C.

MUSCLE POWER
When muscle power is to be tested, the patient is asked to resist pressure exerted by
the examiner. Selected individual muscles are tested in turn, and strength on the two
sides is compared so that minor degrees of weakness can be recognized. Weakness
can result from a disturbance in function of the upper or the lower motor neurons; the
distribution of weakness is of paramount importance in distinguishing between these
two possibilities. Upper motor neuron lesions (e.g., stroke) lead to weakness that
characteristically involves the extensors and abductors more than the flexors and
adductors of the armsand the flexors more than the extensors of the legs. Lower
motor neuron lesions produce weakness of the muscles supplied by the affected
neurons; the particular distribution of the weakness may point to lower motor neuron
involvement at the spinal cord, nerve root, plexus, or peripheral nerve level.
On the basis of the history and other findings, muscles that are particularly likely to be
affected are selected for initial evaluation, and other muscles are subsequently
examined to determine the distribution of the weakness more fully and to shorten the
list of diagnostic possibilities. For instance, if an upper motor neuron (pyramidal)
lesion is suspected, the extensors and abductors of the upper extremity and the flexors
of the lower extremity are tested in more detail as these muscles will be the most
affected.
Weakness may also result from a primary muscle disorder (myopathy) or from a
disorder of neuromuscular transmission. In patients with a motor deficit in all limbs
that is not due to an upper motor neuron lesion, proximal distribution of weakness
suggests a myopathic disorder, whereas predominantly distal involvement suggests a
lower motor neuron disturbance. Marked variability in the severity and distribution of
weakness over short periods of time suggests myasthenia gravis, a disorder of
neuromuscular transmission. Apparent weakness that is not organic in nature also
shows a characteristic variability; it is often more severe on formal testing than is
consistent with the patient's daily activities. Moreover, palpation of antagonist
muscles commonly reveals that they contract each time the patient is asked to activate
the agonist.
For practical and comparative purposes, power is best graded in the manner shown in
Table 5-3. Monoplegia denotes paralysis or severe weakness of the muscles in one
limb, and monoparesis denotes less severe weakness in one limb, although the two
words are often used interchangeably. Hemiplegia or hemiparesis is weakness in both
limbs (and sometimes the face) on one side of the body; paraplegia or paraparesis is
weakness of both legs; and quadriplegia or quadriparesis (also tetraplegia,
tetraparesis) is weakness of all four limbs.

D. COORDINATION
The coordination of motor activity can be impaired by weakness, sensory
disturbances, or cerebellar disease and requires careful evaluation.
Voluntary activity is observed with regard to its accuracy, velocity, range, and
regularity, and the manner in which individual actions are integrated to produce a
smooth, complex movement. In the finger-nose test, the patient moves the index
finger to touch the tip of
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his or her nose and then the tip of the examiner's index finger; the examiner can move
his or her own finger about during the test to change the location of the target and
should position it so that the patient's arm must extend fully to reach it. In the heelknee-shin test, the recumbent patient lifts one leg off the bed, flexes it at the knee,
places the heel on the other knee, and runs the heel down the shin as smoothly as
possible.

Table 5-3. Grading of muscle power according to the system suggested by the
Medical Research Council.
Grade

Muscle Power

Normal power

Active movement against resistance and gravity

Active movement against gravity but not resistance

Active movement possible only with gravity eliminated

Flicker or trace of contraction

No contraction

Reproduced, with permission, from Aids to the Investigation of Peripheral Nerve

Injuries. HMSO, 1943.
The patient should also be asked to tap repetitively with one hand on the back of the
other; to tap alternately with the palm and back of one hand on the back of the other
hand or on the knee; to screw an imaginary light bulb into the ceiling with each arm in
turn; and to rub the fingers of one hand in a circular polishing movement on the back
of the other hand. Other tests of rapid alternating movement include tapping on the
ball of the thumb with the tip of the index finger or tapping the floor as rapidly as
possible with the sole while keeping the heel of the foot in place. During all these

