Motor strength and power indicate the capacity of muscles to exert force and expend energy. Decreased strength is weakness, or paresis; absence of muscle contraction is paralysis, or plegia. Weakness may cause loss of the speed, rapidity, or agility of movement and a decrease in the range, or amplitude, of movement before there is loss of power to formal strength testing. Other manifestations of impaired motor function include fatigability, variation in strength on repeated tests, diminished range and rate of movement, loss of coordination, irregularity and clumsiness of motion, tremulousness, loss of associated movements, and lack of ability to carry out skilled acts.
While judgment of the force exerted in either initiating or resisting movement is the major criterion in the evaluation of strength, observation and palpation of either the contraction of the muscle belly or its movement of its tendon may be helpful adjuncts. The contraction of an extremely weak muscle may sometimes be felt when it cannot be seen. In nonorganic weakness, contraction of the apparently weak muscle may be felt when the patient is asked to carry out movements with synergistic muscles, or the antagonists may be felt to contract when the patient is asked to contract the weak muscle. Weakness may be masked when attempts to contract individual weak muscles are accompanied by activation of other muscles to compensate for the loss of power. In these substitution, or “trick,” movements, the patient exploits a strong muscle with similar function to compensate for the loss of action of a weak muscle. Careful observation for alterations in normal movement patterns and substitution movements may indicate loss of function. Endurance is the ability to perform the same act repeatedly.
The strength examination assesses primarily voluntary, or active, muscle contraction rather than reflex contraction. Strength may be classified as kinetic—the force exerted in changing position—and static—the force exerted in resisting movement from a fixed position. Strength may be tested in two ways. The patient may place a joint in a certain position, and then hold it there as the examiner tries to move it. Alternately the patient may try to move a joint or contract a muscle against the fixed resistance of the examiner. In most disease processes, both are equally affected, and the two methods can be used interchangeably. Some patients may comprehend and cooperate better with the first method, but having the patient initiate movement may better detect mild weakness. There is disagreement about how the examiner should apply force. Some authorities recommend a slow application of resistance in which the patient and examiner match effort; others contend that a rapid movement by the examiner will better detect mild weakness. With very weak muscles, strength may have to be judged without resistance or only against the resistance offered by gravity.
Many factors may complicate the strength examination and make assessment more difficult, such as fatigue, systemic illness, and failure to understand or cooperate with testing. Other conditions may result in a false or distorted impression of weakness, such as extrapyramidal disease, ataxia, impairment of the range of motion due to pain, spasm, joint ankylosis, or contractures, and psychiatric conditions such as hysteria and malingering. Motor impersistence is the inability to sustain voluntary motor acts that have been initiated on verbal command. The patient is unable to sustain an activity, such as keeping the eyes closed or the hand raised. It may be a form of apraxia, and has been said to occur most often with left hemisphere lesions. Passive movements are often helpful to distinguish loss of range of motion due to contractures from other reasons such as weakness, pain, and muscle spasm. With contracture, a muscle cannot be stretched to its normal limits without considerable resistance and the production of pain. Contractures are particularly common in the calf muscles, drawing the foot downward (“tight heel cords”). In evaluating contractures and deformities, it is important to differentiate between those of neurogenic origin and those due to orthopedic disease, congenital abnormalities, habitual postures, occupational factors, or other factors that cause mechanical difficulty with movement.
Strength may be assessed in absolute terms (e.g., the examiner comparing the patient’s power to a belief of what normal should be), or it may be assessed in comparison to the patient’s other muscles. The comparison is most often to a homologous muscle on the other side, as in comparing the two biceps muscles. But proximal strength should be commensurate with distal strength in the same patient. A patient with polymyositis may have weakness of the deltoids on both sides, so one deltoid cannot be judged against the other. But the deltoids may be obviously weaker than the wrist extensors, so there is a proximal to distal gradient of increasing strength that is clearly abnormal. The muscles on the dominant side are usually slightly stronger.
In manual muscle testing (MMT), the strength of individual muscles is tested and graded quantitatively using some scale. Strength is most commonly graded using the 5-level MRC (Medical Research Council) scale, which was developed in Britain in World War II to evaluate patients with peripheral nerve injuries (
Table 18.1). The MRC scale has been widely applied to the evaluation of strength in general. However, because of the original purpose the scale is heavily weighted toward the evaluation of very weak muscles. So the most commonly used strength grading scale has significant limitations when dealing with many patients.
