE MIDTERM AND FINAL EXAM STUDY GUIDE QUESTIONS.

Red Flags for Disease (based on CSPE protocol and class lecture)
Facts & Knowledge

1. What is multiple myeloma?

a. Most common primary bone cancer
b. MRI “+”
c. Bone Scans- appear normal
d. Multiple myeloma is a cancer that forms in a type of white blood cell called a
plasma cell. Plasma cells help you fight infections by making antibodies that
recognize and attack germs. Multiple myeloma causes cancer cells to
accumulate in the bone marrow, where they crowd out healthy blood cells.
(mayo-clinic)
2. Who tends to get it?
a. Patients > 50, w/ chronic LBP and anemia (of chronic disease)
b. Consider multiple myeloma or spinal infection in patients with the above
symptoms + recurrent infections
3. What is the blood test of choice to help diagnose it?
a. Serum protein electrophoresis.
4. What does the radiograph look like?
a. Less dense; affected spinal segments appear with increased translucency.
5. Which advanced imaging would be best to diagnose multiple myeloma, a bone
scan or an MRI?
a. MRI is preferred. Bone scan would be normal, rendering it useless.
b. Multiple myeloma is the exception, bone scan will be positive for most bone
cancers.
6. How common are diseases like cancer and spinal infections as a cause of low
back pain?
a. 3% of LBP due to pathology (1% cancer/spinal infection; 2% referred pain from
GI or GU).
7. What is the single strongest red flag from a patient’s history that their LBP may be
linked to cancer?
a. History of cancer (+LR = 16-23)
b. Weight loss: >10 lbs in three mo (+LR = 2.5)
c. Failure to respond to conservative care for 1 month (+LR = 3.1)
8. How much unexpected weight loss on average is enough to be considered a red
flag for a patient with low back pain?
a. Weight loss: 10 lbs or more over 3 months
9. Is no relief from bed rest a more sensitive or more specific sign for cancer as a
cause of LBP?
a. Highly SENSITIVE (>90%)
b. This means this question is a good cancer screening tool for your patients with
LBP.

1
10. What serious condition can result in a patient having to sleep in chair because of
their LBP?
a. Malignant retroperitoneal lymphadenopathy
11. What is the current thinking regarding night pain as a red flag for cancer? Why?
a. A study of 482 patients found that 42% reported some night pain and 20%
presented with pain “every night.” There was NO correlation with serious disease.
(Harding 2004)
b. A number of guidelines no longer include night pain, although there may still be
concern when the (EXCEPTION) pain is severe, progressive, or unabated by
position.
12. Is unexplained weight loss better at ruling in possible cancer or ruling it out?
a. Ruling in (94% specificity) - +SPIN
b. +LR 2.5
13. In what patient population are neurological deficits an increased risk for possible
cancer?
a. Elderly
b. Any patient over 50 + back and leg pain + neurological deficits = consider
possibility of cancer, order at least an x ray.
14. If you suspect that your patient’s LBP may be due to cancer, what blood tests
should you order first?
a. 1st: ESR and/or CRP
b. 2nd: Complete Blood Count (CBC)
c. 3rd: Blood Chemistry Panel (Serum Ca, ALP, Protein)
d. If suspect urinary problem, 4th: UA & other special blood/urine tests.
15. What finding on a bone scan can signal the presence of cancer? What does it look
like?
a. With radioactive dye-> Malignancy typically show as “hotspots” due to increased
metabolic activity.
16. On average, what are the chances that cancer causing LBP will show up on an
x-ray on the first visit?
a. 68%
b. Note: Plane films are NOT recommended for routine evaluation of ACUTE LBP,
unless a red flag is present.
c. If we suspect pathology + LBP, start by ordering plane films. If suspicion still high,
order MRI, CT, or bone scan.
17. What is LeFebvre’s 20-50 rule for interpreting a patient’s ESR?
a. ESR <20 = not concerning, probably normal.
b. ESR 20-50 = more concerning, might order more tests or keep a close eye.
c. ESR >50 = very concerning, need to dig deeper and order more tests
18. What kinds of disease categories can an elevated ESR signal?
a. Inflammation, cancer, infection, kidney or thyroid disease. (mayo clinic)

2
ESR Reading

0-18 mm= NORMAL

18-50 mm = MODERATE

>50 mm= HIGH RISK

>100 mm = Multiple Myeloma, Temporal

Arteritis, Polymyalgia Rheumatica

19. Your patient has low back pain, loss of calcium as seen on an x-ray, and elevated
ESR of 90mm/hr. What condition do you think of first?
a. Primary or metastatic bone cancer.
b. 40-50% of patients with metastatic cancer have elevated calcium.
i. Elevated calcium might also be due to hyperparathyroidism.
20. What types of bone conditions does ALP go up in?
a. Blastic Lesions, Paget’s Disease, growing bones, pregnancy and liver disease.
b. 50-75% of cancer patients have elevated ALP.
21. What are clues that a patient’s low back pain may be visceral in origin?
a. Periodic and non-associated with movement (not aggravated by bending/lifting).
b. Colicky (cramping).
c. Writhing pain (can’t sit still).
d. Menstrual cycle abnormalities.
e. Little low back muscle spasm, tenderness, or segmental restriction compared to
an MSK issue.
22. Where are pain referral patterns in the back for kidney disease, colon disease,
urinary pain, and pancreatitis? Mark the picture.
a. Pancreatitis: relieved by knees drawn up and forward flexion (high specificity).

3
 b. Pelvic organs: pain may be on opposite side as pathology.

c. Colon: mid lumbar spine.

d. Gynecological disorders: usually L4 and below.
e. Sigmoid colon, rectum, pelvic organs: usually sacral.
23. Your patient has low back pain secondary to spinal cancer. What would be the
likely results in the following tests? (CRP, CBC, blood chemistry panel)
a. Elevated CRP; increased ESR; low hgb and anemia; increased serum calcium or
ALP.

Strategies

24. What is the first step in differential diagnosis of an NMS condition?

a. Determining if Sx derive from an injury or disease, and if there is nerve damage
or not.
25. What are the 3 options you have to choose from when you see red flags + LBP?
a. First need to find out from history and physical exam how many red flags there
are, and decide how serious they are.
i. Treat anyways but monitor patient carefully to see if they worsen or don’t
respond to care.
ii. Worried enough that you order more tests (plane film, blood work, etc).
iii. Red flags are very worrying, might order tests yourself or refer out
immediately.

Applications

26. Your patient has low back pain, and you decide to perform spinal percussion.
What constitutes a positive test? What does it mean if percussion is positive?
a. Patient reports pain that is exquisite and lingers.
b. Spinal infection (most sensitive and specific), cancer, or fracture.
27. You do motion palpation of your patient’s spine, and find severe local muscle
spasm with severe lack of ROM of 3 continuous spinal segments. What might be
the cause?
a. Cord reflex from:
i. Cervical spine: vascular lesion
ii. Thoracic spine: spinal metastasis
iii. Lumbar spine: prostate or uterine cancer

4
 28. You suspect possible cancer in your patient whose ESR came back elevated. Next
you order a CBC. What results might come back that confirm your suspicion of
cancer?
a. Low Hgb/anemia
i. 50% of cancer patients have anemia (14% in all other patients).
ii. Anemia + LBP is a red flag.
b. Increased WBC
i. Signals spinal infection, cancer, or inflammatory disease (just like
elevated ESR).
c. Increased immature WBC
i. Suggests leukemia.
d. Decreased WBC
i. Suggests multiple myeloma or other cancers.
e. Altered WBC + LBP is a red flag.

Sensory Testing (based on Panopto lecture)

Facts & Knowledge

1. In patients with sensory loss and back or leg pain, what three types of
neurological lesions are in your differential diagnosis?
a. Myelopathy: cord lesions (most common in upper lumbar/TL junction)
b. Radiculopathy: nerve root lesions (cauda equina, disc herniation, stenosis)
c. Neuropathy: peripheral nerve lesions (sciatica, femoral, etc)
2. What are the different sensory modalities that are tested? What spinal cord track
does each one travel in?
a. Posterior (dorsal) column: proprioception, vibration, fine touch/2-pt. discrimination
b. Lateral Spinothalamic tract: pain, temperature
c. Anterior Spinothalamic tract: crude touch/pressure
3. What is paresthesia? How does it differ from pain?
a. Paresthesia is not painful; it’s pins and needles; itchy and crawly.
4. What is the proper term for each of the following physical exam findings?
a. Diminished pain sensation? Hypoalgesia
b. Diminished ability to feel a cotton ball? Hypoesthesia (or Hypesthesia)
c. Absence of the ability to discriminate light touch? Anesthesia
d. Increased sensitivity to a noxious stimulus? Hyperalgesia
e. A pain response to a Semmes-Weinstein assessment? Allodynia
f. Exaggerated pain response to a pinwheel? Hyperalgesia
g. Increased sensitivity (but no pain) to light brushing over the skin? Hyperesthesia
h. Unpleasant but not painful reaction to a cotton ball? Dysesthesia

5
5. What does the term dermatome refer to?
a. The area of the skin that is supplied by a specific nerve root.
6. In each of the following circumstances, what nerve root, family of nerves or
peripheral nerve may be implicated?
a. Loss of feeling along the side of the little toe? S1 (pure patch) or Superficial
peroneal n.
b. Loss of feeling on the medial side of the great toe? L5 (L5 pure patch is medial
head of 1st metatarsal), or Deep peroneal n.
c. Loss of feeling along the medial side of the lower leg? L4 or Saphenous n.
d. Loss of feeling along the lateral side of the lower leg? L5 or Superficial peroneal
n.
e. Loss of feeling in the thumb and first finger? C6 or Radial n. (dorsal surface) or
Median n. (palmar surface)
f. In the middle finger? C7 or Radial n. (dorsal surface) or Median n. (palmar
surface)
g. The lateral aspect of the upper arm? C5 or Axillary n. (upper) or Radial n. (lower)
h. Loss of feeling down the midline of the anterior upper thigh? L2 or Anterior
femoral cutaneous n.
i. Loss of feeling just above the knee? L3 or Anterior femoral cutaneous n.
j. Loss of feeling in the 5th finger? C8 or Ulnar n.
k. Loss of feeling in the medial forearm and upper arm? T1 or Medial brachial
cutaneous n. (upper arm) or Medial antebrachial cutaneous n. (forearm)
7. Where is the pure patch for:
a. C8/ulnar nerve? Medial tip of 5th Digit
b. C7? There is none
c. C6/radial nerve? Thumb web (dorsal aspect)
d. C6/median nerve? Lateral tip of index finger
e. C5/axillary nerve? Over Deltoid tubercle
f. L4? Midway medial lower leg
g. L5? Medial head of 1st metatarsal
h. S1? Lateral little toe
8. You discover that your patient has diminished sense of pain at the tip of her
thumb. What’s the very next thing to do before you move on to other procedures?
a. Map out the boundaries of the abnormal pain sensation, work from distal to
proximal to find an area of normal sensation.
i. Next will have to figure out if it is a nerve root, peripheral nerve, if it’s
bilateral or unilateral, etc.
9. Your patient has loss of vibration. What are some diseases that affect the spinal
cord that would be in your DDX (differential diagnoses)? What are diseases of
peripheral nerves that you should consider?
a. Spinal stenosis, upper lumbar disc herniation, TL junction compression
fracture (like from a fall on the buttocks), Tabes Dorsalis, or a tumor.

6
 b. Diabetic polyneuropathy, Multiple Sclerosis, Alcoholic neuropathy, Vitamin B12
deficiency.
10. What is the advantage and disadvantage of hot and cold testing over testing for
pain?
a. Advantages: temperature loss may precede loss of pain perception, and this has
been found to be more discriminatory than loss of pain perception.
b. Disadvantages: pain is easier to assess.
11. How is position sense usually tested?
a. Patients eyes closed, move finger and/or toe up and down and ask which way it
was moved.
12. Where do temperature signals cross the body in the central nervous system?
Where does vibratory sense cross the CNS? Where does pain cross? Where does
proprioception cross?
a. Pain, temperature, and crude touch (lateral/anterior spinothalamic tracts) crosses
immediately at the same spinal cord level.
i. This means that a spinal cord lesion on one side would result in deficits in
the opposite extremity.
b. Vibration, proprioception, and fine touch (dorsal columns) crosses in the medulla
(brainstem).
i. Lesion is on the same side as the deficits.

Applications

13. Your patient has an area where he cannot feel touch, vibration, pain or position
sense. Is the lesion more likely in the spinal cord, a nerve root, or peripheral
nerve?
a. Either the spinal cord was completely severed (nope, there would be more
obvious issues with the patient than just sensory loss), or the injury happened
before the sensory impulse had a chance to split into the different tracts in the
spinal cord. Therefore, a nerve root or peripheral nerve issue is most likely, but
we would need more specific information regarding the sensory loss to
distinguish between the two.

Low Back & Leg Pain: Neurological Assessment (based

on class lecture)

Facts & Knowledge

1. What basic three diagnostic tools do physicians have to figure out what is wrong
with their patients?
a. History, Physical exam findings, and Ancillary studies.
b. You need 3 things to diagnose HeP-A.

7
2. About what vertebral level does the spinal cord end?
a. ~L1-2
3. What are three causes of spinal cord compression in the TLJ region of the spine?
a. TLJ compression fracture.
b. Upper lumbar disc lesion.
c. Spinal canal stenosis.
d. Tumor.
4. Besides leg symptoms, what other symptoms do you need to ask a patient to
screen for cord involvement and LBP?
a. Check for SMR deficits, check for + Babinski, check for + Romberg, check for
negative nerve tension tests and spinal loading tests.
b. Ask about Bowel/Bladder function.
5. How do you perform the Romberg’s test?
a. http://www.neuroexam.com/neuroexam/content37.html
b. Ask the patient to stand with their feet touching one another, and ask them to
close their eyes. With their eyes remained closed, see how long the subject may
stand with minimal to no swaying.
c. Patient should be able to stand for 20 or 30 seconds.
6. What conditions can a positive Romberg test suggest?
a. #1 cause is myelopathy.
b. Less common but possible causes are peripheral nerve lesions, multiple nerve
root lesions, cerebellar disease, or vestibular disorders.
7. What sensory modalities are conducted in the posterior column of the spinal
cord?
a. PVT-2nd Class (Proprioception, Vibration, Touch, 2-point discrimination)
8. What spinal tract does pain and temperature travel in?
a. Lateral spinothalamic tract
9. If you had spinal cord compression on the right, which leg would likely to lose
pain sensation, position sense, two-point discrimination? Vibration?
a. The left leg would lose pain and temperature; these tracts decussate at the level
of the spinal cord.
b. The right leg would lose proprioception, vibration, and 2-point discrimination;
these decussate in the brainstem.
10. What are the key lower extremity reflex changes to check for in the lower
extremity if the patient has myelopathy?
a. Clonus
b. Babinski sign
c. Loss of cremasteric reflex
11. What are the 5 key exam findings suggesting a cauda equina syndrome? Which
one is the most common?
a. Saddle anesthesia: 80% sensitivity
i. Bilateral, but can be unilateral.
ii. Should test light touch and sharp.

8
 iii. Altered perineal sensation may be most important predictor of impending
bowel or bladder dysfunction.
b. Bladder:
i. Painless urinary retention and overflow incontinence (retention is the
most common CES symptom).
ii. Incomplete CES = urinary difficulty, altered urinary sensation, loss of
desire to void, poor urinary stream, need to strain to urinate.
iii. Complete CES = urinary retention, overflow incontinence, complete
saddle anesthesia.
c. Bowel:
i. Inability to control defecation
ii. Sense rectal fullness
iii. Decreased anal sphincter tone
d. Anal “wink”:
i. Normal response (-): contraction of the external anal sphincter when
perianal skin is scratched
ii. Abnormal response (+): no contraction
e. Sexual dysfunction:
i. Decrease in penile/labial sensation
ii. Inability to get or maintain an erection
iii. Reduced sensation during sexual stimulation
f. When both urinary dysfunction AND saddle hypesthesia are present, CES
is strongly suspected.
12. What are the 3 most common causes of cauda equina syndrome (CES)?
a. Midline disc herniation;
b. Severe spinal stenosis;
c. Tumor;
d. Infection;
e. Hematoma;
f. Keep in mind that CES is extremely rare, but requires urgent referral.
13. What nerve roots are affected in CES?
a. S2, S3, S4
b. NOT SPINAL CORD INJURY.
14. An exam finding has +LR of 18. Is that considered a small increase, moderate
increase or large increase in the probability of a particular diagnosis?
a. A large increase
15. A test has a -LR of 0.1. Does that tend to decrease the probability of a specific
disease a small amount, a moderate amount, or a large amount?
a. LARGE
16. What is the relationship of bilateral sciatica to CES? Explain.
a. Bilateral sciatica isn’t unique to CES, but is often present.
17. What peripheral nerve injury can mimic some of the neurological symptoms of
CES? What can cause this condition?

9
 a. Pudendal nerve compression (Alcock’s Syndrome).
b. Caused by a fall on the buttocks, childbirth, chronic defecation straining, vigorous
bicycling.
c. May present as unilateral or bilateral perineal pain (burning/foreign body in
rectum/vagina).
18. What are 4 characteristics of the pain itself that would be consistent with a
neuropathic syndrome?
a. Sharp, electrical, stabbing, lancinating.
19. What are the 5 key findings to look for from the H&P that would support a
radicular syndrome?
a. Pain: past the knee/skin deep/dermatomal (location, Note: dermatomal
distribution is often absent, except in S1 which is very commonly dermatomal),
sharp/stabbing/electrical (quality), worse than back pain (severity), and affected
by spinal positioning.
b. Paresthesia: tingly sensations more often in a dermatomal pattern
c. Compression tests (SMR): deficits or hypersensitivity (usually caused by nerve
root compression from a disc herniation or spinal stenosis).
d. Tension tests: reproduces leg pain
e. Spinal loading: rapid reproduction of leg symptoms (leg pain with forward
flexion, Kemp’s test, or Valsalva).
20. What is a pure patch? Where are the pure patches for S1, L4 and L5?
a. A pure patch is an area innervated by a single nerve root.
i. L4: Middle ⅓ of medial lower leg
ii. L5: Medial big toe and web of 1st/2nd toes
iii. S1: Lateral small toe
21. If your patient had a disc herniation compressing L5, what DTRs might be affected
(affected in what way?), what muscles might be weak? Where might the
paresthesia be felt?
a. L5 DTR: primarily Medial Hamstring reflex (L5-S1, sciatic n.), but also
contributes to the Achilles reflex (L5-S2, S1, sciatic n.).
b. L5 Motor: Big toe extensors (L5-S1, peroneal n.), and hip abductors (L5-S1,
superior gluteal n.), among many others it contributes to.
c. L5 Sensory: paresthesia in the lateral lower leg and large toe.
22. Same questions as above for S1 and L4.
a. L4 DTR: Patellar reflex (L2-L4, femoral n.)
b. L4 Motor: Ankle dorsiflexion and inversion (L4-S1, deep peroneal n.), among
many others it contributes to.
c. L4 Sensory: paresthesia in the medial lower leg.
d. S1 DTR: primarily Achilles reflex (L5-S2, S1, tibial/sciatic n.), but also
contributes to Medial Hamstring reflex (L5-S1, sciatic n.)
e. S1 Motor: Toe flexors (L4-S3, S1, tibial n.), ankle evertors (L5-S2, S1,
peroneal n.), and plantar flexors (L4-S3, S1, tibial n.), among many others it
contributes to.

10
 f. S1 Sensory: paresthesia in the lateral little toe.
23. A positive SLR suggests a lesion is where in the nervous system?
a. SLR and other nerve tension tests provoke inflamed peripheral nerves or its
nerve roots.
24. What is the difference between a hard and soft positive SLR?
a. A hard positive goes past the knee, while a soft positive does not.
b. May follow up a soft positive with something like a maximum SLR.
25. Your patient cannot toe raise. What nerve root could be injured? Which peripheral
nerve?
a. L5, Peroneal n.
26. What nerve roots does the femoral nerve stretch tension?
a. L2,3,4.
b. Also stretches the femoral nerve, which is composed of these nerve roots.
27. What are the key findings that distinguish a radiculitis from a radiculopathy? What
is the difference physiologically between those two nerve root conditions?
a. Radiculitis (inflamed nerve root)
i. Neuropathic pain (dermatomal, sharp, past the knee, leg worse than
back, affected by spinal position).
ii. Paresthesia (dermatomal)
iii. + tension tests
iv. Loading spine reproduces leg pain
v. Increased sensitivity
b. Radiculopathy (compressed/torn nerve root)
i. Motor deficits (weakness, atrophy)
ii. Hyporeflexia
iii. Dermatomal sensory loss
c. Note: pain and deficits often occur together.
28. In what circumstances would pain with Valsalva maneuver or a Kemp’s test be
suggestive of a nerve root problem? Would they also likely suggest a peripheral
nerve injury? How about a myelopathy?
a. These are both spinal loading procedures, which will often rapidly reproduce leg
pain, but peripheral nerve injuries and myelopathy are usually not affected.
29. Your patient has fasciculations—is this more likely due to nerve root compression
or spinal cord compression?
a. Fasciculations, along with fibrillations or muscle atrophy are associated a LMN
lesion, like nerve root or peripheral nerve compression.
30. How are fasciculations detected? How are fibrillations detected?
a. Fasciculations are directly observable/palpable as a muscle twitch under the skin,
while fibrillations require needle EMG.
31. Peripheral neuropathies are divided into what two general categories?
a. Entrapments/Compression
i. Piriformis syndrome, peroneal nerve compression, femoral neuropathy
secondary to pelvic tumor, etc.

11
 b. Diseases (polyneuropathy)
i. Diabetes, alcoholic neuropathy, vitamin B12 deficiency, etc.
32. Your patient has a femoral neuropathy. What are several possible causes to first
consider?
a. Diabetic Mononeuropathy (most common single nerve to be effected)
i. However, Diabetic Polyneuropathy affecting the lumbosacral plexus is
much more common.
b. Tumor
c. Psoas or Iliacus hematoma (or spasm)
d. Injury
e. Inflammatory conditions
33. What would be the pain and sensory loss distribution? What muscle would be
affected? What reflex?
a. Unilateral groin, anterior or medial thigh, and sometimes medial lower leg.
b. Hip flexors and knee extensors (iliopsoas and quads).
i. Knee buckling or locking in hyperextension possible.
c. Patellar reflex
d. Note: the femoral nerve DOES NOT innervate the adductors (obturator n.), so if
they are weak the problem is likely proximal (lumbosacral plexus or L2-4).
e. Note: the femoral stretch test will recreate sharp anterior thigh pain.
34. What would be the common causes and patient presentation for peroneal nerve
entrapment?
a. Most often due to compression/stretching of the nerve near the fibular head.
i. May be caused by prolonged posture (legs crossed), trauma, weight loss
(loss of padding), repetitive running/sports, or caused by some other
medical intervention (casts, surgery, etc).
b. Common symptoms include:
i. Foot drop, weak ankle dorsiflexion, eversion, or big toe extension,
numbness/paresthesia over lateral lower leg and dorsal foot.
ii. Ankle inversion stretches nerve and is painful.
iii. Normal Achilles reflex and usually no distal pain, though there may be
local pain that radiates proximally from the fibular head.
35. How does diabetic amyotrophy first present? What is the dominant symptom?
a. Sudden, severe lower extremity weakness, followed by painful muscle tests.
i. Muscles may test weak in a nerve root/peripheral nerve issue, but a
painful test is more commonly due to a disease process.
b. Painful femoral nerve = potential undiagnosed diabetes.
36. What two blood tests are frequently ordered to test for diabetes? What are the
threshold numbers for making the diagnosis?
a. Hgb-A1C - normal is 5% or lower - 6.5 or 7% or higher is diagnostic.
b. Fasting glucose - normal is 100 mg or lower - 126 mg or higher is diagnostic.
37. Besides blood work, what two ancillary studies may need to be ordered in
suspected femoral neuropathy?

12
 a. EMG/Nerve conduction test to figure out which muscles are affected, thus
where in the nerve a lesion may be.
b. CT to rule out a tumor (next most likely after diabetes).
38. How is “classic” diabetic peripheral neuropathy different than mononeuropathy?
a. Symmetrical sensory loss in extremities, begins in feet, then hands
(stocking-glove distribution).
b. Burning pain, allodynia.
c. Later on autonomic and motor deficits, weakness in distal lower extremities.
d. Gait abnormalities.
e. Gabapentin is a drug that can provide clinically significant pain relief to people
with peripheral diabetic neuropathy and postherpetic neuralgia.
39. What three common diseases that can affect peripheral nerves?
a. Diabetes, alcoholic neuropathy, vitamin B12 deficiency.
40. What peripheral nerve is compromised in meralgia paresthetica?
a. Lateral Femoral Cutaneous n.
b. Due to entrapment under the inguinal ligament.
c. Caused by tight pants/belt, obesity, pregnancy, diabetes, local trauma…
d. Presents with anterolateral thigh pain and paresthesia, but no motor
involvement!
41. What are all of the things necessary to be negative or normal to conclude that a
patient’s leg pain is deep referred from their back?
a. Leg Pain is usually not past the knee, non-dermatomal, achy/dull, not as bad as
the back pain, and may only be affected by prolonged by spinal position.
i. Make sure there is also back pain. If there is ONLY leg pain, it probably
isn’t deep referred.
b. Usually no Paresthesia, but if there is it’s non-dermatomal.
c. Normal SMRs.
d. Negative Nerve Tension Tests.
e. Usually not affected by Spinal Loading.
42. How does the pain territory help differentiate peripheral nerve damage from a
radicular syndrome and from simply somatic referred pain?
a. Peripheral Nerve: stocking distribution if polyneuropathy, but otherwise follows
the territory of the peripheral nerve.
b. Radicular: past the knee and may be dermatomal.
c. Referred: non-dermatomal, usually not past the knee.
43. Based on a study of 187 patients what were the most distinguishing findings for
radicular syndromes?
a. + SLR
b. Reduced Cold temperature detection
c. Hyperalgesia or reduced pinprick response (sharp-dull testing), burning pain,
and tactile allodynia were the best indicators of peripheral neuropathy.
d. Reduced vibration response was the best indicator for diabetic neuropathy.

13
 44. What type of pain was more often associated with peripheral neuritis vs
radiculitis?
a. Radiculitis: more often dermatomal, more often starts proximal and moves
distal, muscle weakness in a more specific myotome.
i. + spinal loading, + nerve tension tests, paresthesia is also more often
dermatomal.
b. Peripheral Neuritis: burning, more often originates from a more distal injury,
NOT dermatomal but rather distinct from a single nerve root, usually no LBP
present, more obvious muscle atrophy.
i. Not aggravated by loading the spine, + nerve tension tests, and very often
paresthesia accompanying the leg pain.
45. What are the various findings for an UMNL?
a. Urinary incontinence, constipation, impotence.
i. Many similar findings as Cauda Equina Syndrome, but remember, the
conus medularis ends at L1-L2. CES is compressing multiple nerve roots,
while a myelopathy is compressing the spinal cord itself above the conus
medularis.
b. Ipsilateral dorsal column sensory loss: vibration, proprioception, 2 pt
discrimination.
c. Contralateral lateral spinothalamic tract sensory loss: pain and temperature.
d. + Romberg test, + Babinski, + Clonus, hyperreflexia, loss of cremasteric reflex.
e. Spastic paralysis or hypertonic hemiparesis.
i. Crampy contraction but still weak muscle test.
46. What are the various findings for a LMNL?
a. Muscle fasciculations or fibrillations.
b. Significant muscle atrophy, flaccid paralysis or paresis, and hyporeflexia.
c. There may be ipsilateral sensory loss or hypersensitivity.

Strategies

47. Your patient has both LBP and symptoms in their foot. What are the 5 possible
diagnostic possibilities you need to explore to solve the patient’s back and foot
complaints?
a. Myelopathy.
b. Radicular/nerve root irritation or compression.
c. Peripheral neuropathy.
d. Deep referred pain.
e. Separate lesions.
48. Once you decide that your patient’s back pain is likely an injury and not a disease,
what is the first clinical puzzle to solve?
a. Is there nerve damage/involvement?
49. What are the 5 key clues from the H&P to focus on to see if your patient has
neuropathic pain or not?

14
 a. History: Leg pain (location, quality, severity, affected by spinal position), and
Paresthesia.
b. Physical Exam: Nerve tension tests, SMR deficits, spinal loading reproducing
leg pain.
50. If you decide your patient has neuropathic/radicular pain, what 3 things must you
figure out?
a. Which nerve root is involved?
b. What is the nature and degree of the nerve root injury?
c. What is the cause?
51. Explain to a 4th quarter student what the SLR is, what it is good for and not so
good for, and what follow-up nerve tension tests you might use and why.
a. The SLR involves lifting the patient’s straight leg at least to 45 or 60 degrees,
looking to see if you can recreate the patient’s leg pain (NOT THE BACK PAIN).
i. This is a passive test without the patient helping you, and it primarily
tensions nerve roots L4, L5, S1, and the sciatic nerve.
b. The sensitivity is very good for posterolateral disc herniations, but more poor
for spinal stenosis, spondylolisthesis, and midline/medial disc herniations.
c. After a positive SLR, you may want to confirm the test by performing Braggard’s,
Bonnet’s, or Bowstring. If you only get a soft positive SLR, you can perform a
Maximum SLR, Seated SLR (Bechetrew), or Slump Test to see if that is enough
to reproduce leg pain past the knee.

Stories

52. What is the story of convergence-projection and the role it plays in deep referred
pain syndromes?
a. When an injury or irritant creates pain in the low back, it synapses on a WDR
neuron, which also receives input from other parts of the body, such as the leg.
When this WDR sends signals to the brain, it can confuse the back pain as
originally coming from the leg.
53. What is the story of central sensitization and the role it plays in the clinical
picture?
a. Pain originating from the low back can hypersensitize the WDR, so that when
non-noxious stimuli from the leg synapse at the WDR, it can be perceived as
painful. This can make the leg both spontaneously painful, and cause any
additional stimulation to be painful.
54. What is the story of sclerotogenous pain referral?
a. Any tissue from the same embryonic origin may or may not share a
neurological connection, but yet when one tissue in the sclerotome is irritated,
pain may be perceived as originating from all the tissues in that sclerotome.

15
 b. Will most often be perceived as deep, dull, achy, hard to localize, and diffuse.
However, besides being sharp/electrical, it can sometimes mimic radicular pain
down the leg, and even past the knee occasionally.

Applications

55. Your patient has neuropathic anterior thigh pain that is reproduced if passive
extend the hip to end range. Is this more likely a nerve root problem or a femoral
nerve problem? How do you know?
a. Most likely a femoral nerve issue since there is no LBP, which would be very
unlikely in a radicular syndrome.

What neurological diagnosis as at the top of your list for each of the following cases?

56. Your 54 year old patient, who has an artificial heart valve and is on coumadin, fell
off a bike and now has sharp anterior thigh pain, loss of patellar reflex, weak hip
flexors, and cannot feel pin prick over his medial lower leg. His spinal exam is
normal. What is the most likely cause of his leg pain? What ancillary study should
be ordered? Why?
a. Because there is no LBP, we suspect femoral neuropathy.
b. Coumadin is a blood-thinner, but may have caused a hematoma which is
compressing the femoral nerve as it passes through the iliac fossa.
c. Order plain film first to rule out fracture due to trauma, then follow up with CT of
the abdominopelvic region to check for hematoma.
57. Your 35-year-old patient has low back pain, positive SLR, loss of sensation along
the medial side of his shin and grade 4 weakness with dorsiflexion muscle test.
a. All symptoms match an L4 radiculopathy (not radiculitis because leg is only
painful with SLR), and there is LBP so not a peripheral nerve.
58. Your 25-year-old patient has had several occasions of “leaking” and wetting his
pants, unilateral tingling and sometimes burning in the perineal region aggravated
by horseback riding, but no back or leg pain and no other neurological findings.
Lumbar examination is normal.
a. Urinary incontinence + saddle paresthesia/pain make us very wary of cauda
equina syndrome, but there is no back or leg pain, which is pretty strange.
b. We would monitor carefully for worsening of these symptoms, and educate the
patient to recognize when these worsen.
c. The more likely diagnosis is Alcock’s Syndrome, aka Pudendal nerve
compression, which can mimic CES, and since there is no LBP which is more
indicative of a peripheral neuropathy.
59. Your 46-year-old patient complains of an annoying “numbness” along his leg
where his pants pocket is. Physical exam reveals mild sensory loss in the same
area, but no motor, or reflex deficits.

16
 a. No back pain, and especially NO MOTOR LOSS, plus the classic sensory
distribution is indicative of Meralgia Paresthetica aka Lateral femoral
cutaneous nerve compression.
60. Your 55-year-old patient has LBP and leg pain down to the lateral side of his foot
and has reduced Achilles reflex on that side and a hard positive SLR.
a. LBP + leg pain matches a radicular syndrome, and all the symptoms point to an
S1 radiculopathy + radiculitis.
61. Your 35-year-old patient has LBP, intense hyperalgesia along the medial border of
his big toe, leg pain that is aggravated when he bends over, and weakness with
hip abduction muscle test.
a. All of these symptoms indicate an L5 radiculopathy + radiculitis.
b. Because his leg pain is worsened with flexion, this may be caused by a disc
herniation.
62. Your 26-year-old patient complains of burning sensation in both feet and has
No LBP mentioned or spine
related synptoms, so bilateral loss vibratory sense in his toes and hypalgesia, but no motor loss and
indicating Peripheral Nerve
related only. So due to
reflexes are all normal.
Bilateralality, indicating more
Diabetic than
a. Bilateral distal extremity burning and vibration loss screams diabetic
Mononeuropathy polyneuropathy.
b. We would send him for bloodwork to check Hgb-A1C >6.5/7 = diabetes.
63. Your 60-year-old patient has intense LBP and achy pain to his heel. The SLR
dramatically increases his LBP, Achilles reflex is 2+, dorsi and plantar flexion are
5/5 and sensory testing is normal.
a. SLR is negative (doesn’t cause leg pain), DTR is normal, muscle and sensory
tests are normal. His pain is achy and even though it goes all the way to his heel,
this matches deep referred pain from the low back.
64. Your 60-year-old patient has LBP, a burning sensation in both feet, and 4+ Achilles
reflex.
a. Older patient with bilateral extremity pain, and clonus. This highly suggests an
UMN lesion/myelopathy, most likely due to spinal stenosis or a tumor due to
older age.
b. Need to order plain films followed by an MRI.

Motor Testing (based on Panopto lecture and CSPE protocol Muscle Testing)

Facts & Knowledge

1. Muscle testing can lead to what four major types of diagnoses?

a. Radiculopathies

17
 b. Peripheral neuropathies
c. Myelopathies
d. Muscle strains
2. What are the technical terms for the following findings:
a. A patient with muscle weakness and associated tremor? Palsy
b. A patient with “partial paralysis” of voluntary movement? Paresis
c. A patient with muscle weakness and loss of muscle tone? Flaccid Paresis
d. A patient with muscle weakness and hypertonia? Spastic Paresis
e. Decreased muscle tone alone? Hypotonia
f. Increased muscle tone alone? Hypertonia
g. A patient with “muscle wasting?” Atrophy
h. A patient with complete loss of voluntary movement? Paralysis
3. Using the muscle grading system, how would you differentiate a grade 2 muscle
weakness from a grade 3? Differentiate a grade 1 from 0?
a. Grade 2 muscle weakness means the patient can move the joint through full
ROM as long as gravity has been eliminated (joint is resting on table moving in
transverse plane), while grade 3 muscle weakness means the patient is able to
move the joint through full ROM against gravity, but cannot withstand resistance
from the doctor.
b. Grade 1 muscle weakness means the patient can cause a voluntary muscle
twitch, but cannot move the joint, while grade 0 muscle weakness is full paralysis
with move contraction or motion at all.
4. What are 3 of the key components of a motor exam?
a. Observe for muscle atrophy/fasciculations.
b. Measure girth.
c. Isometric muscle test.
5. Is resisted range of motion testing more appropriate for neurological assessment
or testing for a tendon or muscle injury?
a. Resisted ROM muscle testing assesses contractile unit itself, checking for a
tendon or muscle injury, while isometric muscle testing can assess the
muscle/tendon AND the neurological innervation.
6. Your patient has foot drop. Where in the nervous system could her lesion be?
What would be two other findings that could help you decide?
a. L4 and/or L5 radiculopathy
i. LBP/disc issues.
ii. L4 or L5 dermatomal sensory loss, paresthesia, or pain.
iii. SMR findings specific to L4 or L5 nerve roots.
b. Common peroneal neuropathy.
i. Injury around fibular head, possible specific local fibular head pain.
ii. Knee degeneration.
iii. Normal DTRs
iv. Non-dermatomal pain, paresthesia, sensory.
v. Motor weakness not specific to L4 or L5.

18
 7. For each of the following weaknesses, indicate the family of nerve roots, the
dominant nerve root, and the peripheral nerve:
a. Ankle inversion
i. L4-S1, Deep peroneal n.
b. Shoulder abduction
i. C5-C6, Axillary n.
c. Walking on heels
i. L4, L5, S1, Deep peroneal n.
d. Extensor hallucis longus
i. L5-S1, Deep peroneal n.
e. Toe flexors
i. S2-S3, Tibial n.
f. Elbow flexion
i. C5-C6, Musculocutaneous n.
g. Wrist flexion
i. C6-C7, Median and Ulnar nn.
h. Triceps muscle
i. C7-C8, Radial n.
i. Peroneus longus and brevis
i. S1, L5-S2, Superficial peroneal n.
j. Ankle plantar flexion
i. S1, L5-S2, Tibial n.

Strategies

8. Your patient has neck and arm pain, but his muscles all test strong. What would
be the next thing to do in terms of your motor testing?
a. Resisted ROM testing, repetitive and/or sustained muscle testing.
9. When doing motor testing and finding a weak muscle, how can you use the
presence or absence of pain during the muscle test to aid your DDX?
a. Muscle weakness w/o pain suggests nerve damage or complete rupture of the
muscle/tendon.
b. Muscle weakness w/ pain suggests a strained muscle or tendon, or that your test
is tensioning an irritated nerve, or compressing an inflamed joint.

Applications

10. Your patient has muscle weakness and loss of muscle tone, where in the nervous
system do you suspect the lesion to be?
a. This is flaccid paresis, which occurs in a LMN lesion, like a peripheral nerve
compression or nerve root radiculopathy.

19
 11. Your patient has had a skiing accident and now has both low back and leg pain.
Knee flexion muscle test is grade 3 but does not hurt. Is this more likely due to a
hamstring strain or nerve damage?
a. Muscle weakness that doesn’t hurt is more indicative of nerve damage, like a
radiculopathy.
12. Your patient has muscle weakness and hypertonia, where in the nervous system
do you expect the injury to be?
a. This is spastic paresis, which occurs in a UMN lesion, like a myelopathy.
13. Your patient has LBP and you notice that hip extension on the right feels mushier
than on the left. If the patient has no nerve damage and no muscle strain, what
would be one likely explanation for the weak muscle?
a. Reflex inhibition from a hypertonic antagonist or a MFTP in the muscle.

Reflex Testing (based on Panopto lecture and CSPE protocol Deep Tendon
Reflexes)

Facts & Knowledge

1. What are the 3 main types of reflexes that you will be testing on patients with
spinal pain?
a. Stretch reflexes (+ when they are diminished or are hyperreflexic)
b. Pathological reflexes (+ when they appear)
c. Superficial reflexes (+ when they disappear)
i. Superficial reflexes involve cutaneous stimulation with subcutaneous
muscle response, instead of muscle stretch like other reflexes.
2. Outline the NINDS scale used for grading reflexes. What is the only grade that
should always be considered pathological?
a. 0 = Areflexia (often pathological, nerve root or peripheral nerve)
b. 1+ = Hyporeflexia (maybe normal, maybe pathological, compare bilaterally)
c. 2+ = Brisk/Normal (everyone’s normal is different)
d. 3+ = Hyperreflexia (maybe normal, maybe pathological, compare bilaterally)
e. 4+ = Clonus (repeating reflex, always pathological, brain or spinal cord)
f. Important Note: absence of one or both ankle reflexes has been associated with
increasing age. Unilateral absence of a reflex is still an important clinical sign, but
bilateral absence may be “normal.” However, this can also be due to bilateral
peripheral neuropathy or other more rare conditions.
3. What are two metabolic diseases that can cause hyporeflexia?
a. Diabetes and Hypothyroidism
i. Hyperthyroidism can cause hyperreflexia.

20
4. How does an UMNL create hyperreflexia?
a. The reflex is caused by a loop from the stretch receptors in the intrafusal muscle
fibers, a single synapse in the spinal cord on an alpha motor neuron, and the
extrafusal muscle fibers.
b. This reflex loop is inhibited by descending motor pathways from the brain, which
get interrupted when there is an UMN above the level of the spinal cord where
this reflex synapses.
5. For each the following stretch reflexes, indicate the group of nerve roots tested,
the dominant nerve root, and the peripheral nerve:
a. Biceps
i. C5-C6, Musculocutaneous n.
b. Brachioradialis
i. C5-C6, Radial n.
c. Triceps
i. C7-C8, Radial n.
d. Patellar
i. L3-L4, Femoral n.
e. Medial hamstring
i. L5-S1, Sciatic n.
f. Achilles.
i. S1-S2, Tibial n.
6. How would you perform a Jendrassik maneuver for an upper extremity reflex? In
what circumstances should you perform this maneuver?
a. UE = clench jaw or cross feet and squeeze ankles together.
b. LE = interlock fingers and pull apart.
c. Both of these would be performed by the patient on command by the doctor, in
which case the doctor would have about 300 ms before the contraction even
begins to test the reflex. This facilitation/reinforcement is done to help elicit
reflexes in patients who have trouble relaxing.
7. What are the four main reflexes that would suggest an injury to the spinal cord or
brain?
a. Babinski sign (and surrogates)
b. Hoffman’s sign
c. Clonus or hyperreflexic DTR
d. Inverted reflex (absent in tested muscle, but reflex in other muscles)
8. Besides using a reflex hammer, what is a common way to test for clonus in the
upper extremity?
a. Wrist extension.
9. How can you tell the difference between a pathological clonus and clonus which
may simply be a normal variant for that patient?
a. Normal = 1 or 2 beats
b. Pathological = >2 beats
10. What are the four Babinski surrogates and how are they performed?

