Normal motor function involves integrated muscle activity that is modulated by the activity of the cerebral cortex, basal ganglia, cerebellum, red nucleus, brainstem reticular formation, lateral vestibular nucleus, and spinal cord. Motor system dysfunction leads to weakness or paralysis, discussed in this chapter, or to ataxia (Chap. 431) or abnormal movements (Chap. 428). Weakness is a reduction in the power that can be exerted by one or more muscles. It must be distinguished from increased fatigability (i.e., the inability to sustain the performance of an activity that should be normal for a person of the same age, sex, and size), limitation in function due to pain or articular stiffness, or impaired motor activity because severe proprioceptive sensory loss prevents adequate feedback information about the direction and power of movements. It is also distinct from bradykinesia (in which increased time is required for full power to be exerted) and apraxia, a disorder of planning and initiating a skilled or learned movement unrelated to a significant motor or sensory deficit (Chap. 26).
Paralysis or the suffix “-plegia” indicates weakness so severe that a muscle cannot be contracted at all, whereas paresis refers to less severe weakness. The prefix “hemi-” refers to one-half of the body, “para-” to both legs, and “quadri-” to all four limbs.
The distribution of weakness helps to localize the underlying lesion. Weakness from involvement of upper motor neurons occurs particularly in the extensors and abductors of the upper limb and the flexors of the lower limb. Lower motor neuron weakness depends on whether involvement is at the level of the anterior horn cells, nerve root, limb plexus, or peripheral nerve—only muscles supplied by the affected structure are weak. Myopathic weakness is generally most marked in proximal muscles. Weakness from impaired neuromuscular transmission has no specific pattern of involvement.
Weakness often is accompanied by other neurologic abnormalities that help indicate the site of the responsible lesion (Table 21-1).
TABLE 21-1Signs That Distinguish the Origin of Weakness |Favorite Table|Download (.pdf) TABLE 21-1 Signs That Distinguish the Origin of Weakness
|Sign ||Upper Motor Neuron ||Lower Motor Neuron ||Myopathic ||Psychogenic |
|Atrophy ||None ||Severe ||Mild ||None |
|Fasciculations ||None ||Common ||None ||None |
|Tone ||Spastic ||Decreased ||Normal/decreased ||Variable/paratonia |
|Distribution of weakness ||Pyramidal/regional ||Distal/segmental ||Proximal ||Variable/inconsistent with daily activities |
|Muscle stretch reflexes ||Hyperactive ||Hypoactive/absent ||Normal/hypoactive ||Normal |
|Babinski sign ||Present ||Absent ||Absent ||Absent |
Tone is the resistance of a muscle to passive stretch. Increased tone may be of several types. Spasticity is the increase in tone associated with disease of upper motor neurons. It is velocity-dependent, has a sudden release after reaching a maximum (the “clasp-knife” phenomenon), and predominantly affects the antigravity muscles (i.e., upper-limb flexors and lower-limb extensors). Rigidity is hypertonia that is present throughout the range of motion (a “lead pipe” or “plastic” stiffness) and affects flexors and extensors ...