Quite apart from spasticity and rigidity, which are caused by
a disinhibition of spinal motor mechanisms, there are forms of muscular
stiffness and spasm that can be traced to abnormalities of the lower
motor neuron and its spinal inhibitory mechanisms or to the sarcolemma
of the muscle fiber. Muscles may go into spasm because of an unstable
depolarization of motor axons, sending volleys of impulses across
neuromuscular junctions—as occurs in myokymia, hypocalcemic
tetany, and pseudohypoparathyroidism. In other states, discussed
in Chap. 54, the innervation of muscle is
normal but contraction persists despite attempts at relaxation (myotonia).
Or, after one or a series of contractions, the muscle may be slow
in decontracting, as occurs in paradoxical myotonia and hypothyroidism.
In the contracture of McArdle phosphorylase deficiency and phosphofructokinase
deficiency, muscle, once contracted, lacks the energy to relax.
In yet another type of muscle stiffness, the muscle may ripple or
respond to percussion by mounding and rapidly contrasting and relaxing.
Cramping should also be differentiated from restless leg syndrome
(Chap. 19), which is primarily a nocturnal
disorder but may carry over into the daytime hours.
Each of these conditions evokes the complaint of cramp or spasm,
which is variably painful and interferes with free and effective
voluntary activity. Each condition has its own identifying clinical
and electromyographic (EMG) characteristics and most of them respond
favorably to therapy.
This subject was introduced in Chap. 48,
where it was pointed out that everyone at some time or other experiences
muscle cramps. Cramps often occur during the night, after a day
of unusually strenuous activity; less frequently they occur during
the day, either during a period of relaxation or occasionally after
a strong voluntary contraction or postural adjustment. A random
restless or stretching movement may induce a hard contraction of
a single muscle (most frequently of the foot or leg) that cannot
be voluntarily relaxed. The muscle is visibly and palpably taut
and painful and the condition is readily distinguished from an illusory
cramp, in which the sensation of cramp is experienced with little
or no contraction of muscle. The latter phenomenon may occur in
normal persons as well as in those with peripheral nerve diseases.
Massage and vigorous stretch of the cramped muscle will cause the
spasm to yield, although for a time the muscle remains excitable
and subject to recurrent cramps. Visible fasciculations may precede
and follow the cramp, indicating excessive excitability of the terminal
branches of motor neurons supplying the muscle. Sometimes the cramp
is so intense that the muscle is injured; it remains sore to touch
and painful upon use for a day or longer. Cramps of precordial chest
muscles or diaphragm may arouse fear of heart or lung disease. In
the EMG, the cramp is marked by bursts of high-frequency, high-voltage
action potentials, and the precramp phase shows runs of activity
in motor units. Why cramps should be painful is not known; probably
the demands of the ...