21
 a. Oppenheim’s = firm stroke of tibial crest from S to I.
b. Chaddock’s = C shaped stroke of lateral malleolus starting inferiorly.
c. Gordon’s = sudden squeeze of the calf.
d. Schaefer’s = pinch the middle ⅓ of the Achilles tendon.
11. What is kappa a measure of? What does a kappa of .30 mean?
a. A measure of inter examiner agreement in regards to a + or - test.
b. .30 means 30% of the time different practitioners agreed with each other on the
result of a test (was it positive or negative).
12. What was an exam procedure that outperformed the Babinski reflex in a small
study of patients with UMNLs?
a. Foot Tapping (asking the patient to rapidly tap your hand with their foot, + when
the patient is unable to do so rhythmically).
i. (FYI) +LR = 5.4, -LR = 0.17
b. Babinski sign has been a traditional method of checking for UMNL, but it isn’t
actually a very good test.
i. (FYI) +LR = 1.3, -LR = 0.91
13. What are the various findings suggesting an UMNL? What neurological findings
would not fit as well?
a. Spastic paresis, hyperreflexia and/or clonus, + pathological reflexes.
i. Muscle fasciculations, significant muscle atrophy, + nerve tension tests,
flaccid paresis, and hyporeflexia are more indicative of an LMNL.
ii. Note: superficial reflexes can be absent in both UMN and LMN lesions,
but for boards and by far the most common cause of absent
superficial reflexes (and + romberg test), is myelopathy.
14. What are four important superficial reflexes, what is the innervation of each, and
how does an abnormal response appear?
a. Plantar reflex/Babinski (L5-S1)
i. When this reflex is +, it is pathological.
b. Abdominal reflex (T7-T12)
c. Cremasteric reflex (L1-L2)
d. Anal wink reflex (S2-S4)
i. When the rest of these are +, it is normal.
e. An abnormal response is the presence of the first reflex, and the absence of the
other three.
15. How are superficial reflexes charted?
a. Present (+) or absent (-)
i. Note: this is reversed from most diagnostic tests, in which + means
pathological, while here + means normal.

Strategies

16. Your patient has a positive Hoffman sign, but all other tests for an UMN lesion are
negative. How do you deal with this fact?

22
 a. When a test comes back +, you still need to look at the big picture. Any given +
test raises our suspicion, but it only might mean the patient has that particular
condition.
b. A + Hoffman sign might imply an UMNL, but it could also be a normal variant for
that patient, or it could be a result of some other unrelated condition.

Introduction to Low Back Pain (based on class lecture and course

notes Introduction to Non-Specific LBP & Low Back Pain Diagnostic Categories)

Facts & Knowledge

1. Most patients with LBP get significant improvement in what period of time?
a. Within the 1st month, with >90% at 8 weeks.
2. Approximately what percent of LBP patients go on to have chronic severe
disabling pain?
a. 10%
3. What percent will have another episode of back pain within a year?
a. 65%
4. What percent will have some moderate to severe pain within a year?
a. 33%
5. What percent will report still some functional limitations a year or longer out?
a. 20%
6. Which of the following patients are generally categorized as acute LBP? 24 hours,
72 hours, 1 week, 1 month?
a. <1 month
b. Acute LBP can also mean an acute flare up of a chronic problem.
7. How long does a patient have LBP pain before it is generally considered to be
chronic?
a. >3 months
b. Subacute = 4-12 weeks
8. What are 4 important messages that should be delivered to patients about their
LBP (hint: PAAP)?
a. First of all, DO NOT promote extended bed rest or overemphasize to the patient
the pathoanatomical damage, which could lead to the patient feeling afraid and
disabled, counteracting our goal of getting back to activity.
b. Pain perception = just because there is pain doesn’t necessarily mean that
physical damage is occurring in the tissues.
c. Active = even when still experiencing pain, need to return to normal activities as
soon as possible (not necessarily high intensity activities like sports).

23
 d. ADLs = improve activities of daily living, not just pain relief (people die of
dysfunction, not pain).
e. Prognosis = function and pain relief improvement is favorable, but there may be
flare ups.
9. What makes up the 4 tool kits for a conservative care treatment approach? Give
an example for each one.
a. Chiropractic Manipulative Therapy (ex. Joint manipulation, flexion-distraction)
b. Soft Tissue Manipulation (ex. PIR, Pin & Stretch)
c. Behavioral Modification (ex. abdominal bracing/hip hinging)
d. Exercise Therapy (ex. Stabilization exercises)
e. A chiropractor can also provide lifestyle/diet advice, orthotic supports, PT
modalities (ultrasound, etc).
10. What are two broad outcome categories that are frequently used to monitor the
patient’s response to treatment? Give some specific examples of each.
a. Pain
i. OPS, pain med consumption, frequency/duration of episodes.
b. Affect on work/ADLs
i. PSFS, improvement in work tasks able to tolerate.
11. What are yellow flags warning you that your patient may have either significant
pain centralization or psychological overlay?
a. This makes treatment difficult and prognosis poor.
b. Nonorganic signs/generalized pain
c. Maladaptive pain coping
d. Psychiatric comorbidities
e. High baseline functional impairment
i. These first 4 are strong outcome predictors.
f. Low general health status
g. High pain intensity
h. Work dissatisfaction
i. High physical work demands
j. Receiving worker’s compensation
k. Radiculopathy or leg pain
i. These 6 are weaker outcome predictors.
12. What is the biopsychosocial approach to LBP?
a. The idea that although a biological/pathoanatomical condition may be the “pain
generator,” or the initial cause of their LBP, how the patient reacts to and
perceives the pain is affected by a variety of psychological and sociological
factors in the patient’s life.
b. We have to approach the patient from these 3 different angles to understand why
the patient is feeling pain, even when the original lesion has long since healed or
is no longer the primary pain driver.
c. In this situation, diagnosing the patient with a specific pathoanatomical diagnosis
may do more harm than good.

24
 13. What is the effect of NSAIDs, muscle relaxants, Tramadol, and Duloxetine on LBP?
a. NSAIDs have NOT shown clinically significant improvement in acute or chronic
LBP.
b. Muscle Relaxants have shown mild improvements in acute LBP.
c. Tramadol (opioid) has shown moderate improvements in chronic LBP.
d. Duloxetine (antidepressant) has shown mild improvements in chronic LBP.
e. However, combination therapy with 2 drugs has shown much larger
improvements in chronic LBP.
14. What are the 5 ways to injury your low back?
a. Repetitive microtrauma
b. Sustained postural load
c. Single traumatic event
d. Sudden unguarded movement
e. Normal activity with unstable spine

Strategies

15. What is the first step in differential diagnosis of an NMS condition?

a. Injury or disease?
b. Second step: nerve damage?

Stories

16. What is the story of “lumbalgia” vs specific pathoanatomical diagnoses? What are
the arguments on both sides?
a. Lumbalgia is a generic term that refers to a nonspecific cause of LBP. The
argument goes that because of potential psychological issues with “labelling” a
patient with a condition, it creates an obstacle to the patient’s recovery. In
addition, they claim that practitioners aren’t able to accurately diagnose these
specific conditions anyways.
b. On the other side of the argument, practitioners claim that patients prefer a
doctor who can tell them exactly what is wrong/damaged, rather than being told
the doctor has no idea what is causing their LBP. Even if this diagnosis isn’t
certain, it allows the patient to wrap their head around and be satisfied that
someone knows what the issue is and how they are going to fix it.

Lumbar Disc Derangement (based on class lecture and course notes

Mechanical Low Back Pain Diagnoses pp 2-7 )

Facts & Knowledge

25
1. What are three main conditions that can affect the lumbar intervertebral discs?
a. Disc Degeneration (common, usually asymptomatic)
b. Disc Derangement (common cause of LBP)
c. Disc Herniation (uncommon, one of the most common sources of radicular pain)
2. What is the prevalence of disc injuries in chronic LBP patients?
a. The disc is responsible for 40% of LBP, with the other most common causes of
LBP being the facet, sprains, strains, and fractures.
3. What exactly happens to a disc with derangement?
a. Tearing of the inner fibers of the annulus fibrosus, most commonly in the
posterior disc due to everyday flexion loads. The nucleus pulposus then
squeezes its way into these fissures in the annulus.
b. There is only nociceptors in the outer ⅓ of the annulus fibrosus, but these pain
fibers will penetrate the inner layers of the annulus when the disc is injured.
i. This means that disc derangement is more commonly painful from
repetitive microtrauma over a longer time period.
4. What’s the most common cause of a disc injury?
a. Most commonly repetitive microtrauma, but can also be due to a single
traumatic event.
5. What key clues from the history are suggestive of an injured disc?
a. When acute, the pain may be sharp/stabbing with movement of the low back.
b. Normally deep, achy, midline, may refer to buttock/leg.
c. Worse when they first get out of bed.
d. Sitting intolerance, may rapidly aggravate LBP, standing may relieve pain.
i. A strain will usually be painful with sitting for a longer period of time.
e. Most commonly sensitive to flexion with a directional preference to
extension, but that can also be painful, especially if the annular tears are
anterior, though this is uncommon. Rotation/lateral flexion may also aggravate.
f. Need to educate patients in hip hinging and avoiding flexion loads (at least
while acute, reintroduce later for rehab).
6. What often is the primary complaint for a patient with a disc derangement?
a. Sitting intolerance that aggravates LBP rapidly.
7. What are some of the key characteristics regarding the referred pain which can be
associated with a disc derangement?
a. Non-dermatomal referral that usually is not past the knee, but can be.
b. Back pain worse than leg pain.
8. What is Dejerine’s triad and why might it aggravate a disc injury?
a. Usually + for LBP aggravation with bowel movement, coughing, sneezing.
b. These 3 increase the intradiscal pressure, causing pain.
9. Based on research studies, what is strongest physical exam clue (i.e., based on
the most evidence) supporting a disc injury? How is it done (be sure to hit all of
the key points of the procedure)? What is the positive finding?

26
 a. Pain centralization with repetitive or sustained end-range loading in a
directional preference.
b. Key Points: must explore multiple directions, prone extension is therapeutic
direction 60-70% of the time, loads can be done actively or passively.
i. A positive finding is either the distal territory shrinks, the distal symptoms
reduce intensity, or AROM increases.
10. What are the key physical exam findings that might be positive in a disc
derangement (be as complete as you can be)?
a. + Valsalva maneuver
b. + Dejerine’s triad (+ for most anything disc related)
i. LBP with bowel movement, coughing, sneezing.
c. Painful and reduced AROM, usually in flexion (extension for anterior
derangement).
d. Painful spinal loading orthopedic tests.
e. Pain centralization
f. Flexion antalgia or lateral pelvic shift.
11. Is extension likely to increase pain in an anterior derangement? Posterior
derangement? What would be the difference in responses?
a. Yes, patients with anterior derangements will most likely be sensitive to
extension, and have a directional preference for flexion.
b. However, more commonly patients will have a posterior derangement, which
will have pain centralization in extension and be sensitive to flexion.
12. If a patient had LBP and no leg symptoms, how do you recognize whether or not
pain centralization is occurring?
a. The pain may change from a large vague area of LBP to more midline, or the
patient’s AROM in the lumbar spine may improve.
13. What are some physical examination procedures that compress the spine?
a. In the acute phase, these may be painful:
i. Active Double Leg Raise
ii. 4 Quadrants Test (similar to Kemp’s test with downward pressure on the
spine in 4 different positions of varying flexion/extension with rotation).
iii. Hip Flexor Muscle Testing
14. What is Minors sign?
a. When a patient is asked to stand from a seated position or return to upright from
a flexed position, they have LBP and use their arms to push up on the arms of
the chair, or “climb” up their legs with their hands.
b. In acute flare ups, all directions of AROM may be painful, and the patient may
display Minor’s sign. Note: Not unique to disc derangements.

27
15. Where might the maximum tenderness be with palpation?
a. Usually in the interspinous spaces surrounding the derangement, may be
aggravated by tapping on SPs.
b. Paraspinal muscles may or may not be tender, sometimes with MFTPs.
16. What would be two antalgic postures that would be consistent with a disc injury?
a. Unintuitively, a patient with a posterior derangement may present with a slight
flexion antalgia, in which there is a “sweet spot” where the posterior disc is not
loaded. Further flexion would be painful, and in these patients repetitive
end-range extension usually centralizes their pain.
b. In patients with a anterior derangement, they may present with a slight
extension antalgia, with further extension aggravating their pain. End-range
flexion usually centralizes these patient’s pain.
c. Patients may also present with a lateral pelvic shift, which should be corrected
as an early treatment goal.
17. What are the key pertinent negative findings that are necessary to support a disc
derangement diagnosis?
a. Normal SMRs.
b. Negative nerve tension tests, but may create LBP or hamstring pain.
c. Absence of a step deformity (seen in spondylolisthesis).
d. Negative SI provocation tests (at least for the patient’s familiar pain).
18. What is an alternate strategy to use when motion palpating the patient’s spine to
find a level and direction to adjust (i.e., different from what you have mostly
learned to do in your technique classes)?
a. Do segmental motion palpation, looking for levels and vectors which centralize
the patient’s pain, or which the patient can most tolerate (not looking for
restrictions).
19. What imaging technique is considered to be the gold standard? What is the
controversy surrounding it?
a. Discography.
b. A 2013 review found only fair evidence supporting discography, and a 2015
German guideline found that the discography’s ability to detect the disc as the
source of LBP as not proven.
c. Note: imaging is usually not indicated for disc derangement unless for surgery,
plain films and CT are usually normal, no disc thinning.
20. What is an HIZ? How well does it correlate with the results from discography?
a. HIZ = High Intensity Zone
b. On an MRI, spots of lighter contrast in the disc can be indicative of annular
tearing, but it was found that the MRI was better at ruling out disc derangement
with the absence of a HIZ (-LR = 0.21, +LR = ~1.5 to 5.9).
c. However, the presence of a HIZ strongly correlated with the results of the
discography.

28
 21. Explain how discography is done. What has to happen for the results to be
considered strongly positive?
a. X-ray guided injection of a contrast dye into the suspected deranged disc.
b. The discography is positive for disc derangement if the test reproduces the
patients familiar pain, and the dye moves in a direction suggesting torn annular
fibers.
c. Some question whether this creates an injury to the disc that can create further
symptoms later on.
22. Using the 4 tool kits recommended from previous lectures, outline the key
ingredients for a treatment plan (be a specific as possible).

CMT STM
- Manipulation in pain centralizing - Stretch hamstrings using PIR, CRAC,
direction or directional preference etc.
(usually extension).
- Flexion-Distraction in a therapeutic
range.

BM Ex
- “Active” bed rest, 2 days or less. - Correct any lateral pelvic shift.
- Strictly limit flexion loads, especially - McKenzie exercises (directional
in the morning and early in treatment. preference), usually repetitive prone
- Reduce time sitting, break up extension stretches (10 reps every hour
prolonged sitting (every 30 mins). when acute).
- Teach patient neutral pelvis,
abdominal bracing, hip hinging, and
instruct on specific situations, like getting
on and off the toilet, getting in and out of
car, and standing at the sink.
- Once patient is not acute: lumbar
stabilization tracks.

23. Explain to your patient with a lumbar disc derangement what their medical options
are if conservative care does not does work for them.
a. Recommend to patient to continue conservative trial for 3-6 months.
b. Next best choice is Epidural injection.
c. Other options are Spinal fusion, Intradiscal electrothermal therapy (IDET),
and Percutaneous intradiscal radiofrequency thermocoagulation (PIRFT).
i. These three have limited evidence to suggest they are better than
conservative care.

Strategies

24. Should x-rays be ordered in suspected disc derangements? Why or why not?

29
 a. No, because disc derangement usually shows up normal on plain films and CT.
b. Exception: when considering surgery like spinal fusion, will order x-rays.
25. Your patient has low back and leg pain. You have him bend backwards 5 times.
What are 3 different findings that would suggest that you found a direction
preference?
a. The pain centralizes (leg pain territory shrinks), leg pain decreases (back pain
may increase), or AROM improves (even though pain remains the same).

Stories

26. What is the story behind why some disc derangements hurt and others do not?
How does this complicate making a discogenic diagnosis?
a. Healthy discs will usually only have tears in the inner annulus fibers, which do not
have any nociceptive nerve fibers innervating them, which means not painful.
b. Previously injured discs can have these nerve fibers penetrate the inner layers of
the annulus, causing further disc derangements to hurt.
c. This makes it difficult to know which deranged discs are causing the patients LBP
and which are not.
27. Explain why patients with a flexion load sensitivity (i.e., flexion makes their back
worse) might nonetheless have a flexion antalgia and benefit from flexion
distraction therapy.
a. Because there is a “sweet spot” where the posterior annulus fibers are not being
stretched from too much flexion, and the posterior disc is also unloaded. This is
why flexion-distraction therapy needs to operate within a therapeutic range,
because too much flexion can aggravate their pain.

Lumbar Facet Syndrome (based on class lecture and course notes

Mechanical Low Back Pain Diagnoses pp 11-15 )

Facts & Knowledge

1. What are the 5 main pathoanatomical diagnoses for patients with LBP and no
nerve damage?
a. Disc
b. FACET
c. Sprain
d. Strain
e. Fracture
2. What is the prevalence of facet syndrome (in general, and age related)?
a. 5%-90%

30
 b. 15% lifetime prevalence (dual facet block study).
c. Older population = 40% prevalence
3. Based on history, how does facet syndrome usually present (be as complete and
descriptive as you can)?
a. Deep achy back pain at paravertebral area > midline.
b. When acute, punctuated w/ transient sharp pain with sudden movement.
c. Morning back stiffness.
i. So far pretty similar to disc derangement, can’t differentiate the two off the
above 3 points.
d. Aggravating factor
i. Hyperextension (walking uphill)
ii. Rotation
iii. Lateral bending
iv. Getting out of bed
v. Stand after prolonged sitting
vi. Inactivity
e. Relieving factor
i. Simply moving around
f. Walking may hurt, but least painful activity
g. Sitting may improve symptoms, least painful position
h. May be caused by trauma, but more commonly chronic postural/repetitive
loads.
i. Ex: line man of football (hyperextension); baseball & golf player (repetitive
rotation)
4. What are the 5 main things to know about referred pain from the facets (these also
apply to referred pain from a disc as well).
a. Overlapping territories (non-dermatomal)
i. Facet is innervated from nerves above & below the facet.
ii. Incoming messages merge in anastomoses between roots.
b. Pain can be referred to the front (groin region) & back of the leg.
c. Sometimes pain can refer to the foot.
d. Referred pain may not be contiguous
e. Referred pain from facets & discs overlap
5. What are the strongest clues against a facet syndrome?
a. Pain centralization with repetitive or sustained spinal loading (suggests disc
derangement).
b. No relief of pain with recumbency.
c. Negative Kemp’s test.
d. Positive Valsalva maneuver.
e. Positive flexion loading tests.
f. + SLR.
g. SMR deficits.

31
6. What are the main clues that would support a facet syndrome but would not work
as well for a disc derangement and sprain? (←but can be)
a. Facet syndrome is aggravated by:
i. Extending up from flexion.
ii. Active hyperextension.
iii. Passive extension.
iv. Extension combined w/ rotation and over pressure = Kemp’s test.
7. When Kemp’s test causes local back pain, what does that mean diagnostically?
a. A positive Kemp’s supports facet syndrome most strongly, but deranged
disc/sprain is still possible.
b. Kemp’s is better at ruling out facet syndrome when negative.
8. What does it suggest if it causes leg pain?
a. “True” positive Kemp’s test
i. Nerve root lesion should be suspected and more likely causes are IVF
stenosis, spur or cyst in IVF, etc.
9. Describe how the presence of a facet syndrome might affect active range of
motion (AROM).
a. Painful and restricted lumbar extension.
10. Back pain aggravated by the active double SLR has been cited in a previous
lecture as supporting a disc derangement. In what circumstances might it also
aggravate a facet syndrome?
a. DSLR (active) can cause LBP if the patient arches back and has weak core
stabilizers.
b. Nachlas or Elys test (especially if done bilaterally) might cause pain.
i. Nachlas - heel to buttock
ii. Elys - heel to opposite buttock
11. What combination of evidence would suggest a pragmatic diagnosis of facet
syndrome?
a. Paraspinal pain (uni/bilateral) who had 1 of the following:
i. Painful extension > flexion
ii. Painful Rotation, extension+rotation, extension+side flexion
iii. Painful palpation over facet with possible joint restriction
b. NO evidence of:
i. Nerve involvement
ii. Pain centralization
iii. Positive painful SI joint challenging
12. What is the role of imaging in making a facet syndrome diagnosis? Should
radiographs be ordered or MRI or CT?
a. Neither plain film nor CT/MRI have much diagnostic value for this condition.
b. Only if there is evidence of nerve involvement, perhaps from a spurs or a facet
cyst, should you order MRI.
13. What is considered the gold standard for making the facet diagnosis?

32
 a. Facet block (intra-articular anesthetic injection) is the most accurate method for
diagnosing facet joint.
14. How are facet blocks done (explain in enough detail that a patient would know
what was going to happen)? What is the difference between a single block and a
double block?
a. Therapeutic facet block
i. For the patients who fail conservative care.
ii. Performed by an anesthesiologist.
iii. Corticosteroid & local anesthetic with contrast medium with
fluoroscopy.
b. 1st injection
i. Short-acting anesthetic (lidocaine)
c. 2nd injection
i. Long- acting anesthetic (bupivacaine)
d. If there is adequate pain relief for both injections, a diagnosis of facet syndrome
is made.
e. Single injection block
i. High false-positive rate.
ii. Not accurate enough.
f. Double or triple block
i. Should be used before aggressive treatments such as surgery.
ii. More accurate diagnosis, but controversial.
iii. For triple block, repeat a third time with a saline injection
15. Using the 4 tool kits recommended from previous lectures, outline the key
ingredients for a treatment plan (be a specific as possible).

CMT STM
- Spinal manipulation (HVLA) to painful Address potential factors of increased
joint restriction. extension load on the lumbar spine:
- Flexion-distraction. - Tight hip external rotators
- Tight hip anterior joint capsule
- Tight hip flexors
- Tight latissimus dorsi
- Impaired thoracic extension

BM Ex
- Avoid repetitive extension and - Core stability exercises
rotation. - Side bridge
- Quadruped
- Curl up

16. Based on lecture, what treatments may also need to be applied to the hip and
thoracic spine? Why?

33
 a. Limitations in thoracic extension and flexibility of hip flexors/anterior capsule need
to be treated (CMT and STM) so that there is more even extension load
distribution in the lumbar spine.
17. What are some extension behaviors that patients may need to avoid?
a. Walking uphill
b. Wearing high heels
c. Prolonged standing
d. Working with arms above shoulder
e. Lying prone on a soft mattress
f. Swimming (crawl)
18. What are some specific positive behavioral recommendations to make?
a. Lean over podium or desk
b. Perform a posterior pelvic tilt
c. Stand with one leg perched on platform
d. Walk at a quicker pace with pronounced arm swing
19. What are two medical interventions that can be done to the facets? How effective
are they?
a. Therapeutic Facet Block Injections
i. There is moderate evidence of long term pain relief.
b. Ablation procedure (radiofrequency ablation)
i. Follows positive facet block, destroys nerve to the facet.
ii. Mixed results, but best evidence available suggests no statistically
significant between this and placebo.
20. How does an acute locked low back present?
a. Sudden onset of agonizing pain and inability to stand erect.
b. Triggered by forward flexion or sudden unguarded movement.
c. Patient must brace when coughing, sneezing, or walking.
d. Flexion/lateral flexion antalgic posture and decreased ROM.
e. Increased pain with extension + lateral flexion towards involved side.
f. Muscle spasm + tenderness.
g. SMRs normal.
21. What is the suggested main treatment of choice?
a. Control pain and inflammation.
i. Cryotherapy and electrotherapy.
ii. Analgesics or short term anti inflammatory medications.
b. Gap the joint to release the entrapped meniscoid with spinal manipulation.
i. Normally patient will present with an antalgic posture. Adjust into that
same direction to gap the joint (they are in that posture to avoid
compressing the facet).
c. SMT to reduce muscle spasm.
22. What is one of the popular mechanisms that has been proposed to explain what is
happening in the locked back?

34
 a. May be due to entrapped meniscoids in the facet joint, or disc fragment
lodged in the end plate.

Strategies

23. What are some clues that would differentiate a deranged lumbar disc from a facet
syndrome? Which clue would be the most useful?
a. Facet syndrome
i. No pain centralization
ii. Extension load sensitivity
iii. Improve with sitting
iv. Tenderness over facet
v. + Kemp’s
b. No pain centralization is the biggest clue that it isn’t disc derangement.

Stories

24. If the accuracy of the H&P is not very good at making a facet syndrome diagnosis
(meaning the pain may not really be coming from the facet), then what is the
advantage of making that particular diagnosis?
a. Because even if the facet isn’t what is causing the patient’s symptoms, the profile
we consider fits with facet syndrome can be treated the same conservatively.
b. For example, if we did a study where we used inclusion criteria that matched
facet syndrome (more paraspinal LBP, sensitive to extension, no nerve damage,
and no pain centralization), and we used facet block injections as our gold
standard to know who did and did not have facet syndrome even when they all
have the same symptoms, there likely would be no difference in treatment
outcomes between groups if everyone received the same conservative treatment.

Applications

For each of the following cases, choose a) facet syndrome, b) disc derangement, or c)
neither.

25. A 72 year old patient has bilateral low back pain and pain into the right buttock.
AROM is limited in both flexion and extension, but worse if he tries to touch his
toes. Valsalva is positive. SLR aggravates his back and buttock pain and he has
grade 3 weakness with big toe extension. SI tests are negative. He has mild
increase of his serum calcium.
a. This looks like a disc derangement up until the motor weakness, where we start
to be suspicious. Then we see the increase in calcium, which is a huge red flag
for possible cancer. Next step is to order an x-ray.
26. Patient has low back pain, groin pain, and pain that extends to his calf. Right
rotation and rotation combined with extension hurts. Sitting is aggravating but not

35
 as much as prolonged standing. SLR is negative and sensory, motor and reflex
tests are unremarkable. Sacroiliac (SI) tests are negative.
a. Pain to calf is unusual in deep referred pain, the presentation doesn’t at all match
a radicular syndrome. Prolonged standing + rotation and extension aggravating
strongly suggest facet syndrome.
27. Patient has low back pain and pain into his left buttock. Sitting brings on his pain
rapidly. Kemp’s test bilaterally is positive for back pain. Valsalva is negative. If he
lies on his back with his knees dropped over to the left, his buttock pain
disappears. SLR is negative and sensory, motor and reflex tests are unremarkable.
SI tests are negative.
a. Kemp’s is positive, but this can apply to both facet syndrome and disc
derangement. Rapidly painful sitting + pain relief in a flexed/rotated position
suggested disc derangement.
28. Patient has low back pain, more on the right. Standing aggravates his pain. AROM
is limited in extension, flexion is full and painless. Kemp’s on the right aggravates
his back and also sends a sharp pain down his leg to the foot. SI tests are
negative.
a. Sharp pain to the foot with Kemp’s is a true positive Kemp’s test, which
suggests radiculitis caused by lateral recess stenosis, or osteophytes, or a facet
cyst, etc.
29. Patient has low back pain. AROM is complete and painless. Kemp’s test is
negative on either side as is the prone extension test. There is palpable
tenderness just lateral to the L5 spinous process and a palpable rotation
restriction. SLR is negative and sensory, motor and reflex tests are unremarkable.
SI tests are negative.
a. Nothing unusual going on except for lumbar joint dysfunction.
30. Patient has low back pain and radiating pain to his foot. AROM is limited in
extension due to pain. Kemps is painful on the right. He cannot tolerate sitting.
Repeated loading into a cobra position aggravates his back but improves his leg
pain (see picture). SLR is negative and sensory, motor and reflex tests are
unremarkable. SI tests are negative.
a. Pain centralization + intolerance to sitting suggests disc derangement.

Lumbar Sprains & Strains (based on class lecture and course notes
Mechanical Low Back Pain Diagnoses pp 8-10 and 23-25)

Facts & Knowledge

1. What is the most common diagnosis for athletes with LBP?

a. Acute muscle strain.

36
 b. Causes up to 60% of low back injuries in college athletes, even more common in
football/gymnastics (80%).
c. Strain/sprain injuries often combined together, associated with high loads
(trauma) or higher reps (overuse).
d. Note: DOMS can mimic a muscle strain, but usually peaks in 24-48 hours and
self resolves within a few days to a week.
2. What are 3 mechanisms of injury that can cause a true extensor strain?
a. Note: true tears likely rare except in sports injuries.
b. Most commonly acute trauma.
i. Sudden eccentric load most common (heavy lifting).
ii. Direct impact trauma, slip and fall, or auto accident
iii. Blunt trauma.
c. Repetitive microtrauma.
d. Sustained end-range postural loading.
3. Where would be the best place to palpate to assess the enthesis (CT of
tendon/ligament to bone) of the quadratus lumborum?
a. ILIAC CREST.
b. If there was a QL strain present, may detect hypertonicity/tenderness, a local
defect, and there shouldn’t be pain with joint play.
4. What is spinal muscle compartment syndrome?
a. Patient presents with elevated spinal muscle pressure that does not normalize
after 20 minutes of rest, exercise induced LBP (relieved by rest) and
hypolordosis.
5. Specifically, which spinal ligaments are most prone to sprains?
a. Supraspinous and interspinous ligaments (most common).
b. Iliolumbar
i. Remember not to specifically denote which ligament tore, in case of
obvious tear.
6. What are the mechanisms for a lumbar sprain?
a. Same as for a muscle strain (trama, repetitive microtrauma, sustained postural
end range loading).
b. Without trauma (like slip and fall), more likely to be disc or facet issue rather than
strain or sprain.
c. Non-traumatic sprains tend to be due to flexion loads, most commonly in a
postural syndrome:
i. Local LBP only.
ii. Normal and pain-free AROM.
iii. Normal orthopedic tests.
iv. Familiar pain is not reproduced until static loading for a longer
duration, usually in flexion.
7. Load bearing sprains are usually due to what kinds of coupled spinal
movements?
a. Lateral bending during flexion.

37
 b. Rotation with lateral bending.
8. What terms or numbers are used to grade the severity of a low back sprain?
a. May be characterized as mild, moderate, or severe.
9. Most patients do not have “point specific tenderness” with palpation when they
have a lumbar sprain, but if they did where would it most likely be located?
a. Pain midline between spinous in case of supraspinous or interspinous ligaments.
b. There may also be pain over joint, pain with joint play, and muscle splinting.
c. If severe supraspinous tear, may be palpable defect.
10. Generally speaking, which of the following would classically be most provocative
in a lumbar sprain: active range of motion, isometric muscle testing, passive load
on the joint at end range?
a. End-range joint loading is most provocative of a sprain.
i. This is not likely to centralize pain, only aggravate it.
b. AROM: painful in direction that stretches ligament (usually flexion).
i. All directions if acute and joints inflamed.
ii. Pain may be sharp, achy, or “stiff.”
c. Muscle test doesn’t usually aggravate pain (+ finding here suggests muscle
strain).
d. Patient may have a guarded slight flexion posture (extension antalgia if sprain
severe).
e. SMRs should be normal.

11. What exam findings would support an iliolumbar sprain? What is the potential
pain referral pattern from this condition?

38
 a. L/S pain and some referrals, tender point(s) along iliac crest or with deep
palpation between L4 TP and crest recreates chief complaint pain, possible
+ FABERs test
b. Referral pattern:
i. Iliolumbar ligament, PSIS area, L4/L5 midline and follows along
posterior/superior border of iliac crest, inguinal area down the groin into
upper medial thigh.
c. Treatment:
i. Acute: Rest, ice, analgesics.
ii. Chronic: ultrasound, heat, cross friction.
iii. Core strengthening.
iv. Corticosteroid, anesthetic, platelet rich plasma injections, or prolotherapy.
12. In what sprain or strain scenarios should ancillary studies be considered?
Exactly what tests and for what purpose?
a. X rays to r/o fractures in cases of trauma.
b. Flexion-extension x rays to rule out structural instability in cases of significant
trauma or post traumatic cases with prolonged period of disability or poor
response to treatment.
13. Explain to your patient what the expected prognosis is for their lumbar sprain.
a. In acute trauma, mild cases may resolve in a couple days.
b. More severe pain tends to resolve within 1-2 weeks, sometimes longer.
c. Not uncommon for patient to feel lower level of pain with intermittent flare-ups
for up to 4-6 weeks after initial injury.
d. Individual recovery times may vary person to person.
14. What are some immediate acute care interventions for a low back sprain or strain?
a. Control pain, spasms, and inflammation.
b. Ice, pain control electromodalities (ultrasound, e-stim), interventions to reduce
muscle spasm.
c. Light effleurage of muscles may be helpful as well as grade I-II joint
mobilizations.
d. Short term use of light weight lumbosacral corset may help control pain
(athletes).
e. Heat therapy (or alternating hot/cold) after 48 hours of initial injury.
f. Pain meds (NSAIDs, acetaminophen).
15. Using the 4 tool kits recommended from previous lectures, outline the key
ingredients for a treatment plan for a sprain and a strain. Divide into immediate
care and then subacute care. Be as specific as possible.
CMT STM
Acute: Acute:
a. None a. Control pain, spasms, inflammation
b. Light effleurage muscles
Subacute: (FEW DAYS-2 WEEKS) c. Grade I-II joint mobilization
a. Joint manipulation as needed Subacute:

39
 a. Deeper sports massage
b. PIR
c. CRAC
d. Pin and stretch
e. Cross fiber
f. Instrument assisted STM

BM Ex
Acute: Acute:
a. Lightweight lumbosacral corset, pain a. Neutral pelvis and hip hinge
meds (NSAIDs, acetaminophen as movement strategy.
needed).
b. Limit end range flexion, lifting, or Subacute:
extension exercises/activities against a. Light home stretching/muscle
resistance. relaxation exercises (PIR)
c. Remain active but avoid offending b. In late subacute phase (especially
sports, high loads, and full ROM recovering extensor strains),
under load until pain free. extension endurance exercises
d. Teach neutral pelvis/hip hinge if (quadruped, superman on ball)
flexion is painful. c. Core stability
e. If postural syndrome, suggest
strategies to break up duration of
offending posture or alternatives that
minimize end range loading

Applications

16. Your patient has a strain of the right quadratus lumborum. Which of the following
muscle tests would hurt the most? Left lateral flexion, right lateral flexion, forward
flexion, extension?
a. Right lateral flexion (QL is ipsilateral lateral flexion).
b. Consider extension too (QL is extension via bilateral contraction).
17. Which type of physical exam procedures would tend to support a strain over a
sprain? Passive orthopedic tests or muscle tests of the low back?
a. Muscle tests may be best clue. Strain may be painful (usually more so than
passive testing) and may be weak.
b. Ortho tests aren’t painful unless muscle is under load.
18. Your patient flinches and says that your palpation was very tender. What grade of
tenderness would you record?
a. II tenderness (tenderness with grimace and/or flinch to palpation)
i. I tenderness = without grimace or flinch.
ii. III tenderness = withdrawal (+ jump sign)
iii. IV tenderness = withdrawal (+ jump sign) to non-noxious stimuli.

40
 19. Your patient has low back pain after a slip and fall on their buttock. Of the two,
what is more likely a sprain or strain?
a. Since trauma case, may be tear in ligaments and sprain diagnosis may be most
appropriate. Lumbar sprains usually caused by torsional loads, direct blows or
ballistic loading associated with violent contractions.
b. Slip and fall on buttock creates significant shear forces, especially across
interspinous ligaments.
20. Your patient reports that she cannot tolerate sitting because almost as soon as
she sits, her back starts hurting. Is this suggestive of a postural sprain?
a. No: pain that increases quickly with sitting (minutes) is suggestive of lumbar
internal disc derangement (discogenic pain, intervertebral disorder) when
primary complaint.
b. A postural sprain would show sitting intolerance after sitting for a longer duration
(probably closer to 30 minutes or more).
21. Your patient is a computer programmer who has back pain at the end of every day.
At the time of the physical his back is not really hurting, but there is mild
tenderness midline from L3 to S1 with palpation, active flexion at end range is
mildly uncomfortable, as is knees to chest if held there for 30 seconds. The rest of
the physical examination is normal. What is the mostly likely Dx?
a. Postural syndrome: longer duration of static loading in at least one direction
provokes familiar pain. Local LBP only.

Spondylolysis & Spondylolisthesis (based on class lecture and

course notes of the same name)

Facts & Knowledge

Spondylolysis
1. What is spondylolysis?
a. Uni/bilateral stress fracture of the narrow bridge between the upper and lower
pars interarticularis. Possible forward body slippage.
i. May be defect in pars or full fracture with separation.
ii. Bilateral in 80% of symptomatic cases
iii. Most common: L5 (85-95%), L4 (5-15%)
iv. Due to repetitive overuse beginning as a fatigue stress fracture.
2. Who is mostly likely to get it?
a. Males/females 2:1
b. Progressive anterior slippage is 4x higher in girls.

41
 c. 75% of cases are athletes <20 years old.
i. Young athletes who train more than 15h/week (overuse); 47% LBP.
3. Is spondylolysis a common cause of low back pain? Explain what we know about
that.
a. NO, only 6-13% of the general population; MOST ARE ASYMPTOMATIC.
b. Only 25% of spondylolysis is associated with spondylolisthesis, with the vast
majority of slippage being <10 mm.
4. What types of spinal motions put the spine at risk for spondylolysis?
a. Repeated flexion and extension.
b. Hyperextension.
c. Twisting and axial load activities.
i. Gymnastics and football are highest risk.
5. Is the onset of pain sudden or gradual?
a. Can be either.
6. What is the most common finding from the history and physical exam in these
patients?
a. Pain associated with hyperextension in athletes is the most commonly
reported history and physical finding.
b. Flexion usually doesn’t aggravate the back, may offer relief or may be limited by
hamstring spasm.
c. Psoas may be short and tight bilaterally.
d. Neurological deficits very uncommon.
7. What is the initial ancillary study to order to make the diagnosis?
a. Radiographs - but often inconclusive in early cases.
i. High specificity, but low sensitivity.

Spondylolisthesis
8. What is spondylolisthesis?
a. Occurs when one vertebra slips forward over an adjacent vertebra (L4/L5).
b. May/not be due to bilateral pars fracture.
c. Usually asymptomatic
i. 10% of adults symptomatic.
d. Unlikely cause of back pain in adults with no history of symptoms before age 30.
9. What are the two most common types? What is the most common location for
each type?
a. Isthmic/lytic: defect in pars from stress fractures or bone remodeling after a
traumatic fracture (71-94% at L5)
i. Most common type in young patients.
b. Degenerative: due to facet arthritis and remodeling (L4)
i. Most common type in older patients (>60 y/o).
ii. Neural arch is intact.
iii. Can result in a dynamic form of stenosis
iv. There may be slippage → unstable if >3-4mm.

42
 v. Treat with conservative care, but may need surgical stabilization.
10. Spondylolisthesis is usually asymptomatic in the adult. In what various
circumstances could it become your primary diagnosis?
a. When associated with a healed but “active” spondylolysis.
b. When the spondylolisthesis is unstable.
c. When it is degenerative and may be associated with spinal canal stenosis.
d. When it is associated with radiculopathy or CES.
11. Describe the Phalen Dixon sign.
a. Pt stands with increased flexion at the hips and knees.
i. Results in functional scoliosis in 60% of patients that self-resolves as
spondylolisthesis symptoms resolve.
12. What would be the most diagnostic finding based on observation or palpation?
a. Tenderness to deep palpation of the SP above the slip (L4) may be present. This
palpation occasionally causes radicular pain.
b. Paraspinal muscle spasm and tenderness.
c. “Step off” defect: test sensitivity standing from 60-88%, specificity of 87-100%.
i. +LR = 4.6
ii. Pt is prone and doc is palpating SP and you feel a “drop” in level.
d. Hamstring spasm (80%); can cause hypolordosis and cause involuntary knee
flexion during SLR.
e. Hypermobility with P-A palpation.
13. Describe how to do the passive leg extension test. In what type of
spondylolisthesis is it most likely positive?
a. Both legs are lifted to about 30 cm and gently tractioned; allows the relaxed
lumbar spine to settle into extension.
b. (+): pain or feeling of heaviness in the low back which disappears when the leg is
lowered → UNSTABLE spondylolisthesis.
c. +LR = 8.8, -LR = 0.17 (radiographic instability).
14. In a 2017 review of the literature, what combination of findings was the most
diagnostic?
a. Intervertebral slip by inspection or palpation
b. Segmental hypermobility by use of manual passive physiological intervertebral
motion test.
15. What radiographic view is diagnostic? How do you measure the severity of the
listhesis (be a specific as possible)?
a. Lateral view.
b. Meyerding Grading System:
i. Grade I: (0-25% displacement)
ii. Grade II: (25-50% displacement)
iii. Grade III: (50-75% displacement)
iv. Grade IV (>75% displacement)
v. Spondyloptosis: complete or 100% spondylolisthesis

43
 16. What would be the imaging tests, findings and measurements that would suggest
structural instability?
a. >3-4 mm of slippage seen on flexion-extension radiographs.
17. What are the indications for surgery? What is done during the surgical procedure?
a. Absolute: progressive neuro deficit and CES.
b. Relative: persistent radiculopathy despite conservative treatment, persistent and
unremitting LBP for more than 6 months, loss of quality of life or neurogenic
claudication.
c. Options are decompression and/or fusion.

Spondylolysis & Spondylolisthesis

18. What muscle most consistently goes into spasm?
a. Hamstrings (Psoas commonly as well).
19. Your patient has leg pain with their spondylolisthesis or lysis: how likely is it that
they have a positive SLR? How likely that they will have neuro deficits?
a. If LE pain present, usually deep referred.
b. SLR rarely positive; neuro deficits NOT common.
c. When there are nerve damage, L5 NR is the most commonly involved.
20. On average, how long before the patient can return to the sport of their choice?
What are the indicators you will use to know when it is safe to do so?
a. Spondylolisthesis w/o fracture:
i. Until pain free and follow-up radiographs document no further
progression of the listhesis.
ii. Safe recommendation >3 months, particularly for junior level or
recreational athletes.
iii. High-level athletes can typically return to sports once symptoms become
tolerable and unlikely to affect performance.
iv. Patients instructed to avoid hyperextension even after symptoms subside.
b. Spondylolysis w/ or w/o listhesis
i. STOP SPORT and all activities involving flexion or hyperextension.
ii. Plain films DO NOT detect fracture + defect only visible on SPECT +
symptoms improving → 2-4 weeks.
iii. True fracture detected on plain films OR symptoms not improving → 3-6
months.
21. Using the 4 tool kits recommended from previous lectures, outline the key
ingredients for a treatment plan for a spondylolysis and spondylolisthesis (they
are very similar). Indicate if there are any differences. Divide into initial phase of
care and then the subacute and rehab phase. Be as specific as possible.

CMT STM
- Should be treated based on totality of their CRAC, PIR, etc to stretch hamstrings and
findings, not the imaging. Psoas.

44
- Treat spinal joint dysfunction and myofascial
pain generators.
- HVLA CMT can offer pain relief.
- Be cautious of P-A thrust adjustments
over the spondylolisthesis, esp if there is
evidence of instability.
- Side posture CMT promoting lumbosacral
flexion.
- Knee-chest stretches/mobilization.
- Drop table adjustments
- Prone treatment utilizing a flexion-biased
table.
- Flexion-distraction

BM Ex
- Avoid hyperextension postures and - Rehabilitation program after adequate rest
activities. period.
- Bracing. - Flexion exercises (knee to chest
exercises), core stabilization exercises,
hamstring stretching, and general aerobic
exercise.
- Use brace as needed, progress to
exercises without as symptoms decrease.
- Cross-training in non-extension activities
can be performed.

