CASE STUDY AND QUESTIONS: To be completed by the 12 th September.

Week 6: Case 6: Joe

Joe is a 60-year-old who works in IT.

Presenting Complaint
Joe presents with neck and right jaw pain of 3 weeks duration. The patient also complained of
headaches in the temporal area which have been present for the last 6 weeks. Within the last 2
weeks the intensity of the headaches has increased. These headaches are worse in the mornings.
The quality of the pain (of the headaches) is dull, throbbing, diffuse and aching. The headaches are
intermittent and may last up to 2-3 hours.

History of Presenting Complaint

He was driving home from work when another car ran a red light and struck his car on the left front
fender. He was wearing a seat belt, had some prior warning that the accident was going to occur,
and braced himself but was still thrown violently against his seat belt. His sunglasses flew off his
head. Estimated impact velocity was about 40 km/hr. Extensive damage was done to the front end
and the left front fender. The patient was able to get out of the car and take information from
witnesses but by the next morning he had developed severe midline neck pain and an inability to
move his right shoulder without discomfort.

Physical Examination
 Joe is an obese male.
 Vitals: pulse 80/min, normal volume; BP 160/95; respiratory rate 18/min; Temp 36.9
 Cervical ROM: He demonstrates limited forward flexion and incomplete extension of the
cervical spine. There is decreased motion on right rotation. Cervical range of motion is
otherwise full.
 The upper extremities demonstrate normal contours and no atrophy.
 There is no point tenderness along the right acromial border.
 Passive range of motion of the right shoulder is comfortable except on forward flexion beyond
90 degrees where there is pain in the acromial region.
 Upper extremity sensory and motor tests reveal no deficits. Supination of the forearm
against resistance (Yergason’s tests for bicipital tendinitis) is painless.
 TMJ examination revealing a translation to the right and difficult placing 3 fingers in his
mouth. There is crepitus and muscles spasm on palpation of masseters and temporalis
X-rays
Cervical and shoulder x-rays are unremarkable.

Questions

1. Questions to ask:
a. When did the accident occur?
b. When you braced, what direction were you looking?
c. Was there anyone else in the car, need more details about the accident – speed,
direction?
d. Possibly movement triggers that bring on the headache
 e. Is there a rust sign? Indicates instability
f.

2. Describe the mechanism of the neck pain and its relationship to the findings.

Joe was driving home and was struck by a car on the left at 40km/hr and through right against the
seat belt. He likely has whiplash which would explain his severe midline neck pain and his shoulder
and jaw pain on the right side.

a. Head glasses flung on his head which indicates his head hip the head rest -> a whiplash injury
where he
i. Hyper- extension injury is dangerous which impacts spinous processes, alar ligaments,
transverse process (all posterior structures), anterior structures could be torn, sympathetic
ganglion and TMJ and spinal cord could also be
ii. Flexion injuries impact traps and sub occipitals which are strong muscles that can take a lot
more force

AKA Hyper flexion/extension injury and acceleration/deceleration injury.

Mechanism of injury:
1. Hyper extension/acceleration -> sudden translation force to trunk produces acceleration of head.
a. Hyper extension forces focus around C5/C6 level – occiput may strike shoulders
b. Head/neck extends beyond normal range causing over-stretch of anterior spinal structures
and compression of posterior structures
2.Hyperflexion/ deceleration injury – usually less severe injury than hyperextension. Causes over
stretch of the posterior structures with compression anterior to spine. Tends to especially involve sub-
occipital region. May occur in combination with hyperextension i.e. recoil effect
3. Lateral Flexion (“sidelash”)
4. Combination of the above

3. How do you explain the lack of pain initially followed by severe pain later?

Joe may have been in shock and also injuries such as whiplash typically present 12-24hours after
trauma due to the swelling and inflammation of the injury as there is a delay in symptom onset:
65% <6hours
285<24 hours
7% <72hours
This may be explained by the gradual build up of oedema +/- Haematoma.
Most patients (75%) will have symptoms which persist more than 6 months
Severity:
95% of the injuries are classed mild. Px develops after interval of several hours or days, and then
intensifies.