tests, the examiner looks for irregularities of rate, amplitude, and rhythm and for
precision of movements. With pyramidal lesions, fine voluntary movements are
performed slowly. With cerebellar lesions, the rate, rhythm, and amplitude of such
movements are irregular.
If loss of sensation may be responsible for impaired coordination, the maneuver
should be repeated both with eyes closed and with visual attention directed to the
limb; with visual feedback the apparent weakness or incoordination will improve. In
patients with cerebellar disease, the main complaint and physical finding are often of
incoordination, and examination may reveal little else. Further discussion of the ataxia
of cerebellar disease and the various terms used to describe aspects of it will be found
in Chapter 3.
E. TENDON REFLEXES
Changes in the tendon reflexes may accompany disturbances in motor (or sensory)
function and provide a guide to the cause of the motor deficit. The tendon is tapped
with a reflex hammer to produce a sudden brisk stretch of the muscle and its
contained spindles. The clinically important stretch reflexes and the nerves, roots, and
spinal segments subserving them are indicated in Table 5-4. When the reflexes are
tested, the limbs on each side should be placed in identical positions and the reflexes
elicited in the same manner.
1. AreflexiaApparent loss of the tendon reflexes in a patient may merely reflect a
lack of clinical expertise on the part of the examiner. Performance of Jendrassik
maneuver (an attempt by the patient to pull apart the fingers of the two hands when
they are hooked together) or some similar action (such as making a fist with the hand
that is not being tested) may elicit the reflex response when it is otherwise
unobtainable. A reflex may be lost or depressed by any lesion that interrupts the
structural or functional continuity of its reflex arc, as in a root lesion or peripheral
neuropathy. In addition, reflexes are often depressed during the acute stage of an
upper motor neuron lesion, in patients who are deeply comatose, and in patients with
cerebellar disease.
2. HyperreflexiaIncreased reflexes occur with upper motor neuron lesions, but they
may also occur with symmetric distribution in certain healthy subjects and in patients
under emotional tension. The presence of reflex asymmetry is therefore of particular
clinical significance. Clonus consists of a series of rhythmic reflex
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contractions of a muscle that is suddenly subjected to sustained stretch, with each beat
caused by renewed stretch of the muscle during relaxation from its previous
contracted state. Sustained clonusmore than three or four beats in response to
sudden sustained stretchis always pathologic and is associated with an abnormally
brisk reflex. In hyperreflexic states, there may be spread of the region from which a
particular reflex response can be elicited. For example, elicitation of the biceps reflex
may be accompanied by reflex finger flexion, or eliciting the finger flexion reflex may
cause flexion of the thumb (Hoffmann sign).
Table 5-4. Muscle strength reflexes.1
Reflex

Segmental

Nerve

Innervation
Jaw

Pons

Mandibular branch, trigeminal

Biceps

C5, C6

Musculocutaneous

Brachioradialis

C5, C6

Radial

Triceps

C7, C8

Radial

Finger

C8,T1

Median

Knee

L3, L4

Femoral

Ankle

S1, S2

Tibial

At the National Institutes of Health, the reflexes are graded on the following scale: 0,
absent; 1, reduced, trace response, or present only with reinforcement; 2 and 3, in
lower and upper half of normal range, respectively; 4, enhanced, with or without
clonus.
3. Reflex asymmetryAlthough the intensity of reflex responses varies considerably
among subjects, reflexes should be symmetric in any individual. Several general
points can be made regarding reflex asymmetries.
a. Lateralized asymmetries of response, i.e., reflexes that are brisker on one side of the
body than on the other, usually indicate an upper motor neuron disturbance, but
sometimes reflect a lower motor neuron lesion on the side with the depressed reflexes.
b. Focal reflex deficits often relate to root, plexus, or peripheral nerve lesions. For
example, unilateral depression of the ankle jerk commonly reflects an S1
radiculopathy resulting from a lumbosacral disk lesion.
c. Loss of distal tendon reflexes (especially ankle jerks), with preservation of more
proximal ones, is common in polyneuropathies.
F. SUPERFICIAL REFLEXES
1. The polysynaptic superficial abdominal reflexes, which depend on the integrity of
the T8-T12 spinal cord segments, are elicited by gently stroking each quadrant of the
abdominal wall with a blunt object such as a wooden stick. A normal response
consists of contraction of the muscle in the quadrant stimulated, with a brief
movement of the umbilicus toward the stimulus. Asymmetric loss of the response may

