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Hyperexcitability of Peripheral Nerve
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This term comprises a set of disorders in which peripheral motor nerve activity is augmented, such that there are excessive, sometimes sustained contractions of the motor unit Its mildest manifestation is benign fasciculation In more severe forms, the result is a group of disorders that includes cramp-fasciculation syndrome, neuromyotonia, Isaacs disease, and a variant of the latter in which there is also involvement of the central nervous system (Morvan disease), a disease of potassium-gated ion channels (page 1273) They are not generally familial but several lines of investigation argue that many of these disorders are of an acquired autoimmune nature (Newsom-Davis) For example, all but benign fasciculations are associated more often than might be expected with other autoimmune diseases such as myasthenia gravis and many respond to anti-immune therapies such as plasmapheresis And, in some of these disorders, the patient s sera possess antibodies to either voltage-gated potassium channels as mentioned or, less frequently, nicotinic acetylcholine (ACh) receptors (Vernino and Lennon) Persistent Benign Fasciculations A few random fasciculations in the muscles of the calf, small muscles of the hand or of the face, or elsewhere are seen in most normal individuals They are of no signi cance but can be a source of worry to physicians and nurses who have heard or read that fasciculations are an early sign of amyotrophic lateral sclerosis A simple clinical rule is that fasciculations in relaxed muscle are not indicative of motor system disease unless there is associated weakness, atrophy, or re ex change Frequently a healthy individual experiences intermittent twitching of a muscle (or even part of a muscle), such as one of the muscles of the thenar eminence, eyelids, calves, or orbicularis oculi It may continue for days Lay persons refer to it as live esh Also, penicillin may destabilize the polarization of distal motor endings and cause twitching Electromyographically, these benign fasciculations tend to be more constant in location and more frequent and rhythmic than the ominous fasciculations of amyotrophic lateral sclerosis, but such distinctions are not entirely reliable Quantitative study of the motor unit size may be helpful in these circumstances by demonstrating normally modeled units in the benign form and abnormally large units due to reinnervation in the case of motor neuron disease (see page 1105) Occasionally, benign fasciculations are widespread and may
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last for months or even years In several of our patients they have recurred in bouts separated by months and lasting several weeks No re ex changes, sensory loss, nerve conduction, EMG abnormality (other than fasciculations), or increase in serum muscle enzymes are found Low energy and fatigability in some of these patients may suggest an endogenous depressive illness, yet the fasciculations are not explained by this mechanism Commonly, patients report a sense that the muscles affected by the twitching are weak but this cannot be con rmed by testing, and several of our patients, curiously the majority of whom were physicians, have complained of equally troubling migratory zones of paresthesias (Romero et al) Pain, of aching or burning type, may increase after activity and cease during rest Fatigue and a sense of weakness are frequent complaints We suspect that this fasciculatory state re ects a disease of the terminal motor nerves, for a few of our patients have shown slowing of distal latencies, and Coers and associates have found degeneration and regeneration of motor nerve terminals However, the majority of these cases are of a benign nature and settle down in a matter of weeks or months In the cases reported by Hudson and colleagues, the condition, even after years, did not progress to spinal muscular atrophy, a polyneuropathy, or amyotrophic lateral sclerosis Eventual recovery can be expected This conforms to our experience and to that reported from the Mayo Clinic where 121 patients with benign fasciculations, followed in some cases for more than 30 years, showed no progression of symptoms and did not acquire motor neuron disease or neuropathy (Blexrud et al) It should be acknowledged, however, that there are infrequent patients with seemingly benign fasciculations in whom the EMG shows some abnormal features (eg, rare brillations) in numerous muscles and who later develop the other features of motor neuron disease Carbamazepine, and to a lesser extent phenytoin, has been helpful in reducing the fasciculations and sensations of weakness Cramp-Fasciculation Syndrome This is a variant of the aforementioned entity in which fasciculations are conjoined with cramps, stiffness, and systemic features such as exercise intolerance, fatigability, and muscle aches Although