4. What injuries of the neck and shoulder might occur in this type of accident, and how would they
be ruled in/out?

Hyper extension
 Muscle strain: Longus coli, SCMs
 Ligament sprain: ALL
 IVD: anterior fibers torn/ rupture
 Vertebral body: - > Fracture/teardrop avulsion
 Facet joints: impaction -> sprain, fracture or dislocation (pillar fractures documented)
 Oesophagus: strain -> oedema
 Pharynx: Retropharyngeal haemorrhage/oedema
 Nerve roots/ sympathetic chain: Traction -> oedema
 Blood vessels: Traction injury of carotid (+carotid bodes)
  TMJ: sprain
 Spinal cord + dura -> oedematous impingement and hemorrhage (moderate/severe injuries)
o Swelling (if oedematous will start to decrease after 72hours. If not suspect oedema and
haematoma)

Hyper Flexion
 Muscle strain -> U. traps, semispinalis capitis, splenius cervices/capitis, lev. Scap, posterior scalenes,
sub-occipitals
 Ligament sprain -> PLL< Interspinous ligaments ligamentum flavum, and sub-occipital ligaments
 IVD – Posterior tear/rupture
 VB -> Fracture/ tear drop
 Facet joint -> Distraction sprain
 TMJ – Sprain
 Spinal cord – oedematous pressure (notably due to PLL damage) and haemorrhage.

 Cervicogenic headache
 Whiplash – get the patient to do a functional proprioceptive assessment. If the patient
sways or is unable to maintain balance a function impairment in proprioception is
indicated which usually occurs with biomechanical dysfunction due to trauma, whiplash.

 Cervical sprain/ strain – O’donoghues Maneuver that uses by resisted and passive
motion to test for cervical sprain

 TMJ dislocation or TMD closed lock – palpation, x-ray

o TMD – acute and commonly extremely painful presentation
o Mouth locked due to muscular guarding/ spasm (Joe can’t put three fingers in his
mouth)
o Possible due to trauma (direct impact, whiplash)

5. Does he have hypertension? Explain your answer.

As an adult (.18years), normal blood pressure is systolic: 110-130 over diastolic 80-90). As
Joe’s BP is 160/95 he has mild to moderate hypertension.

6. What signs would you look for, in order to determine if he has any complications related to his
elevated blood pressure. For each sign named, explain the pathology which it is related to.

 Damage to the sympathetic causing blurred vision, vertigo, tinnitus, nystagmus, deafness

7. What are the possible causes for his headaches? Do you think that they may be related to?
a. His recent MVA?
a. Secondary headaches can definitely be attributed to trauma or injury to the head
and/or neck
b. Tension based headache, primarily C2 that go to the sub occipital region which
may precipice migraines
b. His elevated blood pressure?
a. Headaches of pulsatile or throbbing nature are typically vascular in origin eg.
Hypertension, migraines.

8. How would you treat/manage this patient if he presented to your office

 In the acute phase, stabilize the cervical spine, use a cervical collar in the first 10hours
 Trigger point masseter and temporalis
 Ice to reduce swelling, pain
 Gentle Soft tissue mobilisation to prevent muscle spasm and increase mobility during initial
stage
 Advice on posture, sleeping posture, NSAIDs
 Traction is contraindicated with TMJ symptoms
 Gentle spinal manipulation in the subacute once inflammation has reduced
 Cork stretch to help loosen up the jaw and muscles that you use to chew (temporalis, masseter
and medial pterygoids elevate the mandible)

 Management:
 -Treatment should ideally be initiated no more than 2/3 days after the onset.

Acute phase (first week): -

 Treatment must be aggressive but gentle
 Acute phase is that of a severe sprain
 -Immediate rest of injured area. Patient may benefit from a well-fitted felt or soft collar to splint
the cx spine and support head posture.
 NB. It is very important that the patient remove the collar at regular intervals to allow
normal movement of the neck. It is useful to have a schedule for this. Soft collars used
persistently for more than 72 hours have been shown to prolong the disability due to
whiplash. Ideally used during sleep, and stressful activities eg. prolonged journeys.
 - Ice to reduce pain, blood vessel dilation and the production of histamine like products. (10
minutes per hour is ideal) – better than U.S/Inter. in acute phase
 - Gentle mobilisation – to prevent muscle and ligament contracture and formation of scar tissue
adhesions. Initially it may be best to mobilise away from the pain and restricted ROMs.
 - Adjustment is generally contra-indicated in the acute phase.
 - Advice on posture, sleeping position and px killers/NSAIDs
 - Traction – (contra indicated if there are associated TMJ symptoms)
 - STW

 Sub-acute phase (1-7 weeks): Acute phase symptoms usually start to subside after about 1
week, but tenderness and decreased ROM will normally persist
 - Active exercises to maintain and increase improving ROM are prescribed.
 1st  isotonic exercises to improve active ROM
 2nd  isometric exercises to improve muscle strength

 - Ice for 10 minutes after exercise followed by (moist) heat for 10 minutes.
 This will help to reduce ischaemia within muscle tissue and clear nociceptive metabolites.
 - Adjustments – as indicated, but should be gentle
 - Postural and sleeping advice
 - Modalities U.S/Inter.