There is obviously considerable individual variation in muscle power, affecting examiners as well as patients, dependent in part upon size, gender, body build, age, and activity level. A large, young, powerful physician examining a small, old, sick patient may overcall weakness. Conversely, a small, relatively weak physician examining a large, powerful patient may miss significant weakness because of strength mismatch. As a general principle, reliable strength testing should attempt to break a given muscle. By varying the length of lever and the shortening of the muscle permitted, the examiner may give or take mechanical advantage as necessary to compensate for strength mismatch. Many patients
of different ages, sizes, and strength levels must be examined in this fashion in order to develop an appreciation of the expected strength of a muscle for a given set of circumstances.
PATTERNS OF WEAKNESS
There are common patterns of weakness. Recognition of a pattern may help greatly in lesion localization and differential diagnosis. Identification of the process causing weakness is further aided by accompanying signs, such as reflex alterations and sensory loss.
Table 18.2 reviews the features of upper motor neuron vs. lower motor neuron weakness.
Table 18.3 summarizes some common patterns of weakness and their localization.
Weakness may be focal or generalized. When focal, it may follow the distribution of some structure in the peripheral nervous system, such as a peripheral nerve or spinal root. It may affect one side of the body in a “hemi” distribution. A hemi distribution may affect the arm, leg, and face equally on one side of the body, or one or more areas may be more involved than others. The corticospinal tract (CST) preferentially innervates certain muscle groups, and these are often selectively impaired. When weakness is nonfocal, it may be generalized, predominantly proximal, or predominantly distal. Identification of the process causing weakness is further aided by accompanying signs, such as reflex alterations and sensory loss.
Generalized Weakness
The term generalized weakness implies that the weakness involves both sides of the body, more or less symmetrically. When a patient has truly generalized weakness, bulbar motor functions—such as facial movements, speech, chewing, and swallowing—are involved as well. Weakness of both arms and both legs with normal bulbar function is quadriparesis or tetraparesis. Weakness of both legs is paraparesis. When weakness affects all four extremities, the likely causes include spinal cord disease, peripheral neuropathy, a neuromuscular junction disorder, or a myopathy.
When spinal cord disease is the culprit and the deficit is incomplete, more severe involvement of those muscles preferentially innervated by the CST can frequently be discerned. Reflexes are usually increased (though in the acute stages they may be decreased or absent); there is usually some alteration of sensation; sometimes a discrete spinal “level”; superficial reflexes disappear; and there may be bowel and bladder dysfunction. Generalized peripheral nerve disease tends to predominantly involve distal muscles, although there are exceptions. There is no preferential involvement of CST innervated muscles; reflexes are usually decreased; sensory loss is frequently present; and bowel and bladder function are not disturbed. With a neuromuscular junction disorder, the weakness is likely to be worse proximally; sensation is spared; reflexes are normal; and there is usually involvement of bulbar muscles, especially with ptosis and ophthalmoplegia. When the problem is a primary muscle disorder, weakness is usually more severe proximally; reflexes are normal; sensation is normal; and with only a few exceptions, bulbar function is spared except for occasional dysphagia. These are generalizations. Some neuropathies may cause proximal weakness, and some myopathies may affect distal muscles; not all patients with a neuromuscular transmission disorder have bulbar involvement.
Motor neuron disease is a special case. Amyotrophic lateral sclerosis (ALS) characteristically involves both the upper and lower motor neurons. It produces a clinical picture of weakness and wasting due to involvement of the lower motor neurons in the anterior horn of the spinal cord, combined with weakness and hyperreflexia due to involvement of the upper motor neurons in the cerebral cortex that give rise to the corticospinal tract. There is upper motor neuron weakness (cerebral cortex pathology) superimposed on lower motor neuron weakness (spinal cord pathology).