affected individuals may be to some degree disabled by these symptoms, the prognosis is good The salient nding on physiologic studies is that stimulation of peripheral nerves results in sustained muscle ring due to prolonged trains of action potentials in the distal motor nerve This may be brought out in special electrophysiologic testing as described by Tahmoush and colleagues In effect, this is a mild form of neuromyotonia (see later) In a small number of patients with crampfasciculation syndrome it is possible to demonstrate the presence of autoantibodies directed against voltage-gated axonal potassium channels Carbamazepine or gabapentin may be bene cial There are, in addition to the aforementioned benign states, several syndromes of abnormal muscle activity The main ones are myokymia, a state of successive contractions of motor units imparting an almost continuous undulation or rippling of the overlying body surface, and several syndromes of continuous muscle ber activity Myokymia This state of abnormal rippling muscle activity, as de ned earlier, may be generalized or limited to one part of the body, such as the muscles of the shoulders or of the lower extremities It is observed most often with regeneration of peripheral nerve following injury, as in the facial palsy of Guillain-Barre syndrome,
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and thus it is most often neuropathic in nature In the EMG, myokymic discharges consist of groups of 2 to 10 potentials, ring at 5 to 60 Hz and recurring regularly at 02- to 10-s intervals They arise in the most peripheral parts of the axon of chronically damaged nerves In some patients, cramping is associated and, indeed, muscles about to cramp may twitch or show spontaneous rippling contractions; the cramping may be associated with sweating Thus, myokymia, fasciculation, and cramping are closely related but not clinically identical conditions Continuous Muscle Fiber Activity (Isaacs Syndrome) The relation of myokymia to the state called continuous muscle ber activity is ambiguous Sporadically, in the neurologic literature, there have been described patients whose muscles at some point begin to work continuously (see Isaacs) Terms such as neuromyotonia and widespread myokymia with delayed muscle relaxation are additional names that have been applied to what is essentially the same condition At the moment, there is little reason to distinguish one from another except in gradations of severity In each case the excessive and spontaneous activity can be attributed to hyperexcitability of terminal parts of motor nerve ber, possibly as a result of a partial loss of motor innervation and compensatory collateral sprouting of surviving axons (Coers et al, Valli et al) Twitching, spasms, and rippling of muscles (myokymia) are evident, the latter being the main clinical sign In advanced cases there is generalized muscle stiffness and a sense of weakness Complaints of muscle aching are usual, but severe myalgia is uncommon The tendon re exes may be reduced or abolished Any muscle group may be affected The stiffness and slowness of movement make walking laborious ( armadillo syndrome); in extreme cases, all voluntary movement is blocked The muscle activity persists throughout sleep The continuous visible and painful cramps of Satoyoshi disease are dif cult to distinguish from myokymia General and spinal anesthesia do not always suppress the muscular activity, but curare does; nerve block usually has no effect or may reduce the activity, as in the case described by Lutschg and colleagues The EMG ndings are much the same as those described earlier This syndrome arises in childhood or adult life, sometimes in association either with a polyneuropathy or with an inherited type of episodic ataxia that is variably responsive to acetazolamide or remits spontaneously An inherited form of continuous muscle ber activity has been traced to a gene mutation on chromosome 12 and is attributed to a peripheral nerve K channel abnormality (Gutmann and Gutmann) In addition to the association with polyneuropathy, a state of continuous muscular activity has also been described with lung cancer and thymoma, with or without myasthenia, in which cases an immune mechanism has been inferred (see reviews by Thompson and by Newsom-Davis and Mills) An association of continuous muscle ber activity with psychosis or a severe sleep disorder was described by Morvan under the name choree brillaire as discussed in the previous chapter (see also page 1273, Serratrice and Azalay) Most cases appear to be idiopathic, however Treatment Phenytoin or carbamazepine often abolishes the continuous muscular activity and causes a return of re exes Acetazolamide has been helpful in some other cases (Celebisoy et al) Many of the idiopathic cases, as already noted, will improve spontaneously after several years, but plasma exchange may be tried if the symptoms are intractable
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