22. What are the details regarding prescribing a rigid brace? Address patient
instructions, duration, etc.
a. Bracing = main intervention but high evidence is lacking.
b. No RCTs have been done to clarify the effectiveness of a brace, so the decision
is left to the practitioner/patients/parents.
c. PTS WITH ONLY SPECT SIGNS MAY NOT REQUIRE EXTERNAL BRACING
(although it remains an option).
d. Prescription: 20-23h/day for 3-6 mo.
i. Pt can be weaned off it as symptoms resolve.
ii. Start with 30 min of brace-free time 3x/day for first day; each day for 2
weeks and add 30 more min without brace. Pt allowed to sleep without
brace if symptoms were not exacerbated.
e. Repeat bone scan at 3 mo.

45
Strategies

23. Should you do a neurological exam on a patient with spondylolysis or

spondylolisthesis? Which one(s)? What do you expect to find?
a. Probably not since only 12% of cases have neurological deficits. If history points
in that direction, then consider it.
b. Most likely is L5 nerve root.
24. If your radiographs are normal but you still suspect a spondylolysis, what are your
next choices in imaging? What are the pros and cons for each of these?
a. MRI: preferred initial advanced imaging of choice.
i. Useful to detect early edematous stress reactions of the pars
interarticularis without a fracture line seen on radiograph/CT.
ii. NOTE: order for rare cases of neurological presentation.
b. CT: best test for discovering an occult spondylolysis.
i. More specific than SPECT.
ii. Can reveal other spinal pathologies.
iii. Disadvantages: high radiation, cannot reliably distinguish between active
and inactive lesions.
c. SPECT scan: GOLD STANDARD for occult active spondylolysis, false
positives/negatives may require further testing with CT or MRI.
i. Can identify areas of increased physiological activity; tells you if it’s an
old/new injury.
ii. Disadvantages: high radiation, inability to detect chronic nonunion
fractures, cannot differentiate spondylolysis from facet
arthritis/infection/neoplasm and so CT may need to follow a positive
SPECT test.
25. What radiographs are ordered? What strategy should you use when choosing
your views?
a. Spondylolysis: AP & lateral. If no fracture found, AP axial lumbosacral spot
view, and/or oblique views.
b. Spondylolisthesis: Lateral view allows the measurement of slippage in relation
to lower vertebra.

Stories

26. What is the story behind the controversy surrounding the prescription of rigid
braces?
a. The studies have not shown an advantage to a rigid brace over a softer lumbar
brace, and that the athlete’s compliance with treatment and wearing the
brace is more important.

46
Diagnoses that Cause Radicular Syndromes (based on class
lecture and course notes)

Facts & Knowledge

1. You believe your patient has a lumbar nerve root lesion. What are the first two
diagnoses to consider? (i.e., on your “A” list)?
a. Lumbar disc herniation (NR L5, S1)
b. Spinal canal stenosis
i. Central
ii. Lateral (aka lateral recess)
c. These two combined account for 90% of radicular syndromes.
2. For the same case as above, if those diagnoses do not seem likely, what are the
next less common conditions to consider?
a. Tumors, cysts other SOLs
b. Structural instability (aka dynamic stenosis)
c. Spondylolisthesis (especially if unstable)
d. NR adhesions
e. Fracture
f. Spinal infection (especially abscess)
g. Osteophyte compression
3. For the same case, what are some of the least likely causes of a lumbar radiculitis
(the “c” list)?
a. Disc derangement
b. Facet syndrome
c. Joint dysfunction
d. “Lumbalgia”
4. In what two age groups are tumors causing a nerve root impingement most likely?
a. Patients over 50.
b. Patients under 10.
5. What are some exam findings that are consistent with LBP and leg pain secondary
to a tumor?
a. Breast, lung, and prostate cancer are the most likely to metastasize to the
lumbar spine and cause LBP.
b. Back pain is most common initial complaint.
i. In some it may be radicular pain or spinal cord compression symptoms.
c. Possible presence of red flags (unexplained weight loss, prior history of cancer,
over 50 years old).
d. Pain may be unremitting.
e. LBP may be worse with recumbency.

47
 f. Radicular pain is variable, often relieved or disappears when recumbent.
g. Exquisite percussion tenderness at site of lesion may be present.
h. May be aggravated by valsalva maneuver.
6. What are two kinds of cysts that can compress nerves roots. Where do they tend
to be located? What would be the test of choice to identify them?
a. Meningeal sacral cysts and facet (synovial) cysts.
i. Usually found in the sacral region (most common)
ii. Usually patients >50 y/o.
b. In patients with radicular pain, MRI may demonstrate presence of space
occupying lesion in form of cyst which may be cause.
c. Cysts are common and usually asymptomatic, so usually won’t jump to an
MRI and first diagnose by elimination of other conditions.
d. Radicular pain is often relieved or disappears when recumbent.
e. May be aggravated by valsalva maneuver.
7. Where in the spine do spinal infections usually begin?
a. Disc, then spreads to super/inferior vertebrae, posteriorly.
b. On x-ray, the infection may be seen to “eat” the disc and the bone, which is unlike
cancer (only eats the bone).
i. May take 1 week to 3 months to be visible.
8. What age group is most often affected by a spinal infection?
a. Patients usually over 60 and may have recent history of recurrent infections.
9. What are some of the risk factors for a spinal infection?
a. Diabetes mellitus
b. History of intravenous drug abuse
c. Spinal surgery
d. Spinal or paraspinal injection
e. Epidural catheter placement
f. Recent skin lesions
g. Immunocompromised state
10. What is the classic triad for a spinal infection? How common is it?
a. Fever, back pain, neurologic deficits.
b. Only 20% of patients have classic triad.
c. Usually chief complaint is severe back pain.
11. What physical examination procedure is very frequently positive in a spinal
infection (i.e., high sensitivity)?
a. Spinal percussion is usually positive (90% in one series).
b. WBC and ESR likely elevated.
c. MRI is diagnostic imaging test of choice, but will start with x-ray probably.
12. If a patient recently experienced a trauma and now has LBP with leg symptoms,
what should you rule out? How would you rule it out?
a. Spinal fracture with plain film, and possible follow-up with CT/MRI.
13. In a patient with nerve root adhesions, which of the following tests would more
likely be positive? SLR? DTRs? Muscle tests? XSLR?

48
 a. SLR and XSLR (and other tension tests) should be positive.
b. SMR deficits are unlikely.
c. Diagnosis is by exclusion of other conditions since advanced imaging cannot
usually pick these up.
14. What would be a good test to see if there is lumbar spinal instability? Describe a
positive test.
a. Flexion extension radiograph.
b. Combined findings of 2 views must represent a total sagittal translation >4mm.
15. Sometimes the nervous tissue damage is not in the nerve root after all, but is in
the peripheral nerve instead. List some diagnostic examples of entrapment
/compression causes. List some diseases. Lists some modes of trauma.
a. Entrapments and compression
i. Piriformis syndrome
ii. Peroneal nerve compression
iii. Femoral neuropathy secondary to pelvic tumor
iv. Lateral femoral cutaneous nerve entrapment
b. Diseases (polyneuropathy)
i. Diabetes
ii. Alcoholic neuropathy
iii. Vitamin b12 deficiency
c. Femoral neuropathy:
i. Compression via psoas
ii. Diabetic mononeuropathy
iii. Tumor (vertebral/intrapelvic)
iv. Psoas or iliacus hematoma (complication of anticoagulant treatment,
haemophilia, trauma)
v. Injury (surgery, etc.)
vi. Inflamed conditions (inflamed lymph node, rheumatoid bursitis):
d. Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)
i. Entrapment of nerve as passes inguinal ligament near ASIS
ii. Wearing tight pants, obesity, pregnancy, diabetes, local trauma, extended
sitting cycling or walking
e. Peroneal nerve entrapment:
i. Most due to external compression or stretching of nerve near fibular head
(Most common neuropathy)
ii. Postural factors (sitting with legs crossed, resting knee against console,
bed rest, prolonged squatting or kneeling)
iii. Repetitive motions (sports, running)
iv. Weight loss
v. Trauma (“dashboard” contusion, fracture of femur, fibular, inversion
trauma of foot)

49
 vi. Iatrogenic (plaster casts, tight bandages, various surgeries,
malpositioning during anesthesia, intermittent pneumatic compression for
DVT).
16. For each of the following suspected nerve root lesions, what peripheral nerve
might be injured instead? L3? L5? S1?
a. L3: femoral nerve, obturator nerve, or lumbar plexus.
b. L5: common peroneal nerve, sciatic nerve, or lumbosacral plexus.
c. S1: sciatic nerve, or lumbosacral plexus.
17. How often does Herpes Zoster affect the lower extremity? What are the key
diagnostic features of how it presents?
a. Affect spinal nerve causing symptoms into lower extremity about 5% of time.
b. Onset of pain is frequently severe.
c. Pain gradually decreases as vesicles crust over.
d. 10-15% develop post herpetic neuralgia.
e. Segmental muscle weakness can occur.
f. Complete resolution of motor deficits occur in 50-70% of patients.
18. What other two diseases can very rarely present with neurological symptoms?
What conditions might they be mimic?
a. HIV/AIDS
i. May present with signs of polyradiculopathy or CES.
b. Lyme Disease
i. May mimic disc herniation radiculopathy.

Stories

19. Tell the story of how facet syndromes and disc derangements fit into the
diagnostic process when working up a radicular syndrome.
a. Experiments on animal model suggest inflammation of facet may result in nerve
root becoming chemically irritated, inflamed and symptomatic.
b. Phenomenon could also occur in variety of mechanical low back lesions that
have not typically been associated with true radiculitis, such as disc derangement
c. Neurological deficits, however, especially hard neurological signs, would not be
expected and would signal need for further investigation.
d. Radicular syndromes attributed to facet syndrome, disc derangement or radicular
syndromes should be diagnosis made by exclusion. Other more classic causes
of radiculopathy should be considered first.

Lumbar Disc Herniations, Part 1 (based on class lecture and CSPE

care pathway Herniated Lumbar Disc with Sciatica pp 5-32 & 37-58)

Facts & Knowledge

50
1. What are the 3 conditions that affect intervertebral discs?
a. Disc Degeneration (common, usually asymptomatic)
b. Disc Derangement (common cause of LBP)
c. Disc Herniation (uncommon, one of the most common sources of radicular pain)
2. Morphologically, what is the difference between a disc bulge, disc protrusion, a
disc extrusion, a sequestered disc, a wandering disc, a contained and
uncontained disc?
a. Disc Bulge: NOT a herniation but a general extension of the disc over more than
half of the normal disc circumference, usually <3 mm, very common (>50% of
adults).
b. Disc Protrusion: the base is wider than the depth of the herniation, almost
always considered asymptomatic. Prevalence = 25% of adults <60.
c. Disc Extrusion: “ballooning” herniation with depth greater than base width, may
lead to a sequestered disc. Much more commonly symptomatic.
d. Sequestered Disc: a disc herniation which has separated from the disc.
e. Wandering Disc: a sequestered disc which then moves up or down the spine.
f. Contained Disc: more common, nucleus pulposus is NOT exposed.
g. Uncontained Disc: nucleus pulposus is exposed to spinal canal,
3. What is the clinical impact of a bulging disc? Of a non-contained disc? Of a
wandering disc?
a. Bulging Disc: clinically unimportant.
b. Uncontained Disc: severe inflammatory reaction, Sx more severe.
c. Wandering Disc: can affect nerve roots as levels different than the original
herniation.
4. What is the most common mechanisms of injury for a disc?
a. Usually repetitive flexion + torsion (rotation).
b. However, there is also recent research that supports an individual’s genetic
predisposition as being more influential than exposure to physical loads.
c. Note: smoking for more than 15 years has been shown to increase the risk by 3X
of developing a neuropathic condition, whether a disc herniation or some other
condition.
5. What are the peak age ranges for disc herniations?
a. Some say 30-55, but more likely 20-40.
6. Which discs herniate most often? What percentage of herniations do they
represent?
a. 98% of symptomatic herniations occur or L4-L5 or L5-S1.
7. If an L5 nerve root is impinged by a disc herniation, which disc would it most
likely be? If an L3 nerve root is impinged by a disc herniation, which disc would it
most likely be?
a. This depends on what kind of herniation it is (note: midline herniations can affect
multiple nerve roots).

51
 b. L5 nerve root: if it is a posterolateral (most common) or medial herniation, it is
most likely from a L4-L5 disc herniation, but if it is a far lateral herniation, it is
most likely from a L5-S1 disc herniation.
c. L3 nerve root: posterolateral or medial herniation = L2-L3, far lateral herniation
= L3-L4.
8. If a patient has a posterolateral disc herniation with sciatica down his right leg,
which direction might he lean his body to get some pain relief? Why?
a. Away from the side of the herniation.
b. This is because leaning into the side of herniation more greatly compresses the
nerve root. However, this has been discovered to not be as predictive as once
thought.
9. What physiological mechanism accounts for nerve root pain? Inflammation?
Compression? Both?
a. Both inflammatory (hypersensitizes the nerve root to painful stimuli), and
mechanical (occluding venous return, leading to venous hypertension and
hypoxia, leading to pain) forces can lead to nerve root pain, especially since they
are more sensitive to compression than peripheral nerves.
b. Note: sensory fibers are usually affected before motor fibers, but sensory fibers
also recover more quickly.
10. What are the key signs and symptoms that we associate with an irritated nerve?
a. Leg pain, paresthesia, hyperesthesia, painful SLR = Radiculitis.
11. What physical signs allows us to deduce that there is significant nerve root
compression? What do we call this condition?
a. Lower extremity SMR deficits = Radiculopathy, sometimes leg pain if
compressing the DRG.
b. Note: compression and irritation usually occur together.
c. Note: spinal stenosis or lateral recess stenosis can decrease the size of the
canal, which can make the symptoms more severe and the conservative care
prognosis worse.
12. About what percentage of back pain patients seeing a chiropractic have clinically
important disc herniations?
a. 2-3%.
13. What is an estimated pretest probability that your patient with LBP and leg pain
may have a disc herniation?
a. 14%.
14. Explain the prevalence of urinary symptoms in relation to a disc herniation vs
another diagnosis.
a. Urinary symptoms are not unique to Cauda Equina Syndrome, as 50-80% of
spinal canal stenosis cases will present with urinary symptoms, and are also
more common in otherwise asymptomatic disc herniations compared to
symptomatic ones.

52
 b. Still need to rule out and watch carefully for progression to full blown CES, but in
general since spinal stenosis is so much more common than CES, it is the more
likely Dx.
15. Explain the two ways that the word sciatica is used.
a. True Sciatica: a lesion in the sciatic nerve itself or the L4, L5, or S1 nerve roots
causing sharp leg pain (more precise usage).
b. General Sciatica: any pain (even deep referred) beyond the knee that roughly
follows the distribution of the sciatic nerve.
16. Explain the following numbers regarding sciatica and how much it should affect
your suspicion of a disc herniation. Is this finding stronger at ruling in or ruling
out?
a. Presence of Sciatica to Dx a symptomatic, surgically relevant herniated disc:
i. +LR = 7.9, -LR = 0.06
ii. This question from the history is better an ruling out a disc herniation, but
it is also pretty good at ruling one in as well.
b. If a patient has no lower extremity pain, a clinically significant disc
herniation is unlikely, and should not enter the DDx initially (this may
change after the physical exam).
c. Most individual tests are not very accurate at differentiating lumbar herniated
discs from other similar conditions, so it is best to combine history and physical
findings.
17. For each of the 5 main clues for neuropathic pain (remember? Pain, paresthesia,
SMR, tension tests, spinal load tests causing leg pain), predict what the findings
would be in a classic disc herniation presentation.
a. Dermatomal (especially if S1), sharp, stabbing, electrical leg pain that
crosses the knee, is worse than the LBP.
b. Dermatomal paresthesia.
c. Neurological deficits.
d. Positive SLR and positive confirmatory tension tests.
e. Compressive or lumbar flexing orthopedic tests reproduce leg symptoms.
18. Is a SLR more powerful to rule in a disc herniation when positive, or more
powerful at ruling to when negative? Using the LRs, explain how you know that.
a. +LR = 1.28, -LR = 0.29
b. The SLR is MUCH better at ruling out, as with how small the +LR is, it shows
that the SLR is not at all specific to a disc herniation.
c. This means if the SLR is negative, you can basically forget the possibility of a
disc herniation, but if the SLR is positive, it really doesn’t help you decide what it
is.
19. Explain how the angle of the positive SLR can either support or not support a disc
herniation theory.
a. Reproduction of leg symptoms during the SLR at 35-45 degrees is considered
more specific to a disc herniation, while pain below 30 or above 60 degrees is not
likely due to a disc herniation.

53
 b. Because a disc herniation causes a lot of inflammation compared to spinal
stenosis, a positive SLR due to stenosis usually doesn’t occur until >50 degrees.
i. Note: stenosis usually DOES NOT cause a positive SLR.
20. You want to see if the L4 nerve root is compromised. Where are the main
locations to do your sensory testing? Where is the pure patch? What are two key
muscles to test? What DTR should you do? Now what about L5 and S1?
a. L4
i. Sensory: medial knee and lower leg.
ii. Pure patch: middle ⅓ of lower leg.
iii. Muscle testing: knee extension (quads-L3/L4) and ankle dorsiflexion with
inversion (tibialis anterior-L4/L5).
iv. DTR: patellar reflex (L3/L4).
b. L5
i. Sensory: lateral lower leg, medal dorsum of foot, and medial large toe.
ii. Pure patch: medial large toe/web of 1st and 2nd toe.
iii. Muscle testing: great toe extension (extensor hallucis longus-L5/S1), hip
abduction (glut medius-L4/L5/S1), and heel walk.
iv. DTR: medial hamstring reflex (L5/S1)
c. S1
i. Sensory: small toe and plantar surface of foot.
ii. Pure patch: lateral small toe.
iii. Muscle testing: ankle eversion (peroneus longus/brevis-L5/S1/S2), and
plantar flexion (gastroc-soleus-L5/S1/S2).
iv. DTR: achilles reflex (S1/S2).
d. Note: SMR deficits are better at DDx radicular vs deep referred pain, but not
super accurate at telling you exactly which level the herniation is (so much
crossover for innervations).
21. What would be a key distinction between a severe radicular syndrome and a mild
radicular syndrome?
a. Mild: abnormal sensory, normal DTR, may or may not lose 1 motor grade,
recovery 6-12 weeks.
b. Moderate: absent DTR, loss of 1 motor grade, recovery 3-6 months (DTR
usually never returns).
c. Severe: motor loss at grade 3 or below, recovery 1 year (sometimes only partial
recovery).
22. According to Peterson’s 2017 systematic review, what would be the strongest
combination of exam findings that would support the diagnosis of a lumbar disc
herniation?
a. + SLR and 3 out of 4 of the following corresponding to the same nerve root:
i. Dermatomal pain
ii. Sensory deficit
iii. Motor weakness
iv. Reflex deficit

54
23. List the 8 main clues from the H&P that would support a herniated disc as the
cause of your patient’s sciatica. Which one of those is the best evidence that a
disc is involved?
a. Pain centralization with repetitive/sustained end range loading.
b. Mannequin sign (unique to herniation, doesn’t present in derangement).
c. Flexion load sensitivity.
d. Decreased sagittal TL ROM.
e. Sitting poorly tolerated.
f. + Valsalva.
g. + DeJeurine’s triad.
h. Sensitive to axial loading (ex. DSLR).
24. What does the Mannequin sign look like? What is the mechanism?
a. One leg flat/weight bearing, the other in a slight amount of hip and knee flexion,
and ankle plantar flexion (looks like a posing mannequin). The patient will
apparently assume the position naturally.
b. Relieves some tension from the sciatic nerve/L4-S1 nerve roots.
25. What is the difference between a medial and a lateral disc herniation? Medial and
lateral in relationship to what?
a. A posterolateral herniation occurs lateral to the inferior nerve root, while a medial
herniation occur medial to the inferior nerve root.
b. Medial herniation is much less common.
26. What are some findings that a medial disc herniation might create that are
different from a lateral disc herniation?
a. SLR
i. Positive result doesn’t tell you whether medial or posterolateral, but a
negative result will decrease the likelihood of a posterolateral while a
medial herniation is still possible.
b. XSLR (SLR of the unaffected leg)
i. May suggest a medial herniation, but a positive result (pain in the affected
leg) increases likelihood of every kind of herniation.
ii. +LR = 2.8, -LR = 0.8 (better at ruling in than SLR, but worse at ruling out).
c. Antalgic posture
i. Posterolateral antalgic posture = leaning away from affected side.
ii. Medial antalgic posture = leaning towards affected side.
d. Note: a medial herniation results in a poorer prognosis with conservative
treatment, more likely to need referral for surgery.
27. Why can an L2-L3 disc herniation present with L4 or even L5 nerve root findings?
a. Because higher in the lumbars, the herniation can affect lower nerve roots while
they are higher up and haven’t yet split from the central canal.
b. Upper lumbar herniations are very rare (<5%).
i. Very hard to actually diagnosis since they don’t have strong discriminating
findings and can mimic lower herniations.

55
 ii. Best finding is a positive femoral stretch test, since L2-L3 and L3-L4
herniations most commonly affect the L4 nerve root, and sometimes L5.
28. If your patient has a far lateral disc herniation of the L3-L4 disc, what nerve root
would it most likely impinge? What else do you know about how these far lateral
herniations present?
a. L3 (only herniation to affect the upper nerve root).
b. Deficits are more common, pain is more severe, and very rare.
29. Besides allowing you to see if there is a disc herniation and its location, what
other key piece of information can an MRI provide about the herniation?
a. First of all, no imaging is usually needed for a herniation, unless:
i. Rule out stenosis/spur.
ii. Neurological deficit.
iii. Uncertain Dx.
iv. Surgical consult.
b. MRI can identify nerve damage:
i. (FYI) +LR = 3.1, -LR = 0.23
30. What are 7 situations in which an MRI should be ordered as part of the initial work
up of suspected lumbar disc herniation?
a. Si/Sx of Cauda Equina Syndrome.
b. Progressive muscle weakness.
c. Profound muscle weakness.
d. You or the patient want a surgical consult.
e. Patient doesn’t respond as expected
i. 50% improvement in 4-6 weeks.
ii. 80-100% improvement at 3 months.
f. Suspected upper lumbar disc herniation (rare, so need to rule out SOL).
g. Disc Dx is in doubt, or red flags are present.
i. Order plaims films, followed by MRI.
31. Answer the following questions regarding the natural history and prognosis of a
typical disc herniation:
a. Generally, how long do the severest leg symptoms last?
i. 2 weeks to 2 months.
b. Do most disc herniations resorb? How many? Over what period of time?
i. Yes, 80% over 6-9 months.
c. Do neuro deficits usually improve? Over what period of time?
i. Yes, but functional improvements take 1-2 years, and motor deficits
take months to 1 year.
d. Is the size of a disc herniation related to the prognosis?
i. Larger herniations will resorb more quickly, so no negative effect to the
prognosis.
e. Is the size of the canal related to the prognosis?

56
 i. Yes, the smaller the canal (due to stenosis) + a herniation worsen the
prognosis and may need surgery.

Strategies

32. Your patient has sciatica, neurological deficits, a positive SLR and positive
Valsalva—you have a strong clinical case that she has a herniated disc. Should
you order a radiograph? Should you order an MRI?
a. This seems like a very standard disc herniation diagnosis, so we shouldn’t need
plain films or an MRI unless the neurological deficits worsen or the patient isn’t
responding to care.

Stories

33. Paint the picture of a classic acute lumbar disc herniation.

a. Patient felt sudden LBP (can also come on gradually) after bending over to pick
something up, got better initially but worsens a few hours later.
b. Movement in general is deep, dull, achy pain for a few days, with sharp pain
when leaning forward. Hour or days later, sharp pain into posterior thigh, pins and
needles in the foot.
c. Leg pain is now sharp and worse than the LBP, sitting and having a bowel
movement hurts, but standing and walking aren’t painful anymore.
d. Lumbar muscle splinting and posterior pelvic tilt causing loss of lordosis, possibly
with a flexed antalgic posture.

Applications (what is at the top of your DDX?)

34. Your patient was tackled hard during a football game and now has LBP and right
leg pain, both are aggravated by sitting, flexion hurts the back, lying offers some
pain relief, the SLR is only a soft positive, there is a +1 Achilles reflex on the right
and he has difficulty toe raising on that side.
a. Probably S1 radiculopathy (since both the toe extensor and achilles reflex
receive innervation from S1) caused by a disc herniation (flexion sensitivity,
sitting aggravates).
35. Your patient has left leg pain to the knee, left antalgia, paresthesia along the
lateral aspect of his foot, but no LBP. The symptoms are aggravated by forward
flexion and Valsalva. SLR is negative. XSLR is positive. Toe flexors are +4, medial
hamstring reflex is absent on that side.
a. Probably L5 radiculopathy (medial hamstring reflex absent) caused by a medial
disc herniation (antalgia towards the affected side, XSLR positive but SLR
negative). No LBP is very strange, but the flexion sensitivity and positive valsalva
suggest a disc problem over a peripheral neuropathy.
36. Your patient has LBP and leg pain radiating into the left buttock. Extension and
extension combined with rotation aggravates his familiar pain. There is

57
 tenderness deep in the paraspinal musculature and joint restriction. SLR and
XSLR are negative. SMR are WNL.
a. This doesn’t suggest nerve damage, but rather deep referred pain caused by
facet syndrome.
37. Your patient has LBP from overuse at work where he is required to do a lot of
bending. It hurts at the end of the day. Sitting and lying down gives him pain
relief as well as taking a few days off work. He has no leg symptoms. His SLR and
neuro exam is WNL as is most of the orthopedic exam (Valsalva, Kemps, double
leg raise) except for knees to chest if held for about 30 seconds. Palpation of his
back is negative except for evidence of some joint restrictions.
a. Lumbar sprain, because the only test that recreated the pain was sustained
end-range flexion (a strain would be more likely if the muscle hurt during a
muscle test).
38. Your patient has LBP and left anterior thigh pain. Forward flexion makes his back
and leg hurt worse. He has a sluggish patellar reflex and grade 4 hip flexors on the
left. Passive hip extension gives him a sharp pain in his anterior thigh on that
side. SLR and XSLR are negative. He cannot tolerate sitting.
a. SLR being negative is very unusual, but the inability to tolerate sitting anda
flexion sensitivity point to a disc problem, probably a herniation, causing L4
radiculopathy.

Lumbar Spinal Stenosis (based on Panopto lecture and CSPE protocol

Lumbar Spinal Stenosis)

1. What are 3 degenerative changes that occur in the lumbar spine that together
contribute to spinal canal stenosis?
a. Bulging Disk - degeneration and “pancaking of nerve roots may indent the dural
sac. Doesn’t necessarily mean and symptoms may occur but may have a
cumulative effect with other structures encroaching on the NR.
b. Facet Joint Enlargement - as degeneration of spine increases, osteophytes for
and cause additional bone to be deposited and crowd dural sac.
c. Lig. Flavum Thickening - thickens with age, crowds nerve roots.
d. Also *Severe degenerative spondylolisthesis*
2. What would be a “snapshot” of when to suspect lumbar stenosis in a patient?
a. Patient >60 years old, where thigh pain gets worse with walking, extension
aggravates, flexion/sitting relieves pain (shopping cart sign). Walking with
wide gait (+13 LR)
b. Thigh Pain Dominates.
c. Commonly BILATERAL.
3. Radiographically, what are the different sites of stenosis?

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 a. Typically occurs in mid to lower lumbar region as the spinal cord ends around L1.
Therefore mostly impacts nerve roots than the cord itself.
b. IVF
c. Lateral Recess
d. Central
e. Subarticular
f. However, radiographic stenosis w/o sx’s may be meaningless.
4. Clinically, what are the two neurological presentations of spinal stenosis? What
are key characteristics of each of these?
a. Neurogenic Claudication (more common)
i. Leg Pain w/ walking
ii. Leg Pain sensitive to spinal position
b. Radicular/Sciatica
i. Leg Pain unrelated to activity
ii. Unilateral or bilateral leg pain in ≥ 1 dermatome
iii. May occur alone OR with Neurogenic claudication
5. Based on one study, what is the pre-test probability that a 65-year-old patient with
leg pain and numbness might have lumbar stenosis?
a. 47% in older adults.
b. 15% in patients <60.
c. 25% in patients 60-70.
d. 64% in patients >70.
6. Characterize the leg pain: uni-or bilateral? Location in the leg? Severity of the leg
pain?
a. Lower Extremity Pain- groin, buttock, anterior thigh, posterior thigh, lower leg to
feet.
b. Thigh pain more common than lower leg
c. Commonly Bilateral, may be unilateral
d. Paresthesia, odd sensation usually nondermatomal
e. Patient complains of lower extremity WEAKNESS, “HEAVINESS” or “TIRED
LEGS”, crampy. Itchy, wake up at night.
7. Is it a common cause of surgery in older patients?
a. Most common surgery for patients >65 yo!!!
8. The Panopto lecture suggested that there are 5 basic patterns of the signs and
symptoms of lumbar stenosis. What are they?
a. Leg symptoms made worse by walking (65% of cases)
b. Extension of the spine increases leg symptoms, flexion often improves
symptoms. (Note**: opposite of disk herniation sx’s)
c. Balance and leg proprioception can be affected (large axons conducting
proprioception are more susceptible to compression).
d. Rarely, CES can be present (S2,S3,S4 nerve roots could be affected by the
stenosis).
e. Basic neurology: deficits present about 50% of cases; SLR rarely positive.

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9. What are three of the most useful positive findings from the history (based on
LRs)? Are these very common?
a. Flexion relieves pain- sitting, stooping, leaning over (IVF increases by 12%)
b. Extension reproduces Pain! (IVF gets 15% smaller), walking, prolonged sitting
c. Hyperextension for 1 minute- reproduces pain
10. What are 3 of the most accurate physical exam findings to support the diagnosis
based on LRs? Are these very common?
a. Wide Gait (+LR 13)
b. No Pain When Sitting (+LR 7.4)
c. Burning Sensation in buttock or priapism when walking (erection) (+LR 7.1)
d. Urinary disturbance (+LR 6.9)
11. What clue from the physical carries the most weight in ruling out stenosis (based
on LRs)?
a. ABSENT = Improved walking tolerance with spinal FLEXION (-LR 0.5)
i. If walking with flexion does not relieve symptoms, is the biggest clue
against stenosis.
12. If you suspect that your patient has lumbar stenosis, do you expect them to have
some neurological deficits? Highly likely, about 50/50? Very unlikely?
a. Neuro deficits are 50%.
13. Do you expect the SLR to be positive in patients with stenosis?
a. NO - a positive SLR is very RARE with stenosis.
14. What does flexion do to the size of the central canal? How about the size of the
IVF?
a. Flexion = Central Canal Increases & IVF diameter increases by 12%
b. Extension = Central Canal Decreases & IVF gets 15% smaller
15. What 3 ancillary tests should be ordered in a suspected lumbar stenosis case?
What information does each different test provide?
a. Start with x-ray, check for degenerative changes - not strong enough alone.
b. Confirm with MRI with canal measurements→ measurements don’t guarantee
sx’s either.
i. Relative stenosis: narrowing <12 mm of spinal canal
ii. Absolute stenosis: narrowing <10 mm of spinal canal
c. Electromyographic Paraspinal Mapping -strong clinical recommendation grade B
- for Dx.
d. In order to make diagnosis, need characteristic Si/Sx, MRI evidence, and
exclusion of other causes of back pain.
16. In a 70 year old patient with neurological deficits, leg pain and paresthesia, what
would be 3 other competing diagnoses?
a. Neuropathic Sx’s
i. Nerve Root: Lumbar Disk Herniations, SOL, Osteophytic NR
compression, fracture, spinal infection
ii. Peripheral Neuropathy: Piriformis Syndrome, Diabetes, Herpes Zoster,
compartment syndromes, peroneal nerve compression

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 b. Local Referred Pain Sx’s (No neural damage)
i. Referred pain from Lumbar spine structures
1. Facet joints, deranged disks, MFTP, or hip (trochanteric bursitis,
OA)
c. Lower Extremity Lesion
i. Peripheral Arterial Disease (PAD)
ii. Medial Tibial Stress Syndrome
iii. Stress Fracture tibia or fibula
iv. Muscle strain or tear
17. What are 5 distinguishing findings that could be used from the H&P to
differentiate a possible PAD diagnosis from neurogenic claudication (Stenosis)?

18. What ancillary tests can be used to confirm a suspected diagnosis of leg pain
caused by PAD?
a. Duplex Doppler Ultrasound
i. Detect blood flow on legs, color coded lamination of blood flow, accurate.
b. Ankle-Brachial Index (ABI): blood Pressure and ultrasound detector
i. BP should be higher in leg than in arm
1. If leg is lower <.9 then have PAD.
c. Magnetic Resonance Angiography - most accurate
d. Treadmill Test: Flat then uphill. Stenosis can walk further uphill than flat. PAD
will gets worse or stays same.
19. What are some key examples of activity or behavioral modifications you would
recommend to a patient with spinal stenosis?

Patient Education PAAP: Encourage activity

CMT STM
Won’t affect the stenosis DIRECTLY, but can
treat the peripheral symptoms and Nothing Special - treat spasms, MFTP if
contributors to symptoms. necessary.

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Joint Manipulation
Flexion Distraction
Neuromobilization- flossing

BM Ex
AVOID following: Big Part of conservative management- but
1) Working with arms overhead some mixed research of results
2) Prolonged Standing
1) Flexion Exercises- biking, incline
Modify Home to Prevent falls treadmill
2) Core stabilization - 8-12 weeks
3) Walking Program- maybe supervised
4) Neuromobilization

20. What are a couple of additional things to prescribe for the patient that may
increase their walking distance?
a. Lumbosacral Corset (weak dynamed recommendation)
b. Addition of Ultrasound to exercise may reduce analgesic use.
c. Wheeled Walker - not a walking stick.
21. What are the two main medical approaches to treating lumbar stenosis, especially
when conservative care fails? How strong is the recommendation?
a. Epidural transforaminal steroid injections
i. Short-term symptom relief (Strong Dynamed recommendation)
ii. Repeated injections for recurrent or worsening pain (Weak Dynamed
recommendation)
b. Surgical decompression with or without lumbar fusion for patients with
moderate-to-severe symptoms of lumbar spinal stenosis (Strong Dynamed
recommendation).
c. Decompression alone (without lumbar fusion) is suggested for patients with
leg-predominant symptoms without instability (Strong Dynamed
recommendation).
22. What are some indicators for early surgery in a patient with lumbar stenosis?
a. Severe leg pain, significant difficulty walking, and CES----> REFER FOR
SURGERY!
b. Leg Pain longer than 1 year may have poorer surgical outcome.
c. Note: no real predictor of how patient may respond to surgery.
23. How long might you treat a patient before you decide that conservative care has
not been adequately successful?
a. 4-12 weeks, average visits 13.3 in murphy’s study.
24. What is the success rate of surgery in terms of functional improvement?
a. Not as good of prognosis as disk herniations, or non specific LBP.
b. Mild to moderate stenosis: 30-50% even w/o treatment.
c. 50-70% treated non-surgically either improve or stop progression.

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 d. 20-40% will have surgery eventually.
25. In the study published by Murphy, what were the key components of his approach
to therapy?
a. Flexion Distraction
b. Neuromobilization - seated Flossing
c. Standing Stabilization
d. 2-3x/wk for 3 weeks
i. Based on re-exam: 1-2x/wk, then if resolved, 3 week follow up
ii. Mean Visits = 13.3

Lumbar Disc Herniations, Part 2 (based on class lecture and CSPE

care pathway Herniated Lumbar Disc with Sciatica pp 39-70)

1. What are the 4 main early interventions recommended in class lecture?

a. Manipulation/flexion-distraction.
b. Directional preference exercises.
c. Neutral pelvis, abdominal bracing, hip-hinging.
d. Keep patient active.
i. Can teach patient lumbar stabilization tracks and neuromobilization
stretches once out of the acute phase.
2. What is the difference between manipulation based on joint restriction and
manipulation based on directional preference?
a. In the area of the disc herniation, adjust in a vector which either centralizes the
patient’s leg pain, or at least doesn’t worsen it.
b. In areas other than the disc herniation, you can still adjust in directions that may
be painful at end play if they are restricted.
3. What are the key components of discovering a directional preference for your
patient? What direction is most common?
a. Repetitive or sustained end-range loading, usually in extension (far lateral
herniations may have symptoms increase with extension).
b. Patients who are still very acute may have so much inflammation that you cannot
find a directional preference for a day or two. However, if a directional preference
hasn’t been found after that period of time, it is unlikely that the patient will have
one.
4. What are the various components of teaching a patient a hip hinge strategy?
a. Need to first teach them how to find and hold neutral pelvis, how to abdominal
brace and belly breathe simultaneously, and then walk them through situations
like standing at a sink, getting in and out of the car, etc.
5. How might you progress a patient through a walking prescription?

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 a. Encourage the patient to limit bed rest, and punctuate it with bouts of activity.
b. Start walking 20-60 minutes per day, but reminding patient to decrease
intensity/frequency if walking is aggravating leg pain.
c. Progress to unstable/uneven surfaces, then to carrying a 10 kg pack at the level
of the lumbar spine.
6. What are a couple of sleep aides that might be useful for the patient?
a. Valerian and Melatonin.
7. What recommendations would you make if the patient is constipated and having a
bowel movement increases his low back pain?
a. Increase water and fiber intake, avoid codeine and NSAIDS, take OTC stool
softeners if needed.
8. What 3 medications are usually prescribed for a disc herniation?
a. NSAIDS, acetaminophen, and opioids.
i. There is lack of evidence for the effectiveness to reduce pain from a
herniated disc for all three of these, except for opioids only for severe
short term pain.
b. Epidural glucocorticoid infections have better short term pain relief and
increased function.
9. What medication has been found to be ineffective to treat LBP and lumbar
radicular pain?
a. Anticonvulsants.
10. What is a sciatic slider exercise? When is it prescribed?
a. A neuromobilization exercise prescribed in the post-acute phase, theoretically to
break up adhesions formed during the inflammatory acute phase. If symptoms
get worse between sets, discontinue.
b. Prescription would be 10-15 reps, 3-4 times a day.
11. What are the usual basic floor exercises that you start a patient on a stabilization
program with?
a. Quadruped, side bridge, curl-up/dead bug.
b. Emphasize good, slow control, and for patient to stop if shaking, painful, or lose
form.
c. 10-15 reps, then increase difficulty if patient can handle it.
12. What weight bearing exercises are usually added?
a. Squat, lunge, one leg stand on proprioceptive balance board.
13. About what percentage of patients will require surgery?
a. 10%.
b. 25% will have their sciatica recur within a year.
c. 81% of muscle weakness recover within a year.
d. 50% of sensory deficits recover within a year.
e. 76% of herniations shrink within a year.
14. About what percentage of herniated discs resorb within a year?
a. 80% within 6-9 months.
15. Which neurological deficit is least likely to recover?

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 a. DTRs.
16. You expect patients to be about 50% better in about what time frame?
a. Leg pain should improve in the first 3 days.
b. 50% improvement within 3 weeks (using manual therapy) or 6 weeks (using
functional rehab).
c. If patient has had a profound muscle weakness that has not gotten better by
week 6, refer for surgical consult.
d. Patients with poor response to care at week 8-12, refer for surgical consult.
e. Normally leg pain gets better first, then back pain, then ADLs improve, then
deficits get better.
17. What is usually the first line of invasive treatment when conservative care and
pharmacologic care are insufficient?
a. Epidural steroid infections (3 over a few months).
b. Can then progress to PRP injections (platelet rich plasma), surgical removal, and
artificial disc implantation.
18. In the short term, how does surgical care compare with non-surgical care? How
about in the longer term?
a. Surgery is superior in the short term compared to conservative care (full
recovery in 4 weeks instead of 12 weeks).
b. However, they are equal in the long term.

Biomechanical vs Pathoanatomical Diagnoses &

Lumbar Joint Dysfunction (based on Panopto lecture and course notes
Mechanical Low Back Pain Diagnoses)

1. What are some examples of pathoanatomical diagnoses? What are some

examples of “biomechanical” diagnoses?
a. Pathoanatomical Dx
i. Fracture
ii. Disk Derangement
iii. Strain
iv. Sprain
v. Stenosis
vi. Spondylolisthesis
b. Biomechanical Dx
i. Joint/segmental dysfunction
ii. Myospasm
iii. Myofascial pain syndrome

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 iv. Myofibrosis
2. What is the difference between these two categories?
a. Pathoanatomical Dx
i. Emphasis on structural damage/naming specific tissue.
ii. Does not direct manual therapy interventions.
iii. Usually Primary dx.
b. Biomechanical Dx
i. Emphasis on tissue behavior.
ii. Triggers manual therapy interventions
iii. Usually NOT primary Dx unless it is the ONLY Dx and except for
medicare billing.
3. Which type of diagnosis is usually used as a “primary” diagnosis? This is true
except in what billing situation?
a. Pathoanatomical Dx is PRIMARY except for medicare billing.
4. Explain what each letter in PART stands for and give an example for each.
a. P = Pain (provoked during the physical exam).
i. Palpatory (static or motion) segmental bony or soft tissue
tenderness/dysesthesia.
b. A = Asymmetry
i. Asymmetrical presentation or “misalignment” of various landmarks (e.g.,
spinous deviation, “prominent rib,” superior pubic rami).
c. R = Range of motion
i. Altered segmental range of motion (based on motion palpation)
ii. Decreased global ROM can also be of note, but less valuable.
d. T = Tissue changes
i. Palpable alterations in paraspinal tissue texture and or tone.
e. Medicare needs at least two of the letters for a Dx of joint
dysfunction/subluxation, and one must be either A or R.
f. Joint dysfunction:
i. May present with referred pain to an extremity.
ii. Usually resolves rapidly in response to manual therapy.
iii. Chronic conditions require longer treatment courses.
5. What are some pertinent negatives that would make a joint dysfunction less likely
to be adequate as a diagnosis by itself?
a. Signs of nerve root involvement should signal a search for additional
pathoanatomical diagnoses (e.g., disc herniation, osteophytic compression,
stenosis)—especially when serious nerve root compression signs are present.
b. On the other hand, local pain and/or deep referred pain (or related symptoms)
can be consistent with a joint dysfunction diagnosis.

