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.
Physiology of Reflexes
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
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 lower motor neuron to the target muscle.
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.
This can obviously be of great clinical significance. The Achilles Reflex
(see below) is dependent on the S1 and S2 nerve roots. Herniated disc material
(a relatively common process) 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. The specific nerve roots
that comprise the arcs are listed for each of the major reflexes described
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:
No evidence of contraction
Decreased, but still present (hypo-reflexic)
Clonus: Repetitive shortening of the muscle after a single
The Reflex Hammer
You will need to use a reflex hammer when performing this aspect of the exam. A number of the most commonly used models are pictured below. 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.
Head Oriented Horizontally
Head Oriented Vertically
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 patient?s 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.
This grading system is rather subjective. Additional levels of response can
be included by omitting the ?+? or adding a ?-? to any of the numbers. As you
gain more experience, you?ll have a greater sense of how to arrange your own
Specifics of Reflex Testing ? The peripheral nerves and contributing spinal
nerve roots that form each reflex arc are listed in parentheses:
Achilles (S1, S2 ? Sciatic Nerve):
This is most easily done with the patient seated, feet dangling over the
edge of the exam table. If they cannot maintain this position, have them lie
supine, crossing one leg over the other in a figure 4. Or, failing that, arrange
the legs in 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?), which will cause the calf to contract
and the Achilles to become taut.
Achilles Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
Position the foot so that it forms a right angle with the rest of the lower
leg. You will probably need to support the bottom of the foot with your hand.
Strike the tendon directly with your reflex hammer. Be sure that the calf
if exposed so that you can see the muscle contract. A normal reflex will cause
the foot to plantar flex (i.e. move into your supporting hand).
Positions for Checking Achilles Reflex
Normal Achilles Reflex Exam
Achilles Reflex Exam Comparing Normal with Hyperreflexia
Patellar (L3, L4 ? Femoral Nerve):
This is most easily done with the patient seated, feet dangling over the
edge the exam table. If they cannot maintain this position, have them lie
supine (i.e. on their backs).
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
it?s located, ask the patient to extend their knee. This causes the quadriceps
(thigh muscles) to contract and makes the attached tendon more apparent.
Patellar Tendon: Outlined in pen on left, grasped by forceps (gross dissection)on right.
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.
Patellar Reflex Testing, seated patient
For the supine patient, support the back of their thigh with your hands
such that the knee is flexed and the quadriceps muscles relaxed. Then strike
the tendon as described above.
Patellar Reflex, supine patient
Make sure that the quadriceps are exposed so that you can see muscle contraction.
In the normal reflex, the lower leg will extend at the knee.
Normal patellar reflex exam
Patellar reflex exam comparing normal with hyperreflexia
Biceps (C5, C6 ? Musculocutaneous Nerve):
This is most easily done with the patient seated.
Identify the location of the biceps tendon. To do this, have the patient
flex at the elbow while you observe and palpate the antecubital fossa. The
tendon will look and feel like a thick cord.
Biceps Tendon: Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
The patient?s arm can be positioned in one of two ways:
Allow the arm to rest in the patient?s lap, forming an angle of slightly
more then 90 degrees at the elbow.
Biceps Reflex Testing
Support the arm in yours, such that your thumb is resting directly over
the biceps tendon (hold their right arm with your right; and vice versa).
Biceps Reflex Testing,arm supported
Make sure that the biceps muscle is completely relaxed.
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 patient?s 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.
Make sure that the patient?s sleeve is rolled up so that you can directly
observe the muscle as well as watch the lower arm for movement. A normal
response will cause the biceps to contract, drawing the lower arm upwards.
Normal biceps reflex exam
Biceps reflex exam comparing normal with hyperreflexia
Brachioradialis (C5, C6 ? Radial Nerve):
This is most easily done with the patient seated. The lower arm should
be resting loosely on the patient?s 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.
Brachioradialis Tendon: Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
Strike this area with your reflex hammer. Usually, hitting anywhere in the
right vicinity will generate the reflex.
Observe the lower arm and body of the Brachioradialis for
a response. A normal reflex will cause the lower arm to flex at the elbow
and the hand to supinate (turn palm upward).
Normal brachial radialis reflex exam
Brachial radialis reflex exam comparing normal with hyperreflexia
Triceps (C7, C8 ? Radial Nerve):
This is most easily done with the patient seated.
Identify the triceps tendon, a discrete, broad structure that can be palpated
(and often seen) as it extends across the elbow to the body of the muscle,
located on the back of the upper arm. If you are having trouble clearly identifying
the tendon, ask the patient to extend their lower arm at the elbow while you
observe and palpate in the appropriate region.
Triceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
The arm can be placed in either of 2 positions:
Gently pull the arm out from the patient?s body, such that it roughly
forms a right angle at the shoulder. The lower arm should dangle directly
downward at the elbow.
Triceps Reflex, arm supported
Have the patient place their hands on their hips.
Triceps Reflex, arm unsupported
Either of these techniques will allow the triceps to completely relax.
If you are certain as to the precise location of the tendon, strike this
area directly with your hammer. If the target is not clearly apparent or the
tendon is surrounded by an excessive amount of subcutaneous fat (which might
dissipate the force of your strike), place your index or middle finger firmly
against the structure. Then strike your finger.
Make sure that the triceps is uncovered, so that you can observe the response.
The normal reflex will cause the lower arm to extend at the elbow and swing
away from the body. If the patient?s hands are on their hips, the arm will
not move but the muscle should shorten vigorously .
Triceps reflex exam comparing normal with hyperreflexia
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
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 (the most common
sensory neuropathy seen in developed countries), for example, is a relatively
common reason for loss of reflexes.
Abnormal lower motor neuron (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 upper motor neuron (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.
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)
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.
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.
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
The Babinski response is a test used to assess upper motor neuron dysfunction
and is performed as follows:
Use the handle end of your reflex hammer, which is solid and comes to a
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
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 it?s unlikely to contribute important
information (e.g. screening exam of the normal patient) and they are quite
averse, simply skip it.
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
Babinski Response Present
Newborns normally have a positive Babinksi. It usually goes away after about
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.
The cerebellum fine tunes motor activity and assists with balance. Dysfunction
results in a loss of coordination and problems with gait. The left cerebellar
hemisphere controls the left side of the body and vice versa.
Specifics of Testing: There are several ways of testing cerebellar function.
For the screening exam, using one modality will suffice. If an abnormality is
suspected or identified, multiple tests should be done to determine whether
the finding is durable. That is, if the abnormality on one test is truly due
to cerebellar dysfunction, other tests should identify the same problem. Gait
testing, an important part of the cerebellar exam, is discussed separately (see
Finger to nose testing:
With the patient seated, position your index finger at a point in space
in front of the patient.
Instruct the patient to move their index finger between your finger
and their nose.
Reposition your finger after each touch.
test the other hand.
Interpretation: The patient should be able to do this at a reasonable rate
of speed, trace a straight path, and hit the end points accurately. Missing
the mark, known as dysmetria, may be indicative of disease.
Rapid Alternating Finger Movements:
Ask the patient to touch the tips of each finger to the thumb of the same
Test both hands.
Interpretation: The movement should be fluid and accurate.
Inability to do this, known as dysdiadokinesia, may be indicative of
Rapid Alternating Hand Movements:
Direct the patient to touch first the palm and then the dorsal side of
one hand repeatedly against their thigh.
Then test the other hand.
Interpretation: The movement should be performed with speed
and accuracy. Inability to do this, known
as dysdiadokinesia, may be indicative of cerebellar disease.
Heel to Shin Testing:
Direct the patient to move the heel of one foot up and down along the
top of the other shin.
Then test the other foot.
Intepretation: The movement should trace a straight line along the top of the
shin and be done with reasonable speed.
Realize that other organ system problems can affect performance of any of these
tests. If, for example, the patient is visually impaired, they may not be able
to see the target during finger to nose pointing. Alternatively, weakness due
to a primary muscle disorder might limit the patient?s ability to move a limb
in the fashion required for some of the above testing. Thus, other medical and
neurological conditions must be taken into account when interpreting cerebellar
Ability to stand and walk normally is dependent on input from several systems,
including: visual, vestibular, cerebellar, motor, and sensory. The precise cause(s)
of the dysfunction can be determined by identifying which aspect of gait is
abnormal and incorporating this information with that obtained during the rest
of the exam. Difficulty getting out a chair and initiating movement, for example,
would be consistent with Parkinson?s Disease. On the other hand, lack of balance
and a wide based gait would suggest a cerebellar disorder. In each case, finding
elsewhere in the exam should help point you in the right direction.
