Section 1 Diagnosis of Neurologic

Disorders

Neurologic Disorders PART 13

422 Approach to the Patient

with Neurologic Disease

Daniel H. Lowenstein, S. Andrew

Josephson, Stephen L. Hauser

Neurologic diseases are common and costly. According to estimates

by the World Health Organization, neurologic disorders affect more

than 1 billion people worldwide, constitute 12% of the global burden of disease, and cause 14% of global deaths (Table 422-1). These

numbers are only expected to increase as the world’s population ages.

Because therapies now exist for many neurologic disorders, a skillful approach to diagnosis is essential. Errors commonly result from

an overreliance on costly neuroimaging procedures and laboratory

tests, which, while useful, do not substitute for an adequate history

and examination. The proper approach begins with the patient and

focuses the clinical problem first in anatomic and then in pathophysiologic terms; only then should a specific neurologic diagnosis

be entertained. This method ensures that technology is judiciously

applied, a correct diagnosis is established in an efficient manner, and

treatment is promptly initiated.

THE NEUROLOGIC METHOD

■ DEFINE THE ANATOMY

The first priority is to identify the region of the nervous system that is

likely to be responsible for the symptoms. Can the disorder be mapped

to one specific location, is it multifocal, or is a diffuse process present?

Are the symptoms restricted to the nervous system, or do they arise in

the context of a systemic illness? Is the problem in the central nervous

system (CNS), the peripheral nervous system (PNS), or both? In the

CNS, is the cerebral cortex, basal ganglia, brainstem, cerebellum, or

spinal cord responsible? Are the pain-sensitive meninges involved?

In the PNS, could the disorder be located in peripheral nerves and, if

so, are motor or sensory nerves primarily affected, or is a lesion in the

neuromuscular junction or muscle more likely?

The first clues to defining the anatomic area of involvement appear

in the history, and the examination is then directed to confirm or rule

out these impressions and to clarify uncertainties. A more detailed

examination of a particular region of the CNS or PNS is often indicated. For example, the examination of a patient who presents with

a history of ascending paresthesias and weakness should be directed

toward deciding, among other things, if the lesion is in the spinal cord

or peripheral nerves. Focal back pain, a spinal cord sensory level, and

incontinence suggest a spinal cord origin, whereas a stocking-glove

pattern of sensory loss suggests peripheral nerve disease; areflexia

usually indicates peripheral neuropathy but may also be present with

so-called spinal shock in acute spinal cord disorders.

Deciding “where the lesion is” accomplishes the task of limiting

the possible etiologies to a manageable, finite number. In addition,

this strategy safeguards against making serious errors. Symptoms of

recurrent vertigo, diplopia, and nystagmus should not trigger “multiple

sclerosis” as an answer (etiology) but “brainstem” or “pons” (location);

then a diagnosis of brainstem arteriovenous malformation will not be

missed for lack of consideration. Similarly, the combination of optic

neuritis and spastic ataxic paraparesis suggests optic nerve and spinal

cord disease; multiple sclerosis (MS), CNS syphilis, and vitamin B12

deficiency are treatable disorders that can produce this syndrome.

Once the question, “Where is the lesion?” is answered, then the question “What is the lesion?” can be addressed.

■ IDENTIFY THE PATHOPHYSIOLOGY

Clues to the pathophysiology of the disease process may also be present

in the history. Primary neuronal (gray matter) disorders often present as

early cognitive disturbances, movement disorders, or seizures, whereas

white matter involvement produces “long tract” disorders of motor,

sensory, visual, and cerebellar pathways. Progressive and symmetric

symptoms often have a metabolic or degenerative origin; in such cases

lesions are usually not sharply circumscribed. Thus, a patient with

paraparesis and a clear spinal cord sensory level is unlikely to have

vitamin B12 deficiency as the explanation. A Lhermitte symptom (electric

shock–like sensations evoked by neck flexion) is due to ectopic impulse

generation in white matter pathways and occurs with demyelination in

the cervical spinal cord; among many possible causes, this symptom may

indicate MS in a young adult or compressive cervical spondylosis in an

older person. Symptoms that worsen after exposure to heat or exercise

may indicate conduction block in demyelinated axons, as occurs in MS.