be of diagnostic significance. The response may be depressed or lost on one side in

patients with an upper motor neuron disturbance affecting that side. Segmental loss of
the response may relate to local disease of the abdominal wall or its innervation, as in
a radiculopathy. Bilaterally absent responses are usually of no significance, occurring
in the elderly, the obese, multiparous women, and patients who have had abdominal
surgery.
2. The cremasteric reflex, mediated through the L1 and L2 reflex arcs, consists of
retraction of the ipsilateral testis when the inner aspect of the thigh is lightly stroked;
it is lost in patients with a lesion involving these nerve roots. It is also lost in patients
with contralateral upper motor neuron disturbances.
3. Stimulation of the lateral border of the foot in a normal adult leads to plantar
flexion of the toes and dorsiflexion of the ankle. The Babinski response consists of
dorsiflexion of the big toe and fanning of the other toes in response to stroking the
lateral border of the foot, which is part of the S1 dermatome; flexion at the hip and
knee may also occur. Such an extensor plantar response indicates an upper motor
neuron lesion involving the contralateral motor cortex or the corticospinal tract. It can
also be found in anesthetized or comatose subjects, in patients who have had a
seizure, and in normal infants. An extensor plantar response can also be elicited,
though less reliably, by such maneuvers as pricking the dorsal surface of the big toe
with a pin (Bing sign), firmly stroking down the anterior border of the tibia from knee
to ankle (Oppenheim maneuver), squeezing the calf muscle (Gordon maneuver) or
Achilles tendon (Schafer maneuver), flicking the little toe (Gonda maneuver), or
stroking the back of the foot just below the lateral malleolus (Chaddock maneuver). In
interpreting responses, attention must be focused only on the direction in which the
big toe first moves.
G. GAIT
In evaluating gait, the examiner first observes the patient walking at a comfortable
pace. Attention is directed at the stance and posture; the facility with which the patient
starts and stops walking and turns to either side; the length of the stride; the rhythm of
walking; the presence of normally associated movements, such as swinging of the
arms; and any involuntary movements. Subtle gait disorders become apparent only
when the patient is asked to run, walk on the balls of the feet or the heels, hop on
either foot, or walk heel-to-toe along a straight line. Gait disorders occur in many
neurologic disturbances and in other contexts that are beyond the scope of this
chapter. A motor or sensory disturbance may lead to an abnormal gait whose nature
depends upon the site of pathologic involvement. Accordingly, the causes and clinical
types of gait disturbance are best considered together.
1. Apraxic gaitApraxic gait occurs in some patients with disturbances, usually
bilateral, of frontal lobe function, such as may occur in hydrocephalus or progressive
dementing disorders. There is no weakness or incoordination of the limbs, but the
patient is unable to stand unsupported or to walk properlythe feet seem glued to the
ground. If walking is possible at all, the gait is unsteady, uncertain, and short-stepped,
with marked hesitation (freezing), and the legs are moved in a direction
inappropriate to the center of gravity.
2. Corticospinal lesionsA corticospinal lesion, irrespective of its cause, can lead to a
gait disturbance that varies in character depending on whether there is unilateral or
bilateral involvement. In patients with hemiparesis, the selective weakness and
spasticity lead to a gait in which the affected leg must be circumducted to be
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advanced. The patient tilts at the waist toward the normal side and swings the affected
leg outward as well as forward, thus compensating for any tendency to drag or catch
the foot on the ground because of weakness in the hip and knee flexors or the ankle
dorsiflexors. The arm on the affected side is usually held flexed and adducted. In mild
cases, there may be no more than a tendency to drag the affected leg, so that the sole
of that shoe tends to be excessively worn.