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movements ( dancing eyes of an opsoclonic type) The child is irritable and speech may cease All laboratory tests are normal Treatment Adrenocorticotropic hormone and dexamethasone, the latter in doses of 15 to 40 mg/day, suppress the myoclonus and permit developmental progress Some patients have recovered from the myoclonus but have been left mentally slow and mildly ataxic Others have required corticosteroid therapy for 5 to 10 years, with relapse whenever it was discontinued Ordinary anticonvulsants seem to have no effect The pathology has not been determined A similar syndrome has been observed in conjunction with neuroblastoma in children and as a transient illness of unknown cause (probably viral or postinfectious) in young adults (Baringer et al; see page 641) It is mentioned here because a similar condition is also known in adults, as a paraneoplastic disease with ovarian, breast, gastric, and bronchogenic carcinomas and with other occult tumors In a broader survey of the pediatric opsoclonus-myoclonus syndrome, Pranzatelli and associates reported their experience with 27 cases, some with neural crest tumors, others with viral infections or hypoxic injury (intention myoclonus) In nearly all of their patients there was cerebellar ataxia and mental disorder, and 10 percent had seizures The CSF was normal The investigators have emphasized the pathogenetic heterogeneity and de ned a rare serotoninergic type (low levels of 5-hydroxytryptophan and homovanillic acid in the CSF) that responds to 5-hydroxyindole acetic acid Familial Progressive Myoclonus Five major categories of familial polymyoclonus of late childhood and adolescence have been delineated: (1) Lafora- or amyloid-body type, (2) juvenile cerebroretinal degeneration, (3) cherry-red spot myoclonus (sialidosis or neuraminidosis), (4) mitochondrial encephalopathy, and (5) a more benign degenerative disease (dyssynergia cerebellaris myoclonica of Hunt) Familial myoclonus may also be a prominent feature of two other diseases GM2 gangliosidosis and Gaucher disease which occasionally have their onset in this age period Lafora-Body Polymyoclonus with Epilepsy This disease, which is inherited as an autosomal recessive trait, was rst identi ed by Lafora in 1911 on the basis of the large basophilic cytoplasmic bodies that were found in the dentate, brainstem, and thalamic neurons These inclusions have been shown by Yokoi and colleagues to be composed of a glucose polymer (polyglycosan) that is chemically but not structurally related to glycogen Possibly some of the cases of familial myoclonus epilepsy reported by Unverricht and by Lundborg were of this type, but since these authors provided no pathologic data, one cannot be sure Beginning in late childhood and adolescence (11 to 18 years) in a previously normal individual, the disease announces itself by a seizure, a burst of myoclonic jerks, or both In about half the cases there are focal (often occipital) seizures The illness may at rst be mistaken for ordinary epilepsy, but within a few months it becomes evident that something far more serious is occurring The myoclonus becomes widespread and can be evoked as a startle by noise, an unexpected tactile stimulus (even the tap of a re ex hammer), and also by excitement, or certain sustained motor activities An evoked train of myoclonic jerks may progress to a generalized seizure with loss of consciousness As the disease advances, the myoclonus interferes increasingly with the patient s motor activities until voluntary function is seriously impaired Speech may be marred, much as it is in chorea Close examination may also reveal.

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