A patient with recurrent episodes of diplopia and dysarthria associated

with exercise or fatigue may have a disorder of neuromuscular transmission such as myasthenia gravis. Slowly advancing visual scotoma with

luminous edges, termed fortification spectra, indicates spreading cortical

depression, typically with migraine.

THE NEUROLOGIC HISTORY

Attention to the description of the symptoms experienced by the

patient and substantiated by family members and others often permits

an accurate localization and determination of the probable cause, even

before the neurologic examination is performed. The history also helps

focus the neurologic examination that follows. Each complaint should

be pursued as far as possible to identify the location of the lesion, the

likely underlying pathophysiology, and potential etiologies. For example, a patient complains of weakness of the right arm. What are the

associated features? Does the patient have difficulty with brushing hair

or reaching upward (proximal) or fastening buttons or opening a plastic bottle (distal)? Negative associations may also be crucial. A righthanded patient with a right hemiparesis without a language deficit

likely has a lesion (internal capsule, brainstem, or spinal cord) different

from that of a patient with a right hemiparesis and aphasia (left hemisphere). Other pertinent features of the history include the following:

1. Temporal course of the illness. It is important to determine the precise time of appearance and rate of progression of the symptoms

TABLE 422-1 Global Disability-Adjusted Life-Years (DALYs) and

Number of Annual Deaths for Selected Neurologic Disorders in 2019

DISORDER DALYs DEATHS

Low-back and neck pain 85,766,442 —

Cerebrovascular diseases 143,232,184 6,552,725

Meningitis and encephalitis 21,120,604 326,117

Migraine 42,077,666 —

Epilepsy 13,077,624 114,010

Dementia 25,276,989 1,623,256

Parkinson’s disease 6,292,616 362,907

% of total DALYs or deaths for all

causes that are neurologic

13.7% 16.1%

% change of DALYs or deaths for

neurologic disorders between 2015

and 2019

41.0% 0.0%

Source: Data from Global Burden of Disease Study 2019 (GBD 2019) Data

Resources http://ghdx.healthdata.org/gbd-2019 and GBD 2019 Diseases and Injuries

Collaborators. Global burden of 369 diseases and injuries in 204 countries and

territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study

2019. Lancet 396:1204, 2020.

3278 PART 13 Neurologic Disorders

experienced by the patient. The rapid onset of a neurologic complaint, occurring within seconds or minutes, usually indicates a

vascular event, a seizure, or migraine. The onset of sensory symptoms located in one extremity that spread over a few seconds to

adjacent portions of that extremity and then to the other regions of

the body suggests a seizure. A similar but slower temporal march of

symptoms accompanied by headache, nausea, or visual disturbance

suggests migraine. Less well-localized symptoms that are maximum

at onset and persist for seconds, minutes, or much less commonly

hours, point to the possibility of a transient ischemic attack (TIA).

The presence of “positive” sensory symptoms (e.g., tingling or sensations that are difficult to describe) or involuntary motor movements

suggests a seizure; in contrast, transient loss of function (negative

symptoms) suggests a TIA. A stuttering onset where symptoms

appear, stabilize, and then progress over hours or days also suggests

cerebrovascular disease; an additional history of transient remission

or regression indicates that the process is more likely due to ischemia rather than hemorrhage. A gradual evolution of symptoms over

hours or days suggests a toxic, metabolic, infectious, or inflammatory process. Progressing symptoms associated with the systemic

manifestations of fever, stiff neck, and altered level of consciousness

imply an infectious process. Relapsing and remitting symptoms

involving different levels of the nervous system suggest MS or

other inflammatory processes. Slowly progressive symptoms without remissions are characteristic of neurodegenerative disorders,

chronic infections, gradual intoxications, and neoplasms.