Focal Weakness
Weakness of the arm and leg on one side of the body is hemiparesis. This may range in severity from very mild, manifest only as pronator drift and impairment of fine motor control, to total paralysis. Monoparesis is weakness limited to one extremity, such as the leg contralateral to an anterior cerebral artery stroke. Diplegia is weakness of like parts on the two sides of the body; the term spastic diplegia refers to weakness of both legs that occurs in cerebral palsy; and facial diplegia is weakness of both sides of the face. Spastic weakness of one arm and the opposite leg is referred to as cruciate or crossed paralysis, or hemiplegia alternans. Reflexes—typically increased unless the process is acute—and accompanying sensory loss help identify such focal weakness as central in origin.
Certain patterns of muscle weakness point to a peripheral nerve, plexus, or root lesion. A mononeuropathy, such as a radial nerve palsy, or a spinal root lesion, such as from a herniated disc, causes weakness limited to the distribution of the involved nerve or root. A plexopathy may cause weakness of the entire limb, or weakness only in the distribution of certain plexus components. With such lower motor neuron pathology, reflexes are typically decreased and there is often accompanying sensory loss. Localization of focal weakness due to root, plexus, and peripheral nerve pathology requires intimate familiarity with peripheral neuroanatomy.
With a peripheral nerve lesion, all muscles below the level of the lesion are at risk. When multiple muscles of an extremity are weak in a non-CST distribution, localization depends on recognizing the common innervating structure: root, plexus component, or peripheral nerve.
With lower motor neuron pathology, reflexes are typically decreased, and there is often accompanying sensory loss. Anterior horn cell disease often begins with focal weakness that may simulate mononeuropathy, but it evolves into a more widespread pattern as the disease progresses, culminating in generalized weakness. Except for extraocular muscle involvement in myasthenia gravis, it is rare for a myopathy or neuromuscular junction disorder to cause focal weakness.
NONORGANIC WEAKNESS
The first step in evaluating weakness is often deciding whether it is organic or nonorganic, i.e., due to a psychiatric disorder. This distinction is not always easy. Patients with nonorganic weakness are commonly thought to have neurologic disease, but just as often patients with real weakness are dismissed
as uncooperative, hysterical, or malingering. Coaching is often helpful in improving poor effort, but some patients, in spite of all, will give only erratic and variable effort.
Some things are often useful in distinguishing organic from nonorganic weakness. Patients with bona fide organic muscle weakness will yield smoothly as the examiner defeats the weak muscle. The patient gives uniform resistance throughout the movement. If the examiner decreases his resistance, the patient will begin to win the battle. If the examiner drops the resistance level, the patient with nonorganic weakness will not continue to push or pull. Instead, the patient will also stop resisting so that no matter how little force the examiner applies, there is an absence of follow-through and the patient never overcomes the examiner. When there is nonorganic weakness, resistance is erratic and often collapses abruptly. The muscular contractions are poorly sustained and may give way suddenly, rather than gradually, as the patient resists the force exerted by the examiner. Some patients will give up entirely and allow the muscle or limb to flop; others will provide variable resistance throughout the range of motion with alternating moments of effort and no effort. This pattern of variable strength is referred to as “ratchety,” “give way,” or “catch and give.” It is characteristic of nonorganic weakness. In nonorganic weakness, functional testing may fail to confirm weakness suspected during strength testing. For example, there may be apparent foot dorsiflexion weakness, yet the patient is able to stand on the heel without difficulty. The patient with nonorganic weakness may be calm and indifferent while demonstrating the lack of strength, showing little sign of alarm at the presence of complete paralysis, and smile cheerfully during the examination. If the examiner raises and drops an extremity, a limb with psychogenic paralysis may drop slowly to avoid injury, while an extremity with real weakness would drop rapidly, especially if the paralysis is flaccid.
The Hoover (automatic walking) sign is useful for evaluating suspected nonorganic leg weakness. When a normal supine patient flexes the hip to lift one leg, there is a downward movement of the other leg. The extension counter-movement of the opposite leg is a normal associated movement. An extension movement of one leg normally accompanies flexion of the other leg, as in walking. In organic leg weakness, the downward pressure of the contralateral heel occurs when the patient tries to raise the weak leg, and the examiner can feel the extension pressure by placing a hand beneath the heel that remains on the bed. In nonorganic leg weakness, there is no downward pressure of the contralateral heel, but the extension movement of the “paralyzed” leg may be felt as the good leg is raised (Hoover sign).