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Myofascial Pain Syndromes (based on Panopto lecture and course
notes Mechanical Low Back Pain Diagnoses)

1. What is the difference between myofascial trigger points and a regional

myofascial pain syndrome diagnosis?
a. Lumbar myofascial trigger point syndrome (MFTP) is a local or referred pain
and/or autonomic phenomena initiated by active myofascial trigger points. A
myofascial trigger point is a hyperirritable nodule, usually within a taut band of
skeletal muscle or in the muscle’s fascia, that is painful to compression,
reproduces the patient's familiar pain and that may give rise to characteristic
referred pain, tenderness, and autonomic phenomena.
b. Lumbar regional myofascial pain syndrome (MP) is lumbar muscle pain that is
associated with muscle tenderness that reproduces the patient’s familiar pain but
without palpatory evidence of discrete myofascial MFTP’s. Primary fibromyalgia
and muscle diseases have been ruled out. Myalgia may be an additional
diagnostic term used for this condition.
2. What are the key criteria to consider to make an MFTP diagnosis?
a. At least 2-3 of:
i. Presence of a palpable taut band within a skeletal muscle
ii. Presence of a hypersensitive spot within the taut band
iii. Reproduction of the patient’s familiar pain (this one ALWAYS has to be
present)
iv. Reproduction of a referred pain sensation with stimulation of the spot
b. Presence of a palpable taut band and reproduction of familiar pain are the most
reliable.
c. Trigger points are usually deep, dull and achy.
3. Define the following: myospasm, fibromyositis, muscle strain.
a. Myospasm: an often painful involuntary muscle contraction.
b. Fibromyositis (myofibrositis): muscle or fascia with palpable fibrotic tissue.
c. Muscle strain: a muscle with morphological changes consistent with frank
tearing of muscle fibers.
4. What is the reported prevalence of myofascial pain in a primary care setting?
a. Numbers have been reported as high as 30% of patients consulting a primary
care physician for pain and 85% of patients in a tertiary care clinic.
5. What are some of the autonomic changes that might accompany an MFTP?
a. Vasoconstriction (blanching), coldness, sweating, pilomotor response,
vasodilation, and hypersecretion.
6. To reproduce a patient’s myofascial pain referral, what might you have to do to the
trigger point besides just simply pressing on it? What is the potential lag time?
a. Deep or sustained pressure may be required to reproduce the referral which
might not express itself until after 10-15 seconds delay.

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 b. Stretching, contracting and/or moderate pressure produces local/familiar pain,
but usually not the referred pain.
7. What is a local twitch response? What might you have to do to elicit it?
a. Presence of a local twitch response with snapping palpation of the taut band.
This response is best elicited by plucking or a snapping action across the taut
band/trigger point as opposed to a probing type of palpation.
b. Presence of a jump sign.
8. What is the difference between a latent and an active trigger point?
a. Latent trigger point: when patient reports no spontaneous symptoms, but the
practitioner can find a trigger point.
b. Active trigger point: cause symptoms that the patient is already complaining
about.
9. What are satellite trigger points and what is their clinical importance?
a. Trigger point referral areas may themselves also harbor trigger points called
satellite trigger points.
i. These trigger points will continue to appear until primary trigger point is
eliminated.
10. Cite 6 examples of precipitating or perpetuating factors.
a. Trauma
b. Emotional stress
c. Immobilization, sustained postures
d. Chilling
e. Viscera-somatic reflexes
f. Joint dysfunction
g. Development or congenital anomalies
h. Nutritional inadequacies
11. What are two post interventions steps that are recommended?
a. Having the patient move the muscle through a full range of motion 3 times
b. Applying moist heat
12. What are three common home care self-treatments?
a. Avoid repetitive use of muscle for the first 24 hours after treatment, avoid
holding muscle in a sustained stretch or shortened position.
b. Self treatment includes home stretches of the involved muscle.
c. Intermittent pressure with a tennis ball or pressure applied by lying on
styrofoam rollers.
13. What are some of the broader treatment approaches that may be necessary
especially in a regional myofascial pain syndrome?
a. Increase activity
b. Stress management (management of depression & sleep)
c. Activity modifications
d. Nutrition
e. Address perpetuating factors
14. What lumbar muscle is the most likely to have MFTPs?

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 a. Quadratus Lumborum = lumbar muscle most commonly to have MFTPs
15. What is the referred pain pattern for trigger points in the psoas? The quadratus
lumborum? The gluteus medius?

Sacroiliac Pain Generators (based on Panopto lecture and CSPE

protocol Sacroiliac Orthopedic Tests)

1. What is the concept of “form closure” refer to as it applies to the SI joint?

a. This refers to the structural integrity provided by the bony and ligamentous
anatomy holding joint together. The form “closes” the sacrum between each ilia at
a multi-surfaced joint articulation.
2. What does the concept “force” closure refer to?
a. This refers to the musculotendinous structures that provide biomechanically
sound structure. Based on co-contraction of myofascial slings.

69
3. Which of the main SI ligaments is palpable and is most often symptomatic? Where
would you palpate to find it?
a. Posterior sacroiliac ligament (strongest SI ligament)
b. Palpated below the PSIS.
c. Anterior SI ligament isn’t readily palpable, but it is most commonly injured SI
joint ligament.
4. Which ligament is the key to Logan Basic technique which purportedly can be
stimulated to reduce tension and spasm in the lower back?
a. Sacrotuberous ligament
b. This ligament is also a common source of pain.
5. What muscles contribute to the oblique dorsal muscle-fascia-tendon sling?
a. Latissimus dorsi, gluteus maximus, TL fascia.
6. There is a vertical fascial sling that also helps to stabilize the SI joint. What
structures is it thought to be composed of?
a. Long head of biceps femoris, sacrotuberous and long dorsal sacroiliac ligament,
and erector spinae.
7. What are 4 main seronegative arthropathies? What does the “seronegative” refer
to?
a. Ankylosing spondylitis.
b. Reiter’s syndrome.
c. Enteropathic arthropathies.- reactive, bacterial
d. Psoriatic arthropathy.- thick fingernails
e. Seronegative = negative blood test for Rheumatoid Factor.
8. What are some clinical features they all have in common relative to the following
areas:
a. Spinal:
i. Local SI inflammation
ii. Progressive and insidious
iii. Less mechanical
iv. Episodic pain
b. Musculoskeletal extra-spinal:
i. Concomitant joint pains
ii. Enthesis pain
iii. Synovitis/osteitis
c. General non-MSK findings
i. non-NMS symptoms: fever, malaise, fatigue.
d. Organ-specific non- MSK findings
i. Rash
ii. GI/GU disorders
9. What would be 4 blood test findings that were be useful to see when trying to
decide if your patient had a seronegative arthropathy?
a. HLA-B27
b. ESR

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 c. CRP
d. Absence of RF, negative ANA.
10. Blending the SAS and Berlin criteria, paint a picture of how ankylosing spondylitis
presents.
a. Alternating buttock pain that is episodic and insidious at onset. Pain is
accompanied by morning stiffness, night pain, pain with rest, and relief by
exercise. Typical onset <40. Patient usually has symptoms 3 months or longer.
b. Commonly affects the eyes, neck, ribs, lumbosacral joint, and SI joint.
11. What is uveitis, what are the signs and symptoms and how is it treated?
a. Inflammation of the front side of the eye.
b. Symptoms: redness, photophobia, pain, and blurry vision. Self-limiting, but can
treat with sunglasses, steroids, and antibiotics.
12. What is a bamboo spine? Is it commonly found in AS? How long does it take to
develop?
a. Bamboo spine is the term given to describe a possible presentation of AS,
where the vertebral bodies begin to square due to demineralization, and the
ligaments begin to calcify leaving a rigid spine of bamboo block shaped
vertebra.
b. Takes 10+ years before AS presents this way, and only in a minority of cases.
13. What are some common PE findings in AS?
a. Limited lumbopelvic ROM (especially flexion).
b. Loss of SI joint motion.
c. Positive SI pain provocation tests (when acute)
d. G max or piriformis spasm.
e. Tendon-bone complexes (causing enthesitis).
i. Achilles/heel (most common)
ii. Plantar fascia
iii. Iliac crest
iv. Rotator cuff
v. Costochondral junctions
14. What are two measurements that are commonly done on an AS patient? What is
the cut point for an abnormal finding for each of these?
a. Vertebral separation with Schober’s test.
i. 2 marks, 10 cm apart on spine, look for separation with flexion.
ii. Normal is at least 5 cm separation.
b. Chest expansion.
i. Maximum inspiration vs forced expiration circumference.
ii. Normal is at least 5 cm difference.
15. What is the conservative care treatment approach? What is the medical treatment
approach?
a. Non-Acute: need to keep them moving and focus on joint mobility.
i. Manipulation and soft-tissue mobilization.
ii. Eliminate aggravating environmental factors

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 iii. Exercise and nutrition
b. Acute phase: need to slow down progression/inflammation.
i. NSAIDS or TNF-blockers (tumor necrosis factor)
ii. Stretches as tolerated
iii. Rest
16. What 5 questions are most valuable to screen for AS?
a. Morning stiffness?
b. Improves with exercise?
c. Onset of pain before 40?
d. Slow onset?
e. Pain lasting >3 months?
17. Describe some of the key dermatological findings of psoriasis.
a. Scaly, erythematous plaques with evidence of erythroderma.
b. Commonly affects the hair and nails (nail pitting, cracking, splintering).
18. About what percentage of psoriasis patients get sacroiliitis?
a. About a third, usually asymmetrically.
b. Onset usually 30-50 y/o.
c. Patients may also present with conjunctivitis or uveitis.
19. What two extra-spinal tendons/fascia are most commonly affected? What are
some of the radiographic changes that can occur in the hands with psoriatic
arthritis?
a. Enthesopathy or enthesitis at the Achilles tendon and plantar fascia.
b. Radiographically in the hand:
i. Fusiform soft-tissue swelling.
ii. Terminal tuft and subchondral bone resorption.
1. “Pencil-in-cup” appearance.
20. Suggest 3 different “causes” of enteropathic arthritis.
a. Inflammatory bowel diseases (enteropathic arthropathies)
b. Bacterial infection or Parasites (reactive arthropathies)
i. 75% of reactive form will have episodes for 6 weeks to 6 months before
self-resolving.
ii. The other 25% will have a persistent course requiring treatment.
21. What is the triad of findings suggestive of Reiter’s syndrome?
a. Conjunctivitis/ uveitis
b. Urethritis
c. Sacroiliitis
d. Post-infectious - tends to follow an infection.
e. More common in men (5:1).
f. Asymmetric SI involvement seen on x-ray (AS was bilateral).
g. Lab findings include: + HLA-B27, increased ESR and WBC, mild anemia,
negative SI joint culture.
h. Treatment: (very similar to AS treatment)
i. Acute: rest, NSAIDs, stretching.

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 ii. Non-acute: mobility important via manipulation/mobilization, exercise.
22. What would be some signs suggesting infectious sacroiliitis? What’s the
treatment?
a. Very rare, more common in children and young adults.
b. Unilateral, acutely inflamed SI joint, mimics common LBP.
c. Fever, signs of illness & infection.
d. X-ray indicates SI joint erosion or narrowing.
e. Elevated ESR and WBC
f. Positive SI Joint culture (possible blood culture)
g. Treatment would be IV antibiotics.
23. What 6 orthopedic tests are suggested to perform to identify if the SI joint is the
patient’s pain generator?
a. ASLR to start with, then follow with:
i. Thigh Thrust Test
ii. Sacral Thrust
iii. Gaenslen’s test
iv. SI compression
v. SI distraction
24. Which 5 tests should be interpreted as a group?
a. Laslett’s cluster (the 5 listed above besides ASLR).
b. If 3 or more of these tests are positive → +LR = 4.1
c. If there is NO centralization with repetitive movements → +LR = 6.9
25. A positive active SLR should be immediately followed up by what procedure?
a. Thigh thrust.
26. A positive active SLR offers the physician what 3 pieces of information?
a. SIJ may be the cause of pain or is at least suggestive.
b. SIJ may be the cause of functional instability.
c. Suggests that bracing the SIJ and incorporating abdominal bracing are
therapeutically useful.
d. (FYI only): +LR = 14.5, -LR = 0.14
27. What additional information does joint challenging offer the chiropractor that the
standard SI tests do not?
a. You’ve already reproduced the pain to decide if SIJ is cause, but you don’t know
if the pain centralizes or not. Loading the SI will show if the pain centralizes or
not.
b. According to Lefevbre, it tells you “is the pain coming from the SI or not, and
where do i adjust it?”
28. What are three “injury” diagnoses for the SI joint?
a. SI Syndrome: SIJ w/ leg pain.
b. SIJ Sprain: (+) orthopedic tests.
c. SIJ Dysfunction: palpatory joint challenge findings, (-) orthopedic tests.
d. Clinical presentation:
i. “LBP” aggravated by weight bearing, bending.

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 ii. PI or AS ilium upon palpation.
iii. Pain and paresthesia possible but unlikely past the knee, relieved by lying
down.
iv. Acute: walking is aggravating.
v. Chronic: walking may relieve.
vi. Negative neuro exams, possible local muscle spasm, focal SI
tenderness.
29. What are some causes of SIJ injuries?
a. Microtrauma that is due to repetitive motions/ lifting (overuse), posture,
asymmetrical loading, and anatomical discrepancies.
b. Macrotrauma: fall on the buttock or unguarded movement.
c. Pregnancy (relaxin).
30. SI pain is generally thought not to project above what vertebral level?
a. L4.
31. For a PI ilium (one fixed in flexion and restricted in extension), predict the
following findings in a “textbook” example: PSIS (high or low), iliac crest (high or
low), leg length (long or short), ASIS (high or low) pain felt where in the lower
extremity?
a. PSIS: Low/prominent
b. Iliac crest: High
c. Leg length: Short (except when seated)
d. ASIS: High
e. Pain upper ½ of SIJ.
f. Pain medial knee, sartorius, scrotum, & gluteal muscles.
i. In an AS ilium, pain in lateral knee & TFL.
32. How would you block for a short leg and a PI ilium (prone blocking)?
a. On the affected side, place a block under the ipsilateral greater trochanter and
another under the contralateral ASIS.
33. What might be used to help stabilize a hypermobile joint during pregnancy?
a. On the hypermobile side, fix a trochanteric belt to patient.
b. In non-pregnant patients, one SI joint may be hypermobile and symptomatic
while the other is hypomobile. The hypomobile and asymptomatic joint might be
the one that needs the adjustment, even though it isn’t causing pain.
34. What specifically would be the various treatment interventions for each
component of Janda’s SI muscle imbalance?
a. MET work on the musculature such as, PIR.
b. Address any muscle imbalances (strength and stretch)
i. Ipsilateral tight piriformis
ii. Ipsilateral tight psoas
iii. Ipsilateral inhibited glut max
iv. Contralateral inhibited glut med
c. Treat any LLI.
d. Core stabilization and proprioceptive training.

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 e. Overall GOALS in treating SIJ dysfunction:
i. Restore joint motion & alignment
ii. Control acute pain & inflammation
iii. Treat associated myofascial/muscle problems
iv. Maintain mobility
v. Prevent recurrence/predisposing factors
35. What are 4 medical interventions for SI joint lesions? How does each one work?
Which one is probably the most commonly done?
a. Joint injections: (most common)
i. Inject contrast + anesthetic + steroid.
ii. Reri vs Interarticular
iii. Fluoroscopic vs US-guided
b. Platelet-rich plasma (PPP) injections:
i. Plasma is injected into the joint to activate macrophages, collagen
proliferation, and vascularization to restore the tissues.
c. Prolotherapy:
i. An irritant is injected into the joint, the tendons and ligaments respond
with inflammatory response that repairs joint laxity and increases blood
flow, encourages healing.
d. Intra-articular radiofrequency ablation:
i. RF is employed to destroy the lateral branch of nerves of S1-S3 (that
innervate SIJ). Less pain signaling sent to cortex.

Piriformis Syndrome (based on assigned Panopto video lecture)

1. What are the key differences between a piriformis syndrome, a piriformis spasm,
and a piriformis myofascial pain syndrome?
a. Piriformis spasm (common): involuntary contraction of the muscle causing local
pain.
b. Piriformis syndrome: associated with neuropathic leg pain due to sciatic nerve
irritation
c. Piriformis myofascial pain syndrome: myofascial trigger points associated with
deep referred pain usually into the posterior thigh, but no nerve involvement.
2. What is the reported incidence of a true piriformis syndrome?
a. As little as 0.3-1% and as high as 5-6%.
3. What are some specific mechanisms of injury for a piriformis syndrome?
a. Trauma (pain-spasm-pain cycle): blunt trauma to butt, a fall to butt, twisting with
foot planted, hip or SIJ injury, complications of hip surgery.
b. Chronic repetitive/sustained loads

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 c. “Wallet” sciatica.
d. Prolonged external rotation of hip
4. What are some structural explanations for how the piriformis muscle can entrap
the sciatic nerve?
a. Myofascial band between biceps femoris and adductor magnus
b. Sacrotuberous and sacrospinal ligament size and attachments
c. Relationship of sciatic nerve and piriformis:
i. Passes inferior to the muscle
ii. In 21% of the population, the nerve pierces the muscle.
5. What are some activities that commonly aggravate a piriformis problem?
a. Symptoms may be aggravated by walking / running, walking up stairs,
driving, prolonged sitting.
6. What are some additional symptoms if the piriformis entraps the pudendal nerve?
a. Symptoms of piriformis syndrome:
i. Pain and paresthesia down path of sciatic nerve, deep pain in gluteal
region, relieved by lying supine.
ii. Pain with bowel movements, sitting intolerance.
b. If pudendal nerve is entrapped:
i. Dyspareunia (women)
ii. Erectile dysfunction (man)
7. What are three ways/locations to palpate the piriformis?
a. Palpate tendon near the greater trochanter (may be especially tender near
greater trochanter).
b. Oblique approach to palpating the edge of the piriformis muscle beneath gluteus
max (tender along edge of muscle deep to glut max).
c. Intrarectal palpation (most direct method of evaluation).
8. What is the so-called “piriformis sign?”
a. Piriformis sign: the leg is laterally rotated when patient lies supine.
9. What would be the more likely finding, reduced internal or external rotation of the
leg when the leg is straight out? Why?
a. Limited internal rotation of the lower extremity, because internal rotation would
increase the pain and symptoms.
10. What extra component can be added to the SLR procedure which may make the
test more likely to recreate leg pain?
a. SLR + internal rotation at about 20 degrees may increase local pain or sciatic
symptoms into the foot (common, but not consistent).
11. How common are neurological deficits in piriformis spasm? Myofascial pain
syndrome? Piriformis syndrome?
a. Piriformis spasm: just an involuntary contraction of the muscle causing local
pain. Rare nerve involvement.

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 b. Myofascial pain syndrome: no nerve involvement.
c. Piriformis syndrome: associated with neuropathic leg pain due to sciatic nerve
irritation.
12. What are 3 special piriformis tests? How is each performed? Describe a positive
finding for each.
a. Pace test: Resisted leg abduction in the
seated position. Positive test reproduces
the patient’s back or leg pain.

b. Beatty test (contraction): Patient lies

with painful side up and painful leg is
flexed with knee resting on table. The
patient lifts and holds knee a few inches
above the table and doctor can add
resistance if necessary. Positive test =
buttock pain.

c. FAIR (stretch): Hip about 45 degrees &

knee is bent. A stretch is applied toward
the floor. Positive test is reproduction of
sciatic pain (+LR = 5.2, -LR = 0.14).

13. What muscles have been theorized to create an eccentric load on the piriformis
muscle due to their weakness?
a. If the hip excessively adducts and internally rotates during weight bearing tasks
due to weakness of the gluteus maximus and/or gluteus medius, a greater
eccentric load may be shifted to the piriformis muscle.
14. What are the main treatments for the piriformis muscle recommended in lecture?
a. PIR, CRAC, Rhythmic stabilization.

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 i. Remember, PIR is a relaxation technique - gentle lengthening, not
stretching.
b. Direct pressure therapy (trigger point).
c. Home stretches.
15. What advice was given regarding manipulation?
a. Regarding manipulation, side posture manipulation may aggravate piriformis.

Leg Length Inequality (based on assigned Panopto video lecture)

1. What are the two types of LLI?

a. Functional LLI
i. Pelvic dysfunction or muscular imbalances
ii. Pes planus or pes cavus
b. Anatomical LLI (congenital or acquired)
i. Many different possible causes, including trauma, genetically short
femur/tibia, degeneration of hip, knee, or ankle, etc.
2. What are three methods for identifying LLI in the physical examination?
a. Derefield knees to 90 test.
b. Supine to sitting test.
c. Static observation (standing, or tape measure from umbilicus/ASIS to medial
malleolus).
3. What is a scanogram used for?
a. To check for true anatomic leg length inequalities (the only accurate way of
ensuring someone truly has a LLI).
b. However, 90% of people have an anatomical LLI (5.2 mm average).
4. What are some of the documented effects of LLI on the spine? Be specific.
a. Compensatory lumbar scoliosis.
b. LBP.
c. MSPS.

008 d. Anatomical changes in vertebrae (DJD, spurring, body wedging, etc).

e. Asymmetrical spinal ROM.
f. Spinal EMG imbalance.
5. What are some of the documented effects of LLI on the lower extremity? Be
specific.
a. Hip and knee degeneration, pain, and injury.
b. Foot compression fracture.
c. Risk of chondromalacia patella, iliotibial band syndromes, pronation syndrome
and plantar fasciitis.
d. Altered gait.

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 e. Asymmetrical LE muscle strength.
6. What is the recommended cut point for when to consider adding a heel or sole lift
for a short leg?
a. 10-20 mm.
7. What would be a classic finding when performing a supine to sit test? What
information would it give the practitioner? Be as complete as you can.
a. Supine: short right leg, switches and becomes long leg when sitting.
i. Most likely a functional LLI, caused by a right PI ilium, or a left AS ilium.
b. Supine: short right leg, stays short when sitting.
i. Most likely anatomical LLI.
c. Supine: short right leg, gets longer but still the short leg when sitting.
i. Most likely both an anatomical and functional LLI.
8. What are several factors that need to be considered when deciding how much lift
to add and how fast?
a. The lift should be gradually built up to the desired thickness (promotes
adaptation and decompression).
b. The final height of the lift should be less than the actual LLI.
c. A young patient will more easily tolerate a larger corrective lift than an older
patient.
d. If the patient has a severe compensatory scoliotic curve, the introduction will
need to be very gradual.
e. A short tibia will require greater correction than a short femur (prevents abnormal
knee biomechanics).
f. A sedentary patient will not require as precise of a corrective lift as an athlete or
someone on their feet a lot.
g. The Rule of Logan: ½ inch heel lift will raise ipsilateral femur ½ inch, ipsilateral
sacral base ¼ inch, and ipsilateral L5 ⅛ inch.
h. A heel lift of up to 10 mm is practical in most shoes, but anything greater may
require a sole lift.
i. Throughout introduction and build up of lift, patient should be monitored for
changes in pelvic alignment and lumbar compensation, as every patient may
respond differently to a lift.
j. Patients should also undergo spinal and pelvic manipulation during lift
therapy in order to improve mobility and minimize occurrence of functional LLI.
9. What are two contraindications or precautions to consider when deciding if you
should add a heel lift?
a. If LLI is actually a functional inequality caused by an AS ilium (long leg), a lift may
actually worsen the AS ilium.
b. If a patient has an anatomical LLI but their pelvis does not compensate (unlevel
itself, possibly creating a mild scoliosis), then a lift may make the pelvis unlevel
itself in the opposite direction.

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Maigne’s Syndrome (thoracolumbar syndrome), Psoas
Syndrome & Psoas Myofascial Pain (based on lecture and
powerpoint slides)

1. What is the main pain generator in a thoracolumbar syndrome?

a. T12-L1 joint
i. Treatment involves palpating and adjusting this transitional joint.
ii. Can progress to facet syndrome or disc derangement.
iii. Can also treat by cluneal nerve mobilization, which involves sitting with
ipsilateral leg crossed, and flexing + rotating away from the symptomatic
side. 6-10 reps, several times a day.
iv. Nerve blocks can be injected either to the TL facet or at the level of the
iliac crest.
b. Results in unilateral or bilateral LBP, and non-dermatomal referral (always refers
pain).
c. May be aggravated by contralateral side bending (stretches the irritated nerve).
d. Note: it is also possible for the pain generator to be entrapment of the
cutaneous dorsal ramus of L1 over the iliac crest (via thoracolumbar fascia),
or entrapment of the lateral cutaneous branch of iliohypogastric nerve (no
actual problem with the TL junction).
2. What are the 3 most common pain referral locations for this condition?
a. Ipsilateral iliac crest area via superior cluneal nerve.
b. Groin/inguinal canal area via subcostal or iliohypogastric nerve.
c. Lateral hip area via lateral femoral cutaneous nerve (coming from subcostal or
iliohypogastric rami).
3. What peripheral nerve is most commonly affected?
a. Superior Cluneal nerve.
b. Most valuable findings include painful joint restrictions at TL junction, pain referral
to one or more of these areas, and sharp, excruciating pain (familiar to patient)
with pressure about 7 cm lateral from L5, over the iliac crest.
c. Possible puffy, thickening, nodularity, or hair loss in the skin in this area.
4. What is skin rolling, exactly where should it be applied when assessing a possible
Maigne’s syndrome, and what would be a positive examination finding?
a. Pinching a fold of skin over the iliac crest, lifting it up, and rolling skin over itself.
b. Pain/hyperalgesia is a positive finding.
5. Where is the location of the most common traumatic compression fracture that
causes low back pain? Where might the patient report where they are feeling their
pain?
a. TL junction (due to high flexion load, or fall on buttocks).

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 b. Refers pain to the iliac crest area, same as Maigne’s syndrome, but we Dx a
compression Fx, not a TL syndrome.
6. In what way does a psoas syndrome differ from Maigne’s syndrome? In what way
is it similar?
a. Similarities:
i. Both refer pain to the iliac crest and buttock.
ii. Both caused by TL junction joint dysfunction.
b. Unique to Psoas syndrome:
i. The TL joint dysfunction is still the pain generator, but it was caused by a
tight (often painless) psoas putting an increased load on the TL.
7. How does a psoas syndrome differ from a psoas myofascial pain syndrome?
a. Psoas syndrome = TLJ is the pain generator.
b. Psoas myofascial pain syndrome = Psoas muscle is the pain generator.
8. What two therapeutic interventions are generally done immediately to address the
components of a psoas syndrome? What are the recommended home care
self-treatments?
a. In office: adjust the TL, and stretch/relax psoas.
b. At home: Self stretch of psoas, TL self mobilization.

9. What are the pain referral patterns for a psoas trigger point?
a. Low back/iliac crest/buttock.
b. Anterior thigh, similar to femoral nerve pain distribution.
10. What are the four main components of a lower cross syndrome? What would be
the treatment for each separate component?
a. Stretch tight erector spinae and hip flexors (iliopsoas and possibly quads).
b. Strengthen weak/inhibited abdominals and gluteus maximus.
c. Besides these 4 muscle groups being weak/tight, patient may present with
anterior pelvic tilt, increased lumbar lordosis, and poor hip extension/trunk flexion
movement patterns.

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Congenital & Developmental Defects of the Spine (based
on Panopto lecture)

1. Name 6 developmental and congenital defects of the spine.

a. Bertolotti’s syndrome (transitional segment).
b. Tropism.
c. Baastrup’s disease (kissing spinous syndrome).
d. Spina Bifida (occulta, meningocele, myelomeningocele).
e. Congenital block vertebrae.
f. Hemivertebra.
2. What are the three types if spina bifida? How do they differ from each other in
terms of pathoanatomy and signs and symptoms? How is each managed?
a. Spina Bifida Occulta
i. Congenital separation in one or more vertebrae, possibly resulting in
missing lamina or spinous processes.
ii. Usually no neurological involvement.
iii. Usually discovered on x-ray incidentally, and treated conservatively.
b. Meningocele (rare)
i. Missing part of vertebra creates an opening that the meninges pushes
through, creating a cavity that can be surgically removed since the spinal
cord did not develop into the cavity
ii. Little or no neurological involvement.
c. Myelomeningocele (open spina bifida)
i. Similar to meningocele, but there are several open vertebrae, and both
the meninges and the spinal cord are protruding through at birth (there
may be skin covering the sac).
ii. Must be fixed surgically, but even then very common to have
neurological impairment, such as muscle weakness/paralysis, B/B
problems, seizures, and various related orthopedic problems.
3. What are some of the visible manifestations of spina bifida occulta? What are
some of the treatment contraindications?
a. Over the particular vertebra there may be a tuft of hair, collection of fat, and/or a
small dimple/birthmark.
b. Electrical stimulation or ultrasound over the vertebra is contraindicated.
4. What is Bertolotti’s syndrome? What are the 3 potential pain generators in this
condition?
a. Congenitally one too many or too few vertebrae, usually in transition areas (CT,
TL, LS).
b. Most common at LS area, which may include sacralization, lumbarization,
spatulation with accessory joint, or fusion of TP to sacrum or ilium.

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 i. Fusion of two vertebrae puts more stress of the segment above, leading
to possible disc degeneration, facet syndrome on the side opposite of
fusion, and hypermobility.
c. Pain may be coming from the abnormal fusion/joint (transverse
mega-apophysis), disc degeneration of joint above, or facet syndrome of the
opposite sided joint.
5. What is the test and treatment if conservative care fails?
a. Anesthetic injection to the neo-joint to check for pain relief.

Riffa
b. If this relieves patient’s familiar pain, proceed with Rheumatoid Factor Neurolysis,
or surgical resection.
6. Bertolotti’s’ syndrome is usually asymptomatic. What subset of patients may be
more susceptible to having symptoms?
a. Patients under 30.
7. How might the syndrome influence CMT and the management of the patient?
a. Can start with a trial of adjusting, but this can irritate the joint more.
b. Must determine if adjusting that spot helps, or if you should focus adjusting above
or below.
c. Note: these patients often respond well to flexion-distraction therapy.
8. What is tropism? What is its potential clinical significance?
a. Developmentally asymmetrically facing facet joints.
b. Most asymptomatic, but may increase stress on disc and facet.
i. Symptomatic results in pain/dysfunction unilaterally.
c. Won’t x-ray patient to find these, but it may be an incidental finding on an x-ray.
i. Adjusting can jam the joints, so patients may not respond well to HVLA,
so you should stay away from that joint when it comes to adjusting.
9. What is Baastrup’s disease? Who usually gets it? What is the medical treatment
for it if conservative care fails?
a. Aka Kissing spinous syndrome.
i. Close approximation of adjacent SPs due to spondyloarthritis.
ii. Usually Dx is from imaging.
b. Mainly seen in those >70 years old.
c. Sx include midline LBP, worse with extension and pressure at the involved
segment, relieved with flexion.
d. Normally conservative care is enough, but can proceed with anesthetic injections,
or surgical excision of bursa or osteotomy.
10. Your patient tells you he thinks he felt a “bump” on his low back. He is worried,
wants to know if it is serious or could it become serious and what he should do.
You look and there appears to be lipoma at his sacral base. What are you going to
tell him?
a. Calmly reassure him that although it is a tumor, but it is not cancerous, will never
become cancerous, and it won’t get any larger.

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 b. He can have it removed surgically if he wants, or if it causes him any pain
(usually asymptomatic).
11. What is congenital blocked vertebrae? How about hemivertebra?
a. Congenital blocked vertebrae involves fusion of two or more vertebrae (more
severe fusion than in Bertolotti’s syndrome), resulting in extra stress and
degeneration on the segments above and below the fusion.
i. If the fusion is severe enough, there can be neurological involvement.
b. Hemivertebra results in a wedge due to one or more asymmetrical vertebral
bodies, resulting in a curvature in the spine away from the side of wedging.

Midterm Review Questions

1. Over the last few weeks, you have learned about a number of conditions affecting
the low back, most of which you will treat with manual therapy in the office. What
special advice were you given regarding how to apply the manual therapy or
precautions when doing so for the following conditions?
a. Lumbar disc derangement/herniated disc
i. Manipulation in directions that centralize pain, don’t make leg pain worse.
Find this by motion palpating and loading in end range. Can also do
flexion-distraction.
b. Spondylolisthesis
i. Avoid extension in set up, adjust in flexion vector, avoid P-A over slipped
vertebra if it is acute.
c. Piriformis syndrome
i. Be careful not to aggravate piriformis with a side posture set up.
d. Tropism
i. Might jam the joints together, so if patient isn’t responding or is increasing
pain, stay away from that joint.
e. Bertolotti’s syndrome
i. Flexion-distraction works best, but can do a trial of adjusting to see if it
helps. Might have to experiment with focussing on joints above or below
segment.
f. Spinal stenosis
i. Avoid adjusting in extension, focus on flexion adjustments, and on
flexion-distraction/neuromobilization.
2. What are usually considered the main ancillary tests of choice for:
a. Lumbar disc herniation
i. Start with x-ray, but then MRI. Most likely don’t need any imaging unless it
is a surgical case, progressive motor weakness, CES symptoms, or not
respond to care.
b. Occult spondylolysis

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 i. Start with x-ray, but then MRI (because no radiation) or CT (best at finding
occult fracture) or SPECT (can tell if the fracture is active/symptomatic).
c. Peripheral vs nerve root lesions
i. Nerve conduction.
d. Multiple myeloma
i. MRI.
e. Structural instability
i. Flexion/extension radiographs.
f. Leg length inequality
i. Scanogram.
g. Piriformis syndrome
i. Usually nothing.
h. Spinal infection
i. ESR, CBC, plain films, contrast MRI.
i. Spondylolisthesis
i. Lateral view plain films.
3. For each of the following findings, decide whether they support a spinal stenosis
diagnosis more strongly, a lumbar disc herniation diagnosis more strongly, or are
not particularly useful in differentiating between the two:
a. Positive SLR
i. Disc herniation.
b. Leg pain brought on by walking
i. If there is LBP and leg pain, spinal stenosis. But if the patient is older and
doesn’t have LBP, may be PAD.
c. Mannequin sign
i. Disc herniation because it takes tension off the sciatic nerve.
d. Age of the patient
i. A younger patient, disc herniation. A older patient, spinal stenosis.
e. Positive Romberg
i. Spinal stenosis.
f. Neurological deficits
i. Neither (could be present in either condition).
g. Back pain with lumbar extension
i. Possible spinal stenosis, but not very convincingly. Could be neither.
h. Leg pain with lumbar extension
i. Spinal stenosis.
i. Pain centralization with sustained end range loading of the lumbar spine
i. Disc herniation.
j. Patient stands with feet wide apart
i. Spinal stenosis.
k. Back pain increases rapidly with sitting
i. Disc herniation.
l. Cauda equina syndrome

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 i. Neither (could be present due to either condition).
m. Bilateral leg pain
i. Spinal stenosis.
n. Positive Valsalva
i. Disc herniation.

Midterm summary of poorly performing questions

I. Acute LBP
A. First line: NSAIDS, analgesics (acetaminophen), muscle relaxants
B. Second line: Tramadol (weak narcotic, then may move to stronger ones)
II. Chronic LBP
A. First line: NSAIDS, analgesics, muscle relaxants
B. Second line: antidepressants (duloxetine)
C. Third line: Tramadol (narcotics)
III. EMG and nerve conduction study is for treatment failure leading you to doubt where
the nerve damage really is.
IV. Strongest evidence against disc derangement (rules out)
A. SLR causes leg pain
B. Neurological leg pain
V. NOT evidence against disc derangement (does not rule out)
A. SLR causes low back pain
B. Inability to centralize leg pain
C. Negative Valsalva maneuver
D. LBP with extension
E. Flexion aggravates LBP
VI. Psoas Syndrome: the psoas doesn’t hurt, it is the low back that hurts (the TL junction).
A. We might stretch/relax the psoas, but we first target the pain generator which is
done by adjusting the TL junction.
VII. Central sensitization can lead to deep referred pain, allodynia, and spontaneous pain
even after the injured tissue has healed (chronic pain syndrome).
A. This is why 10% of people with LBP go on to have severe, chronic LBP.

Thoracic Spine Diseases (based on lecture and powerpoint slides)

1. What are the referral location for the following: heart attack, esophagitis,
gallbladder disease, pancreatitis, and an ulcer.
a. May be abdominal/chest pain, or only referral to the back.
i. Not made worse by coughing/deep breathing.

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 ii. NMS exam normal.

2. What are the chances of getting shingles in your lifetime?

a. 1 in 4 (25% chance).
3. Describe the sequence of events as shingles presents.
a. Presents as painful, usually unilateral, dermatomal rash.
b. Itching/tingling with pain 1-5 days before blisters emerge.
c. Rash lasts 7-10 days, a few days later become yellow, flatten, and dry out (scab
over and may leave scarring/loss of skin pigment).
d. Complete healing: 2-4 weeks.
e. Contagious until all blisters have scabbed over.
4. What is postherpetic neuralgia? How does it present? How long does it last? Is
there a way to decrease the chances of getting it?
a. Development of PHN is a complication of shingles, presenting with severe pain
AFTER the rash disappears.
b. Lasts for weeks, months or years.
c. Acyclovir (antiviral) can shorten duration of shingles and lower risk of PHN.
5. What is a home care treatment for shingles? What are the medical options?
a. Home: cover rash with clothing, calamine lotion to reduce itching.
b. Medical: Paracetamol, ibuprofen, codeine.
i. Patients >50 should get vaccine.
6. How quickly must a patient take an antiviral for it to be effective?
a. Within 72 hours of onset.
7. How often does breast cancer metastasize to bone? What kind of effect does it
have on bone? What do you suspect would be the changes in a blood chemistry
panel that you would see?
a. 1/9 women will develop breast cancer.

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 b. >60% survive, but 50% of survivors will later have metastasizing cancer.
c. 40-60% will metastasize to bone.
d. 25% of women who die from breast cancer are due to recurrence of cancer.
e. On x-ray it appears osteolytic.
i. Therefore will likely be elevated blood calcium and ALP.
8. Describe the type of patient that might be at most risk for a spinal hematoma.
a. >50 y/o and taking anticoagulants.
i. However, can also be do to coagulopathies, epidural injections, or
mechanical parts for lumbosacral spinal fusion.
b. Hematoma is usually in thoracic spine (2-4 segments), but patient presents with
leg symptoms.
c. Dx using MRI.
9. Who tends to get Scheuermann’s disease?
a. Men more commonly than women, going through puberty (13-17).
i. Most often presents in thoracic spine over thoracolumbar (75% vs 25%).
ii. 30-40% have associated scoliosis.
iii. Prevalence: 4% clinical Dx, 8.3% radiographic Dx.
10. What are spinal changes that occur?
a. Progressive structural thoracic or thoracolumbar hyperkyphosis.
i. Most common cause of kyphosis in pediatric population.
b. Calcification of vertebral epiphyses, leading to:
i. Vertebral endplate notching.
ii. Vertebral body wedging (leads to hyperkyphosis).
c. Possible causes of Scheuermann’s Disease include:
i. End plate trauma
ii. Heuter-Volkmann Principle (increased axial compression inhibits growth
of epiphyseal plate, the opposite of Wolf’s law)
iii. Malnutrition
iv. Osteoporosis
11. What degree of thoracic hyperkyphosis is problematic?
a. >40-45 degrees (disagreement on exact number).
12. What happens to prominent hyper kyphotic deformity in Scheuermann’s disease
when the patient hyperextends?
a. The hyperkyphosis does not disappear!
13. Describe the elements of the neurological exam that should be done for a patient
with Scheuermann’s disease. Be specific (i.e., what and where).
a. Need to look for evidence of spinal cord involvement (UMNL).
i. DTRs (hyperreflexia)
ii. Pathological reflexes (appearance)
iii. Superficial abdominal reflexes (disappearance)
iv. Presence of hypertonia and weakness (spastic paralysis)
v. Lower extremity sensory loss
vi. Altered sphincter function (B/B problems)

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 b. Also can have patient lie supine with a foam roller under the apex of the
deformity to see how reducible the curve is (hyperkyphosis decreases).
14. What are key elements of the conservative management plan? Include details
regarding the manual therapy and any precautions.
a. Bracing/casting, and physical therapy.
b. CMT: Promote extension, traction/distraction.
c. STM: Reduce myospasms, stretch hamstrings (however, this may aggravate
symptoms).
d. BM: Postural training, and when acute, limit weight bearing and contact
sports.
e. EX: Home exercises to enhance extension and core strength.
i. Combination of manual therapy, Mckenzie, and Brugger exercises have
been found to reduce pain by 16-32%.
15. What are the indicators that surgery might be a better first choice for the patient
with Scheuermann’s disease as opposed to conservative care?
a. Only consider conservative care when:
i. Hyperkyphosis >40 but <60 degrees.
ii. Curve is reducible.
iii. Patient still has >1 year of spinal growth (based on radiographic
findings).
b. Otherwise surgery is the better initial treatment choice.
16. Cite some indications (i.e., different patient scenarios) for getting x-rays to rule
out a possible osteoporotic fracture.
a. Trauma with sudden pain and snapping sound.
b. Patient >70 y/o with sudden, non-traumatic LBP.
c. Patient >50 y/o with low or moderate load, especially if menopausal or
osteoporotic.
17. What is paralytic ileus? Is it common with compression fractures? How long does
it last? How is it managed?
a. A temporary stoppage of intestinal peristalsis, experienced by almost all
compression fracture patients.
i. Patient presents with constipation.
b. Usually lasts 2-3 days.
c. Tell patient to reduce solid food intake, go on a liquid diet.
18. How else might the patient present if they have a compression fracture?
a. Remember that a TLJ compression fracture (most common location) will refer
pain to the iliac crest area, similar to Maigne’s Syndrome, only here you wouldn’t
adjust the TLJ.
b. Associated osteoporosis may be caused by corticosteroid use for 6 months,
leading to rapid bone loss from hip, spine, and forearm.
c. ⅔ of compression fractures are never diagnosed (patient thinks the back pain
is a sign of aging/arthritis).
d. Aggravated by standing, walking, activity.

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 e. Relieved with rest or lying down.
19. In a suspected compression fracture, what exam procedures should you do and
what would be the findings?
a. All AROM decreased and painful (flexion the worst, maybe standing straight).
b. Muscle guarding.
c. Tender/sharp palpation.
d. (+) Spinal percussion.
e. Neurological exam to rule out nerve root or spinal cord damage.
f. Do not perform joint plays or orthopedic tests before taking a radiograph if
you suspect fracture.
20. Are most compression fractures stable or unstable? What is the general
management strategy? When is surgery indicated? What is a common type of
surgery for a compression fracture?
a. Most stable and will heal on their own.
b. Refer to orthopedist, but usually as legal protocol, since management is usually
conservative.
i. Collapse >50% is surgical, <50% responds to conservative care.
c. Treat resulting joint dysfunction and myospasm AFTER acute phase, avoiding
the fracture.
i. Restrict food intake (due to paralytic ilieum).
ii. Ice to reduce inflammation.
iii. OTCs or PT to control pain.
iv. May consider STM to reduce muscle spasm, but may be detrimental if
muscle guarding is stabilizing the fracture.
v. Only unstable fractures require immobilization.
d. Advise patient in “active” rest:
i. Two weeks w/ little weight bearing.
ii. Followed by 1 month of conservative movement.
iii. 3 months with no lifting.
e. Surgery involves making a small incision in the collapsed vertebra, inserting and
inflating a balloon, and then filling the resulting cavity with a bone void filler.
21. How long before the fracture heals?
a. 90 days.
b. All the while, you should be on the lookout for an underlying disease as the
cause of the fracture (multiple myeloma, cancer, or hyperparathyroidism.
c. Retake radiographs after this period to confirm.
22. What occurs in osteoporosis?
a. Loss of cortical bone thickness, and loss in number and size of trabeculae.
b. Most common metabolic bone disorder.
c. Patient may present with LBP being caused by microfractures in the cancellous
bone due to osteoporosis.
d. Many diseases increase the risk for osteoporosis.