2. Patients’ descriptions of the complaint. The same words often

mean different things to different patients. “Dizziness” may imply

impending syncope, a sense of disequilibrium, or true spinning

vertigo. “Numbness” may mean a complete loss of feeling, a positive

sensation such as tingling, or even weakness. “Blurred vision” may

be used to describe unilateral visual loss, as in transient monocular

blindness, or diplopia. The interpretation of the true meaning of the

words used by patients to describe symptoms obviously becomes

even more complex when there are differences in primary languages

and cultures.

3. Corroboration of the history by others. It is almost always helpful to

obtain additional information from family, friends, or other observers to corroborate or expand the patient’s description. Memory loss,

aphasia, loss of insight, intoxication, and other factors may impair

the patient’s capacity to communicate normally with the examiner

or prevent openness about factors that have contributed to the

illness. Episodes of loss of consciousness necessitate that details be

sought from observers to ascertain precisely what has happened

during the event.

4. Family history. Many neurologic disorders have an underlying

genetic component. The presence of a Mendelian disorder, such as

Huntington’s disease or Charcot-Marie-Tooth neuropathy, is often

obvious if family data are available. More detailed questions about

family history are often necessary in polygenic disorders such as MS,

migraine, and many types of epilepsy. It is important to elicit family

history about all illnesses, in addition to neurologic and psychiatric

disorders. A familial propensity to hypertension or heart disease is

relevant in a patient who presents with a stroke. Numerous inherited

neurologic diseases are associated with multisystem manifestations

that may provide clues to the correct diagnosis (e.g., neurofibromatosis, Wilson’s disease, mitochondrial disorders).

5. Medical illnesses. Many neurologic diseases occur in the context of

systemic disorders. Diabetes mellitus, hypertension, and abnormalities of blood lipids predispose to cerebrovascular disease. A solitary

mass lesion in the brain may be an abscess in a patient with valvular

heart disease, a primary hemorrhage in a patient with a coagulopathy, a lymphoma or toxoplasmosis in a patient with AIDS, or a

metastasis in a patient with underlying cancer. Patients with malignancy may also present with a neurologic paraneoplastic syndrome

(Chap. 94) or complications from chemotherapy or radiotherapy.

Marfan’s syndrome and related collagen disorders predispose to

dissection of the cranial arteries and aneurysmal subarachnoid hemorrhage; the latter may also occur with polycystic kidney disease

and fibromuscular dysplasia. Various neurologic disorders occur

with dysthyroid states or other endocrinopathies. It is especially

important to look for the presence of systemic diseases in patients

with peripheral neuropathy. Most patients with coma in a hospital

setting have a metabolic, toxic, or infectious cause.

6. Drug use and abuse and toxin exposure. It is essential to inquire

about the history of drug use, both prescribed and illicit. Sedatives,

antidepressants, and other psychoactive medications are frequently

associated with acute confusional states, especially in the elderly.

Aminoglycoside antibiotics may exacerbate symptoms of weakness

in patients with disorders of neuromuscular transmission, such as

myasthenia gravis, and may cause dizziness secondary to ototoxicity.

Vincristine and other antineoplastic drugs can cause peripheral neuropathy, and immunosuppressive agents such as cyclosporine can

produce encephalopathy. Excessive vitamin ingestion can lead to

disease; examples include vitamin A and intracranial hypertension

(“pseudotumor cerebri”) or pyridoxine and peripheral neuropathy.

Many patients are unaware that over-the-counter sleeping pills, cold

preparations, and diet pills are actually drugs. Alcohol, the most

prevalent neurotoxin, is often not recognized as such by patients,

and other drugs of abuse such as cocaine, methamphetamine, and

heroin can cause a wide range of neurologic abnormalities. A history of environmental or industrial exposure to neurotoxins may

provide an essential clue; consultation with the patient’s coworkers

or employer may be required.

