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Epilepsia Partialis Continua
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This is another special type of focal motor epilepsy characterized by persistent rhythmic clonic movements of one muscle group usually of the face, arm, or leg which are repeated at fairly regular intervals every few seconds and continue for hours, days, weeks, or months without spreading to other parts of the body Thus epilepsia partialis continua is, in effect, a highly restricted and very persistent focal motor status epilepticus The distal muscles of the leg and arm, especially the exors of the hand and ngers, are affected more frequently than the proximal ones In the face, the recurrent contractions involve either the corner of the mouth or one or both eyelids Occasionally, isolated muscles of the neck or trunk are affected on one side The clonic spasms may be accentuated by active or passive movement of the involved muscles and may be reduced in severity but not abolished during sleep First described by Kozhevnikov in patients with Russian spring-summer encephalitis, these partial seizures may be induced by a variety of acute or chronic cerebral lesions In some cases the underlying disease is not apparent (this applies to about half of our cases), and the clonic movements may be mistaken for some type of slow tremor or extrapyramidal movement disorder Most patients with epilepsia partialis continua show focal EEG abnormalities, either repetitive slow-wave abnormalities or sharp waves or spikes over the central areas of the contralateral hemisphere In some cases, the spike activity can be related precisely in location and time to the clonic movements (Thomas et al) In the series of cases collected by Obeso and colleagues, there were various combinations of epilepsia partialis continua and cutaneous re ex myoclonus (cortical mycolonus occurring only in response to a variety of afferent stimuli); these investigators view epilepsia partialis continua as part of a spectrum of motor disorders that also includes stimulus-sensitive myoclonus, focal motor seizures, and grand mal seizures As would be expected, a wide range of causative lesions has been implicated developmental anomalies, encephalitis, demyelinative diseases, brain tumors, and degenerative diseases; but in many instances, as mentioned, the underlying cause is not found even after extensive investigation Epilepsia partialis continua has been particularly common in patients with Rasmussen encephalitis (page 289) As a rule, this type of seizure activity responds poorly or not at all to anticonvulsant medications, but there is little alternative other than to try several drugs in combination Surgical extirpation or circumscription of the discharging cortex is a last resort Whether cortical mechanisms or subcortical ones are responsible for epilepsia partialis continua is an unresolved question The electrophysiologic evidence adduced by Thomas and colleagues favors a cortical origin The pathologic evidence is less de nite In each of eight cases in which the brain was examined postmortem, they found some degree of involvement of the motor cortex or adjacent cortical area contralateral to the affected limbs However, all but one of these patients also had some involvement of deeper structures on the same side as the cortical lesion, on the opposite side, or on both sides
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Physiologically, the epileptic seizure has been de ned as a sudden alteration of central nervous system (CNS) function resulting from a paroxysmal high-frequency or synchronous low-frequency, highvoltage electrical discharge This discharge arises from an assemblage of excitable neurons in any part of the cerebral cortex and possibly in secondarily involved subcortical structures as well Of course, there need not be a visible lesion In the proper circumstances, a seizure discharge can be initiated in an entirely normal cerebral cortex, as when the cortex is activated by ingestion or injection of drugs, by withdrawal from alcohol or other sedative drugs, or by repeated stimulation with subconvulsive electrical pulses ( kindling phenomenon ) Viewed from a larger physiologic perspective, seizures require three conditions: (1) a population of pathologically excitable neurons; (2) an increase in excitatory glutaminergic activity through recurrent connections in order to spread the discharge; and (3) a reduction in the activity of the normally inhibitory GABA-nergic projections The last of these has been challenged, but it is supported by considerable data and serves as a reasonable model, as noted below Understanding of the initial discharges and their spread has been greatly advanced by the identi cation of several rare forms of familial epilepsy that are the direct result of mutations in sodium, potassium, acetylcholine receptor, or GABA channels on neurons These are discussed further under Genetics of Epilepsy
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