Neurologic examination

REFLEX TESTING

REFLEX TESTING
Reflex testing incorporates an assessment of the function and interplay
of both sensory and motor pathways. It is simple yet informative
and can give important insights into the integrity of the nervous
system at many different levels.
Assessment of reflexes is based on a clear understanding of the
following principles and relationships:

Tendons connect muscles to bones, usually crossing a joint.

When the muscle contracts, the tendon pulls on the bone,
causing the attached structure to move.

When the tendon is struck by the reflex hammer, stretch receptors

contained within it generate an impulse that is carried via sensory
nerves to the spinal cord. At this juncture, the message is
transmitted across a synapse to an appropriate lower motor
neuron. An upper motor neuron, whose cell body resides in the
brain, also provides input to this synapse.

The signal then travels down the LMN to the target muscle.

REFLEX TESTING

The sensory and motor signals that comprise a reflex arc travel
over anatomically well characterized pathways. Pathologic
processes affecting discrete roots or named peripheral nerves will
cause the reflex to be diminished or absent. The Achilles Reflex
is dependent on the S1 and S2 nerve roots. Herniated disc
material can put pressure on the S1 nerve root, causing pain
along its entire distribution (i.e. the lateral aspect of the lower leg).
If enough pressure if placed on the nerve, it may no longer
function, causing a loss of the Achilles reflex.
In extreme cases, the patient may develop weakness or even
complete loss of function of the muscles innervated by the nerve
root, a medical emergency mandating surgical decompression.
A normal response generates an easily observed shortening of
the muscle. This, in turn, causes the attached structure to move.

The vigor of contraction is graded on the

following scale:
Grade
Description
0
Absent; No evidence of contraction
1+
Decreased, but still present (hypo-reflexic)
2+
Normal or physiologic
3+
Increased and maybe normal or pathologic
4+
Markedy hyperactive with transient clonus
5+
Markedy hyperactive with sustained clonus
(Repetitive shortening of the muscle after a single
stimulation)

The Reflex Hammer

Technique:
You will need to use a reflex hammer when performing
this aspect of the exam. Regardless of the hammer type,
proper technique is critical.
The larger hammers have weighted heads, such that if
you raise them approximately 10 cm from the target and
then release, they will swing into the tendon with
adequate force.
The smaller hammers should be swung loosely between
thumb and forefinger.

Small Hammers

Large Hammers

REFLEX TESTING
Technique:

The muscle group to be tested must be in a neutral position (i.e.

neither stretched nor contracted).

The tendon attached to the muscle(s) which is/are to be tested

must be clearly identified. The extremity should be positioned such
that the tendon can be easily struck with the reflex hammer.

If you are having trouble locating the tendon, ask the patient to
contract the muscle to which it is attached. When the muscle
shortens, you should be able to both see and feel the cord like
tendon, confirming its precise location. You may, for example, have
some difficulty identifying the Biceps tendon within the Antecubital
Fossa. Ask the patient to flex their forearm (i.e. contract their
Biceps muscle) while you simultaneously palpate the fossa. The
Biceps tendon should become taut and thus readily apparent.

Strike the tendon with a single, brisk stroke. While this is done
firmly, it should not elicit pain. Occasionally, due to other medical
problems (e.g. severe arthritis), you will not be able to position the
patients arm in such a way that you are able to strike the tendon. If
this occurs, do not cause the patient discomfort. Simply move on to
another aspect of the exam.

ACHILLES REFLEX (S1, S2 Sciatic Nerve):

Technique:

This is most easily done with the patient seated, feet dangling
over the edge of the exam table. Other positions: supine, crossing
one leg over the other in a figure 4 or a frog-type position.

Identify the Achilles tendon, a taut, discrete, cord-like structure

running from the heel to the muscles of the calf. If you are unsure,
ask the patient to plantar flex (i.e. step on the gas).

Strike the tendon directly with your reflex hammer.

Be sure that the calf if exposed so that you can see the muscle
contract.