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23. What is the usual screening test for osteoporosis? Why are radiographs not a
good choice?
a. Before deciding to screen them, must decide if they are at risk due to an
epidemiological factor, health status, nutritional status, disease process, or other
cause.
b. Bone density test = Densitometry (DEXA) or Quantitative CT (QCT).
c. X-rays cannot detect bone loss until 30-50% loss in bone density.
24. Basically what is the difference between osteopenia and osteoporosis?
a. Categorization of osteoporosis is by T-Score based on number of standard
deviations the patient is away from the average bone density of a young adult.
i. Normal: >-1
ii. Osteopenia: <-1 and >-2.5
iii. Osteoporosis: <-2.5 (no fractures)
iv. Established Osteoporosis: <-2.5 (with fractures)
25. What are the major goals and some of the interventions for patients with
diagnosed osteoporosis?
a. Assess risk for falls and resulting fracture:
i. Strength testing (grip, quads, ankle).
ii. Wall sit/slide test.
iii. Abdominal strength evaluation.
iv. Muscle tightness.
v. Spinal palpation for joint dysfunction.
b. Manage predisposing medical conditions:
i. Regularly review medications.
ii. Estrogen replacement therapy.
iii. Medical therapies.
c. Reduce fall risk:
i. Vision correction.
ii. Home safety check.
iii. Wear supportive, rubber-soled, low-heeled shoes. Avoid walking in socks
or slip-on slippers.
iv. Advise on side effects of prescriptions, OTCs, and intake of alcohol.
d. Optimize strength, balance, flexibility:
i. Muscle strength exercises.
ii. Balance and gait training.
iii. Weight-bearing exercise to tolerance.
iv. Joint manipulation and STM as needed.
e. Improve nutrition:
i. Moderate protein intake.
ii. Restrict alcohol, salt, and smoking.
iii. Micronutrient support.
26. What is the current evidence on the role of supplementation with Vitamin D and
calcium?

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 a. No significant association of calcium or vitamin D or combined
supplementation with reduced risk of hip fracture compared to placebo or
no treatment.
b. There are still benefits to vitamin D/calcium, like reducing risk of developing
osteoporosis, but not for reducing risk of fracture.
27. Are there any precautions regarding manual therapy for patients with
osteoporosis?
a. Advise patient of the increased risk of fracture manual therapy has when used on
patients with osteoporosis.
b. Assure them and chart what you will be doing differently to minimize risk (like low
force mobilization).
c. Chart the grade of mobilization.

Thoracic Spine Injuries & Conditions (based on lecture and

powerpoint slides)

1. What three types of nervous tissue lesions can occur due to injuries and
conditions of the thoracic spine? Give some common diagnostic causes for each
of these.

a. Nerve root
i. Stenosis
ii. Tumor
iii. Disc herniation
b. Intercostal nerve
i. Trauma
ii. Neuritis
iii. Shingles
c. Thoracic cord
i. Stenosis
ii. Tumor
iii. Disc Herniation
d. Note: these DDx are listed in order of most to least common.
2. What finding during sensory testing of the torso would be strongly suggestive of a
significant spinal cord lesion?
a. Loss of sensation bilaterally below the level of the lesion.
i. Horizontal band below which no sensation is left.
b. Common thoracic dermatome landmarks:
i. Nipples at T4.
ii. Xiphoid process at T7.
iii. Umbilicus at T10.

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3. In someone with a transection of half the spinal cord creating a Brown Sequard
syndrome, what areas would there would be reduced pain and temperature,
reduced vibration, spastic paralysis and flaccid paralysis?
a. Ipsilateral flaccid paralysis at the segmental level of the transection, with
ipsilateral spastic paralysis everywhere below that segment, all the way down
the extremity.
b. Complete ipsilateral sensory loss at the segmental level of the transection,
with ipsilateral loss of proprioception, vibration, and fine touch everywhere
below that segment, and contralateral loss of pain and temperature
everywhere below that segment.
4. What does a positive Beevor’s sign look like? Where in the nervous system could
the lesion be? Be as specific as you can.
a. Patient does a sit up, and the umbilicus deviates away from paralyzed
abdominal muscles.
b. If there is a complete spinal cord transection, the umbilicus will deviate
upward towards the strong muscles and away from the inferior paralyzed
muscles.
c. If there is a nerve root or partial spinal cord injury, the umbilicus will deviate to
the right or left, away from the side of the lesion (away from the weak muscles).
5. What does a normal superficial abdominal reflex look like? Where in the nervous
system could the lesion be that would make the reflex absent?
a. Scratching the skin in one of the 4 quadrants surrounding the umbilicus, normally
umbilicus should deviate towards the stimulus.
b. A (+) finding is if there is no muscle movement/umbilicus deviation.
c. A UMNL is suspected if there is bilateral loss of reflex.
d. A LMNL is suspected if there is unilateral loss of reflex.
6. Using the 5 clues that you always look for to detect neuropathic lesions, predict
what the findings would be for each one if your patient had thoracic myelopathy.
a. Might have generalized leg pain, maybe soles of the feet. Usually burning
quality, but the back pain is usually worse.
b. Might be non-dermatomal paresthesia, but more commonly just sense of
numbness.
c. UMNL signs, +Romberg, +Beevor’s, loss of superficial abdominal reflex, loss of
contralateral pain/temperature, loss of ipsilateral proprioception, vibration, fine
touch.
d. Negative nerve tension tests.
e. Negative spinal loading tests.
7. How common are thoracic disc herniations? At what levels are they usually
located at?
a. Extremely rare (1 in 1 million per year), only 0.25-0.75% of symptomatic disc
herniations.
b. 75% between T8-T12 (most T11-T12).
c. Neurologic deficits rare.

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8. Contrast the presenting symptoms between central and centrolateral protrusions.
a. Central protrusions may compress the spinal cord (UMNL signs).
i. 2% of disc patients will have B/B issues.
ii. If multiple intercostal levels lose sensation, think cord instead of nerve
root.
b. Centrolateral protrusions may resemble Brown-Sequard syndrome.
i. Ipsilateral weakness, ipsilateral sensory loss, contralateral
pain/temperature loss.
9. Cite some of the neurological findings that may occur with a lateral thoracic disc
herniation.
a. Numbness or paresthesia (presenting symptom 25% of the time) along
intercostal spaces.
b. Possible loss of superficial abdominal reflex, or + Beevor’s sign.
10. What is a Schmorl's node? Is it usually symptomatic?
a. Herniation of nucleus pulposus into the vertebral endplate above or below.
b. Usually asymptomatic, but possibility for severe pain from inflammatory
reaction.
11. What are the indications for surgery for a thoracic disc herniation? In general,
what other medical treatment can be tried before surgery?
a. Conservative care is similar to lumbar disc herniations (80% of patients return to
previous activity level).
b. Myelopathic signs indicate need for surgery.
c. In patients who have not responded to conservative care but are experiencing
severe pain, can try thoracic epidural steroid injections before surgery.
12. Your patient has had trauma and now has thoracic pain. What is on your DDX list?
Be as complete as you can be.
a. Thoracic sprain/strain
i. Uncommon.
ii. Strains usually involve middle and upper trapezius caused by unilateral
lifting.
iii. Sprains usually involve rib cage, costovertebral and costotransverse
joints, and anterior costal cartilages.
b. Facet syndrome
c. Disc derangement
d. Spinal fracture or contusion
e. Rib fracture
f. Costovertebral sprain
i. Caused by sudden spinal rotation or extension.
ii. Pain aggravated by breathing/coughing.
iii. Must rule out fracture.
g. Intercostal strain causing intercostal neuritis
i. Strain is a common cause of intercostal neuritis/neuralgia.

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 ii. Strain irritates or entraps spinal nerve, causing severe pain along the
ribs.
iii. May also be caused by post herpetic neuralgia, pregnancy (rib cage
expands to make room for fetus), rib infections or osteomyelitis, tumors
pressing against intercostal nerves, or surgery in or around thoracic
cavity.
13. What are three injuries/diagnoses that can happen to ribs? What are some of the
signs and symptoms that are common to all three conditions?
a. Fracture
i. Onset from trauma (MVA, slip and fall, sports injury) or repetitive
activities (rowers, golfers, etc).
ii. May be secondary to osteoporosis (triggered by coughing).
iii. Pain aggravated by breathing/coughing.
iv. Painful palpation, percussion, tuning fork.
b. Rib sprain or joint dysfunction
i. Due to trauma or overuse.
ii. Pain is sharp, point sensitivity over injury.
iii. Pain aggravated by breathing, worse with deep breathing.
iv. Joint dysfunction: manipulation effective but painful.
v. Sprain: use kinesio tape, but not bracing.
c. Common to all three:
i. Caused by trauma or overuse.
ii. Pain worsened with breathing.
iii. Tender to palpation.
14. How long can it take for a small fracture of the ribs to show up on radiographs?
a. Hairline fractures may take up to 3 weeks to show up on x-ray.
b. Displaced fractures should be more apparent immediately.
c. Will start with AP and lateral radiographs, and can graduate to CT (more
accurate).
i. If initial x-ray is inconclusive, follow up with either another x-ray in 3
weeks, or immediate CT.
15. What are some serious complications of a rib fracture to be aware of and how
would they drive some of your choices regarding physical examination and
ancillary tests?
a. Displaced fractures may puncture:
i. Lung: patient SOB or cough - screen with lung auscultation.
ii. Kidneys: patient has hematuria - screen with UA.
iii. Spleen or Liver: patient in shock due to blood loss - palpate abdomen,
take BP.
16. How long does it usually take a rib fracture to heal? What are the key points of
management? What is the role of a rib belt?
a. Most heal within 6 weeks.
i. Most able to resume ADLs sooner.

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 b. Need to control pain to prevent pneumonia (via splinting/atelectasis).
c. Prevent atelectasis using incentive spirometry aids.
d. After at least 3 days past onset, patient can use rib belts/binders to lessen pain
(earlier use may increase risk of pneumonia).
i. Pain control also in non-acute phase, but still poses risk of atelectasis and
pneumonia.
e. Patient needs to carry a pillow around with them to clutch while coughing
or sneezing to protect ribs.
17. How will a thoracic facet syndrome present? How is it managed if it is
unresponsive to conservative care or analgesics?
a. Less common than lumbar or cervical facet syndrome, but similar findings:
i. Most pain over facet.
ii. Aggravated by extension, extension + rotation.
b. The thoracic facet joint is the source of upper and mid back pain 34-48% of the
time.
c. Treat unresponsive facet syndrome with:
i. Thoracic Medial Branch nerve Block or Radiofrequency Neurotomy.
ii. Intra-articular steroid injection.
18. Where might a patient feel pain in an anterior disc derangement? Lateral
derangement? Posterior?
a. First of all, the thoracic disc is an uncommon source of pain. When there is pain,
>50% of the time the disc had annular tears without significant herniation.
b. For any derangement, pain may be retrogastric, retrosternal, or inguinal
(mimicking cholecystitis, MI, hernia, or nephrolithiasis).
c. Anterior: pain referral to ribs, chest wall, sternum, or viscera.
d. Lateral: pain referral may be visceral or musculoskeletal.
e. Posterior: back pain, locally or diffuse.
19. Cite a number of different factors that can lead to a hyperkyphosis.
a. Forward head carriage
b. Protracted shoulders
c. Slumping
d. Rounded shoulders
e. Upper crossed syndrome
f. Large breasts
g. Very tall individual
h. Structural hyperkyphosis
i. Any of these may cause a postural sprain, which is associated with:
i. Joint dysfunction in Tx, ribs, or SC joint.
ii. Headaches
iii. MFTPs
20. What are the components of an upper cross syndrome?
a. Weak or inhibited:
i. Deep neck flexors

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 ii. Mid/lower trapezius and serratus anterior
b. Tight:
i. Pectorals
ii. Upper trapezius and levator scapula
21. What is the pathophysiology behind a scapulocostal syndrome? What are some of
the key symptoms and physical exam findings?
a. Traumatic or mechanical irritation to soft tissues in the scapulocostal
interspace.
i. Increased friction due to decreased viscosity of serous fluid within
bursae.
b. Local pain along vertebral border and deep to scapula, referred pain down
posterior shoulder/arm.
c. Dysesthesia common in arm/forearm.
d. Painful and decreased shoulder abduction.
e. MFTP and tenderness along vertebral border.
f. Costotransverse joint dysfunction.
22. What are the components of a SICK scapula?
a. Scapular malposition.
i. Usually protracted/forward tilted.
b. Inferior/medial border winging.
i. Due to tight pecs with weak serratus anterior or middle trap.
c. Coracoid tenderness.
i. Tight pec minor.
d. DysKinesis.
i. Abnormal shoulder abduction movement pattern.
23. What are the specific examination procedures and findings that would support the
assessment of a SICK scapula?
a. Posture evaluation
i. Scapula malpositioned forward and protracted.
ii. Inferior angle winging.
b. Palpation
i. Coracoid tenderness.
c. Shoulder abduction assessment
i. Early or late scapula movement.
24. What causes a snapping scapula? What is the medical treatment?
a. Cause may be bony or soft tissue, causing crepitus between the scapula and rib
cage.
b. May be caused by bursitis.
c. May result in scapular dyskinesis.
d. Treatment first involves strengthening of serratus anterior and middle trap. Better
is prolotherapy injections to heal damaged soft tissues, like ligaments.
25. What are the two main components of a T4 syndrome? Cite some signs and
symptoms for each component.

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 a. Joint dysfunction around T4.
i. Joint dysfunction may also be present at rib angles, there may be
interscapular pain/stiffness, cervical/trunk AROM should be pain free.
b. Glove paresthesia in UE(non-dermatomal).
i. Paresthesia should be in whole hand/fingers and forearms, heavy UE
feeling.
ii. Worse at night or in morning (may wake the patient up).
iii. Shaking arm may relieve symptoms.
iv. Pain is more generalized that paresthesia.
v. Raynaud’s phenomenon.
c. Commonly there is a headache in a general, bilateral helmet distribution.
d. Patient may complain of grip weakness, but SMRs are normal.
e. T4 syndrome most often affects:
i. Women > men (4:1)
ii. 30-50 y/o
iii. Associated with frequent sitting in front of a computer.
26. What is the theory as to how a T4 syndrome causes arm symptoms?
a. Sustained or extreme postures lead to ischemia within multiple tissues,
contributing to symptoms of sympathetic origin.
i. The SNS is a pathway for symptom referral from upper thoracic spine to
head/UE.
ii. If the symptoms were originating in SNS, the presentation would be very
different.
27. What is the basic treatment approach to a T4 syndrome?
a. Postural exercise and education.
b. CMT and self-mobilization of upper thoracic spine.
c. STM of hypertonic muscles in CT region.
d. Exercises to strengthen scapulothoracic musculature, and to stretch tight pecs
and upper trap.
28. What is Raynaud’s Phenomenon? What is the difference between primary and
secondary Raynaud’s? How is it treated?
a. Vasoconstrictive disease of distal extremities, often provoked by cold or
emotional stress.
i. Usually hands/fingers, but also possible in feet/toes, nose, ears.
ii. Sequential discoloration (white>blue>red).
iii. Lasts minutes to hours.
iv. Sensation of numbness, swelling, tingling, and possibly pain or
throbbing.
v. Females 9x more common than males.
b. Primary:
i. Most common.
ii. May be symmetrical bilaterally.

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 iii. Etiology unknown, possible familial, but contributed to by smoking,
stress, tight clothing.
iv. Benign.
c. Secondary:
i. Caused by a preexisting connective tissue disease (scleroderma,
Sjogren’s syndrome, lupus, RA), or trauma, or an autoimmune disease.
ii. More likely to experience serious complications: trophic changes, skin
ulcers, gangrene.
iii. Migraines may be part of disorder.
iv. May develop alongside HTN meds, narcotics, or prolonged use of
vibrating tools.
d. Treatment:
i. Stress management.
ii. Stay warm, proper nutrition, heat or chiropractic treatment, movement.
iii. Avoid triggers like smoking/cold.
iv. Determine if caused by a secondary disease needing referral to
rheumatologist.

Scoliosis (based on lecture and powerpoint slides)

1. What is scoliosis? How is the scoliosis named? What is the common cause of
functional or structural scoliosis?
a. Spinal buckling most commonly into a lateral deformity, but can be into lordosis,
or rotation and torsion.
i. Lateral deformity isn’t necessarily the major determinant of progression.
b. Named according to the direction the convexity of the curve.
i. When there is a double curve, we name it based on the the curve with
the larger Cobb angle.
c. Caused by aberrant or misinterpreted sensory information (in spinal cord or
in brain).
i. Leads to inappropriate output response to proprioception.
ii. More common with familial occurrence.
2. What are causes of functional scoliosis?
a. Compensatory
i. LLI
ii. Pelvic subluxation
iii. Anatomical asymmetry
iv. Must rule out short leg - if pelvis levels and curve improves when sitting,
think LLI.
b. Postural

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 i. Muscular imbalance
ii. Handedness (not reliable)
c. Transient
i. Antalgic
ii. Inflammatory
iii. Traumatic
iv. Psychogenic
v. Radiculopathy
d. There are also various “chiropractic” theories.
3. What is the most common cause of structural scoliosis?
a. >80% are idiopathic.
b. Tends to appear at puberty (growth spurt or menarche).
i. Boys 11-16.
ii. Girls 10-12.
c. We want to know if the scoliosis has come on acutely or slowly progressing, if
there is any pain, or any associated muscle spasm (like due to a tumor or
fracture).
d. NOTE: Unless a curve is severe/progressive, be cautious labeling curves as
scoliosis.
4. Since pain is not usually a main complaint, what should you consider if the
scoliosis is accompanied by severe pain?
a. Pain is usually not a main complaint.
i. 25% will have mild, benign pain.
b. Severe pain (aka affecting sleep or daily function) alerts us to search for a
disease process:
i. Spinal infection
ii. Spinal tumor
iii. Chiari type 1 with syrinx
iv. Tethered spinal cord
5. What are the 5 things to include in your physical exam assessment of scoliosis?
a. Observe
i. Check for other associated deformities, neurofibromatosis, or spina bifida.
b. Postural assessment
i. Chest asymmetry
ii. Plumb line (optional)
iii. Shoulder/hip height
iv. Scapular winging
c. Adam’s Test
d. Check leg length
e. Neurological exam
i. Looking for weakness, spasticity, abnormal sensation, abnormal reflexes
→ may indicated tethered cord syndrome or syringomyelia.

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6. What is Adam’s test, how is it performed, how is it interpreted, and how does it
affect management?
a. Have patient bend over to touch their toes, look for a
paralumbar prominence or a rib hump on the side of
scoliosis convexity.
i. If the prominence improves when Adam’s test
is done seated or lying down, the scoliosis is
functional!
ii. This would mean we then look to treat the pelvis
and/or LLI that is causing the functional scoliosis.
b. During Adam’s test you can measure the prominence
using a scoliometer.
c. >7 degrees = scoliosis (ORDER AN X-RAY!)
d. <7 degrees = follow up in 6-12 months.
7. What radiographic views are recommended? How do you measure a cobb angle?
Without consulting your notes, draw the lines on the picture provided necessary
to create the angle that needs to be measured.
a. Full spine and lateral bending into convexity.
i. Measure Cobb angle, check for rotation using
Nash-Moe method, assess bone age with Risser
sign, check for pelvic unleveling, and look for
congenital causes (hemivertebrae).
b. Measured by drawing one line across the top of the superior
vertebral segment, and another across the bottom of the
inferior segment. Perpendicular lines to these two lines
intersect to form the Cobb angle.

8. What is the minimum Cobb angle to be considered evidence of scoliosis?

a. 10 degrees.
9. Does it matter what time the radiographs are taken during the day? Why?
a. Yes, because there is an average difference of 5 degrees between AM and PM
measuring (10-20 degrees in some people.
b. Take the radiographs at the same time every time.
10. What are some key risks for curve progression?
a. Likelihood of structural scoliosis being progressive is 0.2%!!!
b. Female with early onset (11-15 y/o)
i. Before menarche: 50% risk of progression
ii. After menarche: <20% risk of progression
iii. Males less likely to have progressive scoliosis.
c. Before puberty with Risser grade <2.
d. Large curve

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 e. Family history
f. Right sided thoracic curve
g. Marked rotation
h. L5 high in pelvis, or iliac crest line above L4/L5 disc space
i. Double curve
j. Thoracic spine hyperkyphosis
k. Curves >50 degree Cobb angle w/ rotation >30 degrees.
i. This one makes progression into adulthood, after skeletal maturity, more
likely.
11. How is the Risser grade determined? How is it interpreted?
a. Measured by the degree of
ossification/fusion of the iliac
crest epiphysis to the rest of the
ilium.
b. The greater the fusion, the
greater the risser value, the more
skeletal maturity.
c. Risser grade < 3 is considered
pretty immature bone.

12. Besides idiopathic, what are some of the classifications (i.e., causes or types) of
structural scoliosis?
a. Acquired/traumatic
b. Neoplasm
i. Osteoblastoma (malignant) or Osteoid osteoma (benign)
c. Metabolic
i. Rickets, osteogenesis imperfecta
d. Neuromuscular
i. Neuropathic scoliosis
e. Neurofibromatosis
f. Mesenchymal disorders
i. Congenital or acquired.
ii. Marfan’s Syndrome: tall, thin, high arm span to height ratio.
iii. Ehlers-Danlos Syndrome: loose skin, joint laxity.
iv. BOTH HAVE INCREASED RISK OF STROKE FROM MANIPULATION!!
g. Other (Scheuermann's)
h. Congenital
i. Hemivertebrae, spina bifida, dwarfism, congenital rib fusion, sprengel’s
deformity, klippel feil, marfans, ehlers-danlos, lipomas, cafe au lait spots,
club foot, congenital dislocated hip….
ii. 20% have GU abnormalities, 15% have heart defects.

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 i. Idiopathic
13. How does an osteoid osteoma present?
a. Pain worse at night.
b. Relieved by NSAIDs.
14. What are some causes of neuropathic scoliosis? Be specific.
a. LMNL (polio)
b. UMNL (tumor, cerebral palsy)
c. Syringomyelia (syrinx)
d. Cord trauma/disease
e. Progressive left thoracic primary curve may indicate neuropathic scoliosis.
15. What is the significance of a left primary thoracic curve?
a. >90% of curves are to the right.
b. A left curve is more likely to be caused by a disease process!
16. What are some indications for ordering an MRI for a structural scoliosis?
a. Severe or progressive curve
b. Left thoracic curve
c. Patient <11 y/o
d. No family history of scoliosis
e. Neurological abnormalities
f. Radiographic findings
g. Painful, unresponsive to treatment
17. What are the 3 types of idiopathic scoliosis?
a. In idiopathic scoliosis, vertebrae rotate into convexity (SP deviated toward
concavity).
i. Remember, 80% of structural scoliosis is idiopathic.
b. Infantile: before age 3 - 80-90% resolve spontaneously.
c. Juvenile: age 3-10 (or puberty onset) - more worrying, may be very
progressive.
d. Adolescent (AIS = Adolescent Idiopathic Scoliosis)
18. What is the most common type of idiopathic scoliosis? What age groups?
a. AIS (2% of scoliosis)
b. Age 10-18 (or skeletal maturity)
19. What sex is most common to have AIS? What curve is most common in this
group?
a. Most common in women.
i. Most likely a genetic predisposition.
b. Right thoracic curve is most common.
20. What are the ages and timing to screen for AIS?
a. NOT AN X-RAY SCREEN! This is a scoliometer screen!
b. Twice for girls (At 10 and again at 12).
c. Once for boys (13-14).
21. What is the overall treatment goal in terms of limiting curve progression?
a. Keep scoliosis <50 degrees by skeletal maturity.

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22. What are the 4 main factors that affect treatment decisions?
a. Cobb angle
b. Age/Riser grade
c. Symptom severity (or nerve involvement)
d. Speed of progression
23. What are the 3 main treatment objectives?
a. Improve strength and flexibility.
i. Improve ROM towards convexity.
ii. Improve strength, endurance, and postural control of convex muscles.
iii. Stretch and relax concave muscles.
b. Improve motor control.
i. Improve vestibular and proprioceptive deficiency.
ii. Improve balance and coordination.
iii. Improve vestibular-visual integration.
c. Normalize biomechanics.
i. Improve SROM.
ii. Normalize LE weight bearing.
iii. Correct forward head carriage/upper crossed syndrome.
d. With any condition: what is the treatment objective, and what treatments
are needed to reach that objective?
24. How does scoliosis affect breathing?
a. 60% of curves >60 degrees have decreased vital capacity.
b. Teaching patient breathing exercises is associated with a 20% increase in chest
expansion, and increased vital capacity.
25. In general, about how often should the patient under care for AIS come back to
monitor curve progression?
a. <10 degrees
i. Not considered scoliosis, follow up every 6 months until skeletal maturity.
ii. Treat patient when symptomatic, treat functional scoliosis components,
CMT/STM/exercises when appropriate, educate patient and parents
about possibility of progression.
b. 11-20 degrees
i. Monitor every 3-6 months with neuro/ortho evaluation + radiographs.
ii. Watch for significant progression (5-6 degrees) → if noted and bone age
still young, refer for bracing.
iii. Continue treatment until skeletal maturity.
c. 21-30 degrees
i. Monitor every 3-6 months (neuro/ortho + radiographs) until skeletal
maturity.
ii. Intensify chiropractic management, including exercises, home regimen,
co-management with orthopedist.
iii. If 25-30 degrees (or >20 degrees according to Canadian guidelines),
OR Risser grade <3, OR rapid progression, refer for bracing!

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 d. 30-40 degrees
i. Monitor every 3-6 months as clinically indicated.
ii. Brace and co-treat.
iii. Same chiropractic treatment.
iv. If bracing has not yet been done, consider if there is >5 degrees of
progression in one year + at least 1 year of bone growth remaining.
v. Adults in this range should continue to be monitored.
e. 40-50 degrees
i. Evaluate risk factors for progression.
ii. Gray zone: bracing may not be effective, surgery may not be necessary.
iii. Monitor every 3-6 months, co-treat, periodically monitor adults in this
range.
iv. Refer for surgery if: >45 degrees + Risser grade < 3, OR >50 degrees.
f. >50 degrees
i. Surgery more likely necessary, refer for surgical consultation
regardless of other factors.
ii. Bracing/support can help relieve symptoms in adults.
iii. Chiropractic treatment still indicated in reducing symptoms, improving
function, and increasing successful outcome of surgery.
iv. More likely to continue progressing (0.5-1 degree per year or more).
v. Respiratory difficult more likely.
26. At about what Cobb angle is should the patient seek a surgical consultation?
a. >45 degrees + Risser grade < 3, OR >50 degrees.
27. What is recommended when deciding which direction to adjust the spine?
a. Adjust INTO the convexity!
i. Ex. A right scoliosis means you should adjust L-M on the right side.
28. What are some examples of specific exercises that would be aimed at the concave
side vs the convex side of the curve? What about deciding on rotational
exercises?
a. Stretch concave side
i. Lay side posture with pillow/roll/balance ball under the apex of the convex
side.
b. Strengthen convex side
i. Lay side posture on the opposite side (concave side on the floor) and do
trunk raises
c. Can also do neutral spine trunk exercises, and rotation exercises to the side
opposite the convexity (usually to the left).
29. Besides ROM, strengthening and stretching exercises, what other type of
exercises would be a key element of any management plan?
a. Main goal is preventing progression, lucky if we can reverse scoliosis.
b. Rocker board, one legged proprioceptive training.
c. Balance ball exercises to improve proprioception, re-educate CNS.
d. Heel lift to balance weight bearing (not pelvis leveling).

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 e. If there is pelvic unleveling, consider exercise program:
i. Elevated right ilium (due to short left leg): strengthen left QL, stretch
right QL.
f. Can use Electrospinal Muscle Stimulation to re-establish muscle
proprioceptive balance.
30. What are some of the types of braces used for scoliosis patients?
a. 93% of patients with scoliosis who braced for 23 hrs/day had a successful
outcome.
i. In general, effectiveness increases with number of hours worn.
ii. Quality of evidence is low.
b. Milwaukee Brace
c. Boston Brace (most commonly used)
d. Charleston Bending Brace
e. Copes Brace
f. SpineCor Dynamic Brace
g. Braces recommended for curves 25-45 degrees.
h. Need to educate patients that braces will help prevent progression, but not
reverse/improve the curve cosmetically.
31. Describe the typical surgical treatment.
a. Spinal fusion using bone grafts + Harrington rods.
b. Greatly decreases deformity.

Cervical Diseases/Red Flags Part 1 (based on lecture and

powerpoint slides)

1. How much unexplained weight loss over the period of 3 months might be a red
flag in a typical patient?
a. 10 lbs or more.
2. For each of the following, indicate what type of disease or disease process might
concern you?
a. Prior history of cancer
i. Recurrence of cancer.
b. Unexplained weight loss
i. Cancer, infection, autoimmune/inflammatory disease.
c. Symptoms not influenced by rest or activity, same during the day/night (or
worse at night)
i. Cancer, infection.
d. Sharp, severe, intolerable pain
i. Cancer, infection.

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 e. Fever/chills
i. Infection.
f. Recent bacterial infection, or history of recurrent infections
i. Spinal infection.
g. Pain unimproved with 1 month of treatment
i. Cancer, infection, inflammatory disease.
h. Multiple extra-spinal joint involvement
i. Autoimmune/inflammatory disease.
i. Chronic shoulder/arm pain in a smoker over the age of 50-60
i. Pancoast tumor.
j. Fever + neck stiffness
i. Meningitis.
k. Mid back, neck, or joint pain + fever
i. Cancer, infection, autoimmune/inflammatory disease.
l. Neck/arm pain with neurological deficits in patients over 50-60
i. Cancer.
m. Neck pain plus nuchal rigidity
i. Meningitis.
3. In simple English, what are the 3 components of Horner’s syndrome? What are
some of the serious causes of Horner’s syndrome?
a. Ptosis (unilateral droopy eyelid)
b. Miosis (unilateral pupil constriction)
c. Anhidrosis (lack of sweating)
d. Most Horner’s syndrome cases are idiopathic!
i. Most common causes are tumor (brain, neck, spinal cord), cluster
headache, and head/neck procedures.
ii. When it is a tumor, it invades and ascends the cervical sympathetic
chain, causing this symptoms.
e. Even though internal carotid dissection is an extraordinarily rare cause of
Horner’s syndrome, an acute onset of painful Horner’s syndrome + ipsilateral
eye, face, or neck pain should be treated as an internal carotid artery
dissection until proven otherwise.
4. What percentage of palpable neck masses are malignant?
a. 75% in patients >40 y/o.
b. Unless there are signs of infection, a lateral neck mass is considered
metastatic squamous cell carcinoma or lymphoma until proven otherwise.
5. Most carcinomas that cause cervical lymph node enlargement come from what
part of the body?
a. 74% from head and neck.
b. 11% come from elsewhere.
6. What ancillary studies should you consider ordering when you suspect a disease
causing neck symptoms?
a. Radiograph (followed by MRI/CT)

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 b. ESR/CRP
c. CBC
d. Blood chemistry panel
e. Worried if ESR/CRP come back elevated, or if the CBC reports anemia
(normocytic normochromic or microcytic), or increased/decreased WBCs.
7. What is a Pancoast tumor? Who tends to get it?
a. A tumor that starts in the lung and migrates to the brachial plexus, wrapping
around and engulfing it. Might also migrate to the 1st or 2nd rib, or a vertabrae
(pain intensity goes up).
b. First presents as chronic shoulder pain in a smoker over 50 y/o.
8. What is the pain & paresthesia distribution for a typical Pancoast tumor? What
accounts for this particular distribution?
a. Starts in the shoulder and vertebral border of scapula.
b. Then may extend along the ulnar nerve distribution down the medial half of the
arm and forearm all the way to the 4th and 5th fingers (C8 dermatome).
c. Pain is relentless and unremitting, relief only with narcotics.
9. What antalgic position might a patient adopt if he has arm pain due to a Pancoast
tumor?
a. Affected arm elbow supported in opposite hand (eases tension on affected side
shoulder/arm).
10. What are some of the neurological findings that can accompany a Pancoast
tumor?
a. Horner’s syndrome on the ipsilateral face and upper extremity due to invasion
of the sympathetic chain.
b. Triceps reflex absent.
c. Hand muscles weak and atrophied.
d. Spinal cord/canal may be invaded, leading to UMNL signs.

Cervical Diseases Part 2 (based on assigned outside of class Panopto

lecture and powerpoint slides)

1. What is the most common inflammatory arthritis? How does it present?

a. Rheumatoid Arthritis
b. Prevalence: 1-2%
c. Most common presentation: neck and suboccipital pain (40-85%).
i. Next most common: radiculopathy and myelopathy.
ii. Younger patients (<34 years) are less likely to have neck pain and more
likely to have a shorter disease duration (3.5 years).
iii. There is a correlation between neck pain and the amount of subluxation -
patients without neck pain have less subluxation.

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 iv. The degree of cervical involvement correlates with the degree of
hand/wrist erosion, the presence of rheumatoid nodules, and the use of
corticosteroids.
d. Neurological symptoms are reported in 5-67% of cases.
i. Weakness, decreased endurance, gait difficulty, paresthesias of the
hands, loss of fine dexterity, incontinence.
e. Neurological deficits are present in 7-34% of cases.
i. If they have a deficit, must evaluate for a history of myelopathic
symptoms.
f. Patients may also present with vertebrobasilar artery insufficiency (especially
with C1-C2 instability), vertigo, loss of equilibrium, visual disturbances, tinnitus,
dysphagia (symptoms similar to brainstem compression), or shock-like symptoms
into torso/extremities with neck motion (Lhermitte sign).
g. Multiple subluxations is the most common radiological presentation.
2. What three types of structural instability can be caused by rheumatoid arthritis
(RA)? Which is the least common?
a. C1-C2 instability - 49% of RA patients.
i. Sliding/subluxation of the atlas into the spinal cord.
b. Proximal migration - 38% of RA patients.
i. Superior migration of the odontoid into the brainstem.
c. Subaxial instability - very common when present with one of the other two
types, but only 10-20% of RA patients have ONLY this type.
i. Sliding/subluxation of vertebrae below C2.
3. You are treating a patient with RA. What are the chances that it has affected his
cervical spine? Give a range of probability.
a. 19-71%.
b. Point is that this is very common.
4. What two blood tests are ordered to help diagnose RA?
a. + Rheumatoid factor
b. + Anti-CCP antibody
5. What is the cut point for an abnormal ADI interval in an adult? In a child?
a. >3-4 mm for an adult.
b. >4 mm for a child.
c. Surgery may not be indicated until 8, 9 or 10 mm.
d. Surgery should be considered, however, BEFORE the onset of neurological
symptoms.
i. New subluxations appear and old ones may progress as RA goes on.
6. How does an RA neck affect in-office chiropractic management?
a. Nonsurgical care of RA involvement in the neck is supportive.
i. Cervical involvement is associated with disease activity, early aggressive
medical management is recommended.
b. Patients need to be carefully monitored for long-tract signs or radiographic
findings suggesting impending neurologic compromise.

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 c. Prior to manipulation, must order flexion-extension radiographs to evaluate
for RA cervical instability (not 100% sensitive).
i. Can change over time, must order new x-rays in old patients who return.
ii. Low force techniques if symptoms/radiographs suggest no inflammatory
changes.
iii. NO MANIPULATION if evidence of inflammatory involvement.
iv. Can also prescribe rigid cervical collars for comfort (not to prevent
subluxation), or cervical stabilization exercises.
d. Chin retraction and protrusion causes more flexion/extension at C0-C1 and
C1-C2 than full cervical flexion/extension, and therefore should be avoided.
i. Chin retraction causes: posterior muscles to stretch, upper cervicals go
into flexion, lower cervicals go into extension.
7. What is syringomyelia? Where is it located?
a. Rare disorder in which a syrinx (a cyst) forms inside the spinal cord,
compressing it from the inside out slowly.
8. What is the classic neurological presentation for this condition?
a. Pain/temperature loss in diffuse, cape-like distribution in one or both
hands, arms, shoulders.
b. Slow, progressive weakness in arms and legs.
i. May be sudden with coughing/straining.
c. Chronic, severe pain.
d. Stiff back, shoulders, arms, or legs.
e. Headaches.
f. Loss of bladder function.
g. LMNL or UMNL findings in upper extremity; UMNL findings in lower extremity.
h. May affect the brainstem: Syringobulbia.
i. Respiration and heartbeat control compromised.
9. What are the two major ways that a syrinx is formed (i.e., what are the two types of
causes)?
a. Most common: Chiari 1 Malformation.
b. Less common: complication of trauma, meningitis, hemorrhage, a tumor, or
arachnoiditis.
10. When a syrinx is formed associated with a Chiari Type 1 malformation, what is the
key additional anatomical change?
a. Inferior cerebellum protrudes through foramen magnum into cervical spinal
canal.
i. Leads to syringomyelia developing in spinal cord.
b. Most common onset at 25-40.
c. Symptoms may worsen with straining/activities that cause CSF pressure to
suddenly change.
d. Some may have long periods of functional stability.
11. What is the dominant feature of post traumatic syringomyelia?
a. Pain that may spread upwards from the site of injury.

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 i. Symptoms may not appear for months or years after injury, including pain,
weakness, and sensory impairment starting the the site of trauma.
b. Bilateral or unilateral pain, motor/sensory loss, numbness, weakness, loss of
temperature sense.
c. Possible ANS symptoms: sweating, loss of sexual function, B/B control.
12. What are key components of a management strategy for syringomyelia? What
drugs may be prescribed?
a. Diagnosis using MRI, CT, myelogram.
b. Refer patient for surgical consult, and for gabapentin/neurontin prescription
for nerve related pain.
i. Goal is to stop progression.
ii. Delay may result in irreversible spinal cord injury.
c. Surgery:
i. Drainage or repair of syrinx.
ii. If Chiari malformation, will try to create more space at foramen magnum.
iii. Recurrence of syrinx is possible.
13. Where are the typical pain locations during a dissection of the carotid artery?
a. Back of the eye, the temple, and at the level of the carotid bifurcation.
b. Vertebral artery dissection is more suboccipital.
14. What is the classic triad of a dissecting carotid? How common is the triad?
a. Unilateral pain of head/face/neck.
b. Partial Horner’s syndrome (ptosis + meiosis)
c. Cerebral or Retinal ischemia
15. What would be a bright red flag about the pain that could signal a dissection was
occurring (in either the carotid or vertebrobasilar artery?)
a. Sudden, severe pain in the side of the head or neck, unlike any pain
experienced before.
i. Gradual onset is more common, but less indicative of of dissection.
16. What ancillary studies can make a diagnosis of a carotid artery dissection?
a. Conventional angiography, duplex scan, magnetic resonance angiography
(MRA) or CT angiography.
17. What are some risk factors making one more prone to a carotid or vertebral artery
dissection?
a. Blunt trauma to neck
b. Hereditary connective tissue disorders
i. Ehlers-Danlos syndrome
ii. Marfan syndrome
iii. Autosomal dominant polycystic kidney disease
iv. Osteogenesis imperfecta
c. Hyperhomocysteinemia
d. Oral contraceptives
e. Infection
f. Elevated high-sensitivity CRP

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 g. Age <45
h. History of migraines
18. What are some signs and symptoms you may see in carotid dissection? In VBA
dissection?
a. Carotid dissection
i. Headache
ii. TIAs, stroke Si/Sx, transient monocular blindness, numbness, weakness
aphasia, ataxia, pulsatile tinnitus.
iii. Meiosis + Ptosis (Acute onset of painful Horner’s syndrome with
ipsilateral eye, face, or neck pain should be treated as internal
carotid artery dissection until proven otherwise)
iv. Visual scintillations
v. Subjective bruit
vi. Neck pain
vii. Taste impairment
viii. Anterolateral cervical tenderness, bruit, cranial nerve palsies possible.
b. VBA dissection
i. Posterior neck pain (more common than neck pain in carotid dissection).
ii. Neck pain usually precedes other symptoms by 2 weeks.
iii. Headache that can be unilateral or bilateral, usually occipital, with
throbbing pressure quality. Usually comes on gradually, but may be
abrupt thunderclap onset.
iv. Headache usually precedes other symptoms by 15 hours.
19. If a patient suddenly gets neck pain in your office and it is a dissecting VBA, will
your neurological exam likely have positive findings? Explain.
a. No, since if it really is a dissecting VBA with presenting neck pain, other
symptoms, including neurological deficits, shouldn’t show up for around 2 weeks.
20. What is the A, 5 Ds and 3 Ns that may accompany a VBA dissection? (Lateral
medullary signs)
a. Ataxia
b. Dizziness/vertigo
c. Drop attacks
d. Diplopia
e. Dysphagia
f. Dysarthria
g. Nausea
h. Numbness (unilateral)
i. Nystagmus
j. Note: an isolated symptom, lightheadedness + absence of neurological signs,
episodes of vertigo lasting >3 weeks = rarely VBI.
21. According to Canadian Practice Guidelines, what are the 3 emergency
referrals/absolute contraindications to all treatment modalities?

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 a. Sharp neck/occipital pain with sudden, severe onset unlike anything
before.
b. Severe, persistent headache unlike anything before.
c. 1 or more of the following:
i. Unilateral facial paresthesia
ii. Objective cerebellar signs
iii. Lateral medullary signs
iv. Visual field defects
v. If a patient presents with 1 of these + vertigo, send them for diagnostic
imaging.

Nonspecific Neck Pain Diagnoses Part 1 (based on Panopto

lecture and reading from CSPE care pathway Neck and Arm Pain, pp 7-8.)