A lot of information about neurological (and other) disorders
can be gained from simply watching a patient stand and then walk. For the screening
exam, simply observing while the patient walks into your office and gets up
and down from the exam table will provide all of the relevant information. If
there is suspicion of neurological disease (based on history, other exam findings,
observation of gait) then more detailed testing should be performed. Proceed
Ask the patient to stand. If they are very weak or unsteady, make sure that
you are in a position and capable of catching and supporting them if they
fall. Enlist the help of a colleague if you need an extra pair of hands. If
you are still unsure as to whether standing/walking can be performed safely,
skip this area of testing. No test result is worth a broken hip!
Have the patient stand in one place. As mentioned above, make sure that
you are capable/in position to catch and support them if they fall. This is
a test of balance, incorporating input from the visual, cerebellar, proprioceptive,
and vestibular systems. If they are able to do this, have them close their
eyes, removing visual input. This is referred to as the Romberg test. Loss
of balance suggests impaired proprioception, as it is this pathway which should
provide input that allows the patient to remain stably upright.
Ask the patient to stand from a chair, walk across the room, turn, and come
back towards you. Pay particular attention to:
Difficulty getting up from a chair: Can the patient easily arise from
a sitting position? Problems with this activity might suggest proximal muscle
weakness, a balance problem, or difficulty initiating movements.
Balance: Do they veer off to one side or the other as might occur with
cerebellar dysfunction? Disorders affecting the left cerebellar hemisphere
(as might occur with a stroke or tumor) will cause patient?s to fall to
the left. Right sided lesions will cause the patient to fall to the right.
Diffuse disease affecting both cerebellar hemispheres will cause a generalized
loss of balance.
Rate of walking: Do they start off slow and then accelerate, perhaps losing
control of their balance or speed (e.g. as might occur with Parkinson?s
Disease)? Are they simply slow moving secondary to pain/limited range of
motion in their joints, as might occur with degenerative joint disease?
Atttitude of Arms and Legs: How do they hold their arms and legs? Is there
loss of movement and evidence of contractures (e.g. as might occur after
Heel to Toe Walking: Ask the patient to walk in a straight line, putting
the heel of one foot directly in front of the toe of the other. This is referred
to as tandem gait and is a test of balance. Realize that this may be difficult
for older patients (due to the frequent coexistence of other medical conditions)
even in the absence of neurological disease.
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
If it?s 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?
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
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.
Information from the sensory, motor and reflex examinations should correlate
with one another, painting the best picture of where the level of dysfunction
is likely to exist. A few examples of injuries resulting in characteristic patterns
of motor and sensory loss are described below:
In the setting of a suspected acute spinal cord injury at the T 10 vertebral
level, for example, the following might be identified on detailed neurological
Absence of ability to sense pin prick, vibration or propriocetion
below the level of the umbilicus.
No movement of the lower extremities (e.g. paralysis).
Initially, decreased. Over weeks, tone increases with progression
to spasticity and contractures of the lower extremities.
Initially, absent Achilles and Patellar reflexes. After a
few weeks, these will become hyperreflexic and demonstrate clonus.
Toes will be up-going bilaterally (i.e. Babinski response
will be present).
Partial Cord Transection – The Brown-Sequard Lesion: A knife injury, for example,
might damage only the right half of the cord at the T 10 level. This would result
in the following findings on detailed exam:
The patient would be unable to identify the pin stimulus on
the left side of his body (remember that the spinothalamacs cross soon after
entering the cord) below the level of the injury. Vibratory sensation would
be impaired on the right side of the body below the level of the injury,
as these paths do not cross over until they reach the base of the brain.
The patient would be unable to move their right leg.
Initially, decreased in the right leg. Over weeks, tone increases,
with progression to spasticity.
Initially, absent at the right Patellar and Achilles. After
a few weeks becoming hyper-reflexic.
Up-going toe on the right
Several additional examples of specific patterns of nerve injury/dysfunction
can be found via the following links:
A few final comments about diagnosing neurologic disorders:
It is also important to note that the pace at which a particular
disorder develops will have a dramatic effect on symptoms and exam findings.
Acute dysfunction (as might occur with a stroke) generally causes obvious symptoms
as the loss of function is abrupt, allowing the patient no time to develop compensatory
mechanisms. Patient presentation will also be affected by the size and location
of the lesion. Larger lesions or those affecting critical areas of function
tend to generate more overt problems. Additionally, patients with pre-existing
medical or neurological dysfunction may well tolerate new lesions poorly. In
contrast, disorders which occur more slowly tend to cause relatively subtle
symptoms. For example, toxin induced damage to the cerebellum can result in
profound atrophy of this region of the brain. While imaging may reveal significant
volumetric loss, exam findings can remain relatively minimal. These same principles
apply to most other aspects of the physical examination.