Muscle strength

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No contraction

Flicker or trace of contraction

Active movement, with gravity eliminated

Active movement against gravity

Active movement against gravity and resistance

Normal power

From Medical Research Council: Aids to the Examination of the Peripheral Nervous System Memorandum No. 45. London, Crown Publishing, l976

discover whether there is a particular pattern of weakness that can be used to localize the lesion. Is it a hemiparesis, suggesting a hemispheric lesion, a paraparesis, which is consistent with a spinal cord lesion, or a proximal pattern of weakness compatible with a myopathic process versus a distal pattern that is consistent with neuropathy? (... Table...15-2 ).

Even more important than tests of the strength of individual movements are tests of the ability of the patient to perform functional movements that bring out more subtle deficits escaping detection when muscle strength is tested against resistance. For example, a very subtle weakness of the leg may be noticed if the patient has some difficulty in hopping in one place. Because the leg and thigh muscles are so powerful, the patient's ability to walk, hop on either foot, and walk on the heels and toes is important. A mild upper motor neuron weakness may be betrayed by a slight circumduction or external rotation of the leg or even by an occasional scuffing of the sole against the floor. One may be able to differentiate an L5 from an S1 radiculopathy due to a herniated disc if weakness of dorsiflexion of the foot reduces the ability to walk on the heels (L5 lesion), whereas a weakness of the gastrocnemius diminishes the ability to rise on the toes (S1 lesion). Walking may demonstrate a decrease in arm swing that is consistent with an upper motor neuron or basal ganglia lesion of one hemisphere.

A variety of functional tests of the upper extremities can be used to bring out subtle weakness or spasticity. Probably the most widely used test is the one is which the patient is asked to extend the arms in the fully supinated position while keeping the eyes closed. A mildly paretic arm gradually

TABLE 15-2 -- PATTERNS OF WEAKNESS THAT AID IN LOCALIZATION

Distribution of Weakness, UMN or LMN Signs

Location of Lesion

Limbs and lower face on same side (spastic hemiparesis, UMN)

Contralateral cerebral hemisphere

All four limbs (spastic tetraparesis, UMN), speech (spastic dysarthria), swallowing with hyperactive jaw and facial jerks

Bilateral cerebral hemispheres

(pseudobulbar palsy, UMN)

Hemiparesis (UMN) plus cranial nerve signs (LMN)

Brain stem

Tetraparesis (UMN) plus cranial nerve signs (LMN)

Brain stem

All four limbs (spastic tetraparesis, UMN)

Mid or upper cervical cord

Lower limbs (UMN) and hands (LMN)

Low cervical cord

Lower limbs (spastic paraparesis, UMN)

Thoracic spinal cord

Bilateral, medial motor cortex

All limbs, proximal > distal (LMN)

Muscle (myopathy or dystrophy)

Legs, distal > proximal (LMN)

Nerve (polyneuropathy)

Ocular muscles, eyelids, jaw, face, pharynx, tongue (LMN)

Neuromuscular junction (NMJ)

Jaw, face, pharynx, tongue; sparing ocular muscles, eyelids (UMN and LMN)

Motor neuron disease

Specific muscle groups in one limb (LMN)

Nerve root, plexus or peripheral

nerve

UMN, Upper motor neuron; LMN, lower motor neuron.

UMN, Upper motor neuron; LMN, lower motor neuron.

becomes pronated and sometimes flexed and drifts downward, showing the "pronator drift." Other tests not as well validated by widespread use are the digiti quinti minimi sign (hyperabduction of the outstretched fifth finger on the paretic side) and the forearm rotator sign (the patient rotates the forearms around each other; the paretic arm tends to stay fixed while the good arm rotates around it). Because paretic muscles move more slowly with reduced amplitude, some repetitive tasks, such as finger tapping or the forearm rotator test, are used to look for asymmetrical movements. However, interpretation of these tests may be more difficult because it may be hard to differentiate an abnormality from the bradykinesia of Parkinson's disease or even from problems with coordination secondary to cerebellar disease.

