A Practical Guide to Clinical Medicine

A comprehensive physical examination and clinical education site for medical students and other health care professionals

Web Site Design by Jan Thompson, Program Representative, UCSD School of Medicine.
Content and Photographs by Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, California 92093-0611.
Send Comments to: Charlie Goldberg, M.D.

Introduction Breast Exam Write Ups
History of Present Illness Male Genital/Rectal Exam The Oral Presentation
The Rest of the History The Upper Extremities Outpatient Clinics
Review of Systems The Lower Extremities Inpatient Medicine
Vital Signs Musculo-Skeletal Exam Clinical Decision Making
The Eye Exam The Mental Status Exam Physical Exam Lecture Series
Head and Neck Exam The Neurological Exam A Few Thoughts
The Lung Exam Physical Exam Check Lists Commonly Used Abbreviations
Cardiovascular Exam Medical Links References
Exam of the Abdomen    

The "daVinci Anatomy Icon" denotes a link to related gross anatomy pictures. DaVinci's Anatomy Symbol

The Neurological Examination

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 move.
  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 below.
  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 stimulation

For more information about anatomy and physiology of reflexes, see the following link:

Washington University Review of Anatomy and Physiology of Reflexes


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 Hammers

Large 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 scale.

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.
  3. Achilles Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.

  4. 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.
  5. 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).
  6. Positions for Checking Achilles Reflex

To see a video of the normal achilles reflex exam, click on the movie icon.
To see a video of the achilles reflex exam comparing normal with hyperreflexia, click on the movie icon.

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.
  3. Patellar Tendon: Outlined in pen on left, grasped by forceps (gross dissection)on right.

  4. 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.
  5. Patellar Reflex Testing, seated patient

  6. 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.
  7. Patellar Reflex, supine patient

  8. 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.
  9. To see a video of the normal patellar reflex exam, click on the movie icon.
    To see a video of the patellar reflex exam comparing normal with hyperreflexia, click on the movie icon.

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.
  3. Biceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.

  4. 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.
    2. Biceps Reflex Testing

    3. 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).
    4. Biceps Reflex Testing,arm supported

  5. Make sure that the biceps muscle is completely relaxed.
  6. 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.
  7. 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.

To see a video of the normal biceps reflex exam, click on the movie icon.
To see a video of the biceps reflex exam comparing normal with hyperreflexia, click on the movie icon.

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.
  3. Brachioradialis Tendon: Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.

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

  6. 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).

To see a video of the normal brachial radialis reflex exam, click on the movie icon.
To see a video of the brachial radialis reflex exam comparing normal with hyperreflexia, click on the movie icon.

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.
  3. Triceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.

  4. 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.
    2. Triceps Reflex, arm supported

    3. Have the patient place their hands on their hips.
    4. Triceps Reflex, arm unsupported

    Either of these techniques will allow the triceps to completely relax.
  5. 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.
  6. 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 .
To see a video of the triceps reflex exam comparing normal with hyperreflexia, click on the movie icon.

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:

  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 disease.

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 point.
  2. The patient may either sit or lie supine.
  3. Start at the lateral aspect of the foot, near the heel. Apply gentle, 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 area.
  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 remember:

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.

To see a video of an exam showing Babinski response absent, click on the movie icon.
To see a video of the comparing Babinski response present and absent, click on the movie icon.
To see a video of a dorsiflexion exam showing clonus, click on the movie icon.


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 hand.
    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.

If the movement is accurate and smooth but slow, the likely problem is weakness.

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.

Gait Testing

The ability to stand and walk normally is dependent upon input from multiple systems, including: visual, vestibular, cerebellar, motor, and sensory. The precise cause(s) of gait dysfunction can be determined by identifying which aspects are abnormal and then incorporating this information with that obtained during the rest of the exam to paint the best picture. Difficulty getting out a chair and initiating movement, for example, could be consistent with Parkinson's Disease. On the other hand, lack of balance and a wide based gait might suggest a cerebellar disorder. In each case, historical features coupled with findings elsewhere in the exam should help point you in the right direction.

For the screening exam, simply observing as the patient walks into your office and gets up and down from the exam table should provide you with 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:

A few common gait disorders and their causes are described below.

Ataxic gait: This is an unbalanced, uncoordinated gait. It can result from diseases affecting the cerebellum (e.g. stroke, degenerative disease, multiple sclerosis, metabolic deficienciesthiamine, tumor, toxic effectetoh, other), vestibular system, and other motor or sensory disorders.

An ataxic gait is notable for being wide based, with lurching/staggering to keep balance, truncal instability, and impaired tandem walking. If it is the result of cerebellar disease, the patient may also have difficult-to-understand speech (dysarthria), problems with fine movements like picking up small objects, buttoning clothes, or drawing, difficulty with finger to nose movement and impaired rapid alternating movements. Nystagmus and tremor may also be present. A common reversible cause for ataxia is acute alcohol intoxication. In fact, sobriety testing done by police officers is designed to identify the acute cerebellar dysfunction caused by this toxin.

Hemiplegic Gait: Notable for patients walking with their arm abducted, elbow flexed, hand closed, and hip circumducted in order to move their leg. Exam will be remarkable for weakness, increased tone and hyper-reflexia of limbs on the affected side of the body. Common causes include motor cortex stroke or other structural brain disease affecting that area of the brain
This video demonstrates the gait of a patient status post stroke. Note the way that they hold their left arm and circumduct their left hip

Neuropathic Gait (from foot drop): Notable for lifting affected leg high to keep foot from dragging. The shoe on the affected side is often scuffed at the toe. Exam is remarkable for weakness in dorsiflexion on the affected side. This is often the result of peroneal nerve dysfunction.

Neuropathic Gait (from sensory neuropathy): Notable for raising the leg high and striking it firmly on the ground with each step, done in order to help identify the precise location of the feet. On exam, sensation will be impaired (e.g. light touch, pin prick, vibratory, proprioception). Etiology can be from toxic effects (e.g. ETOH), metabolic disorders (e.g. diabetes), deficiency states (e.g. B12), autoimmune and other diseases affecting the sensory system.

Parkinsonian gait: Gait is remarkable for stooped forward posture, narrow base, shuffling nature, difficulty initiating movement, impaired ability to stop and turn, balance problems, and limited arm movement. Other findings can include masked/inexpressive facies and resting tremor of hand or head.

Antalgic (limping) Gait: Gait is notable for placing weight on the affected leg for the least amount of time possible due to pain or other impairment. This is typically due to injury or degenerative disease of the hip, knee or leg. The exam will be notable for pain or other abnormality affecting the leg on that side.
This video demonstrates an antalgic gait secondary to to chronic left hip arthritis.

Diplegic gait (typically associated with cerebral palsy): This gait is associated with flexed knees and hips, knees crossing in scissor-fashion with walking, circumduction of hips, and arms often abducted and bent at elbows. Other exam findings include hyper-reflexia and increased tone of affected limbs, with the legs impacted to a greater extent than the arms

A wide array of other conditions can affect gait including visual impairment, muscle weakness, disorders of the peripheral or central nervous system, or other acute or chronic processes. Note that as patients age, multiple conditions can contribute simultaneously to gait problems. A comprehensive history and exam should help to identify the cause(s).

NeurologicExam for more info and videos about assorted gait disorders

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 pattern?
    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 examination:

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.
Babinksi Toes 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.
Babinksi Up-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.

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