 Chronic phase (more than 7 weeks):
 -Continuation of the above. A gradual reduction of intensity of Rx
 -Studies have shown around 10% of patients involved in rear end collisions suffer some
permanent medical disability or do not achieve full functional recovery.
 -Balla (1980) found most patients would recover within 6 months and that little difference was
noted in the patients’ clinical picture between 6 months and 2 years.
 -Between 40 and 70% retain some “nuisance symptoms” after 6 months

 -The prognosis is worse if there is a previous history of cervical dysfunction or DJD

 -The Quebec Taskforce researching whiplash (early 90s) graded whiplash 0-IV according to the
severity of the injury, with 0 being no complaint/physical signs and IV involving fracture and
dislocation of the spines.

 Their study suggested the average recovery time (i.e. resolution of signs and symptoms) as
follows:
 0 < 4 days
 I 4-21 days
 II 22- 45 days
 III 46-180 days
 IV > 6 months recovery prognosis

Chiropractic Treatment Protocol for Neck Injury.

Phase 1

Objective – pain reduction, Treatment of inflammation and muscle spasm.

Operational end–point – No pain at rest.
-Acute - ice 24 hours (joints and muscle spasm). A collar may be used in the initial stages of the acute phase.
-Chronic – heat.
-Decreased heavy manual activity.
-Soft tissue therapy: trigger points and stretching.
-Electrical therapy -acute – codeton, ultrasound (pulse)
-chronic – ultrasound (continuous)
-Manipulation of related areas.
-Education of the patient stressing their abilities.
-Ergonomic: sleeping, posture, back support.
-Nutritional advice for healing and stress
-Exercises: passive for range of motion
-The cervical collar is worn in this phase only. The more severe the degree of whiplash injury, the longer the
cervical collar is worn in phase 1.

Phase 2

Objective – recovery of movement function. Operational end-point-the capacity to perform unstressed

basic daily activities.
-Electrical therapy -acute – codeton, ultrasound (pulse)
-chronic – ultrasound (continuos)
-Ergonomic: sleeping, posture, back support.
-Mobilisation of the specific and traumatised segments: ice.
-Nutritional advice for healing and stress.
-Manipulation of related areas.
- Exercises: active for stretching and passive for range of motion.

Phase 3

Objective – restore the normal movement patterns along with conditioning of normal strength and
function. Operational end-point-the capacity to perform normal activities under some constraints and
conditions.
-Manipulation to traumatised areas using a lateral break, toggle, Gonstead (technique using minimal rotation is
preferable)
-Begin walking. This improves the C.V.F: increases the endorphins and serotonin causing a decrease in the
pain and patient depression.
-Psychological counselling
-Ergonomic: sleeping, posture.
-Exercises: isometric strengthening for the injured area.

Phase 4

Objective – the return of the patient to full and active lifestyle and help in the prevention of future
episodes.
Operational end–point – the recovery of the full normal, and uncontrollable activities, and release from
active care.
-Manipulation as indicated.
-Soft tissue therapy: trigger points, massage etc.
-Walking for C.V. F.
-Lifestyle management
-Exercises: isotonic or isometric for strengthening

Study
Guide

Questions: 6.6

The questions for this week will focus on components of a cranial nerve and
TMJ assessment.

1. Which branches of the trigeminal nerve supply each region in the

image below?
A: Ophthalmic branch

A
B: Maxillary branch

C: Mandibular branch
 B

CASE STUDY 6 CHIR13009

1. Complete the following table:

Examination Finding Nerve(s) involved

C
Wasting/weakness of Trigeminal nerve, V3 mandibular branch
temporalis and masseter innervates the muscles of mastication
muscles

Weakness of jaw opening Trigeminal nerve, V3 mandibular branch.

– jaw deviates to side Contraction of each muscle causes deviation of
the jaw to the opposite side, so that weakness of
the pterygoid muscle would cause deviation of
the open jaw to the ipsilateral side.

Loss or diminished jaw Trigeminal nerve, V3 mandibular branch

reflex The jaw jerk is one of the deep tendon or stretch
reflexes. When it is normal, tapping the mandible
produces a brisk contraction. 

Loss of corneal reflex – Corneal light reflex tests cranial nerves

neither eyes blink III, IV and VI.
If neither eyes can blink, CN III most
likely affected.
2. What is the possible cause of each of the following?

a. pain in the distribution of either V1, V2 or V3 when

touching that area
Trigeminal neuralgia

b. pain, vesicle formation and hyperaesthesia in the region

of V1, V2 or V3
Herpes Zoster – reactivation of varicella zoster virus
at the geniculate ganglion of CN 7 which supplies the
facial nerve.

The questions will now focus on components of cranial nerve IX, X,

XI and XII structure, function and significance of the findings.