Because walking requires not just strength but the interplay of all the motor and sensory systems that are necessary for balance and the execution of motor programs, it is one of the most important parts of the neurological examination. A normal gait excludes a wide variety of neurological disorders (see Chapter.18 ). Abnormal gait patterns may provide powerful clues to the localization of a lesion. Upper motor neuron weakness is generally accompanied by spasticity, which produces a gait with a stiff jerky quality. The classic example of a lower motor neuron weakness is the steppage gait typical of a motor neuropathy in which weakness of dorsiflexion of the feet requires the patient to lift the legs higher to prevent the toes from scuffing the pavement. This appearance is accompanied by an excessive slapping of the forefoot against the floor. It may occur unilaterally in a patient with a pressure palsy of the peroneal nerve. The incomplete dorsiflexion of the foot combined with the slapping of the forefoot on the ground gives rise to the appearance of the "drop foot." The foot may also be inverted because of the unopposed action of the posterior tibial muscle. However, one must be careful to differentiate this condition from dystonia of the foot, which commonly produces a posture of flexion and inversion of the foot. The ability to dorsiflex the foot should be carefully examined in such patients; in patients with dystonia it will be normal, whereas in those with a peroneal palsy it will not.

A characteristic gait and posture are apparent in patients with myopathic weakness, in which the proximal muscles are much weaker than the distal ones. The weakness of the lumbar paraspinal muscles results in a hyperlordosis, and failure of the myopathic girdle muscles to fix the pelvis on one side when the other leg is being advanced gives rise to a ducklike waddling appearance. When a proximal myopathic weakness is suspected, other important functional tests include tests of the ability to rise from a squat or out of a chair, or to step up onto a stool or chair. Another helpful test in children with suspected muscular dystrophy is rising from a supine to a standing position. They cannot simply sit up and then push themselves to a standing position because truncal and hip girdle weakness prevents it. Instead, they roll to a prone position, push themselves up on all fours, and then quickly grab their thighs and walk up the thighs to a standing position ( Gower's sign).

FATIGABILITY

Normal fatigue associated with intense muscular contraction is accompanied by a reduction in the motor-unit firing

rate, which is thought to be the result of a reduction in the excitatory drive to the motor neurons, which is a central mechanism. y The phenomenon of fatigability with normal levels of muscle activity is a specific characteristic of disorders of the neuromuscular junction and is accompanied by a decrement in amplitude, not frequency, of the muscle action potential. This phenomenon is demonstrated most easily with electrophysiological techniques in the clinical neurophysiology laboratory. However, there are methods for bedside testing of the ability to produce a repetitive forceful movement or tonic muscle contraction. Jolly devised a grip ergometer connected to a smoke drum that could demonstrate the classic decrement in force produced by each attempt by the patient to produce a maximum grip. The Jolly test has subsequently been modified, depending on the availability of material at the bedside and the ingenuity of the examiner. One readily available method is to inflate a blood pressure cuff, which the patient can grip and squeeze repetitively. The height of the excursions of the mercury manometer can be readily monitored, and the decrement in pressure produced by each squeeze is readily appreciated.

Such methods of quantitating fatigability are especially important when one is assessing the patient's response to the acetylcholinesterase inhibitor edrophonium chloride (Tensilon) as a test for myasthenia gravis. For example, one may test how many squats can be performed before and after the injection of Tensilon. The muscles or movements to be tested depend to a great extent on the patient's symptoms, but whenever possible a movement should be chosen that can be quantitated as accurately as possible. Another quantifiable method is the length of time a posture can be held. For example, if the patient complains of ptosis or double vision, the length of time the patient can maintain upward vision before ptosis or diplopia occurs can be estimated. Another is the length of time a patient can hold the arms out before they fall below a horizontal 90 degrees. Sometimes the fatigability of the muscles involved in myasthenia gravis cannot be readily quantified. For example, weakness of the face has to be judged on a more subjective basis. Usually the weakness is bilateral and symmetrical, and milder examples may escape notice until after Tensilon clearly produces a change in facial movements and expression. Reading a standard passage can help in measuring the time it takes for the speech to become mushy and dysarthric.

The Tensilon test is performed by giving incremental intravenous injections of 10 mg (1 ml) of the drug. A test dose of 2 mg (0.2 ml) is given first to monitor the heart rate (preferably with electrocardiography [ECG]) to avoid bradycardia and vasodepressor syncope, which occasionally occur with higher doses. If this dose is tolerated and no definite improvement in strength occurs, another 3 to 4 mg is given. If there is still no response, the final 4 to 5 mg is given.

ASSESSMENT OF REFLEXES

Tendon jerks are conventionally graded on a scale of zero to 4, with zero representing absent jerks and 4 representing hyperactivity with clonus. A commonly used scale with accompanying definitions is shown in Table, 15:3, . Superficial

TABLE 15-3 -- SCALE FOR AMPLITUDE OF TENDON REFLEXES

Scale

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