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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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that these potentials, which were a re ection of presynaptic inhibition or excitation, modulated the activity of secondary transmitting neurons (T cells) in the dorsal horn, and that this modulation was mediated through inhibitory (I) cells The essence of this theory is that the large-diameter bers excite the I cells, which, in turn, cause a presynaptic inhibition of the T cells; conversely, the small pain afferents inhibit the I cells, leaving the T cells in an excitatory state Melzack and Wall emphasized that pain impulses from the dorsal horn must also be under the control of a descending system of bers from the brainstem, thalamus, and limbic lobes At rst the gate-control mechanisms seemed to offer an explanation of the pain of ruptured disc and of certain chronic neuropathies (particularly those with large ber outfall), and attempts were made to relieve pain by subjecting the peripheral nerves and dorsal columns (presumably their large myelinated bers) to sustained transcutaneous electrical stimulation Such selective stimulation would theoretically close the gate In some clinical situations, these procedures have indeed given relief from pain, but not necessarily due to stimulation of large myelinated bers alone (see Taub and Campbell) But in a number of other instances relating to pain in large- and small- ber neuropathies, the clinical behavior has been quite out of keeping with what one would expect on the basis of the gate-control mechanism As with preceding theories, aws have been exposed in the physiologic observations on which the theory is based These and other aspects of the gate-control theory of pain have been critically reviewed by P W Nathan During the last few decades there has been a signi cant accrual of information on cutaneous sensibility, demanding a modi cation of earlier anatomic-physiologic and clinical concepts Interestingly, much of this information is still best described and rationalized in the general framework of the oldest theory, that of speci city, as will be evident from the ensuing discussion on pain and that on other forms of cutaneous sensibility in the chapter that follows.

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In terms of peripheral pain mechanisms, as already implied, there is indeed a high degree, though not an absolute, of speci city in the von Frey sense In keeping with distinctions between nerve types, the sensory (and motor) bers have been classi ed according to their size and function (Table 8-1) It is now well established that two types of afferent bers in the distal axons of primary sensory neurons respond maximally to nociceptive (ie, potentially tissue-



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