1. Name the 5 most common pathoanatomical diagnoses to consider when your

patient has neck pain but no neurological involvement.
a. Facet syndrome (causes 36-67% of persistent neck pain)
i. The facets are richly innervated with nociceptors.
ii. A patient with chronic neck pain will more often have both a facet
syndrome and a deranged disc at the same segment than only a facet
syndrome.
b. Sprain
c. Strain
d. Disc derangement
e. Fracture
2. Where do the C2-3 facets usually refer pain? What about the C4-5 facets? C6-7?
What about deranged discs at about the same level?
a. Upper cervicals tend to refer upwards to the head.
b. Mid cervicals tend to refer to the rest of the neck.
c. Lower cervicals tend to refer to the shoulder or down the arm/hand (even with
no nerve damage).
d. Disc derangements can also refer down the arm/hand, but otherwise tend to
stay more midline than facet syndromes.
3. Describe the neck pain which often accompanies a facet syndrome.
a. There may be an acute phase with inflammation and muscle splinting.
b. Unilateral or bilateral.
c. May be episodes of sharp pain/all directions are painful, but others a dull
background ache.
d. Persistent, with painful episodes and “catches.”

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 e. Feeling of neck weakness.
f. Headaches.
g. Aggravated by weight bearing, especially extension.
4. What physical examination findings are typically used to justify a facet syndrome?
What combination of these findings can be used to make a cervical joint
dysfunction diagnosis? What additional findings might justify adding a facet
syndrome diagnosis?
a. Palpatory findings alone: joint dysfunction.
b. Palpatory findings + positive orthopedic tests: facet syndrome and joint
dysfunction.
c. Palpatory findings:
i. Tenderness over facet
ii. Palpable local spasm
iii. Joint restriction
d. Facet loading procedures recreate pain:
i. Active/passive extension or rotation
ii. Quadrant position
iii. Cervical compression
iv. Cervical Kemp’s
5. What are 3 pertinent negatives that would help support a facet diagnosis, but if
positive would call the diagnosis into question?
a. Neurological deficits.
b. Distal arm symptoms reproduced by cervical orthopedic/tension tests.
c. Pain centralization with repetitive/sustained end range loading.
6. What features do maximum cervical compression, cervical Kemps, and the
quadrant position all have in common?
a. Rotation, extension, and lateral flexion towards the symptomatic side.

7. What combination of findings did one small study suggest was most accurate at
predicting who should be referred for a diagnostic facet block? Be sure to provide
all of the pertinent details.
a. + Quadrant position/Kemp’s - must reproduce familiar pain >3/10 OPS.

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 b. Pain with static palpation over facet - must reproduce familiar pain >3/10 OPS.
c. Restricted P-A joint glide
d. All 3 positive → +LR = 4.95.
8. In the same study, which of the findings were most useful to help rule out a
positive facet block response? Which one was the best at helping to rule out?
a. Negative palpatory tenderness over facet → -LR = 0.08.
b. Negative palpatory P-A restriction → -LR = 0.11.
9. Which is more likely effective: A medial nerve branch block to the facet or an
intra-facet injection?
a. Medial nerve branch block is more supported by medical literature as a better
facet block.
10. Explain how RF denervation works and why it might not be permanent.
a. The medial branch of the dorsal ramus is denervated by coagulating and
denaturing proteins in the nerve.
i. This should block conduction of pain signals to the DRG, but the nerve is
not actually destroyed, and may grow back/pain return after 6-9 months.
11. How has the concept of the cervical disc anatomy changed?
a. The anterior annular fibers are more similar to an interosseous ligament than
concentric rings.
b. The posterior annular fibers are a thin layer of vertically oriented fibers.
c. The posterolateral fibers are essentially deficient.
12. What set of 5 clues from the history and physical is recommended for making a
cervical deranged disc diagnosis? Which is considered the most useful clue?
a. Deep referred arm pain improved by repetitive/sustained end range
movements into chin retraction, extension, or another direction.
i. If there is no arm pain, focus on the neck pain.
b. Neck flexion/chin protrusion may aggravate, extension/chin retraction
improves.
c. More tender midline than over facets.
d. + Valsalva
e. Relieved by cervical distraction, aggravated by cervical compression.
f. Any of these alone being negative does not rule out a disc derangement.
g. Additional findings:
i. Patients often 20-55 y/o.
ii. Pain worse in the morning, better during the day, then worse again in the
evening.
iii. Possible torticollis.
13. If you are checking for a directional preference, what is the order of directions that
you should load the patient’s neck in? How do you know you found it?
a. Start with repetitive chin protrusion (will likely aggravate).
b. Repetitive chin retraction.
c. Repetitive chin retraction + neck extension (remove retraction once neck is
extended).

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 d. Supine repetitive chin retraction + extension combined with manual traction.
e. Repetitive ipsilateral flexion to the side of pain.
f. If you found it:
i. The distal pain centralizes.
ii. The distal symptoms improve.
iii. AROM improves (likely in direction opposite of centralization, not doesn’t
have to be).
14. What would orthopedic testing tell you about the source of non-specific neck
pain? Which supports a cervical sprain the most?
a. Cervical compression
i. Collapse sign - indicates of moderate to severe sprain.
b. Cervical distraction
i. Pain relief suggests disc derangement or facet syndrome.
ii. Pain aggravation could suggest multiple sources, including sprain-strain.
c. Soto Hall
i. Local pain = joint dysfunction, sprain-strain, vertebral fracture.
d. Joint play
i. Local pain = joint dysfunction, sprain.
ii. Increased movement = instability/hypermobility.
15. What positive clues could support a cervical strain in a trauma case?
a. Isometric contraction of neck muscles is painful and may be weak.
b. Muscle is tender to palpation.
c. Painful when stretched.
d. AROM painful and limited if it stretches muscle.
e. Muscle may appear inflamed.
16. What physical examination clues would be most useful in trying to differentiate a
cervical sprain from a strain?
a. Sprain
i. Muscle test is strong and painless, except sometimes in the set phase
(the very beginning of the test where the joint is first loaded).
ii. Passive ROM is painful/limited, especially in midrange.
b. Strain
i. Muscle test is painful/weak.
ii. Passive ROM is painless, unless the muscle is stretched.
17. What kinds of residual effects can sprains and strains cause?
a. Sprain
i. Chronic facet syndrome or disc derangement
ii. Chronic instability
b. Strain
i. Myofascial pain syndromes
c. Both
i. Adhesions

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 ii. Joint dysfunction

Nonspecific Neck Pain Part 2: Treatment and

Myofascial Pain Syndromes (based on lecture and powerpoint slides)

1. What are some causes of benign, acute, severe neck pain?

a. Facet syndrome
b. Meniscoid entrapment
c. Torn annular fiber
d. Joint dysfunction
e. Patient may have severely limited AROM and PROM in all directions, sharp pain
if they move their neck, may or may not have torticollis.
2. What is the NDI?
a. Commonly used tool for measuring the impact of pain on the patient’s lives,
including ADLs.
3. What are the 6 recommended treatment approaches for patients with acute severe
neck pain?
a. Manipulation, mobilization, and home exercises in a patient’s directional
preference.
b. Manual cervical traction.
c. PIR/massage to relax muscles so you can palpate a direction to adjust.
d. Adjust joint dysfunctions in the thoracic spine.
e. Pain reducing electromodalities.
f. NSAIDs.
4. Using the 2 by 2 table to organized a treatment approach to routine neck pain,
describe the differences and similarities between treating a suspected facet
syndrome vs a suspected deranged disc.

CMT STM
Facet syndrome Both Facet syndrome and Disc
- CMT/mobilize painful restrictions derangement
- If every direction hurts, you can adjust - Stretch cervical extensors, SCM,
in the direction that hurts the least. and/or pectoralis muscles.
- STM to treat muscle spasms.
Disc derangement
- CMT into directional preference or
painful restriction.
- Cervical traction.
- Cervical flexion-distraction.

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BM Ex
Facet syndrome Disc derangement
- Decrease extension loads (forward - Directional preference exercises.
head carriage, sustained upward
looking - upper cervical extension Both
load). - Rehab program.

Disc derangement
- Decrease flexion loads (forward head
carriage, sustained downward
looking - lower cervical flexion load.

5. What are the three immediate exercise prescriptions that might be assigned to
patients when they are still in acute neck pain?
a. First of all, these are can be done on the first visit because the patient is acute
and in pain. If the patient can do all 3 of these without any pain, start them with
resistance exercises.
b. AROM exercises.
c. Isometric exercises into flexion, extension, lateral flexion, and rotation against
the patient’s own hand.
d. Directional preference exercises (likely chin retraction).
e. For all 3 of these, the limiting factor is pain. Only do them within a range/intensity
that is pain free.
6. Generally speaking, about how long does a structured rehab program for the neck
take?
a. First of all, this doesn’t start until the subacute or chronic phase of moderate/ or
severe cases.
b. At least 6-12 weeks is needed to allow for hypertrophy of muscle fibers.
c. Some patients may benefit from a program lasting 3-6 months.
d. Patients must do lighter maintenance training to maintain these gains.
7. What are the 4 main strategies that would make up a comprehensive physical
rehabilitation program for a patient with chronic neck pain?
a. Evaluate and strengthen deep neck stabilizers.
b. Assess posture and respiration, teach patient Brugger’s and abdominal
breathing.
c. Address muscle imbalance of large torque producers (like in upper crossed
syndrome).
d. Retrain sensory motor response loop (proprioceptive exercises).
i. Helps strong muscles get “smart” so they know when to contract.
8. What are the components of an upper cross syndrome? How would each
component be treated?

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 a. Weak deep neck flexors, lower trap, and serratus anterior (need to be
strengthened).
b. Tight pectorals, upper trap, and levator scapula (need to be stretched).
9. What criteria should athletes and normal people follow before “returning to play?”
What if they return before meeting these criteria?
a. Minimal or no tenderness.
b. Full AROM.
c. Neck strength is within normal limits.
d. Absence of neurologic Si/Sx.
e. The likelihood of a recurring injury is extremely high if the player returns to
action before pain, tenderness, and ROM have returned to normal.
10. What muscles and their myofascial trigger points were covered? Where were their
referral patterns? How would you stretch each one? How would your patient do a
home stretch?
a. Scalenes
i. May mimic C6 radiculitis or thoracic outlet syndrome.
ii. Refers pain to the medial border of the scapula, and down the
shoulder/lateral arm into hand (C6 dermatome).
iii. Can perform a scalene cramp test (turn head towards painful side), length
test (doctor stretches head into contralateral rotation/lateral flexion), or
relief test (shoulder abduction relieves pain, also true for a radicular
syndrome, but opposite in a thoracic outlet syndrome).
iv. Patient can laterally flexion/rotate head to opposite side, and use hand to
provide overpressure.
b. Levator scapula
i. Only refers to shoulder/medial scapula, doesn’t go down the arm.
ii. Pin and stretch.
iii. Patient can flex, rotate and laterally flex to opposite side, and use arm to
pull head into further flexion overpressure.
c. Trapezius
i. Trigger points most often in vertical fibers in upper trap.
ii. Can cause joint dysfunction in C2-4, hypermobile C4.
iii. MFTPs may cause posterolateral neck pain, temporal headache, jaw
pain.
iv. Patient can use pressure with a ball/roller, or stretch by bringing arms into
maximum horizontal adduction.

Cervical Spine Trauma & “Whiplash” Part 1 (based on lecture

and powerpoint slides)

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1. How might a patient present if they have an acute cervical sprain or strain?
a. Cervical Strain
i. CC is pain and stiffness.
ii. Reactive spasm in the muscle that is injured.
iii. Poorly localized burning or cramping pain.
b. Cervical Sprain
i. CC is jammed neck sense, local pain (sometimes sharp).
ii. Muscle splinting in the whole area.
c. Both
i. Swelling, tenderness, motion restriction, referred pain to occipital area or
shoulder (not to extremities).
ii. Possible torticollis, but more commonly decreased ROM.
iii. AROM limited if it stretches the muscle or ligament.
iv. Pain during rotation, flexion, or extension against resistance
indicates damage of muscles.
v. No neurologic deficits.
2. What are some common types of traumatic mechanisms of injury that lead to
cervical sprains?
a. Macro trauma producing derangement of ligaments beyond anatomical limits.
i. Compressive injury to top of head or forehead (compression fracture
or sprain more likely than strain)
ii. Flexion / extension or lateral flexion injury (whiplash)
iii. Hx of head trauma with associated loss of consciousness (could tear
muscles, ligaments, traction a nerve, or fracture)
3. How long does it usually take for the muscle spasm that can accompany sprains
and strains to resolve?
a. Should be fully resolved within a few days up to 2-3 weeks.
i. May cause a temporary loss of cervical lordosis.
4. What is the usual amount of C1-C2 translation that is suggested to be the cut
point for Atlas instability in adults and children?
a. The C1-C2 translation is normally between 2-3 mm, although some authors
suggest 2.5 mm for adults and 4.5 mm for children as the upper limit of
normal motion.
b. Should not exceed 3.5 mm horizontally or 11 degrees of angular displacement.
5. If a patient has evidence of possible structural instability, what is the first
treatment intervention?
a. If any evidence of ligamentous instability exists, the patient must be placed in a
rigid collar.
b. Take neutral, flexion, and extension radiographs to measure degree of
movement.
i. Must retake these radiographs 2-4 weeks later (after muscle spasm
has resolved).

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6. What 5 exam procedures and their findings would help to make a cervical muscle
strain diagnosis?
a. Observe: possible bruising or visible swelling.
b. Palpation: tenderness.
c. AROM: painful in plane using the muscle.
d. Stretching: painful with end range lengthening of muscle.
e. Contract: pain and/or weakness with isometric muscle testing.
7. What are the goals of treatment for cervical sprains and strains?
a. Control pain and inflammation in acute phase.
b. Support and prevent further injury.
c. Prevent adhesion, atrophy, and erosion of motor control programming.
d. Restore proper muscle balance.
8. What in-office and home treatments are used to prevent adhesions, atrophy, and
loss of motor control programming in a sprain or strain?
a. CMT
b. Isometric muscle exercises
c. Home ROM exercises
9. What type of in-office manual therapy would be helpful in relaxing a muscle
spasm? What type of manual therapy would be helpful in stretching muscles and
their fascia?
a. PIR for painful spasms, CRAC/stretching for tight muscles.
b. Activation and strengthening of weak muscles.
10. What are some of the late effects of a cervical sprain?
a. Periarticular Fibrosis
i. Tight fibrous tissue
ii. Decreased segmental ROM at end play.
11. What are some of the last effects of a cervical strain?
a. Myofibrosis
i. Muscle inelasticity, tenderness/trigger points.
ii. Decreased and painful ROM as muscle is lengthened.
iii. Usually will muscle test strong, maybe pain with full contraction.
iv. Treat using cryotherapy, MET, CMT, electrotherapies, home
stretching/exercises.
12. Tell the story of the S curve, the loads it produces in different parts of the cervical
spine, and why a well-positioned head rest likely will not prevent it.
a. The “S” curve is created during a rear end collision at 60 msec, causing the
cervical spine to form an S shape. The upper cervicals bend into flexion, while
the lower cervicals bend into extension.
i. This may cause the upper cervicals (C0-2) to be restricted, while the
lower cervicals (C4-6) become hypermobile.
b. Head contact with the head piece occured between 70-100 msec (the “S” whip
occurs at 60 msec). Proper positioning of a head rest (aligned with EOP) can
decrease the amount of hyperextension, but won’t prevent the “S” curve.

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13. In an upper cervical injury, what may be the repercussions of injury to nociceptors
and mechanoreceptors?
a. Balance disorders
b. Dizziness
c. Mild Traumatic Brain Injuries (MTBI)
14. Moving layer by layer, predict the different types of injuries that can occur to
anterior neck structures during the hyperextension phase of an acceleration
injury.
a. Strains of anterior paravertebral & superficial muscles.
b. Sprains of anterior longitudinal ligament.
c. Tears of anterior disc and avulsion fractures of anterior vertebral bodies.
d. Tractional injuries to the vertebral artery and sympathetic plexus (possible
Horner’s syndrome).
e. Tears / swelling in scalenes, SCM, deep flexors (longus colli, longus capitis)
f. Note: there is also debate around the possibility of the TMJ being damaged.
15. What can result if the deep neck flexors are weak, injured, or inhibited?
a. Functional instability
i. May contribute to persistent pain or increase susceptibility to future injury.
16. What is a structural cause of dysphagia?
a. Tensile loads (due to hyperextension) may tear the smooth muscle of the
esophagus, which can cause dysphagia.
i. However, most dysphagia after CAD is psychological in nature. Use
radiographs and look for retropharyngeal swelling to rule out.
17. What other structures might be injured due to a hyperextension injury?
a. ALL sprain
i. Can cause structural instability if severe.
b. IVD tears
i. Disc and ALL tears are the most common injuries.
ii. Typically either disc avulsion from the end plate, or annular fiber tearing.
iii. Usually at C4-5, or C6-7.
iv. Anterior disc more common in rear end collision, posterior disc (with
resulting herniation/nerve root compression) less common, but may occur
in a head on collision.
c. “Rim” lesions
d. Avulsion fractures
i. Occurs are the lower corner of vertebral body.
e. Nerve root directly traumatized (causing a radiculitis).
18. About what percentage of neck pain is due to the facets in chronic whiplash
patients?
a. Based on double block studies about 60% of the chronic pain in “late whiplash”
comes from the facet joints.
i. The facets are rich in nociceptors, and shear force/hyperextension places
a tensile load on the facet capsule.

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 19. What syndrome can be caused by damage to the sympathetic plexus?
a. Most likely Horner’s Syndrome, but a dissecting carotid aneurysm or Pancoast
tumor can present with these symptoms. Because these are much more serious,
need to rule them out.

Cervical Spine Trauma & “Whiplash” Part 2 (based on lecture

and powerpoint slides)

1. What structures are most at risk in a head on collision? What are the diagnostic
terms for these different lesions?
a. Head rotates forward, forcibly flexing the neck; followed by degree of recoil
resulting in hyperextension (based on elastic properties of posterior neck);
deceleration is first applied at C0-C1, then at C6; neck will undergo shear force.
b. Sprains: alar ligaments, PLL, nuchal, supra and interspinous ligaments, facet
capsule.
c. Strains: posterior thoraco cervical muscles (semispinalis, splenius capitis, rectus
capitis, suboccipital, trapezius, levator scapulae).
d. Chip fracture: anterior superior vertebral bodies.
e. Orthopedic subluxations and dislocations.
f. Traction injuries to nerve root or spinal cord.
i. Upper cervical nerve roots may be under increased tension.
g. Greater occipital nerve traction injury neurapraxis (may contribute to
headaches or pain radiating up the posterior skull).
h. Note: the alar ligaments go from the tip of the dens to the skull - sprained by
upward projection of body during CAD (head hitting roof of car).
i. Note: muscles are most injury resistant tissue in the neck, and heal fairly well.
2. What are 7 long term effects of a CAD injury?
a. Persistent facet syndromes (about 60%) most common C5-6 and C2-3.
b. Joint dysfunction
c. Spinal instability (x rays may not be positive for months).
d. Myofascial pain syndromes/myofibrosis
e. Persistent post traumatic headaches
f. CNS and PNS dysfunction
g. Altered cervical biomechanics (may have less kinesthetic awareness)
3. Demonstrate the body attitude to prepare for a rear end collision if you are the
driver.
a. Put head and back against the seat.
b. Straight arm on steering wheel and get a good grip.
c. If stopped, put food on brake as hard as possible.
d. Look straight ahead and slightly at top of windshield.

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 e. Scrunch shoulders toward ears to brace for impact.
4. Describe the Quebec classification system for grading whiplash. (FYI ONLY)
a. Grade 0: no complaint of neck problems, no physical signs
b. Grade 1: complaint of neck pain, stiffness or tenderness only. No physical signs
(no decreased ROM, point tenderness etc)
c. Grade 2: neck complaint and musculoskeletal signs (decreased ROM, point
tenderness etc)
d. Grade 3: neck complaint and neurologic signs (deficits)
e. Grade 4: neck complaint and fracture or dislocation
5. What are the four main components of information you need to get from the
patient regarding the details of the accident and effect on their body? For each
component, list the specific questions you need to ask your patient.
a. Magnitude and direction of forces:
i. Direction of impact
ii. Make and model of vehicles
iii. More than one impact
iv. Vehicle speed: estimates of damage, body damage, drive away or tow,
glove compartment fly open, objects fly from back.
b. Position and attitude of body
i. Were you the driver
ii. Which way was head turned: head turned and flexed, head turned and
extended
iii. Hit top of head
iv. Which way was body turned
c. Force dampeners and accelerators
i. Use of seat belt (dampener for body and augmenter for head and neck-
injury to spine 3x more likely with seatbelt)
ii. Airbag (dampener)
iii. Brakes applied (augmenter for head and neck but prevents double
impact)
iv. Damage to seat (dampener)
v. Did you know you were going to get hit (dampener- unaware 15x higher
risk for symptoms at 6 months)
d. Detailed list of symptoms (need to know all of these)
i. Head and neck: headache, dizziness, vision changes, neck pain,
dysphagia, when did each symptom come on?
ii. Higher brain centers: trouble concentrating or remembering, trouble
sleeping or sleeping too much, irritability, fatigue, depressed, anxious,
moody, when did each symptom come on?
iii. Rest of body: symptoms in arms, legs, or back, when did each symptom
come on?
6. What is the clinical significance of finding out if the patient’s head was turned at
the time of a rear end collision? Be as specific as you can.

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 a. Rotated or laterally flexed head at time of impact is primary feature related to
symptom persistence.
i. Often worst kind of CAD injury.
b. If head is rotated right: more load on right facet, more tearing of left SCM.
7. What are the key indicators from the history that suggest that cervical radiographs
should be taken? (need to memorize the bolded terms, understand the others)
a. Age 65 and over.
i. High risk for C/s injury following blunt trauma
b. Dangerous mechanism of injury.
i. 1) fall from height >1m, 2) axial load injury (diving injury), 3) high speed
(>62 mph, 100 km/h) MVA, 4) motorized recreational vehicle or bicycle
collision
c. Presence of paresthesia in extremities.
i. Report of numbness, tingling or weakness
d. NOTE: Patients with any of the above 3 MUST get radiographs before
undergoing AROM testing!
e. Painful, distracting injury elsewhere in body.
i. Important to consider C/s radiographs if alert patient presents with severe
associated injuries that may distract him/her from focus of C/s discomfort.
Some clinicians have found this to be poorly reproducible
f. Altered level of alertness.
i. 1) Glasgow coma scale < or equal to 14, 2) orientation x3, 3) can’t
remember 3 objects at 5 minutes, 4) delayed or inappropriate response to
external stimuli
g. Evidence of intoxication.
h. Patients with known vertebral disease.
i. Fused spinal segments, spinal stenosis, RA, AS, down’s syndrome,
marfan’s syndrome, os odontoideum, klippel-feil syndrome and morquio
syndrome
8. Describe what is meant by a “dangerous mechanism of injury.”
a. Refer to #7b..
9. In order from most common to least common, what are some immediate
symptoms following a CAD?
a. Neck pain
b. Headache
c. Shoulder pain
d. Back pain
10. What is Rusts sign? What does it suggest?
a. Patient holds his/her neck with both hands.
i. May be all the time, or only in transitional movements like standing to
sitting, lying to sitting, etc.
b. Suggests fracture.

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11. What are some of the key physical exam findings that suggest a radiographs
should be taken? (need to memorize the bolded terms, understand the others)
a. Unable to actively rotate neck 45 degrees to left or right.
i. Patients 65 and over, dangerous mechanism of injury, or paresthesia
must undergo C/s radiography PRIOR to undergoing active range of
motion testing!
b. Midline cervical spine tenderness.
i. Midline cervical spine tenderness is defined as pain on palpation at
midline from nuchal ridge to prominence of first thoracic vertebra or if
patient evinces pain with direct palpation of any cervical spinous process
c. Focal neurologic deficit.
i. Focal deficit (could be in spinal cord or spinal nerve distribution) may be
elicited by history or finding on motor or sensory examination. Prevalence
of C/s fractures in patients with focal deficit has been reported at 19-55%
of patients presenting with motor deficits had an associated C/s fracture
12. What is the opening sequence of performing the physical examination? In what
circumstances should the sequence of process be altered?
a. Observation
b. AROM (patients 65 and over, dangerous MOI, paresthesia must undergo C/s
radiography PRIOR to undergoing AROM!)
c. Light, superficial palpation
d. Neuro: SMRs (emphasis on upper extremities), cranial nerves, mental status if
head trauma.
e. Passive ROM, muscle test the neck, orthopedic tests
f. Deeper palpation and segmental ROM.
13. Describe the components of the neuro exam that should be done. What parts of
the nervous system are at risk?
a. Neuro exam - clues indicating further assessment.
i. Loss of consciousness? How long?
ii. Post traumatic HA (R/O subdural hematoma especially in older patients,
especially worried about this if they head their head, the headache has
steadily gotten worse, an older patient, on anticoagulation medication.
iii. Dizziness/vertigo
iv. Nausea
b. Myelopathy, damage to occipital nerve, radiculopathy, post concussive syndrome
(loss of coordination or balance, visual changes, auditory changes), sympathetic
nerve injuries (CRPS, Raynaud phenomenon, Horner’s syndrome, Barre Lieux
syndrome).
14. List some physical neuro signs and symptoms, mental status symptoms and
mood presentations that can suggest TBI.
a. Physical neuro signs and symptoms: loss of coordination or balance, visual
changes, auditory changes.

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 b. Mental status: cognitive problems, difficulty solving problems, difficult
concentration, impaired memory, forgetfulness, language difficulty.
c. Mood: personality changes, mood swings, irritability, anxiety, reduced motivation,
unusual amount of fatigue.
15. What is the significance of LOC?
a. <10% of concussions lose consciousness, but LOC presumes concussion.
16. What are the parts of a Davis series?
a. Complete 7 view study.
b. AP, APOM, Lateral, 2 obliques, flex/extension.
i. Flex/extension taken AFTER static films in severe trauma.
17. What is a teardrop fracture? A clay shoveler’s fracture?
a. Teardrop: fracture of anteroinferior aspect of cervical vertebral body.
b. Clay shoveler: spinous process fracture.
18. Describe the two types of instability and what can cause each type.
a. Structural: significant disruption of ligaments, bony structures, discs leading to
joint laxity and excessive motion beyond usual anatomical barriers.
i. Causes included congenital, trauma, inflammatory diseases, and an
instability phase of spinal degeneration.
b. Functional: damaged muscles, mechanoreceptors, or altered motor control
leading to poor stability within usual anatomical barriers (neutral zone).
i. Causes include trauma, repetitive microtrauma, sustained postural loads.
19. What are some positive findings that would suggest structural instability on a
flexion-extension series of radiographs? AP and lateral?
a. Flexion and extension views
i. Listhesis > 3.5 mm
ii. Forward displacement > 11 degrees
iii. C1-C2 translation > 2.5 mm
b. AP and lateral views
i. Widening of interspinous space
ii. Subluxation of facet joints
iii. Compression fractures of subadjacent vertebrae
iv. Loss of cervical lordosis
c. Treatment for structural instability includes a rigid collar and surgery.
20. What are two exercises that you might send a patient home with even in the acute
phase of a CAD injury?
a. Active ROM.
b. Isometric exercises (flexion, extension, lateral flexion, rotation)
c. These are only within a pain free range.
d. Prescription is 10 reps every 1-2 hours.
21. What are the operational end points for each phase of care?
a. Acute: no pain at rest
i. Treatment aims to reduce pain, inflammation, spasm.

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 ii. CMT, PIR, PT modalities, NSAIDs, cervical collar if needed to allow
activity.
b. Subacute: capacity to perform unstressed basic ADLs
i. Control pain, promote flexible healing, restore function.
ii. Continue CMT, PIR, PT modalities, progress to resistance exercises,
rehab deep flexors, address any upper cross syndrome.
c. Rehab-repair: capacity to perform normal activities under some constraints
i. Decrease adhesions, restore normal movement patterns, restore
strength, endurance, and motor control, increase physical work capacity.
d. Rehab-remodel: full recovery (“pre injury status) or functional recovery
i. Prevent future injury through reduction of risk factors.
e. Following these steps is important, since soft tissue injuries are often permanent
otherwise. 70% of patients still have symptoms 15 years after injury.

Torticollis (based on lecture and powerpoint slides)

1. What are the two basic types of torticollis?

a. Acquired
b. Congenital
i. Presents in infants within hours to weeks following birth.
ii. Caused by birth trauma or bony anomaly.
iii. 90% respond to passive stretching in first year of life.
2. What is atlantoaxial rotary subluxation? What are some causes of AARS in a
child?
a. Predominantly in children, the head in is the cock robin position, where the head
is rotated to the side opposite the facet dislocation and laterally flexed toward the
lesion.
i. Precipitated by retropharyngeal edema, leading to laxity of ligaments and
structures at the atlantoaxial level, permitting the rotational deformity.
ii. May complain of unilateral occipital pain.
b. May be caused by:
i. Minor trauma
ii. Pharyngeal surgery
iii. Inflammatory process
iv. Upper respiratory tract infection
3. What is the usual prognosis of uncomplicated acute adult “wry neck”?
a. Self limiting, and symptoms resolve in a few days up to 1-2 weeks.
b. Most common type of torticollis.
c. Painful neck spasms that develop overnight.

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 d. Need to make sure this is the uncomplicated case, and not something more
serious.
4. In simple uncomplicated torticollis what is generally the cause and the treatment?
a. Cause: usually unprovoked, but could be from exposure to cold or sleeping in
awkward position.
b. Treatment: conservative care using analgesics, massage, exercise, and
stretching.
i. CMT for joint dysfunction in upper cervical spine.
ii. Relax the SCM that is spasming (stretching, heat, electromodalities)
iii. Botox (botulinum toxin) injections a go to treatment as well.
5. What muscle is most often involved?
a. SCM
6. How does acute traumatic torticollis differ from uncomplicated torticollis?
a. The result of blunt trauma to head and neck.
i. Need to rule out atlas subluxation, fracture, structural instability!
b. Torticollis may present immediately or a few days after.
i. Immediate torticollis indicates need for immobilization and
radiographs!
c. Patient presents with local pain immediately following trauma, followed within
days by marked decrease in neck ROM, abnormal head posture, shoulder
elevation, and eventual trapezius hypertrophy.
7. Torticollis has been associated with retropharyngeal abscesses which can be life
threatening—what are some of the signs and symptoms?
a. Most common in children 2-4 y/o.
b. Neck discomfort
c. Fever
d. Stridor (high pitched whistle sound when taking breath)
e. Dysphagia
f. Drooling
g. Odynophagia (painful swallowing)
h. Respiratory distress
8. What are some of the infectious diseases you need to rule out when considering
torticollis patient? Non-infectious diseases? Other causes?
a. Infectious
i. Upper respiratory infection
ii. Tooth infection
iii. Pharyngitis
iv. Tonsillitis
v. Systemic infection
vi. Meningitis
vii. Osteomyelitis
viii. Upper lobe pneumonia
b. Non-infectious

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 i. Spinal epidural hematomas (especially worried if patient is on heavy
anti-coagulant + presents with torticollis)
ii. Neurogenic
iii. Tumors
iv. Psychiatric disease
c. Other
i. Side effect to some medications
ii. Any biomechanical abnormality of cervical spine
9. What is dystonia?
a. A movement disorder that causes involuntary muscle contractions, resulting in
twisting and/or repetitive movements.
b. May or may not be painful.
c. May affect one muscle, groups of muscles, or all muscles.
i. Affects the entire muscle, which is different from a tick (only part of the
muscle).
d. Symptoms may include: tremors, voice problems, or a dragging foot.
e. Unclear etiology, but suspected thalamic or basal ganglia lesion, leading to a
problem in muscle contraction messaging.
10. What are some if the characteristics of idiopathic spasmodic torticollis?
a. Chronic, slowly progressive.
b. Most common in females 30-60 y/o.
c. Acquired, non traumatic origin consisting of episodic tonic and/or clonic
involuntary contractions of neck muscles.
i. Tonic: continuous contraction
ii. Clonic: on and off again, possible jerking or twitching
d. May progress to hand, arm, oromandibular region, clinical dysphagia.
e. Tremor and pain are very common symptoms.
f. Usually worsened by standing, walking, emotional stress.
g. Better in the morning.
h. Sensory tricks may be present that the patient can use to reduce head and neck
movement (like touching their face in a particular spot, but this varies from patient
to patient).
i. Only present in idiopathic and delayed post-traumatic types, so can
use to differentiate from acute traumatic and nondystonic types.
i. Prognosis: symptoms last >6 months, resulting in considerable somatic and
psychological disability.
i. However, 10-20% of patients experience spontaneous remissions that
may be brief or last up to 2-3 years.
11. What are some clues that would help you differentiate late post traumatic
torticollis from idiopathic spasmodic torticollis?
a. They are nearly identical in symptoms, and both present with sensory tricks.
b. Post-traumatic Torticollis will present 3-12 months after head and neck trauma.
c. No trauma in idiopathic type.

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12. How can you DDx the dystonic torticollis (idiopathic or delayed post-traumatic)
from nondystonic torticollis (acute traumatic or noncomplicated)?
a. Dystonic
i. SCM in spasm
ii. Head “fixed” in antalgia
iii. Self-limiting
iv. No neurological signs
v. Good chiropractic case
b. Nondystonic
i. Chronic/recurrent
ii. Tonic or clonic
iii. Triggered by physical or emotional stress
iv. Sensory tricks to inhibit
v. Possible tremors
13. What physical exam procedures can you do to help make a DDx?

14. Will you need ancillary studies to evaluate a torticollis case?

a. X-ray only needed in trauma cases, to rule out atlas subluxation, or suspected
retropharyngeal infection.
b. MRI or CT if suspect CNS disease.

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Cervical Neurological Assessment (based on lecture and
powerpoint slides)

1. What are the 5 parts of the nervous system where a lesion could be that could
cause arm symptoms in a patient with neck pain?
a. Nerve roots
b. Spinal cord
c. Brachial plexus
d. Peripheral nerve
e. Sympathetic nerves
2. What are the 5 main clues that you look for in an history and physical (H&P) to
decide if arm symptoms may be neuropathic?
a. Pain (especially if dermatomal, classic sharp electrical presentation not often
seen, may be diffuse and non-dermatomal)
b. Paresthesia (especially if dermatomal, starts distal and spreads proximal - the
opposite as the pain, and it is more often dermatomal than the pain)
c. SMR deficits
d. Change in arm symptoms by any of the big 5 cervical orthopedic tests.
i. This is different from the low back, where we used nerve tension tests.
e. Rapid reproduction of arm symptoms with AROM or any load to the cervical
spine.
3. What are four characteristics of just the pain that would make it sound
neuropathic?
a. Location
i. Past the elbow, dermatomal, superficial.
b. Quality
i. Sharp, stabbing, electrical, painful cold (like frostbite).
c. Severity
i. Worse than neck pain.
d. Rapidly aggravated by spine position
4. Which clues from the H&P would be most accurate at predicting which particular
nerve root might be injured?
a. Deficits and dermatomal paresthesia is more predictive than the pain
distribution (especially C6 or C7 nerve roots).
5. Where is the pure patch for the C5, the C6 and the C8 nerve roots? What is the
pure patch of the ulnar nerve, median nerve and radial nerve?
a. Note: dermatomal distributions of C6, C7, and C8 aren’t reliable until they cross
the elbow.
b. C5/axillary nerve: over deltoid tubercle
c. C6/radial nerve: dorsal surface of thumb web or lateral thumb
d. C7: none

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 e. C8/ulnar nerve: medial tip of 5th finger
f. Median nerve: lateral tip of index finger
6. Where are the “signature zones” for C6, C7, and C8 nerve roots? How strong can
we trust a deficit in one of these zones as being caused by a lesion to that
particular nerve root?
a. C6: lateral surface of thumb and web - +LR = 8.5
b. C7: middle finger - +LR = 2.3
c. C8: medial surface of 5th finger - +LR = 41
7. Describe the peripheral nerve territories for the median nerve, ulnar nerve and
radial nerve on the palmar surface of the hand. What about the dorsum?
a. Median nerve: Palmar - lateral palm, pad of thumb, and 2nd, 3rd, and half of 4th
digits. Dorsal - distal fingertips starting at PIP of 2nd, 3rd, and half of 4th digits.
b. Ulnar nerve: Palmar - medial palm, and 5th and half of 4th digits. Dorsal - medial
hand, and 5th and half of 4th digits.
c. Radial nerve: Palmar - lateral aspect of thumb/thenar. Dorsal - lateral thumb and
web of thumb, lateral hand, and 2nd, 3rd, and half of 4th digits up until the PIP.

8. Your patient has motor weakness of the triceps muscle—what are three other
muscle tests to perform that might also be weak?
a. Could be a C7 or C8 lesion, so check wrist flexion, finger flexion, and finger
extension.
9. What nerve roots are you testing when you do a biceps muscle test? What
peripheral nerve?
a. C5-C6, Musculocutaneous n.
10. What would be a key muscle test to perform for C8? How about T1?
a. C8: finger flexion
b. T1: interossei
11. What is the advantage of adding pronation to your muscle tests?
a. In patients with a C6 radiculopathy, weak pronation is the most common
muscle weakness.

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 b. In patients with a C7 radiculopathy, weak pronation is sometimes the only
weak test.
12. Your patient has a +1 biceps reflex. Where could the neurological lesion be
located (be specific)?
a. C5 or C6 nerve root, or the musculocutaneous nerve.
13. What neurological deficit would be the most accurate predictor of a C6 nerve root
lesion? C7? C8? Which of those deficits has the highest +LR?
a. C6
i. Decreased biceps or brachioradialis reflex - +LR = 14.2
ii. Sensory loss over thumb - +LR = 8.5
iii. Weak wrist extension - +LR = 2.3
b. C7
i. Decreased triceps reflex - +LR = 28.3
ii. Weak elbow extension - +LR = 4.0
iii. Sensory loss over middle finger - +LR = 2.3
c. C8
i. Sensory loss over little finger - +LR = 41
ii. Decreased triceps reflex - +LR = 28.3
iii. Weak finger flexion - +LR 3.8
14. What are the big 5 orthopedic test most useful in helping to rule in or out a
radicular syndrome? On average how much would one of these tests increase the
probability of a nerve root lesion in a patient with arm pain and dermatomal
paresthesia?
a. Cervical compression
i. Maximum cervical compression (Spurling’s test) - if it aggravates arm
symptoms, +LR = 3.5 for a radicular lesion, possibly due to a disc
herniation.
b. Cervical distraction - if it improves arm symptoms, +LR = 4.4 for a radicular
lesion.
c. Shoulder abduction - if it improves arm symptoms, helps rule IN a radicular
lesion, possibly due to a disc herniation.
d. Upper limb tension test (ULTT) - median nerve - if it DOES NOT aggravate
arm symptoms, helps rule OUT neuropathic irritation (97% sensitivity)!
e. Valsalva maneuver - if it aggravates arm symptoms, +LR = 3.5 for a radicular
lesion, possible due to a disc herniation.
f. On average, a positive finding from one of these tests that rule a radicular
syndrome IN would increase the probability by between 15% and 30%.
15. Your patient has an inflamed nerve root that appears to be very sensitive to
tension. Predict what tests or postures might affect their arm symptoms.
a. Lateral bending to opposite side.
b. Flexion AROM.
c. ULTT-median.

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16. Your patient has an inflamed nerve root that appears to be very sensitive to IVF
compression. Predict what tests and ranges of motion might affect their arm
symptoms.
a. Extension or quadrant position.
b. Lateral bending to same side.
c. Kemp’s test.
d. Maximum cervical compression.
17. What are two ways the doorbell sign might be positive? What would each different
positive mean to you?
a. Pain down the arm - nerve root lesion.
b. Classic: pain between the shoulder blades - cervical deep referred pain.
18. What was the test cluster that in one study could predict a radicular syndrome
with up to 90% probability?
a. ULLT-median nerve
b. Cervical rotation <60 degrees to symptomatic side
c. Cervical distraction
d. Maximum cervical compression
e. 3 out of 4 = 65% post-test probability
f. 4 out of 4 = 90% post-test probability
19. Why might some radicular syndromes show no pattern in symptoms?
a. Injured, ischemic, denervating, or regenerating roots may have ectopic sites of
spontaneous firing.
b. The peripheral nerve becomes hypersensitized rather than the CNS/WDR.
20. How might your treatment be tailored to a patient with a radicular syndrome which
respond to opening or closing the IVF?
a. Avoid manipulative positioning and thrusts that close down the IVF.
b. Consider cervical traction therapies.
21. When should you be suspicious of a radicular syndrome that responds to traction
on and off the nerve root?
a. When the patient presents with Bakody’s sign, and shoulder abduction
reduces arm symptoms.
b. ULLT likely positive.
22. Your patient has a C7 radiculopathy. What is on your “A” differential diagnosis list
of causes (in order of probability)? What is on your “B” list?
a. Osteophytes
i. Most spurs don’t affect the nerve root unless it is in the IVF.
ii. On an X-ray, a spur in the IVF must correlate with the same side as the
arm symptoms, and must correlate with the nerve root level that is
suspected from the history and physical.
iii. However, need MRI to confirm Dx.
b. Disc herniations
i. Tend to compress/irritate nerve roots more than a spur does.
c. Spinal stenosis

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 d. Trauma to the nerve root (compression or traction).
e. Structural instability (trauma, inflammatory arthritis, degeneration).
f. Tumor/SOL (metastatic cancer, facet cyst, ossified PLL).
g. Infection (disc, bone, meninges)
h. Nerve root adhesions
23. If you suspect cervical myelopathy, what are 2 things you immediately are certain
of?
a. There is a relative or absolute contraindication to HVLA.
b. Need to order an MRI.
24. How much spinal cord volume can be lost, and yet may still have a normal
neurological exam? How does the degree of compression change the likelihood of
pain in healthy vs injured nervous tissue?
a. 30%.
b. When you compress healthy nervous tissue, including the spinal cord, often
there is no pain or neurological deficits until greater amounts of compression.
c. In previously injured nervous tissue, pain and deficits are more likely with less
compressive force.
d. First symptom in spinal cord compression are neurological deficits, not pain!
25. What are some symptoms in the legs that would suggest cervical myelopathy?
a. LMN signs are level of compression, UMN below.
b. Bilateral findings like paresthesia, proximal leg pain, proximal muscle weakness.
c. Clumsy gait.
i. Stumbling, awkward shuffling, frequent falls.
ii. Stooped, wide gait, + Romberg, + single leg stand.
d. Bladder dysfunction:
i. Frequency, urgency, incontinence, retention.
ii. As many as ⅔ of patients with cervical disc herniations may have
some bladder dysfunction!
26. What are some observations or tests in the hands that might be positive in
cervical cord compression?
a. Unilateral neurological findings.
b. Clumsy numb hands.
c. Selective atrophy of muscles on the back of the hand.
d. Inability to open and close hand 20x in 10 seconds.
e. Finger escape sign - patient asked to squeeze fingers together and into
extension.
27. How is Lhermitte’s sign elicited? What is a positive finding? What does it mean?
a. Doctor flexes patient’s neck forward.
b. Positive when patient feels an electric shock run down the back and limbs.
c. Associated with cervical cord lesions, including:
i. Compression
ii. Multiple sclerosis
iii. B12 deficiency

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28. What test should be done to check the integrity of the posterior column? Where
on the body should these be performed?
a. Vibration and Proprioception on the DIP of the 3rd finger/toe.
29. Besides performing a DTR, what is another way to elicit clonus?
a. Rapid and sustained ankle dorsiflexion, or wrist extension.
30. Describe some paradoxical reflexes for the biceps and brachioradialis?
a. Biceps: wrist extension instead of elbow flexion.
b. Brachioradialis: elbow extension or finger flexion instead of elbow flexion.
c. These suggest spinal cord compression.
31. What is the key response that you would see in a positive Babinski?
a. Big toe extension.
b. Can also do:
i. Hoffman’s sign: flick finger tip downwards
ii. Tromner sign: flick finger tip upwards
iii. Dynamic Hoffman’s: doctor performs Hoffman’s while patient flexes and
extends their neck.
iv. For all 3, look for thumb and index to approximate.
32. In a patient with suspected cervical spinal cord compression, what are the earliest
muscle weaknesses?
a. Weak heel walking (one forefoot does not raise as high as the other).
b. Proximal muscle weakness (like hip flexors or knee extensors).
33. Your clinician asks you to do a very thorough neurological examination for
suspected cervical myelopathy. What procedures will you be sure to do? Which
ones are optional? (You need to know this well enough to do on a patient without
an exam form telling you which tests to do)
a. DTRs
b. Sensory (sharp, vibration, proprioception)
c. Muscle testing
i. The above 3 are done in the UE and LE.
d. UE Hoffman’s/Clonus
e. LE Babinski/Clonus
f. Romberg
g. Neck flexion (Lhermitte’s sign)
h. Cranial nerve exam (rule out cerebral involvement)
i. Observe hand intrinsics
j. Finger escape sign
k. Rapid hand open and close
l. Single leg stand or run in place
34. Why can’t you stop after getting a positive Babinski? That means they have an
UMNL, right? What if you only had a positive clonus?
a. All these tests mostly suck, there is no one test or combination that is sensitive
enough to rely on. So you need to do as many as possible to not miss a
myelopathy.