3.Consider examination of the pharynx. Complete the following table:

Finding Possible significance

Uvula moves to one side
Unilateral nerve lesion When the patient says
"ah" there is excessive nasal air escape. The
palate elevates more on the left side and the
uvula deviates toward the left side because the
right side is weak. This patient has a deficit of
CASE STUDY 6 CHIR13009

the right 9th & 10th cranial nerves.

Uvula does not move on Bilateral vagus nerve deficit.

saying ‘ahh’ or gag

4.Consider examination of the larynx. Complete the following table:

Finding Possible significance
When asking patient to cough, it is Suggests vocal cord palsy
of gradual onset

‘Bubbly’ voice Combined cord palsy and pharyngitis pooling

due to CN X nerve lesion

Swallowing is followed by Indicates aspiration due to poor airway

coughing protection: suggests X-nerve lesion

Hoarse voice Recent laryngeal palsy or vagal lesion

5.Consider examination of the spinal accessory nerve. Complete

the following table:

Finding Possible significance

Weakness of
sternocleidomastoid and
trapezius on the same side
Weakness of sternocleidomastoid CN IX, X, XI palsy
and trapezius on the same side,
plus
ipsilateral loss of gag reflex and
uvula deviation
Weakness of ipsilateral
sternocleidomastoid and
contralateral trapezius
Unilateral delayed shoulder
shrug
Peripheral accessory palsy. Look for
associated ipsilateral IX and X lesions:
suggests a jugular foramen lesion (glomus
tumour or neurofibroma)
Upper motor neuron weakness on ipsilateral
side
Indicates unilateral trauma, unilateral XI nerve
weakness or upper motor neuron weakness (check
opposite trap)

Bilateral wasting and weakness of Myopathy (such as myotonic dystrophy,

sternocleidomastoid
Unilateral sternocleidomastoid
abnormalities
fascio-scapulo-humeral dystrophy or
polymyositis) or motor neuron disease (look
for associated bulbar abnormalities)
SCM muscle weakness/ paralysis
CASE STUDY 6 CHIR13009

Abnormal head position and Cervical dystonia

hypertrophy of neck muscles

6.Undertake some research of neurological disorders and name a condition

associated with each of the cranial nerve provided.

Neurological Disorders Name

CN V Trigeminal Neuralgia
CN VII Lower Motor Neuron CN VII dysfunction is
the most serious as the inability to close
the eye or produce tears (lacrimation) can
lead to corneal ulceration if the eyes are
not kept moist and closed.

CN VIII Vestibular neuritis

C5-T1 Brachial plexus lesion

C5-6

C7-8
T1

7. What is the difference between mandibular deviation and mandibular deflection

when assessing the TMJ joint?

Deflection of the mandible is movement away from the midline during opening

without return to center during the movement. Deviation of the mandible is
movement away from midline followed by a return to center and is often described as
either a “C” or “S” pattern

9. What are the articular surfaces in the TMJ joint covered by in order to reduce
the effects of compressive forces placed upon it.
 All articulating surfaces are covered by fibrocartilage, which is dynamic in that it
recovers from injury quickly.
 Helpful due to the demands put upon joint by repetitive compressive force

9 Name the ligamentous structures in the TMJ joint

 Articular capsule
 Temporomandibular ligament (lateral ligament)
CASE STUDY 6 CHIR13009

 Accessory ligament
 Stylomandibular
 Sphenomandibular

10. How does the disc stay on the condyle while moving?
The disc stays on the condyle (composed of dense fibrocartilage) because of its
concave shape and collateral ligaments

11. The muscles of mastication include

Temporalis, masseters, lateral and medial pterygoids

true or false

12. The upper TMJ joint is a sliding joint (ginglymus) - False

The upper TMJ joint is a sliding joint but is it amphiarthroses – it doesn’t move

13. The disc of the TMJ joint is avascular and derives its nutrition from the
synovia?

False – the capsule (lined by synovium) provides lubrication, nutrition and

immune functions.

14. The TMJ motion of depression is generated by the contraction of

temporalis, masseter and medial pterygoids? – False, the contraction of
temporalis, masseter and medial pterygoids cause mandibular elevation

15. What kind of head position may cause the mandible to close differently
than it should, thus causing mal- occlusion?

Forward head posture

16. What are some of the symptoms that can occur with forward head posture
and TMJ mal occlusion?

 Teeth grinding or clenching

 Neck and back muscle tension which may produce head, neck and
back pain

17. What is the cause of the noises heard in the TMJ like (popping, snapping,
clicking)?
The noise is produced by the cartilage disc being caught between the two
bones of the TMJ as the lower jaw moves, there may or may not be pain
With clicking, there is a displaced disc and this implies that the muscles that
more the jaw are more tense than normal
CASE STUDY 6 CHIR13009
CASE STUDY 6 CHIR13009