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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.

Physiology of Reflexes

Assessment of reflexes is based on a clear understanding of the following principles and relationships:

  1. Tendons connect muscles to bones, usually crossing a joint. When the muscle
    contracts, the tendon pulls on the bone, causing the attached structure to
  2. 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.
  3. The signal then travels down the lower motor neuron to the target muscle.
  4. 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
  5. A normal response generates an easily observed shortening of the muscle.
    This, in turn, causes the attached structure to move.
  6. The vigor of contraction is graded on the following scale:
No evidence of contraction
Decreased, but still present (hypo-reflexic)
Super-normal (hyper-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.

Small HammerSmall HammerLarge Hammer,
Head Oriented Horizontally
Large Hammer,
Head Oriented Vertically


  1. The muscle group to be tested must be in a neutral position (i.e. neither
    stretched nor contracted).
  2. 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.
  3. 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.
  4. 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):

    1. 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.
    2. 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.


    1. 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.
    2. 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 ExamAchilles Reflex Exam Comparing Normal with Hyperreflexia

Patellar (L3, L4 ? Femoral Nerve):

    1. 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).
    2. 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.
    1. 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
    1. 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
  1. 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 examPatellar reflex exam comparing normal with hyperreflexia

Biceps (C5, C6 ? Musculocutaneous Nerve):

    1. This is most easily done with the patient seated.
    2. 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.
    1. The patient?s arm can be positioned in one of two ways:
      1. 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
      1. 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
  1. Make sure that the biceps muscle is completely relaxed.
  2. 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.
  3. 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 examBiceps reflex exam comparing normal with hyperreflexia

Brachioradialis (C5, C6 ? Radial Nerve):

    1. This is most easily done with the patient seated. The lower arm should
      be resting loosely on the patient?s lap.
    2. 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.
    1. Strike this area with your reflex hammer. Usually, hitting anywhere in the
      right vicinity will generate the reflex.
Brachioradialis Reflex
  1. 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 examBrachial radialis reflex exam comparing normal with hyperreflexia

Triceps (C7, C8 ? Radial Nerve):

    1. This is most easily done with the patient seated.
    2. 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.
    1. The arm can be placed in either of 2 positions:
      1. 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
      1. Have the patient place their hands on their hips.
Triceps Reflex, arm unsupported

Either of these techniques will allow the triceps to completely relax.

  1. 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.
  2. 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

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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

  1. If you are unable to elicit a reflex, stop and consider the following:
    1. 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.
    2. 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.
    3. 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).
    4. 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.
  2. 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

Babinski Response

The Babinski response is a test used to assess upper motor neuron dysfunction
and is performed as follows:

  1. Use the handle end of your reflex hammer, which is solid and comes to a
  2. The patient may either sit or lie supine.
  3. 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.
  4. When you reach the ball of the foot, move medially, stroking across this
  5. Then test the other foot.
  6. 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
  1. Newborns normally have a positive Babinksi. It usually goes away after about
    6 months.
  2. 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.
  3. 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 ?-?.
  4. Withdrawal of the entire foot (due to unpleasant stimulation), is not interpreted
    as a positive response.

Babinski response absentComparing Babinski response present and absentDorsiflexion exam showing clonus

Adapted, with permission from University of California, San Diego School of Medicine By Charlie Goldberg, M.D.

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Cerebellar Testing


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
next section).

  1. Finger to nose testing:
    1. With the patient seated, position your index finger at a point in space
      in front of the patient.
    2. Instruct the patient to move their index finger between your finger
      and their nose.
    3. Reposition your finger after each touch.
    4. Then
      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.

  1. Rapid Alternating Finger Movements:
    1. Ask the patient to touch the tips of each finger to the thumb of the same
    2. Test both hands.

Interpretation: The movement should be fluid and accurate.
Inability to do this, known as dysdiadokinesia, may be indicative of
cerebellar disease.

  1. Rapid Alternating Hand Movements:
    1. Direct the patient to touch first the palm and then the dorsal side of
      one hand repeatedly against their thigh.
    2. 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.

  1. Heel to Shin Testing:
    1. Direct the patient to move the heel of one foot up and down along the
      top of the other shin.
    2. 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
test results.

Adapted, with permission from University of California, San Diego School of Medicine By Charlie Goldberg, M.D.

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Gait Testing


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
as follows:

  1. 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!
  2. 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.
  3. Ask the patient to stand from a chair, walk across the room, turn, and come
    back towards you. Pay particular attention to:

    1. 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.
    2. 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.
    3. 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?
    4. 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
      a stroke)?
  4. 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.

Gait of a patient status post stroke

Adapted, with permission from University of California, San Diego School of Medicine By Charlie Goldberg, M.D.

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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.

  1. Is there evidence of motor dysfunction (e.g. weakness, spasticity, tremor)?
  2. If so, does the pattern follow an upper motor neuron or lower motor neuron

    1. 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).
    2. 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?
  3. Do the findings on reflex examination support a UMN or LMN process (e.g.
    hyper-reflexic in UMN disorders; hyporeflexic in LMN disorders)?
  4. Do the findings on Babinski testing (assuming the symptoms involve the lower
    extremities) support the presence of a UMN lesion?
  5. Is there impaired sensation? Some disorders, for example, affect only the
    Upper or Lower motor pathways, sparing sensation.
  6. 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?
  7. 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?
  8. 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:

Example 1

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

Sensation:Absence of ability to sense pin prick, vibration or propriocetion
below the level of the umbilicus.
Strength:No movement of the lower extremities (e.g. paralysis).
Tone:Initially, decreased. Over weeks, tone increases with progression
to spasticity and contractures of the lower extremities.
Reflexes:Initially, absent Achilles and Patellar reflexes. After a
few weeks, these will become hyperreflexic and demonstrate clonus.
BabinksiToes will be up-going bilaterally (i.e. Babinski response
will be present).

Example 2

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:

Sensation: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.
Strength:The patient would be unable to move their right leg.
Tone:Initially, decreased in the right leg. Over weeks, tone increases,
with progression to spasticity.
Reflexes:Initially, absent at the right Patellar and Achilles. After
a few weeks becoming hyper-reflexic.
BabinksiUp-going toe on the right

Several additional examples of specific patterns of nerve injury/dysfunction
can be found via the following links:

University of Wisconsin, Anatomy and pathophysiology of spinal cord copression syndromes

University of Wisconsin, Anatomy and pathophysiology of motor weakness

University of Wisconsin, Examples of various radiculopathies

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.

Adapted, with permission from University of California, San Diego School of Medicine By Charlie Goldberg, M.D.

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