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 35. How can you tell if a neurosurgeon will be worried about a cervical myelopathy
patient you send them?
a. The neurosurgeon is likely only worried if the compression is severe.
b. Mild - sensory symptoms, subjective weakness, hyperreflexia,
Babinski/Hoffman’s/Clonus, no functional impairment.
c. Moderate - objective motor or sensory signs, no or only mild functional
impairment (like mild slowing of gait).
d. Severe - objective motor or sensory signs with functional impairment (hand
weakness, unsteady gait, sphincter disturbance, etc).
36. What are the two most common causes of cervical spinal cord compression? How
common is it for herniation to compress the spinal cord?
a. Large central disc herniation.
i. Most common if patient <50-60 y/o.
ii. 15% of disc herniations cause cord damage.
iii. If a patient has a disc herniation, radiculopathy, or radiculitis in
cervical spine, need to evaluate for a possible myelopathy on the
FIRST VISIT.
b. Severe spondylotic changes with central canal stenosis.
i. Most common if patient >50-60 y/o.
ii. Caused by disc degeneration/bulging, facet thickening, ligament
thickening.
37. What is on your secondary list of conditions that can cause spinal cord
compression?
a. Trauma
i. Single event tractioning the cord into flexion.
b. Structural instability
i. Trauma, inflammatory arthritis, degeneration.
c. Tumor/SOL
d. Infection
e. Fracture
f. Spinal cord adhesions
g. Spurs/osteophytes are unlikely to cause a cervical myelopathy on their own.

Causes & Treatment of Cervical Radicular and

Myelopathic Syndromes (based on lecture and powerpoint slides)

Facts & Knowledge

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1. What are the three conditions at the top of your DDX list for a patient with a
cervical nerve root lesion?
a. Osteophytes
b. Disc herniation
c. Spinal Stenosis
2. Predict how a patient with a radicular syndrome due to a spur in the IVF might
respond to the common cervical orthopedic tests and various directions of AROM
of the neck.
a. Patients usually >50-60 y/o.
i. Clinical Tip: in older patients with radicular signs, consider spondylotic
spurs as first DDx.
b. Positions that close down the IVF may aggravate arm symptoms: Rotation,
extension, quadrant position or any test performed on the side of the arm
symptoms.
c. Positions that open the IVF may improve arm symptoms: this includes flexion,
rotation, and lateral flexion away from the symptomatic arm.
d. Cervical compression may aggravate arm symptoms (especially in disc
herniation).
e. Shoulder abduction doesn’t relieve symptoms and Valsalva doesn’t aggravate
symptoms (unless it is a disc herniation).
3. Besides radicular signs and symptoms, what are some of the osteoarthritic
findings that might be present in a patient with osteophytes?
a. Brief morning stiffness (< 1 hour).
b. Cervical crepitus.
c. Significant reduced rotation symmetrically even without being limited by
pain.
4. What are 3 positive findings in the physical that would cast doubt on osteophytic
compression being the best diagnosis for a radicular syndrome?
a. Little evidence of degenerative changes on a radiograph
i. Note: large percentage of asymptomatic patients show degeneration (like
spurs) on x-ray.
b. Arm pain centralizes with repetitive or sustained neck positioning (AKA McKenzie
evaluation).
c. Bakody’s sign or positive shoulder abduction test is more suggestive of a disc
herniation.
d. Positive Valsalva maneuver.
5. What is a “hard disc” and “soft disc?”
a. Osteophyte formation that includes part of the vertebral end plate/an old
herniation = hard disc.
b. A typical herniated disc = soft disc.
6. What are some signs of chronic radicular syndromes, likely from osteophytes?
a. Root pain rarely extends beyond elbow.
b. Paresthesia starts distal, pain starts proximal.

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 c. Muscle atrophy and hyporeflexia common, objective findings uncommon.
7. What are the sagittal canal measurements on a radiograph suggesting relative vs
absolute stenosis? What are the clinical implications of these measurements?
What follow up test would be necessary to confirm the diagnosis of spinal
stenosis?
a. Normal is >15 mm.
b. 10-12 mm relative radiographic stenosis
c. <10 mm absolute radiographic stenosis
d. MRI or CT is needed to see if the stenosis or osteophytes are really the cause of
neuro deficits.
8. What does cervical flexion do to the spinal canal? To the IVFs? What does cervical
extension do to the spinal canal? To the IVFs?
a. Flexion makes the central spinal canal larger throughout the spinal column,
makes IVD larger.
b. Extension makes the central canal smaller throughout the spinal column, IVD are
smaller, ligamentum flavum folds in with more extension.
9. What are potential effects of stenosis? How does stenosis affect the patient’s
prognosis?
a. Might cause myelopathy, radicular syndromes, or no symptoms.
b. Could be congenital or degenerative.
c. Could be the primary cause of a radicular or cord syndrome, or might be a local
complicator. Will usually affect the central canal, not an IVF.
i. Stenosis hurts the prognosis of conservative care.
d. Spurs are more likely if it is a radicular syndrome, stenosis is more likely if it is a
cord syndrome.
10. What is the most important component in a disc herniation that causes
symptoms?
a. Inflammation.
b. After a few weeks of treatment, a patient’s pain/symptoms might be much better
even though the herniation is still pushing against the nerve root. This is because
the inflammation has gone way down.
11. What structures might a disc herniation irritate/compress? What does this mean
clinically?
a. Nerve roots, spinal cord, or both!
b. Whenever a radicular syndrome is diagnosed in the cervical spine, you
must also evaluate for spinal cord involvement.
c. There could be both UMNL and LMNL findings.
12. Which two cervical discs most commonly herniate?
a. C6-C7 is the most commonly herniated discs, followed by C5-C6.
13. If your patient had C8 radiculopathy, what disc level would you suspect might
have herniated?
a. C7-T1

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 b. The radiculopathy is the bottom segment of the disk herniation in the cervical
region.
14. About what percentage of disc herniations are traumatic? <1/3? About 1⁄2? More
than 2/3rds?
a. Rare, about <⅓ (15-33%).
15. Where is a common sclerotogenous referral for a cervical disc herniation?
a. The neck, suprascapular, scapular, and interscapular regions.
b. Uncommonly, there may be no neck pain!
c. Otherwise, the pain, paresthesia, etc follow similar patterns to lumbar disc
herniations (worse than neck pain, paresthesia more commonly dermatomal,
etc).

16. What is Bakody’s sign? What does it mean? Is it common?

a. Bakody’s sign (placing the patient’s hand on their head) or positive shoulder
abduction test is more suggestive of a disc herniation. It is very uncommon but is
considered almost pathognomonic for a herniated disc!
b. May also be torticollis.
c. Chronic cases may have normal ROM.
d. Acute cases may have: flexion is most aggravating, quadrant position/Kemp’s
narrows IVF and may compress nerve root, lateral bending may increase pain
towards or away from symptomatic side.

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17. Predict the exam findings for each of the big 5 cervical orthopedic tests. Indicate if
each one is more specific or more sensitive?
a. For a herniated disk a patient would present with the following:
i. Cervical compression and Valsalva make the arm worse (positive test,
more specific). Cervical distraction and Shoulder abduction make the
arm better (positive test, more specific). → for all 4 of these, positive test
supports a radicular syndrome caused by a disc herniation, negative test
doesn’t tell us much.
ii. ULTT-median nerve makes the arm worse (positive test, more sensitive)
→ positive test doesn’t tell us where it’s coming from, but a negative test
makes us doubt a radicular syndrome.
18. About what percentage of cervical disc herniation patients also have cord
compression? Which level of disc herniation most commonly affects the cord?
a. 15%
b. C5-C6
19. You diagnose your patient with a disc herniation causing a radiculopathy, but you
know you need to look out for myelopathy when the herniation is in the cervical
spine. What might make you worried about spinal cord compression as well?
a. Spastic gait
b. Clumsy hand
c. UMNL signs, atrophy and sensory impairment
d. Sphincter disturbances
20. What are 5 indications for radiographs in patients with neck or neck and arm
pain?
a. Moderate to high load trauma (to R/O fractures & structural instability).
b. Red flags for disease
c. Cord signs/symptoms (then MRI)
d. Radicular signs/ symptoms
e. Unresponsive cases (perhaps after 1 month or more of failed care).
21. Under what circumstances would ordering an MRI for suspected disc herniation
be most advisable?
a. LOWEST requirement: signs/sx of radiculitis.
b. MODERATE: only if there are deficits.
c. HIGHEST: only if there is suspicion of myelopathy, progressive motor deficit,
non-response to conservative care, presurgical exam.
22. What are 3 key outcomes to monitor when treating a patient with a cervical disc
herniation?
a. Arm and neck symptoms (especially arm)
b. Neurological status (especially motor)
c. Effects on ADLs
23. What are the main conservative treatment interventions for the initial phase of
care of a cervical disc herniation? What two subacute interventions are
suggested?

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 a. Manipulation in direction of centralization.
i. When looking for a centralizing direction, can follow McKenzie protocol,
starting with 10 reps in protrusion/retraction, followed by retraction +
extension.
ii. Doctor can choose whether to adjust in a non-peripheralizing or
centralizing direction, or only to use graded mobilization in those
directions, or to not adjust/mobilize in the acute phase at all if they have
neurological deficits.
b. Traction or flexion-distraction.
i. Traction wasn’t part of the lumbar herniation management.
c. Repetitive end range loading (McKenzie).
d. Cervical collar (<3 days).
e. In subacute phase: neuromobilization, and cervical stabilization exercises
(same as in lumbar herniation).
f. Most disc herniations will resorb, and should be managed conservatively for at
least 2-3 months.
24. When manipulating a cervical disc, what are some of the set up
recommendations?
a. Position the neck to centralize peripheral Sx.
b. Rotate and laterally flex away from symptomatic side.
c. Try chin retraction.
d. Consider abducting the symptomatic arm.
e. Consider adjusting with distraction.
f. Could also modify adjustment to focus on distraction with the vector, or adjust the
upper thoracics supine or seated.
25. What are some of the parameters for performing traction on a patient with a disc
herniation? What is a situation when traction is generally not recommended for a
cervical disc herniation?
a. Start with chin retraction, then traction the patient’s neck towards a bit of flexion.
i. Should be flexed 15-20 degrees.
ii. The amount of pressure in the traction needs to be at least 20 lbs of
force.
b. Try with rotation and lateral flexion away from side with arm symptoms.
c. Traction in extension can also be helpful.
d. Main contraindications:
i. Midline disk herniation with acute torticollis
ii. Suspected cord compression (this one is also a contraindication to
adjusting in a cervical cord case).
e. Home care can include repetitive chin retractions given on first or second visit.
f. Rehab program is the same as for nonspecific neck pain: see nonspecific neck
pain part 2, question 7.
26. What is the prognosis for most cervical disc herniations?
a. Prognosis is generally favorable.

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 b. Most patients (up to 90%) will improve with conservative treatment.
c. 40% of disk herniations will resorb, usually after about 1 year.
i. However, symptoms will usually improve without resorption of the disc.
d. The worst period is the first 1-3 weeks, or up to 4-5 weeks.
i. Improves gradually afterwards for up to 3 months or longer.

Applications

(For each of the following, decide on a working diagnosis, and what kind of ancillary
studies may need to be order, and highlight areas in the history/physical which help rule
in your Dx and rule out opposing Dx)

27. 25-year-old forest ranger whose whole neck is stiff, especially in the upper
cervicals. Neck aches 3/10 OPS, punctuated with sharp pain in the posterior neck.
No radiation, numbness, tingling or weakness in the arms. Started a few days ago
and has been getting worse. End range extension causes neck pain. Cervical
compression in neutral doesn’t hurt, but with rotation and extension to the right it
hurts a lot in the right side of C4-C6 spinous processes. There is much palpatory
tenderness there as well as multiple segmental restrictions.
a. Cervical Facet Syndrome + joint dysfunction.
28. 65-year-old patient has neck pain and left arm pain intermittently for the last six
months. Neck pain is dull and achy, mostly on the left. Sharp pain will sometimes
radiate down lateral arm past the elbow. Sometimes a “cold feeling” in thumb and
first finger of left hand. History of three whiplash injuries over the last 10 years. All
were treated and all resolved. No idea what brought it on this time, and it is getting
worse. Cervical ROM limited in rotation by 50% bilaterally without pain. Cervical
compression in neutral and passive extension causes local neck pain. Maximum
cervical compression to the left side reproduces sharp arm pain. Diminished
feeling (both light touch and pain over lateral hand).
a. C6 radiculopathy due to osteophytes.
29. 40-year-old barber has bouts of severe neck and arm pain for the last month. Pain
radiates down the inside of right arm all the way to the hand. Neck ROM guarded
in all directions (reduced by about 50%). Abduction of arm toward end range
reduces arm pain. Cervical compression reproduces arm pain and so does
doorbell sign performed in lower part of neck. Loss of sensation to all modalities
over right middle finger. Triceps muscle weaker on left than on right. Valsalva
maneuver reproduces pain. Positive Babinski on the right foot.
a. C8 radiculopathy due to disc herniation, possible myelopathy that needs to
be evaluated.
30. 35-year-old computer programmer has a sense of numbness in his whole right
hand that gets worse throughout the day. He notices that his fingers sometimes
blanch very white when he enters a cold room. He also complains of a general
lower neck and upper back ache. Cervical ROM is complete and painless. Cervical

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 compression, distraction, ULLT test-median nerve, and shoulder depression are
all negative. SMR tests are WNL. The only findings are atlas has a tender and
prominent TP on the right side, and T3-T4 is restricted in extension with palpable
muscle spasm on the left.
a. T4 syndrome + Raynaud’s phenomenon.
31. 35-year-old teacher has LBP that radiates into the buttock along with some groin
pain. It came on slowly over the last week. Now sitting is very uncomfortable and
it hurts getting in and out of the car. She finds that if she hyperextends her back
doing a Yoga “cobra” posture she gets some relief. She denies NTW. AROM is
limited in extension and flexion, but more in flexion. The SLR aggravates her back
and buttock. SMRs are WNL. Active double leg raise is too painful to perform.
a. Lumbar disc derangement.
32. 35-year-old professional dancer was rear-ended while sitting in her car at a stop
light. The next day she started having neck pain and pain and paresthesia in her
right medial hand. AROM is limited in extension and flexion, but more in flexion
due to neck pain. Cervical compression is unremarkable but cervical Kemp’s
aggravates the hand symptoms. Cervical flexion muscle test is moderately painful
and mildly weak. Pin prick reveals hyperalgesia along her little finger. The rest of
the neuro exam is normal. The Davis series of radiographs are normal except for a
slight loss of lordosis. MRI is normal.
a. C8 radiculitis due to direct trauma to the nerve root, associated multiple
muscle strains.

Causes & Treatment of Cervical Radicular and

Myelopathic Syndromes, Part 2 (based on out of class Panopto
lecture and powerpoint slides)

1. Your patient has a cervical radiculopathy. What is on your DDX from the “B” list of
causes?
a. Trauma directly to the NR (single event compressing or traction the nerve root)
b. Structural instability (due to trauma, inflammatory arthritis, degeneration)
c. Tumor/SOL (e.g., metastatic spinal cancer, facet/synovial cyst, ossification of the
posterior longitudinal ligament)
d. Infection (starts as discitis, then migrates to the bone, where we call it infectious
spondylitis)
e. NR adhesions (Dx by exclusion since x-ray/MRI can’t see this)
2. Describe 3 traumatic mechanisms that can directly injury a nerve root.
a. Compression
b. Hyperextension (especially with rotation)

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 c. Lateral flexion with shoulder depression (think brachial plexus first, then NR)
d. Could also be hyperflexion, but this is uncommon since the chin hits the chest. If
it does happen, the spinal cord is tractioned.
3. List 3 muscles with myofascial trigger points that can mimic a C6 radicular
syndrome. Name two that can mimic a C8 radicular syndrome.
a. C6
i. Scalenes
ii. Supraspinatus
iii. Subclavius
iv. Infraspinatus
b. C8
i. Latissimus Dorsi
ii. Serratus anterior
c. Subscapularis doesn’t mimic any specific nerve root.
4. What is cervical cord neuropraxia?
a. Transient neurological syndrome occurring in athletes with cervical spine injury.
b. Lasts 15 minutes to 48 hours, complete recovery.
c. Could cause bilateral paresthesias, or in the worse case complete quadriplegia.
d. Caused by brief spinal cord compression during a cervical spine injury.
5. Your patient has a cervical myelopathy. What is on your DDX from the “B” list of
causes?
a. Tumors
b. Structural instability
c. Cord trauma injury
d. Fracture/dislocation
e. Cord adhesions
f. Infection
6. How does a myelopathy change your management plan? What is the prognosis?
a. Majority of the time, manipulation is contraindicated!
b. Up to ⅔ of myelopathy patients will have deteriorating or unchanging
conditions, with only ⅓ completely recovering.
c. Cervical decompression surgery is treatment of choice.

TOS and Cervicobrachial Plexus Injuries (based on in-class

Panopto lecture and powerpoint slides)

1. Describe 2 traumatic mechanisms that can directly injure the brachial plexus.
a. Traumatic traction: Traumatic Brachioplexopathy

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 i. Lateral flexion and contralateral shoulder depression as result of fall
on head/shoulder → traction of upper trunks C5-C6 (nerve roots also
at risk).
ii. A fall and grab injury, like from a ladder → traction injury of the
lower trunks C8-T1 (nerve roots are probably safe).
b. Slow postural load traction:
i. Sleeping in lateral flexion and contralateral shoulder depression.
2. What usually is the prognosis for most brachial trauma cases?
a. Usually self-limiting with or without sequelae. Recurrent injuries to the affected
area poses the greatest risk for long-term side-effects.
3. What ancillary study would be most helpful to differentiate a nerve root injury from
a brachial plexus injury?
a. EMG
4. Your patient has traumatized the upper trunk of the brachial plexus. What muscles
might test weak? What deformity might be observed if the damage was serious?
What does this deformity look like? What symptoms might be observable on the
face?
a. Elbow flexors, shoulder abductors, and external rotators are weak.
b. Waiter’s tip posture (adduction, internal rotation, pronation, wrist flexion)
c. If the sympathetic chain was damaged then possible Horner’s syndrome.
i. Meiosis, ptosis, and anhidrosis.
d. Follow C5-C6 distribution.
e. Note: middle trunk injuries are rare but possible, and will follow a C7 nerve root
pattern.
5. Your patient has traumatized the lower trunk of the brachial plexus. What muscles
might test weak? What deformity might be observed if the damage was serious?
What would it look like? What sympathetic nerve symptoms might be observable
in the arm?
a. Wrist/finger flexors and intrinsic hand mm.
b. Claw hand deformity (flexion at the 1st, 2nd, and 3rd fingers because the 4th
and 5th fingers are too weak).
c. Edema and trophic changes in forearm/hand.
d. Horner’s syndrome.
e. Follow C8-T1 distribution.
6. Your patient has an brachial plexus upper trunk lesion. What are some specific
causes? Lower trunk lesion?
a. Upper trunk
i. Traction injury (traumatic or postural).
ii. Stab wound
b. Lower trunk
i. Hyperabduction of shoulder
ii. Clavicle fracture
iii. Dislocation/fracture of humeral head

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 iv. Pancoast tumor
v. Aortic aneurysm
vi. Cervical rib
7. List some differences between nerve root injuries and brachial plexus injuries
(types of mechanisms of injury, predisposing factors, aggravating factors).
a. Root injury
i. Compression within IVF
ii. Extension w/ compression
iii. Neck pain common
iv. Associated w/ stenosis in adults
v. More common in college sports
b. Plexus injury
i. Traction Injury
ii. Lateral bending + shoulder depression
iii. Neck pain not usually prominent
iv. No spinal stenosis predisposition
v. More common in high school sports
8. What structures can be compressed in a TOS case? What structures are usually
doing the compression?
a. Brachial plexus and subclavian A&V are compressed.
b. Structures are within the thoracic inlet (superior thoracic aperture).
c. Usually postural or overuse, but may be due to trauma.
d. Bony margins:
i. Posterior: T1 vertebra
ii. Laterally: 1st ribs
iii. Anteriorly: 1st costal cartilage and manubrium
iv. These are potential areas to manipulate if locked/tender.
e. Structures doing the compression:
i. Anterior scalene muscles
ii. Pectoralis minor
iii. May have costoclavicular compression
iv. Subclavius or middle scalene may also contribute.
f. Common areas of compromise:
i. Interscalene triangle (supraclavicular)
1. Scalenus anticus syndrome
2. Cervical rib
ii. Between the first rib and clavicle (costoclavicular)
iii. Between the coracoid process and the tendon of pec minor
(infraclavicular)
1. Hyperabduction = pectoralis minor syndrome
9. Describe some specific postural contributors to TOS.
a. “Drooping” shoulder girdle posture/forward head carriage (rolled forward
shoulders) - intrinsic posture

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 b. Tight pectoralis major
c. Upper cross syndrome
d. Poor work postures - extrinsic posture
e. Long periods of hyperabduction of the arm due to job/recreation/sleeping
posture - extrinsic posture
f. Carrying heavy weights on back or arms (single strap book bag).
10. What are the three main types of TOS?
a. Non specific (AKA neurogenic TOS)
i. Typical TOS (85% of cases)
ii. W/ infraclavicular pec minor hyperabduction TOS, neuro symptoms are
prominent (but are not signs unless it’s true neurogenic TOS)
b. True neurogenic
i. Objective evidence of nerve damage (deficits)
ii. OR EMG nerve conduction study showing nerve damage
c. Vascular
i. Uncommon, arterial version slightly more common.
ii. Arterial: requires surgery - resection of cervical rib (time sensitive, but not
urgent).
iii. Venous: risk of thrombus/embolism formation (urgent, same or next day
referral)
1. If patient is SOB, possible pulmonary embolism → emergency
referral!
iv. MUST REFER OUT!
v. Note: The diagnosis is not based on loss of pulse during TOS
orthopedic tests, but on combination of vascular signs and
symptoms.
11. Describe key signs and symptoms that would suggest significant arterial
compromise.
a. Symptoms:
i. Ischemic pain
ii. Cold sensation
iii. Complaints or signs of mm cramping or fatigue with repetitive use
b. Signs:
i. Pallor of fingertips (may feel cold)
ii. Asymmetrical radial pulses
iii. Asymmetrical blood pressures
iv. Subclavian bruit
v. Splinter hemorrhages
12. Describe key signs and symptoms that would suggest significant venous
compromise.
a. Symptoms (Hx):
i. Fatigue, heaviness in the extremity
b. Signs (PE):

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 i. Nonpitting edema of hand or arm
ii. Cyanosis
iii. Ecchymosis (discoloration of skin from ruptured blood vessels)
iv. Distended engorgement of superficial veins in the infraclavicular area,
upper extremity and chest (not varicose veins).
13. Describe a “Gilliatt- Sumner hand.” What condition is it associated with?
a. Atrophy of the abductor pollicis brevis muscle.
b. Thenar eminence has a scooped out appearance.
c. It is associated with true neurogenic TOS.
14. What are the minimum requirements to make a “true” neurogenic TOS diagnosis?
a. A reproducible neurological deficit seen in the PE.
b. OR
c. A positive EMG-NCV study demonstrating plexus damage.
i. Stick a needle in muscles, check for action potentials. Look at grouping of
conduction to figure out where the nerve damage is.
15. TOS is most common among what gender and age group?
a. True neurogenic : Young thin females
b. Extremely rare (1/1,000,000)
c. Non-specific : 20-40 females
i. In this type, primary sign is pain and paresthesia.
ii. ULNAR nerve distribution usually, but median nerve distribution possible.
iii. May have neck pain.
iv. Sometimes pallor in fingers.
v. Worse after activity or at night.
vi. Caused by trauma, posture, or repetitive microtrauma.
vii. Catching pain in shoulder.
viii. UE fatigue on exertion, heavy/weak feeling.
ix. 1st rib and A-P lower cervical rotation restrictions are common.
x. Commonly associated with a congenital cervical rib —> impingement
d. Neurologic signs dominate in true neurogenic:
i. Little or no pain or intermittent pain
ii. Sensory paresthesias/dysesthesias
iii. Sx usually restricted to the ULNAR aspect of the hand (lower branch).
iv. Aggravated by overhead activities, carrying heavy objects, and may be
worse at the end of the day and when sleeping.
16. What 5 orthopedic tests are recommended to perform to make a TOS diagnosis?
How many are recommended to be positive? What would be the strongest positive
finding for each test (reproducing pain? paresthesia? pulse loss?)
a. Adson’s test
i. Strongest positive is cc pain reproduction in the upper extremity
ii. Paresthesia is a softer positive.
iii. Least useful is loss of pulse.
iv. Lots of healthy people lose pulse (little clinical meaning).

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 b. Hyperabduction test (Wright’s test)
i. Positive test reproduces arm pain/paresthesia - may need to maintain for
30-60 seconds
ii. Loss of pulse alone is clinically meaningless.
iii. If arm sxs improve, think possible nerve root (positive shoulder abduction
test).
c. Costoclavicular test (Eden’s)
i. Compression of the clavicle down on the first rib may reproduce pts hand
or arm Sxs.
ii. Arm down and back, chest out.
d. Roos test
i. Tell patient to hold arms up and open and close hands for up to 3 minutes
ii. Positive finding is arm dropping due to exacerbation of symptoms (has to
be asymmetrical).
e. Tinel’s (or deep pressure)
i. Tap or apply pressure just superior to the clavicle, reproduce arm Sxs.
f. To minimize false positives:
i. Pain used to define a positive Adson’s test, costoclavicular test or
supraclavicular pressure (then paresthesia).
ii. A patient discontinues Roos test d/t pain before 3 minutes
iii. At least 2 of the TOS Tests reproduced pain in the upper extremity or
at least 3 tests produced any symptoms in the same arm.
17. What three key muscles should be assessed? What methods should you use to
assess each one?
a. Scalenes (length test) - supraclavicular
i. Neuro Sx more common than Vascular Sx.
b. Pectoralis major (length test) - less likely - infraclavicular
c. Pectoralis minor (length test and palpate, harder to isolate for a stretch) - least
likely - infraclavicular
i. Neurologic Sxs prominent, but not signs unless it is a true
neurogenic TOS.
d. Costoclavicular entrapment also possible.
i. Vascular Sx more common than Neuro Sx.
18. What would be your key differential diagnosis in a TOS case?
a. Carpal tunnel
b. Cubital tunnel
c. Cervical radicular syndromes
d. Myofascial pain syndromes
19. What are some general steps to assess possible TOS?
a. Use history and TOS ortho tests to suggest TOS, rule out more common Dx.
b. R/O true neurogenic TOS (SMRs) and arterial/venous compromise (vascular
exam).
c. Assess compressing structures (scalenes, pecs).

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 d. Assess thoracic spine and shoulder girdle joints.
e. Decide if influenced by: intrinsic posture, extrinsic posture, faulty breathing
patterns, or elements of upper cross syndrome.
20. Outline your management plan for a typical TOS case. Be as specific as possible.

CMT STM

Joint manipulation to: Stretch:

- Rib 1 - Scalenes
- Cx (esp. A-P of lower cervicals) - Pec. Minor
- Upper Tx - Levator Scapula
- AC, SC, GH, scapulothoracic - Suboccipitals
Intermittent ischemic compression:
- Pec. Minor
PIR, CRAC
Pin and Stretch (ART)
IASTM
“Nerve flossing”

BM Ex

- Adapt job, sport or environment to - Correct forward head carriage

decrease risky posture. - Correct rounded/drooping shoulders
- Find alternate ways to carry packs, - Address upper cross syndrome
bags. Home stretches:
- Assess need for proper bra support - Pectoralis muscles
and width of straps. - Scalenes
- Consider avoiding long bike rides, - Brachial plexus nerve mobilization
swimming, long periods of driving. Brugger Relief Position:
- Perch at edge of chair
- Abduct & externally rotate your legs
- Lift your sternum slightly
- Tuck your chin in & look straight
ahead
- Supinate your arms as you exhale
actively
- Repeat 3-4X
Teach proper breathing:
- Vertical breathing may be associated
with overactive scalenes
- Belly breathing with lateral rib
excursion w/ inhalation
- Avoidance of substitution patterns
involving upper trapezius and
scalenes

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Headache Neurology (including ataxia and vertigo)
(based on in-class lecture and powerpoint slides)

Facts & Knowledge

1. When assessing a patient with headaches or central nervous system symptoms,

what are three major parts of the brain that need to be screened and what are the
types of tests that are used to screen each part?
a. Cerebrum
i. UMNL signs
ii. Cognitive dysfunction or mood problems
b. Cerebellum
i. Ataxia
ii. Vertigo
iii. Dysarthria
iv. Problems w/: rate, range and force of movement, equilibrium,
coordination of eye and neck movement.
c. Brainstem:
i. Cranial nerves w/ presentation contralateral to lesion
2. What is an example of a neurological exam when you suspect a more serious
headache?
a. Orientation, mental status, mood
b. Gait/cerebellar tests
c. Cranial nerve exam + fundoscopic exam
d. UE and LE light touch, sharp/dull
e. Muscle testing both proximal and distal muscles in all 4 extremities
f. DTRs (biceps, triceps, patella, Achilles)
g. Pathological reflexes
3. What are some of the components of a mini mental status exam?
a. Level of consciousness
b. Orientation (X3)
i. Who are they?
ii. Where are they?
iii. What year is it?
c. Mood
i. Inappropriate affect?
ii. Depressed?
iii. “Cooperative” in a report implies that mood is normal.
d. Registration and short term memory

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 i. Remember 3 common objects for at least 3 minutes.
e. Calculation
i. 100-7 taken out for 5 subtractions
ii. Or spell a word backwards
iii. If pt gets mad and refuses —> non cooperative —> inappropriate mood
4. What is ataxia? What are the 3 types of ataxia? What are some tests for each
type? What are some causes of each type?
a. Ataxia = lack of coordination of voluntary muscle movements
i. “Lack of order” (Greek)
b. Sensory ataxia
i. Corrupted input from peripheral nerves through the posterior column of
the spinal cord.
ii. Wide-based & tentative gait. Watches foot placement.
iii. Station = normal w/ eyes open. Abnormal w/ eyes closed (+ Romberg).
iv. Decreased sensation in distal extremities (glove & stocking)
v. Depressed / absent Achilles DTR
vi. Speech, vertigo and nystagmus all normal.
vii. Causes:
1. Cord damage (posterior column)
2. Multiple nerve root damage (Lx spinal stenosis)
3. Polyneuropathy (diabetic neuropathy)
c. Vestibular ataxia
i. Inner ear or CN VIII lesion
ii. Head sxs
iii. Gait driven by the “spins” - “true” vertigo
iv. Station - may be abnormal with eyes open, often abnormal with eyes
closed, swaying/balance issue.
v. Speech normal.
vi. Nystagmus and “True” vertigo present.
vii. Caused by inner ear problems.
1. Viral labyrinthitis
2. Ménière’s disease
a. Acute recurrent attacks (several hours) or hearing loss,
tinnitus, fullness in one ear.
d. Cerebellar ataxia
i. Very wide-based and very irregular w/ possible arms out for balance.
ii. May be afraid to walk. Most trouble turning (may only be abnormal when
turning in one direction and not the other).
iii. Station - abnormal w/ eyes open and closed.
iv. Limb ataxia in various limbs
v. Dysmetria - past-pointing
vi. Truncal ataxia - flexed at waist
vii. Normal sensory exam

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 viii. Achilles DTR is intact but “pendular” (repeating)
ix. Slurred speech
x. “True” vertigo and nystagmus - possible
xi. Causes: cerebral lesion (MS, stroke, trauma, tumor, alcohol)
5. What is dysmetria? How would you test for it?
a. Dysmetria (limb ataxia) is an UE finding in cerebellar disorders/ataxia.
b. Have pt touch their finger to a target and then finger to their nose.
i. Dysmetria/past pointing is seen w/ an ipsilateral lesion of cerebellar
hemisphere.
ii. Test can elicit even mild limb ataxia.
c. Intention tremor
d. Heel to shin
i. Pt tries to run heel along shin up and down several times
ii. If cerebellar disorder, will not be able to keep heel on shin
6. How would you test for stereognosis? What lobe of the brain does it test? What
about a test for graphesthesia?
a. Stereognosis = ability to recognize familiar objects by sense of touch w/ eyes
closed.
i. Eyes closed - put object in patients hand. Ask to identify. Test two objects
in each hand.
ii. Astereognosis = abnormal. Pt cannot identify object by feeling it in their
hand, or failure to grasp.
b. It tests the contralateral parietal lobe affecting association center OR posterior
column cord lesion.
c. Graphesthesia = ability to recognize letters or numbers being traced on the skin.
i. Patient closes their eyes while you trace on their hand.
ii. Agraphesthesia = inability to identify letter or number (also a test of the
contralateral parietal lobe).
7. What does a “focal deficit” refer to?
a. Cranial nerve deficits are considered to be “focal deficits” and suggest a
patient’s headache is due to a serious cause.
8. What is papilledema? What can cause it?
a. Optic disc swelling d/t increased intracranial pressure (ICP).
b. Causes:
i. Tumor
ii. Optics neuritis
iii. Pseudotumor
9. Compare and contrast pronator drift and cerebellar drift and their respective
causes.
a. Pronator drift = important early indicator of UMNL
i. Generalized extremity weakness as might be seen in a stroke
ii. Note: UMNL tend to cause weak gross movements/positions, while LMNL
tend to cause specific weak muscles/muscle groups.

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 iii. Hold both palms up for 2 min.
iv. Pt will have one or both arms drop, internally rotate and flex at the elbow,
while the wrist flexes & hands pronates.
b. Cerebellar drift = indicates cerebellar lesion
i. Arms may drift in any direction, though their eyes must be closed.
10. What are some conditions that can cause spasticity via an UMNL?
a. Stroke
b. Traumatic Brain Injury (TBI)
c. Spinal cord injury
d. Less common: (FYI)
i. Cerebral palsy
ii. MS
iii. Amyotrophic lateral sclerosis
iv. Brain damage d/t oxygen debt, encephalitis, meningitis
11. What are some of the key symptoms associated with cervicogenic vertigo?
a. Most common in females, 30-50 y/o.
b. Dizziness (80-90%)
c. Neck pain (must be present)
d. Headache (common)
i. May be occipital, TMJ, forehead, orbital regions, tension like headache.
e. Tinnitus (30%)
f. Hearing loss (less common)
g. Earache
h. Feeling of unsteadiness when standing
i. Pts experience “room is spinning”
j. Can be due to
i. Trauma (CAD injury common)
ii. Chronic musculoskeletal problems (Cx or shoulder dysfunction)
iii. Anxiety
12. What are 3 key physical examination findings to support cervicogenic vertigo?
a. Neck movement may include nystagmus.
b. Pain with palpation of lateral mass of atlas & suboccipital muscles.
c. Induced by neck rotation while the head is stationary.
d. Swivel Test = used to decipher cervicogenic vertigo from the inner ear caused
vertigo.
i. If moving the body while the head is stationary causes unsteadiness,
dizziness, recreation of symptoms = positive for cervicogenic vertigo.
13. What is thought to cause Barré-Lieou Syndrome? What are some of the
presenting symptoms? What are some findings that would help differentiate it
from cervicogenic vertigo?
a. Barre-Lieou Syndrome (Posterior cervical sympathetic syndrome)
i. Suboccipital pain and vertigo precipitated by head rotation.
b. Symptoms:

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 i. Suboccipital pain, tinnitus, unilateral facial pain or eye pain.
ii. Vertigo made worse by turning head —> cervicogenic vertigo
iii. Visual symptoms
iv. Acute episodes of hoarseness that disappear suddenly
v. Severe fatigue
vi. X-ray changes at C4-C6
1. Both help differentiate from cervicogenic vertigo.
14. What is thought to cause Meniere’s Syndrome? What is the triad of exam findings
suggestive of this condition?
a. No pain
b. Acute attacks may last for several hours:
i. Recurrent attacks of vertigo
ii. Hearing loss
iii. Tinnitus (ringing or buzzing)
c. Fullness in one ear.
d. Residual symptoms may remain for days or longer.
e. Associated with a change in fluid volume (endolymph) within the labyrinth.
f. Diagnosis is by exclusion.
g. Treatment: low salt diet, no caffeine or alcohol.
15. What would your management plan look like to treat cervicogenic vertigo?
a. CMT to Cx to stimulate mechanoreceptors.
b. Rehab to balance muscle dysfunction, increase proprioception/ROM.
i. Start with AROM reps in different directions on a stable surface, with the
eyes leading the movement before moving the head.
ii. Progress to an unstable exercise ball.
c. 85% of patients have favorable outcomes from those 2 treatments.
16. How do you perform the following tests, what is a positive test, and what does that
indicate?
a. Hoffman’s - Flick the nail of the third digit. Positive sign is finger snapping sign of
the flexion of the thumb and the index finger. Possible cord lesion.
b. Sitting Swivel test - Patients on a chair that swivels and closes their eyes. They
shake their head from side to side → if symptoms of vertigo return, the vestibular
system or cervical spine may be responsible. Wait for the symptoms to subside.
Hold the patient’s head still while they swivel themselfs side to side in a chair.
Positive for cervicogenic vertigo if the symptoms return.
c. Scalene length test - One hand on clavicle, and the other hand pulls head
diagonally into opposite LF and extension. May or may not be painful, but
decreased LF due to tight scalenes is a positive test. Could indicate a TOS.
d. Roos test - Hold arms up and tell the patient to open and close their hands for
up to 3 minutes. Positive if arm is dropping due to exacerbation of symptoms, but
must be a unilateral finding. Possible Plexus injury.

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Applications

17. A 45-year-old female presents with intermittent dizziness and tinnitus for the past
2 years. Intermittent and worse when shopping at Costco. Pressure over atlas
recreates vertigo. Globally decreased cervical ROMs. Cervical spine rotation is
provocative for vertigo.
a. Cervicogenic vertigo
18. 35 yo female w/ dizziness, extensive fatigue, with neck, suboccipital and right
temporal pain for the past 10 years. History of cervical disc herniation at C5-6. All
exam findings normal. Observation of minimal Horner’s syndrome. No provocative
test findings.
a. Barre-Lieou Syndrome
19. For each of the following injuries, indicate which orthopedic tests, if positive,
would support your diagnosis:
a. Cervical compression injury
i. Nerve root may be damaged, test using the big 5 orthopedic tests
(cervical compression, cervical distraction, shoulder abduction,
ULTT-median nerve, and valsalva).
b. Hyperabduction traction injury
i. Brachial plexus may be damaged, test using Tinel’s sign in clavicular
fossa, shoulder depression, ULTT-median nerve.
ii. TOS tests will probably be negative.
c. CAD hyperextension injury
i. Nerve root may be damaged, same big 5 as before.
d. Lateral flexion with shoulder depression injury
i. Brachial plexus may be damaged (probably upper trunk), test the same
as the traction injury.