7. Formulating an impression of the patient. Use the opportunity while

taking the history to form an impression of the patient. Is the information forthcoming, or does it take a circuitous course? Is there

evidence of anxiety, depression, or hypochondriasis? Are there any

clues to problems with language, memory, insight, comportment, or

behavior? The neurologic assessment begins as soon as the patient

comes into the room and the first introduction is made.

THE NEUROLOGIC EXAMINATION

The neurologic examination is challenging and complex; it has many

components and includes a number of skills that can be mastered only

through repeated use of the same techniques on a large number of individuals with and without neurologic disease. Mastery of the complete

neurologic examination is usually important only for physicians in

neurology and associated specialties. However, knowledge of the basics

of the examination, especially those components that are effective in

screening for neurologic dysfunction, is essential for all clinicians,

especially generalists.

There is no single, universally accepted sequence of the examination that must be followed, but most clinicians begin with assessment

of mental status followed by the cranial nerves (CN), motor system,

reflexes, sensory system, coordination, and gait. Whether the examination is basic or comprehensive, it is essential that it is performed in an

orderly and systematic fashion to avoid errors and serious omissions.

Thus, the best way to learn and gain expertise in the examination is to

choose one’s own approach and practice it frequently and do it in the

same exact sequence each time.

The detailed description that follows describes the more commonly

used parts of the neurologic examination, with a particular emphasis

on the components that are considered most helpful for the assessment

of common neurologic problems. Each section also includes a brief

description of the minimal examination necessary to adequately screen

for abnormalities in a patient who has no symptoms suggesting neurologic dysfunction. A screening examination done in this way can be

completed in 3–5 min. Video demonstrations of the neurologic screening

examination (V6) and the detailed neurologic examination (V7) can be

found in the Harrison’s Video Collection included in this textbook.

Several additional points about the examination are worth noting.

First, in recording observations, it is important to describe what is

found rather than to apply a poorly defined medical term (e.g., “patient

groans to sternal rub” rather than “obtunded”). Second, subtle CNS

abnormalities are best detected by carefully comparing a patient’s performance on tasks that require simultaneous activation of both cerebral

3279Approach to the Patient with Neurologic Disease CHAPTER 422

hemispheres (e.g., eliciting a pronator drift of an outstretched arm with

the eyes closed; extinction on one side of bilaterally applied light touch,

also with eyes closed; or decreased arm swing or a slight asymmetry

when walking). Third, if the patient’s complaint is brought on by some

activity, reproduce the activity in the office. If the complaint is of dizziness when the head is turned in one direction, have the patient do this

and also look for associated signs on examination (e.g., nystagmus or

dysmetria). If pain occurs after walking two blocks, have the patient

leave the office and walk this distance and immediately return, and

repeat the relevant parts of the examination. Finally, the use of tests

that are individually tailored to the patient’s problem can be of value in

assessing changes over time. Tests of walking a 7.5-m (25-ft) distance

(normal, 5–6 s; note assistance, if any), repetitive finger or toe tapping

(normal, 20–25 taps in 5 s), or handwriting are examples.

■ MENTAL STATUS EXAMINATION • The bare minimum: During the interview, look for difficulties with

communication and determine whether the patient has recall and

insight into recent and past events.

The mental status examination is underway as soon as the physician

begins observing and speaking with the patient. If the history raises

any concern for abnormalities of higher cortical function or if cognitive

problems are observed during the interview, then detailed testing of

the mental status is indicated. The patient’s ability to understand the

language used for the examination, cultural background, educational

experience, sensory or motor problems, or comorbid conditions must

be factored into the applicability of the tests and interpretation of

results.

The Mini-Mental State Examination (MMSE) is a standardized

screening examination of cognitive function that is extremely easy

to administer and takes <10 min to complete (Chap. 29). Using

age-adjusted values for defining normal performance, the test is ~85%

sensitive and 85% specific for making the diagnosis of dementia that

is moderate or severe, especially in educated patients. When there is

sufficient time available in the outpatient setting, the MMSE is one

of the best methods for documenting the current mental status of the

patient, and this is especially useful as a baseline assessment to which

future scores of the MMSE can be compared.