NORMAL RESPONSE: plantar flexion (contraction of the

Gastrocnemius).

ACHILLES TENDON

PATELLAR REFLEX (L3, L4 Femoral Nerve):

Technique:

This is most easily done with the patient seated, feet dangling
over the edge the exam table.

Identify the patellar tendon, a thick, broad band of tissue

extending down from the lower aspect of the patella (knee cap). If
you are not certain where its located, ask the patient to extend
their knee. This causes the quadriceps (thigh muscles) to contract
and makes the attached tendon more apparent.

Strike the tendon directly with your reflex hammer. If you are
having trouble identifying the exact location of the tendon (e.g. if
there is a lot of subcutaneous fat), place your index finger firmly
on top of it. Strike your finger, which should then transmit the
impulse.

For the supine patient, support the back of their thigh with your
hands such that the knee is flexed and the quadriceps muscles
relaxed.

NORMAL RESPONSE: The lower leg will extend at the knee.

(contraction of the Quadriceps)

Patellar Tendon

PATELLAR REFLEX TESTING

BICEP REFLEX (C5, C6 Musculocutaneous Nerve):

Technique:

Identify the location of the biceps tendon in the antecubital fossa.

The tendon will look and feel like a thick cord.
The patients arm can be positioned in one of two ways:
A. Allow the arm to rest in the patients lap, forming an angle of
slightly more then 90 degrees at the elbow.
B. Support the arm in yours, such that your thumb is resting
directly over the biceps tendon (hold the right arm with your right)
It may be difficult to direct your hammer strike such that the force
is transmitted directly on to the biceps tendon, and not dissipated
amongst the rest of the soft tissue in the area. If you are
supporting the patients arm, place your thumb on the tendon and
strike this digit. If the arm is unsupported, place your index or
middle fingers firmly against the tendon and strike them with the
hammer.
NORMAL RESPONSE: elbow flexion

BICEP TENDON

BICEP REFLEX TESTING

BICEP REFLEX TESTING

BRACHIORADIALIS REFLEX (C5, C6 Radial Nerve):

Technique:

This is most easily done with the patient seated. The lower arm
should be resting loosely on the patients lap.

The tendon of the Brachioradialis muscle cannot be seen or well

palpated, which makes this reflex a bit tricky to elicit. The tendon
crosses the radius (thumb side of the lower arm) approximately
10 cm proximal to the wrist.

Strike this area with your reflex hammer. Usually, hitting anywhere
in the right vicinity will generate the reflex.

NORMAL RESPONSE: elbow flexion and supination of the

forearm (turn palm upward).

BRACHIORADIALIS REFLEX

BRACHIORADIALIS REFLEX

TRICEP REFLEX (C7, C8 Radial Nerve):

Technique:

Identify the triceps tendon, a discrete, broad structure that can be

palpated as it extends across the elbow to the body of the
muscle, located on the back of the upper arm. Ask the patient to
extend their lower arm at the elbow while you observe and
palpate in the appropriate region
The arm can be placed in either of 2 positions:
A. Gently pull the arm out from the patients body, such that it
roughly forms a right angle at the shoulder. The lower arm should
dangle directly downward at the elbow.
B. Have the patient place their hands on their hips.
NORMAL RESPONSE: the lower arm to extend at the elbow and
swing away from the body. If the patients hands are on their hips,
the arm will not move but the muscle should shorten vigorously .