Serious Headaches (based on out of class Panopto lecture and powerpoint

slides)

1. What group of 3 symptoms is suggestive of a brain tumor headache? How

commonly does it is it present this way?
a. 20% have a headache initially, 90% will get a headache eventually.
b. Classic Triad - only occurs 17% of the time.
i. High Severity
ii. Worse in the morning
iii. Associated with Vomiting
2. Cite 5 additional clues that are consistent with a tumor generated headache.
a. HA increased with Valsalva

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 b. Resistance to analgesics (i.e. acetaminophen)
c. Patients have had a seizure or epileptic episode (Cardinal Sign) + Loss of
consciousness (LOC).
d. Focal neurological deficits - CN Exam findings
e. Slow Growing Tumor - grow over months to years
i. Esp. Frontal Lobe of brain: Personality change
1. Mistreatment for depression.
3. How often due ischemic strokes present with headaches?
a. Headache occurs in 20% of ischemic STROKES.
i. Bottom line: most don’t get headaches.
4. What clues from the history or physical suggest that the patient’s headache is
associated with an ischemic stroke or TIA?
a. Half will be unilateral, focal, mild to moderate severity.
i. Associated Sx’s
1. Nausea
2. Vomiting
3. Photophobia + Phonophobia
ii. Aggravating Factors
1. Valsalva
2. Nitroglycerine
iii. Lasts about 4 days.
b. Headaches w/ TIAs
i. Lasts about 17 hours (much shorter than ischemic stroke headache).
5. What are the hallmarks of a subarachnoid hemorrhage? What other
life-threatening conditions share the same hallmarks?
a. Subarachnoid Hemorrhage
i. Key presenting Sx: SEVERE and SUDDEN HEADACHE (98% of cases)
1. Similar to Vertebrobasilar or Carotid dissection.
ii. Usually unrelenting, bilateral.
6. What is the most common age range for a subarachnoid hemorrhage?
a. 40-60 y/o
7. What are some the other associated symptoms (from the history) that may be
present with a subarachnoid hemorrhage?
a. May come on sudden (i.e. bolt up in middle of night) OR may come on during
exertion.
b. Remain for hours to several days, subside over a couple weeks.
c. Nausea/vomiting
d. Transitory LOC
e. Transitory Muscle weakness
f. Nuchal Rigidity
g. Photophobia
h. Seizures
i. DIzziness

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 j. Change in mental status or alertness
k. Warning Sign: Sentinel Bleed (50% of cases)
i. Hours or days before
ii. Maybe absent in elderly
iii. Similar symptoms but milder
iv. May have facial pain or local deficits (eye field, eye movement).
v. So if patient starts with mild versions of the above symptoms, then a
few hours or days later, it becomes much more severe, might be
full-blown subarachnoid hemorrhage.
8. What are some the other associated signs (from the physical) that may be present
with a subarachnoid hemorrhage?
a. Patient appears ill.
b. At time of physical exam: ***NO PROMINENT NEUROLOGICAL FINDINGS***
i. DDx Migraine - don’t confuse.
ii. Signs may take HOURS to DAYS to manifest.
c. Si’s of Meningeal irritation
i. Trouble flexing neck or unable to.
d. Lethargy
e. Hypertension
f. Fever (up to 102 deg F)
g. Visual FIeld Defects
h. Double Vision
i. Oculomotor Paralysis
j. Bilateral Babinski reflex
k. Hemiparesis
l. Subhyaloid Hemorrhage (Pathognomic)
i. Seen in fundoscopic exam
ii. Smaller deceptive bleed
iii. Severe abrupt hemifacial pain during exercise or sexual intercourse
iv. Slight alteration in awareness
v. Subtle meningeal Irritation
vi. Asymmetry in pupillary response, equivocal Babinski, pronator drift
9. If you indeed think your patient is having a subarachnoid hemorrhage after the
history and physical, what will you refer your patient out for?
a. Immediate CT!
i. However, 10% of the time there will be a false negative, so will follow up a
normal CT with a spinal tap looking for blood.
10. What are the two main sets of findings suggestive of a cluster headache. Describe
each set in detail.
a. PAIN
i. EXCRUCIATING
ii. SWARMS of brief headaches
1. Duration: 15 min-3 hours, 1x-8x per day

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 2. Nocturnal manifestation
iii. Unilat eye, temporal, forehead
iv. Quality: stabbing, burning, pulsating
b. Associated Sx’s - UNILATERAL
i. Ipsilateral facial sweating
ii. Lacrimation - tears
iii. Nasal Discharge or congestion
iv. Ptosis and Meiosis (Partial Horner’s Syn)
v. Swelling of Eyelid
vi. Conjunctival Injection
11. Who tends to get a temporal arteritis headache? What other symptoms can be
associated with this condition?
a. >50-55 years old (<40 yo → don’t even include on DDx list)
b. AVG age: 72 years old
c. More common in women than men (3:1)
d. Very rare
e. New primary complaint of Headache with:
i. Jaw Claudication (pain near TMJ after chewing firm foods)
1. DDx with TMJ condition or poor fitted dentures.
ii. Vision complaints
1. Diplopia, sudden transient monocular blindness!
iii. Polymyalgia Rheumatica (PMR - 50% of cases)
1. Abrupt morning stiffness - neck, shoulder girdle, or low back!
2. Myalgia with significant tenderness or proximal arms and thighs.
iv. Fever, fatigue, unexplained weight loss
v. Scalp Tenderness (combing hair)
12. What key examination procedures would you perform and what are the findings
that would suggest temporal arteritis? Describe in detail.
a. Temperature: low grade fever
b. Ophthalmoscopic Exam
i. Pale swollen disk
ii. Retinal occlusion
c. Visual field testing: loss of visual field
d. Upper and Lower Ext. Joint Assessment
i. PMR also Present?
1. Decreased ROM for shoulder and hip
2. Muscles significantly TENDER
e. Visual Inspection Of Scalp
i. Nodules, redness along temporal artery
ii. Scalp/tongue ischemic or necrotic changes
f. Palpation of Scalp
i. Lightly palpate anterior to tragus of ear, follow temporal pulse up and
anteriorly.

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 ii. Compare side to side for:
1. Tenderness
2. Swelling
3. Decreased pulse on one side
4. String of hard nodules
5. Prominent nodule
13. Why is temporal arteritis an urgent referral?
a. Associated w/ SUDDEN IRREVERSIBLE BLINDNESS!
i. Suspected? → Urgent referral for assessment and BIOPSY.
14. What ancillary tests can be ordered for this condition and what would be the
findings? T.A.- inflammatory
a. ESR >50 - could be >100
i. Can’t use by itself - 10%-20% have normal ESR
ii. Example: 72 yo patient with HA has normal ESR - still has 12% risk of
T.A.
iii. Jaw claudication and tenderness → risk goes up to 78%.
b. C-Reactive Protein: could be elevated, but cannot R/O
c. CBC
i. Normocytic Anemia present in 44%
ii. Platelet count may be increased.
d. Temporal Artery Biopsy = GOLD STANDARD
i. Mandatory to make diagnosis.
ii. Sn= 85%, Sp=100%
15. What are the key signs and symptoms of meningitis?
a. Classic Triad (not all will have all 3)
i. Painful, Stiff neck
ii. Fever
iii. Headache
16. Describe Brudzinski and Kernig’s tests. How accurate are they for a meningitis
diagnosis?
a. Brudzinski
i. Passive head flexion: positive if knees come up.
b. Kernig's
i. Supine: thigh to 90 degrees, try to extend knee, patient won’t let you.
c. Both Tests: LITTLE or NO VALUE (LR = 1.0)
d. Note: an additional test is if the patient has a rash, you can press a glass against
it. In a meningitis case, the rash will stay visible, but non-meningitis rashes will
disappear.
17. Describe each of the SNOOP4 red flags.
a. Systemic
i. Unexplained fever, chills, weight loss.
ii. New onset headache in a cancer, immunosuppression, or HIV patient.
b. Neurologic Findings

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 i. Motor weakness, sensory loss, diplopia, ataxia.
c. Onset of headache suddenly
d. Onset of new headache >50 y/o
e. Pattern change
i. P1 - Progressive evolution to daily headache
ii. P2 - Made worse by Valsalva
iii. P3 - Postural aggravation
iv. P4 - Papilledema
18. Which conditions that can cause a headache would need a referral?
a. Subarachnoid hemorrhage or hematoma
b. Tumor
c. Stroke/TIA/aneurysm
d. Temporal Arteritis
e. Meningitis

Headache (based on in-class lecture and powerpoint slides)

1. What are some causes of benign acute headaches (lasting <10 days)?
a. Acute infection
b. Eye strain
c. Stress or lack of sleep
d. Caffeine withdrawal
e. Dehydration
f. Constipation
g. Medication
2. What important headaches must you consider in trauma patients? Which are the
most serious?
a. Subarachnoid hemorrhage (from trauma or congenital predisposition)
b. Subdural or Epidural hematoma (trauma)
c. Post-traumatic HA, post-concussive syndrome, or traumatic brain injury
d. Patients with a headache may not remember the trauma, so you can’t rule it out
just based on them not reporting a trauma. Need to be vigilant.
3. What percentage of patients with a subdural hematoma have a headache? How
severe are they usually? How does the severity compare with a subarachnoid
hemorrhage?
a. 80%
b. Usually mild to moderate intensity.
i. Usually no focal deficits/head pain besides headache, but may have
confusion or changes in alertness/consciousness.
c. DDx: Subarachnoid hemorrhage HA is sudden and severe!

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4. How long does it take from the traumatic event for someone to start to experience
headache due to a subdural hematoma?
a. Up to 3 months after the trauma!
b. This also applies to post-traumatic HA or post-concussive syndrome.
5. What type of patients are more at risk to get a subdural hematoma due to trauma?
a. Elderly
b. Alcoholics
c. Epileptics
d. Patients on dialysis or warfarin
e. Patients with coagulopathies
6. Post-traumatic headache symptoms fall into 3 groups: what are they and what are
some examples?
a. Physical (headache, dizziness, diplopia, blurred vision, nausea, photophobia,
phonophobia, sleep disturbance)
b. Emotional (irritability, frustration, depression, restlessness)
c. Cognitive (forgetfulness, poor concentration, taking longer to think)
d. Mild head injury: Sxs are common, self limiting, may be similar to a migraine.
e. Acute post-traumatic HA: develops within 7 days, resolves in a few weeks.
f. Chronic post-traumatic HA: lasts longer than 3 months.
7. What are some red flags a headache patient may present with that could make you
suspect something more serious?
a. New HA in older patient
b. Trauma
c. Progressive HA
d. Thunderclap headache (sudden and severe)
e. Cognitive changes
f. Vomiting without nausea
g. Changes in vision
h. Double vision
i. Unexplained weight loss
j. Fever
k. Horner’s syndrome
l. Nuchal rigidity with or without fever
m. Valsalva
n. Positive jolt test
o. Very high BP (>180 SBP/>110 DBP)
p. Neurological signs
q. Papilledema
8. What are 5 quick screening questions to screen headache patients for serious
conditions?
a. Is the HA of recent onset (less than 6 months)?
b. Is there any progression in the frequency or severity of the headaches?
c. Was the onset sudden and severe?

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 d. Are there any clues suggesting focal neurologic signs associated with the
headaches?
e. Are there any cognitive changes associated with the headaches?
f. If the answer to all 5 is NO, low change of a serious disease causing the HA.
9. What are the 8 components of a neurological exam for a headache patient?
a. Orientation & mental status
b. Cranial nerve exam + fundoscopic exam
c. Gait & cerebellar tests
d. Sensory: light touch, sharp/dull (UE and LE)
e. Motor: proximal and distal muscle testing (all 4 extremities) + pronator drift
f. Reflex: DTRs (biceps, triceps, patella, Achilles)
g. Reflex: pathological reflexes
h. Meningitis tests (jolt maneuver, Brudzinski, Kernig’s)
10. What are the 3 most common types of headaches, from most to least common?
a. Tension-type
b. Migraine
c. Cervicogenic
11. What is the prevalence of cervicogenic headache?
a. As low as 1-2%, up to 15-20% of chronic/recurrent HA (numbers are FYI).
b. Higher in a chiropractic setting.
12. What are criteria for making a cervicogenic headache diagnosis?
a. Pain is aggravated by special neck movements or sustained posture.
b. 1 or more of the following:
i. Resistance to or limitation of passive neck movements.
ii. Changes in neck muscle contour, texture, tone, or response to
active and passive stretching and contraction.
iii. Abnormal tenderness of neck muscles
c. Additional Si/Sx:
i. Neck stiffness/decreases AROM
ii. Triggered by prolonged awkward neck posture or specific AROM
iii. Digital pressure can aggravate or induce the HA
iv. Abnormal SROM
v. May have a history of trauma
vi. Usually more severe than tension-type, but less severe than migraine
vii. Dull, background pain that is non-throbbing
viii. Doesn’t interfere with sleep
ix. Tend to last longer than migraines (hours to days), can become chronic
d. CGH can trigger a classic or common migraine!
13. What are some typical locations for this headache?
a. Unilateral HA that starts in the neck, and spreads to forehead, or
frontotemporal regions.
i. Doesn’t shift from side to side.

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 ii. Can be bilateral (and confused with migraine), but CGH will tend to
have one side more intense.
b. The reason for this pattern is because the C1-3 spinal nerves converge with the
trigeminal nerve.
14. What are some special physical examination procedures that are more commonly
positive in cervicogenic headaches compared to migraine or tension-type
headaches? Describe how they are done and what a positive test look like.
a. Painful, hypomobile upper Cx SROM (C0-3)
i. Palpation of occipital region and upper Cx reproduces CC head/neck
pain.
b. Restricted Cx AROM
i. Usually not restricted in other headaches, or at least not to the same
degree.
c. Impaired deep neck flexors
i. + Jull’s test (tuck chin and lift barely off the table, get patient to hold their
head there; positive if they cannot hold, pokes their chin, or shakes within
10 seconds)
ii. Cervical flexion movement pattern (positive if patients pokes their chin out
during first 10-20 degrees of flexion)
iii. Craniocervical flexion test (a pressure sensitive pillow device is placed
under the neck; patient slowly nods head, which changes pressure on the
pillow, which is read on a pressure gauge; patient needs to be able to
move 5 consecutively larger points on the gauge with each nod, and hold
the last one steady for 10 seconds; this tests the patient’s motor control)
d. + Cervical flexion rotation test
i. Patient supine, doctor passively flexes neck, the rotates to either side.
ii. A positive test is if one side has 10 degrees or less rotation than the other
side.
iii. Also positive if it reproduces the patient’s familiar headache or neck pain.
iv. This means the upper cervicals are likely restricted, and the cause of the
CGH.
v. Inter-examiner reliability is excellent: ICC = 0.93
15. What are some of the associated symptoms that can accompany cervicogenic
headaches that overlap with migraines?
a. Mild nausea, vomiting, ipsilateral periocular edema (but more rare and less
severe than in a migraine).
b. Phonophobia OR photophobia (not both, as in a migraine).
c. Dizziness, ipsilateral blurring, difficulty swallowing (rare, but mimics a
migraine).
d. Ipsilateral lacrimation, conjunctiva irritation, and rhinitis rare, but mimics a
cluster HA).
16. What is greater occipital neuritis? Where is a good method to find this nerve and
palpate it? What are some causes of greater occipital neuritis?

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 a. Palpate using a thumb 2 cm inferior, and 2 cm lateral of the EOP.
b. Paroxysmal stabbing pain radiating up the back of the head.
c. Caused by trauma or infection (including herpes zoster).
17. Outline your management plan for a typical cervicogenic headache case. Be as
specific as possible.

CMT STM

Manipulation (especially C0-3) Suboccipital muscles.

- 4 week treatment period

BM Ex

Use of a cervical pillow. Sustained chin retractions with gentle

Avoidance of aggravating neck postures. overpressure for 1 minute.

Home exercises to:

- Strengthen deep neck flexors
- Maintain cervical lordosis
- Correct forward head carriage
- Address upper cross syndrome

18. What are 4 key outcomes to measure when treating a patient with cervicogenic,
migraine and tension-type headaches?
a. Frequency of HA
b. Duration of HA
c. Intensity of HA
d. Analgesic usage
e. Cx AROM and SROM
f. Soft tissue tenderness
19. What are the two types of migraine? What are the phases of a migraine? How are
the two types similar when it comes to the headache itself?
a. Classic migraine: an aura (neurological symptoms) precedes the headache.
b. Common migraine: aura is absent due to less severe vasoconstrictive phase
(which is what causes the aura symptoms).
c. Prodrome: Nausea, a feeling of doom/dread/anxiety.
d. Aura: only in classic; motor or sensory perversions.
e. Head pain
f. Post headache “hangover”
g. Headache symptoms:
i. Usually unilateral (may be bilateral), frontotemporal location
ii. Throbbing or pounding
iii. Severe or incapacitating

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 iv. Nausea, maybe vomiting
v. Photophobia, phonophobia
vi. Often morning onset
vii. Usually relieved by sleep
20. List the parts of the quick migraine screen called migraine ID.
a. Step one:
i. 2 or more headaches in the last 3 months?
b. Step two:
i. Bad enough that it limits your ability to work, study, or enjoy life, or at least
made you want to have the HA assessed?
c. Step three: YES to at least 2 of the following questions
i. HA limited activities for a day or more in the last 3 months?
ii. Nauseated or sick to stomach during HA?
iii. Light bother you when you have HA?
21. Which of the following headaches is least likely to shift sides: cervicogenic,
migraine or tension-type headaches?
a. Cervicogenic
22. List some things in the history that differentiate a cervicogenic headache from a
migraine? List some things from the physical.
a. Only in migraine:
i. Unilateral HA that shifts from side to side
ii. Pulsatile HA
iii. Pain begins in head
iv. HA responds to ergotamine or sumatriptan
v. HA improves or goes away during pregnancy
vi. Prodrome before HA
b. Only in CGH:
i. Pain begins in neck
ii. Possible vague, non-radicular pain in shoulder or UE
iii. Reduced cervical rotation with neck in flexion
iv. HA provoked by manual pressure on upper Cx, or with continuous neck
extension
v. Weak deep neck flexors
vi. Upper Cx joint dysfunction, other special tests (+)
vii. Favorable response to nerve block
c. Both:
i. Nausea, vomiting, photophobia, phonophobia (severe in migraine, mild in
CGH)
ii. Decreased Cx AROM (worse in CGH)
iii. Pain with upper Cx joint play/palpation (worse in CGH)
23. What is the POUND mnemonic for a migraine? What is the +LR for a migraine if 3
of the letters are present? 4 or more?
a. P: Pulsatile pain

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 b. O: Hours of HA: 4-72
c. U: Unilateral
d. N: Nausea or vomiting
e. D: Disabling pain
f. 3 features: +LR = 3.5
g. 4 or more: +LR = 24
24. What are the criteria for making a tension-type headache diagnosis?
a. Diagnose a tension-type HA when history, physical, and neurological exam
DO NOT suggest another type of HA!
b. Needs at least 2 of the following:
i. Pressure/tight (non-pulsating) quality
ii. Mild or moderate intensity (may impair, but doesn’t prevent activities)
iii. Usually bilateral.
iv. Not aggravated by routine physical activity.
c. May overlap with a CGH.
d. Most common HA type.
i. Different from a tension HA, which is primarily psychological.
e. Lasts between 30 minutes to 7 days.
i. Can last up to 1 week, longer than a migraine!
f. No nausea or vomiting, but may have mild photophobia OR phonophobia
(not both).
g. Causes:
i. Muscle stress
ii. Unphysiological working position
iii. Long lasting tonic muscular contraction
iv. Lack of sleep
25. What physical examination findings might be positive in a tension-type headache?
a. Palpation of the scalp may reveal associated pericranial tenderness.
26. What are the headache patterns for the following MFTPs?
a. Upper trapezius
i. Inframastoid, mastoid, supramastoid, angle of the mandible, temple, and
supraorbital.
b. Splenius capitis
i. The top of the head.
c. Splenius cervicis
i. Similar to suboccipital pattern/tension-type, but doesn’t go all the way to
forehead.
d. Suboccipital muscles
i. Up the neck, and around the head (occipital, temple, forehead).
ii. Similar pattern to tension-type HA.
iii. Caused by forward head posture, sustained flexion posture, sustained
extension posture, sustained head rotation + tilt.
e. SCM

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 i. Suboccipital and supraorbital (this is the same pattern as a CGH, and
similar to a rhinosinusitis HA).
1. Sinus HA: along with HA, has nasal discharge (from nose or
down throat), OR nasal obstruction/congestion.
f. These are all treated with gentle ischemic compression, otherwise the HA
can get worse.
27. What are the steps for doing a quick TMD screen?
a. HA with associated pain with chewing + jaw popping.
b. Palpate the jaw:
i. Tender/crepitus
ii. Jaw deviation
iii. Inability to fully open mouth
c. Palpate TMJ muscles:
i. Tender masseter
ii. Tender temporalis
28. Based on each of the following locations, what headaches might present?
a. Forehead
i. Rhinosinusitis, cervicogenic, occipital or suboccipital MFTPs
b. Side of head
i. Migraine, TMJ, temporal arteritis
c. Occipital
i. Myofascial, disc pain, eyestrain, hypertension, greater occipital neuralgia,
cervicogenic
d. Parietal
i. Meningitis, migraine, tumor
e. Face
i. Sinusitis, trigeminal neuralgia, tumor
f. Vertex
i. Rhinosinusitis, splenius capitis MFTP
g. Around the head
i. Tension-type, T4 syndrome
29. Based on each of the following times and positions, what headaches might
present?
a. Morning
i. Sinusitis, migraine, hypertension, sleeping position, hangover
b. Afternoon
i. Eyestrain, muscle tension
c. Night
i. Cluster HA
d. Bending
i. Rhinosinusitis
e. Laying horizontal
i. Rhinosinusitis, cluster HA

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 f. Exertional
i. Brain tumor
30. Based on location and description, what would be at the top of your DDX list for
each of the following headaches?
a. TMD
b. Sinusitis
c. Migraine
d. Tension-type
e. Trigeminal neuralgia
f. Splenius capitis MFTP

Complex Regional Pain Syndrome (based on out of class Panopto

lecture and powerpoint slides)

1. List the key major components of CRPS and cite at least 3-4 signs and symptoms
for each component.
a. Pain
i. VERY SEVERE - WORSE THAN CHILDBIRTH!
1. Big distinction: this is continuing pain that is disproportionate
to any inciting event.
ii. Burning quality.
iii. Non-dermatomal, usually in an extremity.
iv. Comes on as a second, more severe pain weeks after trauma.
v. Allodynia and hyperalgesia.
vi. Starts at injury site, but then spreads due to central sensitization,
sometimes even to bilateral limbs.
b. Autonomic dysfunction (ipsilateral affected limb only)
i. Swelling: significant, non-pitting edema, limb pale white or bright red,
limb becomes cold or warm.

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 ii. Trophic changes: hair darken and proliferate (hypertrichosis), later hair
falls out (hypotrichosis), nails rigid/brittle, osteopenia on x-ray.
iii. Sweating: abnormal sweating.
c. Motor dysfunction
i. Hyperreflexia
ii. Tremor
iii. Movement disorders
iv. Dystonia leading to contractures
v. Paresis or clumsiness
vi. Rapid limb fatigability
vii. Pain or motor deficit leads to decreased ROM
viii. Muscle spasm
2. What are the two different types and what can cause each type?
a. Type 1: no nerve damage (most common)
i. Caused by MSK trauma, brain injury, MI, or other injuries.
b. Type 2: nerve damage present (aka causalgia)
i. Caused by nerve injury.
3. Describe the process of how the condition develops and progresses over time
after the initiating event.
a. Usually develops following trauma to a limb.
i. Usually symptoms begin immediately, days, or weeks later, but can rarely
begin months later.
b. Tissue injury → peripheral sensitization → central sensitization
i. Leads to aberrations in motor control and sympathetic nerve
overactivity.
ii. Augmented inflammatory response, neuronal membranes have lower
thresholds, so spontaneous pain/allodynia.
c. More common in females 37-50 y/o.
i. Very uncommon.
4. What is the prognosis for this condition?
a. 80% of CRPS type I achieve complete, spontaneous relief (with or without
treatment) within 18 months.
b. In cases of CRPS with prolonged and persistent Si/Sx, there is an increased
chance of poor outcomes and disability.
5. What is dystonia? What are some examples that can occur in CRPS? Describe the
movement disorder that can occur.
a. A neurological movement disorder in which sustained or repetitive muscle
contractions result in twisting and repetitive movements, or abnormal fixed
positions (may resemble a tremor).
i. Ex. 4th and 5th finger flexion, wrist adduction and flexion, foot inverted
with plantar flexion.
b. May lead to inability to initiate movement (or need to look at limb to initiate),
and limb may feel “foreign.”

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6. What are the different stages of CRPS?
a. Stage 1: local injury or entire extremity symptoms within weeks.
i. Constant burning pain, allodynia, hyperesthesia.
ii. Altered temperature regulation.
b. Stage 2: within months of injury.
i. Edema, thickened skin, abnormal sweating, stiff joints, bone loss.
c. Stage 3: for years.
i. Marked changes in muscle/joint adhesions, waxy skin, brittle/rigid nails,
tremors, dystonic posture, joint contracture.
7. Compare and contrast CRPS with posttraumatic neuralgia.
a. Posttraumatic neuropathy
i. Pain in territory of injured nerve (similar to CRPS type II).
ii. Spontaneous burning pain, hyperalgesia, mechanical allodynia.
iii. Lacks swelling, progressive symptom spread, or autonomic/motor findings
like in CRPS.
8. Describe the overall strategy and some of the treatment interventions used for
CRPS.
a. Consult with different medical experts to manage patient: pain specialist, PT,
neurologist, anesthesiologist, psychologist, neurosurgeon.
b. Pain relief via medication and procedures.
c. Physical and vocational rehab.
d. Psychological interventions.
i. Hand laterality, recognition training, imagination of movements, mirror
movements.
e. Patient education to support self-management.
9. One study reported an advantage of graded motor imagery over usual care and PT
to be MD -21.00 (95%CI -31.17 to -10.83). Explain what each of those numbers
means.
a. Graded motor imagery had very low quality evidence that it improved pain by
21 points on a 100 point scale, and this difference was statistically significant.
i. This also improved functional disability by MD 2.30 on an 11 point scale.
b. Other treatments that found statistical significant improvements (albeit with very
low quality evidence) included:
i. Multimodal physiotherapy improved “impairment.”
ii. Mirror therapy improved pain and function.
iii. Laser therapy improved pain in the short term.
10. What is the controversy surrounding vitamin C and CRPS? How much is
recommended and for how long?
a. 3 RCTs have been done.
b. 2 found benefit of vitamin C (but were done by the same author).
c. 1 found no benefit, but had a large loss to follow-up.
d. Professional organizations support vitamin C use, but this was before the RCT
showing no benefit.

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 e. 500 mg 1x/day for 50 days.
11. What are some of the more aggressive medical treatments for this condition?
a. Bisphosphonates
b. Sympathetic nerve block, sympathectomy, spinal cord stim, hyperbaric oxygen
treatment.
c. Electric acupuncture + massage and manipulation.
12. What condition did we study this term that sometimes triggered a Raynaud’s
phenomenon?
a. T4 syndrome.

Spinal Degeneration (based on in-class Panopto lecture and powerpoint

slides)

1. Tell the story of the progression of disc degeneration and how it affects the facet.
a. Annular fiber tears from micro trauma leads to disc separation from the vertebral
endplate, with the disc losing its blood/nutrition supply.
b. This leads to proteoglycan breakdown, loss of hydrostatic properties over time
(plus disc height loss with age).
c. Shifts center of rotation posteriorly, and axial load moves posteriorly to the
facets, which are not built for primary weight bearing.
i. Articular and subchondral cartilage, capsule, and synovium may
degenerate (may encroach on IVF or cause facet syndrome).
ii. Degenerated disc is less shock absorbing → more likely to herniate
posterolaterally.
2. What are Kirkaldy-Willis’ 3 stages of spinal degeneration? What specific
diagnoses that we have studied this term can the different stages lead to?
a. Dysfunction phase
i. May have no symptoms.
ii. May lead to: disc derangement, disc herniation, facet syndrome.
b. Instability phase
i. May have no symptoms.
ii. May lead to: degenerative spondylolisthesis, structural instability.
c. Stabilization phage
i. May have no symptoms.
ii. May lead to: osteophytic radicular syndromes, degenerative facet
syndrome, osteoarthritis, spinal stenosis.
3. What are two environmental factors that are thought to increase the risk of disc
degeneration?
a. Smoking and Vibration.

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4. What are some reasons that we think that spinal degeneration itself is not an
appropriate diagnosis in most cases?
a. Disc/joint degeneration is usually asymptomatic. Cannot look at an x-ray, see
degeneration, and predict if that is causing their pain.
i. There is a connection between pain and spinal degeneration, but it
usually isn’t the direct cause.
ii. Unless degeneration is severe, is should be a cofactor to another Dx.
iii. Treat the patient, not the x-ray.
b. If there is sufficient local inflammation due to degeneration to be the cause of
pain, we call it osteoarthritis, spondylitis, degenerative joint disease, or
degenerative disc disease.
i. This can be difficult to determine.
c. Degeneration is very common, especially with age, but there is only a weak
correlation between this and LBP.
i. However, in the Cx, degeneration is more strongly correlated with
higher disability ratings in women, and higher likelihood of
chronicity.
5. What did we learn from Birrell’s 2005 hip study? (Be as specific as you can.)
a. Mild/moderate degenerative changes are very common, and not related to
pain.
b. However, severe degenerative changes are rare, and ARE related to pain.
i. Excluding young males.
6. Even when spinal degeneration is not the main diagnosis what are some ways it
might affect the patient or their condition?
a. It may be an underlying factor that either amplifies symptoms, or makes a
patient more susceptible to injury.
b. It may affect duration of care.
c. It may affect the management strategy.
i. Avoid rotational adjusting in favor of traction in severe degeneration
patients.
7. What are 4 scenarios in which spinal degeneration become the main
pathoanatomical diagnosis?
a. Spinal stenosis
b. Structural instability
c. Spondylotic nerve root compression
d. Osteoarthritis
8. What are some of the more common symptoms and signs of osteoarthritis of the
neck? What are some of the more unusual signs and symptoms of osteoarthritis
of the cervical spine?
a. Common Si/Sx
i. Worse in AM, again in PM, and with activity
ii. Chronic forward head posture
iii. Reduced AROM (may be painless, stiff, with crepitus, but spares flexion)

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 iv. Morning stiffness <30 minutes (longer than that, think big inflammatory
conditions)
v. Head rotation markedly reduced if atlas is involved
vi. Radiographic evidence of degeneration
b. Unusual Si/Sx
i. Cervicogenic dizziness/vertigo
ii. Dysphagia
iii. Pupillary signs
iv. Ear symptoms (relieved by traction)
v. Pseudoangina (pain referred to chest)

Chronic Pain (based on in-class lecture, powerpoint slides, and assigned

reading)

1. What are the three kinds of pain? Which one is often the dominant player in
chronic pain cases?
a. Nociceptive pain
i. Based on damaged tissues, and lasts as long as the injured tissues
continue to stimulate the nociceptors.
b. Neuropathic pain
i. From damage directly to nervous tissues, which can become
“programmed in” to the central nervous system.
c. Central sensitivity
i. Long-standing amplification of neural signaling within the CNS, leads to
pain hypersensitivity.
2. What three key factors affect the degree and experience of pain that a patient feels
from their injury?
a. Peripheral sensitization due to initial tissue damage that is painful and needs to
heal.
b. Amplified pain signals in the CNS due to central sensitization.
c. Influence of higher brain centers and psychological/emotional factors.
3. What are the “unholy” four potential results when central sensitization sets in?
a. Exaggerated pain response to noxious stimuli.
b. Enlargement of the area of pain due to convergence-projection.
c. Pain response when there shouldn’t be one from non-noxious stimuli.
d. Spontaneous pain even though the tissue is healed.
4. What is “chronic pain syndrome?” How does someone’s psychosocial experience
affect the pain?

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 a. Patients who have a significant overlay of central sensitization and psychosocial
challenges that have swamped the underlying injury or have completely replaced
the initial injury which has since healed.
i. Much more challenging to treat.
b. Someone with pain that is bad enough that they are having trouble sleeping →
this lack of sleep can make the pain even worse.
5. Give an example illustrating each component of the biopsychosocial model?
a. Bio: actual biological considerations (injury or illness).
b. Psycho: how the patient thinks/feels or is stressed by the problem.
c. Social: how family or work expectations may contribute to the problem.
6. What are Nij’s criteria for identifying central sensitization?
a. Pain is disproportionate to the injury/pathology, and is not changed by
mechanical variables.
b. At least 1 of the following:
i. Bilateral mirror pain
ii. Large areas or widespread pain
iii. Allodynia and hyperalgesia outside the main nociceptive region
iv. Non-segmental diffuse areas of palpatory tenderness
v. Inconsistent pain response to movement/mechanical challenges
c. Central Sensitization Inventory (CSI) of 40 or more.
7. Name and describe 3 different “maladaptive pain coping behaviors.”
a. Fear avoidance behavior
i. If I move, it will hurt, which will cause more damage.
ii. Lack of movement and fear of pain can lead to increased sensitivity to
pain, turning up their pain alarm.
b. Catastrophizing
i. Magnifying the threat of the pain, seeing the worst possible outcome.
c. Somatization
i. Worrying about common somatic symptoms, like dizziness, nausea, etc.
8. Besides the above, what are some other yellow flags that should be screened?
a. Widespread pain
i. Pain that moves around to other areas
ii. Sensitive to light or foods
iii. Readily flares up
b. Non Organic signs
c. Depression
d. Return to work perception
e. Sense of health status
f. Sleep quality
g. Functional impairment
9. What is the STarT tool?
a. A screening tool to establish a prognosis for chronic pain.
10. What are some do’s and don’ts when it comes to your messaging to the patient.

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 a. Avoid negative messaging, emphasize what is to be gained.
b. Don’t overemphasize a pathoanatomical diagnosis, which has probably already
healed.
c. Avoid the “bone out of place” model of subluxation.
11. What are some of the key messages you want the patient to hear regarding their
chronic pain?
a. Their pain is more hypersensitivity than actual tissue damage.
i. Hurt DOES NOT equal harm.
b. Help patient acknowledge that pain centralization and their psychosocial factors
are playing a large role in their pain.
c. Help them explore movements they fear, slowing exposing themselves to reduce
fear and sensitivity.
d. Set small goals in activity and movement.
e. Convince them there is hope, they have power over their pain, and are stronger
than they think.
f. These messages should be a part of every visit with this chronic pain patient.
g. Consider referring them for psychosocial interventions, but emphasize to the
patient that this is to help manage the stress of their pain, not that the pain is in
their head.
12. What should you emphasize in your continued treatment of the patient?
a. Function, tolerance to normal activities, weaning off of passive treatment.
13. What is some advice you can give a patient to help them distinguish “acceptable”
pain when doing an activity vs pain suggesting that the patient is overdoing?
a. Try to modify a movement that was hurting, and continue the activity for 3-5
minutes if the pain is mild. If the pain is worse than mild, or it flares up for days,
then back off to slowly build up tolerance.
b. Some pain is fine, but if it keeps increasing in intensity or flares up, ease it back.
14. If the advice to practitioners is not to “chase the patient’s pain,” what should be
done instead?
a. Treat the person, not the pain. The pain could be in a different location at each
visit.
b. Use manual therapy and exercise to restore function.
c. Emphasize self-efficacy.
d. Recommend healthy lifestyle.
15. When explaining the diagnosis to a patient with an acute problem, besides
offering them a diagnosis, what are other important messages?
a. Avoid or minimize bed rest (doesn’t mean immediate return to work, it just
means light activity).
b. If they are able, keep them at work with light workload.
c. Encourage normal activities to tolerance.
d. Instruct patient in spine-sparing strategies.
e. Reassure patient some discomfort is normal.

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 f. Consider a formal exercise program in patients whose condition does not
resolve in 4 weeks of care.
g. Reassure the patient the condition is not serious, and has a favorable prognosis.
16. When should you consider a more formal assessment for central sensitization or
yellow flags in a patient who comes in with a new, acute musculoskeletal
problem?
a. In a patient who has already had disabling back pain for 4 or more weeks,
immediately screen them.
b. Screen them if the patient has not made satisfactory progress by the 4th week of
care.
c. In a patient who displays worrisome yellow flags, screen them at any point.
d. At 3 months of disability, there is increased risk of permanent disability.
17. What is perceived disability and what role does it play in recovery?
a. The patient’s perception of how disabled they are due to their condition, when
they will return to work.
b. The worse the patient’s perception of when they would return to work, the worse
their prognosis.

Fibromyalgia (based on in-class lecture and powerpoint slides)

1. Describe the key signs and symptoms of fibromyalgia.

a. Widespread pain in muscles/connective tissues.
b. Associated with central sensitization.
c. Tender points, sleep disorder, other systemic Sxs.
2. What is the old diagnostic criteria for fibromyalgia?
a. Chronic widespread pain: on both sides of body, above and below the waist,
axial skeletal pain present.
b. 11 of 18 tender points with <4 Kg pressure using an algometer: not a trigger
point nodule, only based on patient report of pain; don’t need to know the specific
points.
i. These tender points have been shown to have no soft tissue pain
generator, no tissue changes, and don’t respond to medications. They are
tender due to central sensitization.
3. According to the 2010 criteria, three conditions must be met to make a diagnosis
of fibromyalgia. What are they?
a. Widespread Pain Index (WPI) >7 AND Symptom Severity (SS) score >5
i. OR WPI 3-6 AND SS score >9.
ii. Don’t need to know these specific numbers.
b. Similar symptom severity present for at least 3 months.
c. Does not have a disorder to explain the pain.

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4. What are some key differences between myofascial trigger point diagnosis and
primary fibromyalgia?
a. MFTP
i. Specific muscles + referred pain
ii. Related to trauma
iii. No sleep disturbance
iv. Local trigger points, decreased ROM, local edema
v. No systemic Sxs
vi. Male/female equal incidence
b. Primary Fibromyalgia Syndrome
i. Generalized aching/stiffness
ii. Chronic, progressive
iii. Fatigue and chronic sleep disorder
iv. Multiple bilateral tender points
v. IBS, HA, etc
vi. 80% female
5. What are the 3 therapeutic interventions that seem to have the most clinical
research evidence
a. Mild aerobic exercise + gentle stretching
b. Cognitive behavioral therapy
c. Low dosage antidepressant medications
6. What are other interventions that have the most recommendations?
a. Massage
b. Muscle strength training
c. Balneotherapy (hot water spa)
d. Acupuncture
e. SSRIs and Tramadol
f. NOT NSAIDs or Corticosteroids!
i. These two are not recommended as primary medications for FMS.
7. What is the purpose of the Revised Fibromyalgia Impact Questionnaire?
a. An outcome measure to track improvement over baseline - NOT TO FOR
DIAGNOSIS.

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Final Exam Practice Test
This sample is not comprehensive and does not cover all of the material that may be on
the final exam. When using this to study, be sure to use it as a gateway to the topics the
questions cover—not just limited to the narrow focus of each question.

1. What is the checklist for determining if there is a neuropathic lesion in a patient

with low back and leg pain?
2. What are the main clues for a lumbar facet syndrome?
3. What are the main clues for a lumbar disc derangement? The strongest clue?
4. What are the indications for lumbar and cervical radiographs?
5. What are recommended tests for the sacroiliac joint?
6. What are the main diseases of the SI joint, what signs and symptoms do they
share? What are some of the signs/symptoms unique to each separate disease?
7. What are the 3 most common pain referral locations for thoracolumbar syndrome.
What peripheral nerve is most commonly affected?
8. How does a psoas syndrome differ from a psoas myofascial pain syndrome?
9. What is the pain referral location for pancreatitis?
10. What is postherpetic neuralgia? How does it present? How long does it last? What
are ways to decrease the chances of getting it?
11. What are spinal changes that occur in Scheuermann’s disease?
12. What are two indicators that surgery might be a better first choice for the patient
with Scheuermann’s disease as opposed to conservative care?
13. What is a paralytic ileus? What causes it?
14. What does a positive Beevor’s sign look like? Where in the nervous system could
the lesion be?
15. What is a Schmorl's node? Is it usually symptomatic?
16. What are three injuries/diagnoses that can happen to ribs? What are some of the
signs and symptoms that are common to all three conditions?
17. What are the components of a SICK scapula?
18. What are the three main components of a T4 syndrome? What are some of the
minor signs and symptoms? What are the findings of a neurological exam for T4?
19. How does Bertolotti’s syndrome differ from Baastrup’s disease and various types
of spina bifida?
20. What is Adam’s test, how is it performed, how is it interpreted, and how does it
affect management?
21. What are the 4 main factors that affect treatment decisions for scoliosis?
22. What are some of the neurological findings that can accompany a Pancoast
tumor?
23. How does an RA neck affect in-office chiropractic management?

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24. What are the classic signs of syringomyelia?
25. What are 3 pertinent negatives that would help support a facet diagnosis, but if
positive would call the diagnosis into question?
26. What physical examination clues would be most useful in trying to differentiate a
cervical sprain from a strain?
27. What muscles with MFTPs refer to the medial hand? How about to the lateral
hand?
28. What exercises are used in acute neck cases to prevent adhesions, atrophy, and
loss of motor control programming in an acute traumatic sprain or strain?
29. What is Rusts sign? What does it suggest?
30. What are some of the key physical exam findings in a neck trauma case that
suggest a radiographs should be taken?
31. What are some if the characteristics of idiopathic spasmodic torticollis (AKA
cervical dystonia)?
32. Which clue from the H&P would be most accurate at predicting that a C8 nerve
root was damaged?
33. Describe the peripheral nerve territories for the median nerve, ulnar nerve and
radial nerve?
34. Your patient has a paradoxical biceps reflex. Where could the neurological lesion
be located?
35. Your patient has a C7 radiculopathy. What is on your “A” differential diagnosis list
of causes (in order of probability)?
36. What does cervical flexion do to the spinal canal? To the IVFs?
37. What are the big 5 cervical orthopedic tests to assess a patient for a possible
cervical radiculopathy? Predict the exam findings for each. Indicate if each one is
more specific or more sensitive.
38. Under what circumstances would ordering an MRI for suspected cervical disc
herniation be most advisable?
39. What are 3 key outcomes to monitor when treating a patient with a cervical disc
herniation?
40. Describe 3 traumatic mechanisms that can directly injury a nerve root.
41. Your patient has traumatized the upper trunk of the brachial plexus. What muscles
might test weak?
42. What are the three main types of TOS? How is each one treated?
43. What 5 orthopedic tests are recommended to perform to make a TOS diagnosis?
44. What is ataxia? What are the 3 types of ataxia? What are the various tests for
ataxia? What are the tests for an UMNL? Do they overlap?
45. What the symptoms and signs to check to screen patients for cerebral disease or
trauma?
46. What are 3 key physical examination findings to support cervicogenic vertigo?
47. What group of 3 symptoms is suggestive of a brain tumor headache?
48. What are the hallmarks of a subarachnoid hemorrhage? What other
life-threatening conditions share the same hallmarks?

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49. What are the key signs and symptoms of meningitis? How accurate are they?
50. List some things in the history that differentiate a cervicogenic headache from a
migraine? List some things from the physical.
51. What are the criteria for making a tension-type headache diagnosis?
52. What physical examination findings might be positive in a tension-type headache?
53. What is the headache pattern for a splenius capitis headache?
54. List the 3 key major components of CRPS and cite at least 1-2 signs and
symptoms for each component.
55. What is the controversy surrounding vitamin C and CRPS? How much is
recommended and for how long?
56. What are 4 main ways spinal degeneration can cause symptoms?
57. What are some of the more common symptoms and signs of osteoarthritis of the
neck?
58. What are some key differences between myofascial trigger point diagnosis and
primary fibromyalgia?
59. What are the 3 therapeutic interventions for fibromyalgia that seem to have the
most clinical research evidence?
60. Name and describe 3 different “maladaptive pain coping behaviors.”
61. What are the signs and symptoms of spondylolisthesis and spondylolysis? What
are the treatment approaches?
62. What are the key signs and symptoms of cauda equina syndrome What are the
most common causes?
63. How are the key signs and symptoms of VBI and a vertebral dissection and a
carotid dissection?
64. Which MFTPs refer pain to the forehead? Which refer to the top of the head?
65. What are the two types of LLI? How are they tested?
66. What is the protocol for adding a heel lift or a sole lift?
67. What blood tests are ordered for suspected RA? For suspected multiple
myeloma?
68. What is the STarT questionnaire? What is it used for?
69. What is Nij’s criteria for central sensitization and chronic pain syndrome?
70. What are the main testament strategies for chronic back pain?
71. What are the cerebellar tests?
72. What the components and the specific treatments for each component of an upper
cross syndrome? How about a lower cross syndrome?
73. What are the signs and symptoms for a spinal infection? Which ones are most
common?
74. What is the test for osteoporosis, what is a treatment approach?

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