Individual elements of the mental status examination can be subdivided into level of consciousness, orientation, speech and language,

memory, fund of information, insight and judgment, abstract thought,

and calculations.

Level of consciousness is the patient’s relative state of awareness of the

self and the environment, and ranges from fully awake to comatose.

When the patient is not fully awake, the examiner should describe

the responses to the minimum stimulus necessary to elicit a reaction,

ranging from verbal commands to a brief, painful stimulus such as a

squeeze of the trapezius muscle. Responses that are directed toward

the stimulus and signify some degree of intact cerebral function (e.g.,

opening the eyes and looking at the examiner or reaching to push away

a painful stimulus) must be distinguished from reflex responses of a

spinal origin (e.g., triple flexion response—flexion at the ankle, knee,

and hip in response to a painful stimulus to the foot).

Orientation is tested by asking the person to state his or her name,

location, and time (day of the week and date); time is usually the first

to be affected in a variety of conditions.

Speech is assessed by observing articulation, rate, rhythm, and prosody (i.e., the changes in pitch and accentuation of syllables and words).

Language is assessed by observing the content of the patient’s verbal

and written output, response to spoken commands, and ability to read.

A typical testing sequence is to ask the patient to name successively

more detailed components of clothing, a watch, or a pen; repeat the

phrase “No ifs, ands, or buts”; follow a three-step, verbal command;

write a sentence; and read and respond to a written command.

Memory should be analyzed according to three main time scales:

(1) immediate memory is assessed by saying a list of three items and

having the patient repeat the list immediately; (2) short-term memory

is tested by asking the patient to recall the same three items 5 and 15 min

later; and (3) long-term memory is evaluated by determining how well

the patient is able to provide a coherent chronologic history of his or

her illness or personal events.

Fund of information is assessed by asking questions about major

historic or current events, with special attention to educational level

and life experiences.

Abnormalities of insight and judgment are usually detected during

the patient interview; a more detailed assessment can be elicited by asking the patient to describe how he or she would respond to situations

having a variety of potential outcomes (e.g., “What would you do if you

found a wallet on the sidewalk?”).

Abstract thought can be tested by asking the patient to describe similarities between various objects or concepts (e.g., apple and orange,

desk and chair, poetry and sculpture) or to list items having the same

attributes (e.g., a list of four-legged animals).

Calculation ability is assessed by having the patient carry out a

computation that is appropriate to the patient’s age and education (e.g.,

serial subtraction of 7 from 100 or 3 from 20; or word problems involving simple arithmetic).

■ CRANIAL NERVE EXAMINATION • The bare minimum: Check the fundi, visual fields, pupil size and reactivity, extraocular movements, and facial movements.

The CNs are best examined in numerical order, except for grouping

together CN III, IV, and VI because of their similar function.

CN I (Olfactory) Testing is often omitted unless there is suspicion

for inferior frontal lobe disease (e.g., meningioma). With eyes closed,

ask the patient to sniff a mild stimulus such as toothpaste or coffee and

identify the odorant.

CN II (Optic) Check visual acuity (with eyeglasses or contact

lens correction) using a Snellen chart or similar tool. Test the visual

fields by confrontation, i.e., by comparing the patient’s visual fields to

your own. As a screening test, it is usually sufficient to examine the

visual fields of both eyes simultaneously; individual eye fields should

be tested if there is any reason to suspect a problem of vision by the

history or other elements of the examination, or if the screening test

reveals an abnormality. Face the patient at a distance of ~0.6–1.0 m

(2–3 ft) and place your hands at the periphery of your visual fields in

the plane that is equidistant between you and the patient. Instruct the

patient to look directly at the center of your face and to indicate when

and where he or she sees one of your fingers moving. Beginning with

the two inferior quadrants and then the two superior quadrants, move

your index finger of the right hand, left hand, or both hands simultaneously and observe whether the patient detects the movements. A single

small-amplitude movement of the finger is sufficient for a normal

response. Focal perimetry and tangent screen examinations should be

used to map out visual field defects fully or to search for subtle abnormalities. Optic fundi should be examined with an ophthalmoscope,

and the color, size, and degree of swelling or elevation of the optic disc

noted, as well as the color and texture of the retina. The retinal vessels

should be checked for size, regularity, arteriovenous nicking at crossing

points, hemorrhage, and exudates.