TRICEP BRACHII TENDON

TRICEP REFLEX (C7, C8 Radial Nerve):

TRICEP REFLEX (C7, C8 Radial Nerve):

DEEP TENDON REFLEXES

Pectoralis Reflex C5 T1
have patient elevate arm; place fingers of your left hand upon the pts
shoulders with your thumb extended downwards. Strike your thumb
directed slightly upwerd toward the pts axilla.
NORMAL RESPONSE: muscle contraction can be seen or felt

Pronator Reflex C6 C7
grasp pts hand and hold it vertically so the wrist is suspended
from the medial side, strike the distal end of the radius directlywith
horizontal blow
NORMAL RESPONSE: pronation of the forearm

Upper Abdominal Muscle Reflex T8 T9

tap the muscles directly near their insertions on the costal margins and
xiphoid process

Mid Abdominal Muscle Reflex T9 T10

tapping an overlaid finger

Lower Abdominal Muscle Reflex T11 T12

tap the muscle insertion directly near the symphysis pubis

DEEP TENDON REFLEXES

Adductor Reflex L2 L4
patient supine, arrange the lower limb in slight abduction. Tap directly on
the Adductor magnus, just proximal to its insertion on the medial
epicondyle of the femur
NORMAL RESPONSE: the thigh adducts

Hamstring Reflex L4 S2
Patient supine with hips and knees flexed at 90 degrees, and thigh
rotated slightly outward.
place your left hand under the popliteal fossa to compress the medial
hamstring
NORMAL RESPONSE: flexion of the knee and contraction of the medial
mass of hamstring

Making Clinical Sense of Reflexes:

Normal reflexes require that every aspect of the system function
normally. Breakdowns cause specific patterns of dysfunction.
These are interpreted as follows:

Disorders in the sensory limb will prevent or delay the

transmission of the impulse to the spinal cord. This causes the
resulting reflex to be diminished or completely absent. Diabetes
induced peripheral neuropathy, for example, is a relatively
common reason for loss of reflexes.

Abnormal LMN function will result in decreased or absent reflexes.

If, for example, a peripheral motor neuron is transected as a result
of trauma, the reflex dependent on this nerve will be absent.

If the UMN is completely transected, as might occur in traumatic

spinal cord injury, the arc receiving input from this nerve becomes
disinhibited, resulting in hyperactive reflexes. Of note, immediately
following such an injury, the reflexes are actually diminished, with
hyper-reflexia developing several weeks later. A similar pattern is
seen with the death of the cell body of the UMN (located in the
brain), as occurs with a stroke affecting the motor cortex of the
brain.

Making Clinical Sense of Reflexes:

Primary disease of the neuro-muscular junction or the muscle

itself will result in a loss of reflexes, as disease at the target organ
(i.e. the muscle) precludes movement.
A number of systemic disease states can affect reflexes. Some
have their impact through direct toxicity to a specific limb of the
system. Poorly controlled diabetes, as described above, can
result in a peripheral sensory neuropathy. Extremes of thyroid
disorder can also affect reflexes, though the precise mechanisms
through which this occurs are not clear. Hyperthyroidisim is
associated with hyperreflexia, and hypothyroidism with
hyporeflexia.
Detection of abnormal reflexes (either increased or decreased)
does not necessarily tell you which limb of the system is broken,
nor what might be causing the dysfunction. Decreased reflexes
could be due to impaired sensory input or abnormal motor nerve
function. Only by considering all of the findings, together with their
rate of progression, pattern of distribution (bilateral v unilateral,
etc.) and other medical conditions can the clinician make
educated diagnostic inferences about the results generated
during reflex testing.

Trouble Shooting
If you are unable to elicit a reflex, stop and consider the
following:

Are you striking in the correct place? Confirm the location of the
tendon by observing and palpating the appropriate region while
asking the patient to perform an activity that causes the muscle
to shorten, making the attached tendon more apparent.
Make sure that your hammer strike is falling directly on the
appropriate tendon. If there is a lot of surrounding soft tissue
that could dampen the force of the strike, place a finger firmly
on the correct tendon and use that as your target.
Make sure that the muscle is uncovered so that you can see
any contraction (occasionally the force of the reflex will not be
sufficient to cause the limb to move).
Sometimes the patient is unable to relax, which can inhibit the
reflex even when all is neurologically intact. If this occurs during
your assessment of lower extremity reflexes, ask the patient to
interlock their hands and direct them to pull, while you
simultaneously strike the tendon. This sometimes provides
enough distraction so that the reflex arc is no longer inhibited.

