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Harrison’s Manual of Medicine



Paralysis or Weakness
Movement Disorders

GENERAL CONSIDERATIONS   The loss of power or control of voluntary muscle is usually described by pts as “weakness” or as some difficulty that can be interpreted as “loss of dexterity.” The diagnostic approach to such a problem begins by determining which part of the nervous system is involved. It is important to distinguish weakness arising from disorders of upper motor neurons (i.e., motor neurons in the cerebral cortex and their axons that descend through the subcortical white matter, internal capsule, brainstem, and spinal cord) from that arising from disorders of the motor unit (i.e., the lower motor neurons in the ventral horn of the spinal cord and their axons in the spinal roots and peripheral nerves, the neuromuscular junction, and the skeletal muscle). In general:

Upper motor neuron dysfunction: increased muscle tone (spasticity), brisk deep tendon reflexes, and Babinski’s sign.

Lower motor neuron dysfunction: reduced muscle tone, diminished reflexes, and muscle atrophy.
Table 11-1 presents patterns of weakness and signs associated with weakness arising from lesions of different parts of the nervous system. Table 11-2 lists common causes of weakness by the primary site of pathology.

Table 11-1 Clinical Differentiation of Weakness Arising from Different Areas of the Nervous System

Table 11-2 Common Causes of Weakness

EVALUATION   The history should focus on the tempo of development of weakness, presence of sensory and other neurologic symptoms, medication history, predisposing medical conditions, and family history. The physical exam aids in localization of the abnormality by criteria such as described above and in Table 11-1. An algorithm for the initial workup of a patient with weakness is shown in Fig. 11-1.

FIGURE 11-1. An algorithm for the initial work-up of a patient with weakness. CT, computed tomography; EMG, electromyography; LMN, lower motor neuron; MRI, magnetic resonance imaging; NCS, nerve conduction studies; UMN, upper motor neuron.

Movement disorders are often divided into akinetic rigid forms, in which there is muscle rigidity and slowness of movement, and hyperkinetic forms, in which there are involuntary movements. In either case, preservation of strength is the rule. Most movement disorders arise from dysfunction of the circuitry in the basal ganglia and can occur by virtually any pathogenic mechanism; common causes are degenerative diseases (hereditary and idiopathic), drug-induced, organ system failure, CNS infection, and ischemia. Clinical features of the various movement disorders are summarized below.
BRADYKINESIA   Inability to initiate changes in activity or perform ordinary volitional movements rapidly and easily. There is a slowness of movement and a paucity of automatic motions such as eye blinking and arm swinging while walking. Usually due to Parkinson’s disease.
TREMOR   Rhythmic oscillation of a part of the body about a fixed point, usually involving the distal limbs and less commonly the head, tongue, and jaw. May be divided according to amplitude and relationship to posture. Most common—a coarse tremor at rest, 4–5 beats/s, usually due to Parkinson’s disease; a fine postural tremor of 8–10 beats/s, which may be an exaggeration of normal physiologic tremor or indicative of familial essential tremor. The latter often responds to propranolol or primidone.
ASTERIXIS   Brief, arrhythmic interruptions of sustained voluntary muscle contraction, usually observed as a brief lapse of posture of wrists in dorsiflexion with arms outstretched. This “liver flap” may be seen in any encephalopathy related to drug intoxication, organ system failure, or CNS infection. Therapy is correction of underlying disorder.
MYOCLONUS   Brief, arrhythmic muscle contractions, or twitches. Like asterixis, usually indicative of a diffuse encephalopathy. Following cardiac arrest, diffuse cerebral hypoxia may produce multifocal myoclonus. Clonazepam, valproate, or baclofen may be effective.
DYSTONIA   Involuntary, sustained posture or slowly changing involuntary postures. Postures attained are often bizarre, with forceful extensions and twisting about individual joints. Dystonias may be generalized or focal (e.g., spasmodic torticollis, blepharospasm). Symptoms may respond to high doses of anticholinergics, benzodiazepines, baclofen, and anticonvulsants. Local injection of botulinum toxin is effective in certain focal dystonias.
CHOREOATHETOSIS   A combination of chorea (rapid, jerky movements) and athetosis (slow writhing movements). The two usually exist together though one may be more prominent. Choreic movements are the predominant involuntary movements in rheumatic (Sydenham’s) chorea and Huntington’s disease. Athetosis is prominent in some forms of cerebral palsy. Chronic neuroleptic use may lead to tardive dyskinesia, in which choreoathetotic movements are usually restricted to the buccal, lingual, and mandibular areas. Benzodiazepines, reserpine, and low-dose neuroleptics may suppress choreoathetotic movements but are often ineffective.
TICS   Stereotypical, purposeless movements such as eye blinks, sniffling, and clearing of the throat. Gilles de la Tourette syndrome is a rare but severe multiple tic disorder that may involve motor tics (especially twitches of the face, neck, and shoulders), vocal tics (grunts, words), and “behavioral tics” (coprolalia, echolalia). The cause is unknown. Treatment with haloperidol usually reduces the frequency and severity of the tics.

For a more detailed discussion, see Olney RK, Aminoff MJ: Weakness, Myalgias, Disorders of Movement, and Imbalance, Chap. 22, p. 118, in HPIM-15.

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