CN III, IV, VI (Oculomotor, Trochlear, Abducens) Describe

the size and shape of the pupils and reaction to light and accommodation (i.e., as the eyes converge while following your finger as it moves

toward the bridge of the nose). To check extraocular movements, ask

the patient to keep his or her head still while tracking the movement

of the tip of your finger. Move the target slowly in the horizontal and

vertical planes; observe any paresis, nystagmus, or abnormalities of

smooth pursuit (saccades, oculomotor ataxia, etc.). If necessary, the

relative position of the two eyes, both in primary and multidirectional

gaze, can be assessed by comparing the reflections of a bright light

off both pupils. However, in practice it is typically more useful to

determine whether the patient describes diplopia in any direction of

gaze; true diplopia should almost always resolve with one eye closed.

Horizontal nystagmus is best assessed at 45° and not at extreme lateral

3280 PART 13 Neurologic Disorders

gaze (which is uncomfortable for the patient); the target must often

be held at the lateral position for at least a few seconds to detect an

abnormality.

CN V (Trigeminal) Examine sensation within the three territories

of the branches of the trigeminal nerve (ophthalmic, maxillary, and

mandibular) on each side of the face. As with other parts of the sensory

examination, testing of two sensory modalities derived from different

anatomic pathways (e.g., light touch and temperature) is sufficient for a

screening examination. Testing of other modalities, the corneal reflex,

and the motor component of CN V (jaw clench—masseter muscle) is

indicated when suggested by the history.

CN VII (Facial) Look for facial asymmetry at rest and with spontaneous movements. Test eyebrow elevation, forehead wrinkling, eye

closure, smiling, and cheek puff. Look in particular for differences in

the lower versus upper facial muscles; weakness of the lower two-thirds

of the face with preservation of the upper third suggests an upper

motor neuron lesion, whereas weakness of an entire side suggests a

lower motor neuron lesion.

CN VIII (Vestibulocochlear) Check the patient’s ability to

hear a finger rub or whispered voice with each ear. Further testing for

air versus mastoid bone conduction (Rinne) and lateralization of a

512-Hz tuning fork placed at the center of the forehead (Weber) should

be done if an abnormality is detected by history or examination. Any

suspected problem should be followed up with formal audiometry.

For further discussion of assessing vestibular nerve function in the

setting of dizziness, coma, or hearing loss, see Chaps. 22, 28, and 34,

respectively.

CN IX, X (Glossopharyngeal, Vagus) Observe the position and

symmetry of the palate and uvula at rest and with phonation (“aah”).

The pharyngeal (“gag”) reflex is evaluated by stimulating the posterior

pharyngeal wall on each side with a sterile, blunt object (e.g., tongue

blade), but the reflex may be absent in normal individuals.

CN XI (Spinal Accessory) Check shoulder shrug (trapezius

muscle) and head rotation to each side (sternocleidomastoid) against

resistance.

CN XII (Hypoglossal) Inspect the tongue for atrophy or fasciculations, position with protrusion, and strength when extended against

the inner surface of the cheeks on each side.

■ MOTOR EXAMINATION • The bare minimum: Look for muscle atrophy and check extremity

tone. Assess upper extremity strength by checking for pronator drift

and strength of wrist or finger extensors. Assess lower extremity

strength by checking strength of the toe extensors.

The motor examination includes observations of muscle appearance,

tone, and strength. Although gait is in part a test of motor function, it

is usually evaluated separately at the end of the examination.

Appearance Inspect and palpate muscle groups under good light

and with the patient in a comfortable and symmetric position. Check

for muscle fasciculations, tenderness, and atrophy or hypertrophy.