Trouble Shooting
Occasionally, it will not be possible to elicit reflexes, even
when no neurological disease exists. This is most
commonly due to a patient's inability to relax. In these
settings, the absence of reflexes are of no clinical
consequence. This assumes that you were otherwise
thorough in your history taking, used appropriate
examination techniques, and otherwise identified no
evidence of disease.

BRAINSTEM REFLEXES
Direct Pupillary Reaction to Light - the iris constricts when bright light
is shone upon the retina
Consensual Pupillary Reaction to Light - stimulation of one retina
causes contralateral constriction of the pupil
Ciliospinal Reflex - pinching the skin of the back of neck causes
pupillary dilatation
Corneal Reflex - touching the cornea causes blinking of the eyelids
Orbicularis Oculi Reflex - the eyelids close when the retina is
exposed to bright light
Auditocephalogyric Reflex - the head and eyes turn toward the
source of a loud sound
Jaw Reflex - when the mouth is partially opened and the muscles
relaxed, tapping the chin causes the jaw to close.
The reflex center is in the midpons
Gag Reflex - gagging occurs when the parhynx is stroked.
The reflex center is is the medulla

SUPERFICIAL REFLEXES
have reflex arcs whose receptor organs are in the skin
rather than in muscle fibers
adequate stimulus is stroking, scratching or touching
these reflexes are lost in disease of the pyramidal tract

SUPERFICIAL REFLEXES
Upper Abdominal Skin Reflex T5 T8
with patient supine, stroke the skin with blunt handle towards the midline
watch for ipsilateral contraction of muscles or umbilical deviation towards
the stimulated side

Mid Abdominal Skin Reflex T9 T11

Lower Abdominal Skin Reflex T11 T12
Cremasteric Reflex L1 L2
stroke the inner aspect of the thigh from the pubis distad
prompt elevation of the testis on the ipsilateral side

Plantar Reflex L4 S2
stroke the sole near its lateral aspect from the heel towards toes
produces plantar flexion of the toes

Superficial Anal Reflex L1 L2

stroke the skin of the perianal region
the external and anal sphincter contracts

Glabellar Reflex (Corticopontine)

- lightly tapping the forehead between the eyebrows with the fingers
Abnormal response: persistent blepharospasm and closing of the
eyes

Snout Reflex (Corticopontine)

- tapping the nose
Abnormal response: excessive grimace of the face

Sucking Reflex (Frontal cortex)

- stroking the lip with the finger or a tongue depressor
- present in infants but disappears after weaning; reappears in diffuse
lesions of the frontal lobe and commonly noted in dementias
Abnormal response: lips pout and make sucking movements

Chewing Reflex (Frontotemporal cortex)

- placing a tongue depressor in the mouth
- seen in dementia, general paresis and anoxic encepalopathy
Abnormal response: chewing movement of the teeth and jaw

ABNORMAL REFLEXES IN PYRAMIDAL TRACT DISEASE

Babinski Sign (Hallucal Dorsiflexion Reflex)

The Babinski response is a test used to assess upper motor

neuron dysfunction and is performed as follows:

The patient may either sit or lie supine.

Start at the lateral aspect of the foot, near the heel. Apply steady
pressure with the end of the hammer as you move up towards the
ball (area of the metatarsal heads) of the foot.

When you reach the ball of the foot, move medially, stroking
across this area.

Then test the other foot.

Some patients find this test to be particularly noxious

/uncomfortable. Tell them what you are going to do and why. If its
unlikely to contribute important information (e.g. screening exam
of the normal patient) and they are quite averse, simply skip it.

Babinski Response Present

Babinski Sign (Hallucal Dorsiflexion Reflex)

Interpretation: In the normal patient, the first movement of the great
toe should be downwards (i.e. plantar flexion). If there is an upper
motor neuron injury (e.g. spinal cord injury, stroke), then the great
toe will dorsiflex and the remainder of the other toes will fan out. A
few additional things to remember:
Newborns normally have a positive Babinksi. It usually goes away
after about 6 months.
Sometimes you will be unable to generate any response, even in
the absence of disease. Responses must therefore be interpreted in
the context of the rest of the exam.
If the great toe flexes and the other toes flair, the Babinski
Response is said to be present. If not (i.e. normal), it is recorded as
absent. For reasons of semantics, the Babinski is not recorded as
+ or -.
Withdrawal of the entire foot (due to unpleasant stimulation), is not
interpreted as a positive response

ABNORMAL REFLEXES IN PYRAMIDAL TRACT DISEASE

Grasp Reflex
Stroke the pts palm so he grasps your index finger. If present, he
cannot release the fingers; lesions of the premotor cortex

Hoffmanns Sign
Have pt present pronated hand with fingers extended and relaxed.
With your thumb, press his fingernails to flex the terminal digit and
stretch his flexor
Abnormal response: flexion and adduction of thumb

Mayers Reflex
Have pt present his supinated hand with thumb relaxed and
abducted. Grasp his ring finger and firmly flex the
metacarpophalengeal
joint
Normal response: adduction and apposition of the thumb

Palm-Chin Reflex (Radovicis sign)

Vigorous scratching or pricking of the thenar eminence causes
ipsilateral contraction of the muscles of the chin

SIGNS OF MENINGEAL IRRITATION

Nuchal Rigidity
- pt cannot place the chin upon the chest
- passive flexion of the neck is limited by involuntary muscle spasm

Spinal Rigidity
- movements of the spine are limited by spasms of the Erector spinae

Kernigs Sign
- with pt supine, passively flex the hip to 90 deg while the knee is
flexed at about 90 deg
- attempts to extend the knee produce pain iun the hamstring and
resistance

Brudzinskis Sign
- with pt supine and the limbs extended, passively flex the neck
- produces involuntary flexion of the hips

Making Sense of Neurological Findings

While compiling information generated from the motor and sensory

examinations, the clinician tries to identify patterns of dysfunction
that will allow him/her to determine the location of the lesion(s).
What follows is one way of making clinical sense of neurological
findings.
Is there evidence of motor dysfunction (e.g. weakness, spasticity,
tremor)?
If so, does the pattern follow an upper motor neuron or lower motor
neuron pattern?
If its consistent with a UMN process (e.g. weakness with spasticity),
does this appear to occur at the level of the spinal cord or the brain?
Complete cord lesions will affect both sides of the body. Brain level
problems tend to affect one side or the other. It is, of course, possible
for a lesion to affect only part of the cord, leading to findings that
lateralize to one side (see below, under description of Brown Sequard
lesion).
Is it consistent with an LMN process (e.g. weakness with flaccidity)?
Does the weakness follow a specific distribution (e.g. following a spinal
nerve root or peripheral nerve distribution)? Bilateral? Distal?

Making Sense of Neurological Findings

Do the findings on reflex examination support a UMN or LMN

process (e.g. hyper-reflexic in UMN disorders; hyporeflexic in LMN
disorders)?
Do the findings on Babinski testing (assuming the symptoms involve
the lower extremities) support the presence of a UMN lesion?
Is there impaired sensation? Some disorders, for example, affect
only the Upper or Lower motor pathways, sparing sensation.
Which aspects of sensation are impaired? Are all of the ascending
pathways (e.g. spinothalamic and dorsal columns) affected equally,
as might occur with diffuse/systemic disease?
Does the loss in sensation follow a pattern suggestive of dysfunction
at a specific anatomic level? For example, is it at the level of a
Spinal nerve root? Or more distally, as would occur with a peripheral
nerve problem?
Does the distribution of the sensory deficit correlate with the
correct motor deficit, assuming one is present? Radial nerve
compression, for example, would lead to characteristic motor and
sensory findings.

THE END