Involuntary movements may be present at rest (e.g., tics, myoclonus,

choreoathetosis, pill-rolling tremor of Parkinson’s disease), during

maintained posture (essential tremor), or with voluntary movements

(intention tremor of cerebellar disease or familial tremor).

Tone Muscle tone is tested by measuring the resistance to passive

movement of a relaxed limb. Patients often have difficulty relaxing

during this procedure, so it is useful to distract the patient to minimize active movements. In the upper limbs, tone is assessed by rapid

pronation and supination of the forearm and flexion and extension at

the wrist. In the lower limbs, while the patient is supine the examiner’s

hands are placed behind the knees and rapidly raised; with normal

tone, the ankles drag along the table surface for a variable distance

before rising, whereas increased tone results in an immediate lift of the

heel off the surface. Decreased tone is most commonly due to lower

motor neuron or peripheral nerve disorders. Increased tone may be

evident as spasticity (resistance determined by the angle and velocity

of motion; corticospinal tract disease), rigidity (similar resistance in

all angles of motion; extrapyramidal disease), or paratonia (fluctuating changes in resistance; frontal lobe pathways; or normal difficulty

in relaxing). Cogwheel rigidity, in which passive motion elicits jerky

interruptions in resistance, is seen in parkinsonism.

Strength Testing for pronator drift is an extremely useful method

for screening upper limb weakness. The patient is asked to hold both

arms fully extended and parallel to the ground with eyes closed. This

position should be maintained for ~10 s; any flexion at the elbow or

fingers or pronation of the forearm, especially if asymmetric, is a sign

of potential weakness. Patients with shoulder pain or a limited range

of motion may have an apparent pronator drift that is not due to true

weakness. Muscle strength is further assessed by having the patient

exert maximal effort for the particular muscle or muscle group being

tested. It is important to isolate the muscles as much as possible, i.e.,

hold the limb so that only the muscles of interest are active. It is also

helpful to palpate accessible muscles as they contract. Grading muscle

strength and evaluating the patient’s effort is an art that takes time and

practice. Muscle strength is traditionally graded using the following

scale:

0 = no movement

1 = flicker or trace of contraction but no associated movement at

a joint

2 = movement with gravity eliminated

3 = movement against gravity but not against resistance

4– = movement against a mild degree of resistance

4 = movement against moderate resistance

4+ = movement against strong resistance

5 = full power

However, in many cases, it is more practical to use the following terms:

Paralysis = no movement

Severe weakness = movement with gravity eliminated

Moderate weakness = movement against gravity but not against

mild resistance

Mild weakness = movement against moderate resistance

Full strength

Noting the pattern of weakness is as important as assessing the magnitude of weakness. Unilateral or bilateral weakness of the upper limb

extensors and lower limb flexors (“pyramidal weakness”) suggests a lesion

of the pyramidal tract, bilateral proximal weakness suggests myopathy, and

bilateral distal weakness suggests peripheral neuropathy.

■ REFLEX EXAMINATION • The bare minimum: Check the biceps, patellar, and Achilles reflexes.

Muscle Stretch Reflexes Those that are typically assessed include

the biceps (C5, C6), brachioradialis (C5, C6), triceps (C6, C7), and

sometimes finger flexor (C8, T1) reflexes in the upper limbs and

the patellar or quadriceps (L3, L4) and Achilles (S1, S2) reflexes

in the lower limbs. The patient should be relaxed and the muscle

positioned midway between full contraction and extension. Reflexes

may be enhanced by asking the patient to voluntarily contract other,

distant muscle groups (Jendrassik maneuver). For example, upper

limb reflexes may be reinforced by voluntary teeth-clenching, and the

Achilles reflex by hooking the flexed fingers of the two hands together

and attempting to pull them apart. For each reflex tested, the two sides

should be tested sequentially, and it is important to determine the

smallest stimulus required to elicit a reflex rather than the maximum

response. Reflexes are graded according to the following scale:

0 = absent

1 = present but diminished

2 = normoactive

3 = exaggerated

4 = clonus