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an alteration in muscle tone and a slight degree of cerebellar ataxia At this time, or even before the onset of myoclonus and seizures, the patient may experience visual hallucinations or exhibit irritability, odd traits of character, uninhibited or impulsive behavior, and, ultimately, progressive failure in all cognitive functions Deafness has been an early sign in a few cases Rigidity or hypotonia, impaired tendon re exes, acrocyanosis, and rarely corticospinal tract signs are late ndings Finally the patient becomes cachectic and bedfast and succumbs to intercurrent infection Most do not survive beyond their 25th birthday Nonetheless there are isolated reports of Lafora-body disease in which symptoms began as late as 40 years, with death as late as 50 years These late cases may constitute a separate genetic type No abnormalities of the blood, urine, or CSF have been detected The EEG shows diffuse slow waves and spikes as well as bursts of focal or multifocal discharges Altered hepatocytes with homogeneous PAS-positive bodies that displace the nuclei have been observed in both the presymptomatic and symptomatic stages of the disease These inclusions have been seen in skin and liver biopsies, even though liver function tests were normal Neuropathologic examinations have shown a slight loss of granule and Purkinje cells and loss of neurons in the dentate nuclei, inner segment of globus pallidus, and cerebral cortex in addition to the Lafora bodies The latter may also be seen in the retina, cerebral cortex, myocardium, and striated muscles Anticonvulsant drugs, especially methsuximide and valproic acid, help in the control of the seizures but have no effect on the basic process Polyglycosan Body Disease (See also page 914) This is another closely related disease, the features of which have been reviewed by Robitaille and coworkers, in which glycosamine bodies are found in the central and peripheral nervous system The clinical syndrome includes dementia, chorea, and amyotrophy with or without sensory loss in the limbs Similar bodies are found in the cells of the liver and heart This is a progressive disease usually beginning in adult life It has been attributed to the accumulation of polymers of glucose Diagnosis is con rmed by the nding of the polyglycosan bodies in the axons of peripheral nerves or liver cells The causative mutation in most cases affects the gene for glycogen branching enzyme Juvenile Ceroid Lipofuscinosis (Cerebroretinal Degeneration) As stated earlier, this is one of the most variable forms of the lipidoses The salient clinical features of the later-onset types are severe myoclonus, seizures, and visual loss In the juvenile type, the rst lesions are seen in the maculae; they appear as yellow-gray areas of degeneration and stand in contrast to the cherry-red spot and the encircling white ring of Tay-Sachs disease At rst, the particles of retinal pigment are ne and dust-like; later they aggregate to resemble more the bone-corpuscular shapes of retinitis pigmentosa The liver and spleen are not enlarged and there are no osseous changes The usual development of these and other manifestations of the disease was outlined by Sjogren, who studied a large number of the late infantile and juvenile types of cases in Sweden He divided the illness into ve stages: 1 2 Visual impairment, sometimes preceding retinal changes by months After approximately 2 years, the onset of generalized seizures and myoclonus, often with irritability, poor control of emotions, and stuttering, jerky speech Gradual intellectual deterioration (poor memory, reduced mental activity, inattentiveness) By this stage the move-.

FIGURE 10-13

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ments have usually become slow, stiff, and tremulous, resembling somewhat those of Parkinson disease to which are added elements of cerebellar ataxia and intention tremor, coming in this respect to resemble Wilson disease 4 Stage of severe dementia in which the patient needs assistance to walk, no longer speaks, and may scream when disturbed or forced to move The muscles are wasted, though the tendon re exes remain lively, and the plantar re exes are extensor 5 Finally the patient lies curled up in bed, blind and speechless, with strong extensor plantar re exes, occasionally adopting dystonic postures Life usually ends in 10 to 15 years In the early stages the EEG picture of random, high-voltage, triphasic waves is diagnostic; later, as the seizures and myoclonic jerks become less frequent and nally cease, only delta waves remain The electroretinographic waveforms are lost once the retina is affected The lateral ventricles are slightly dilated in CT scans and on MRI The CSF is normal Diagnosis can be con rmed by the appearance of inclusions of a curvilinear ngerprint pattern in electron microscopic study of biopsy material, particularly of the eccrine sweat glands of the skin A defective membrane protein has been identi ed that forms the inclusion material in the most common, or classic, juvenile phenotype The genetics of the lipofuscinoses have been reviewed by Mole Late Juvenile and Adult Ceroid Lipofuscinosis (Kufs disease) The Kufs type of ceroid lipofuscinosis, which develops later (15 to 25 years of age or older), is often unattended by visual or retinal changes and is even slower in its evolution It is presented here for ease of exposition, but it becomes relevant mostly in relation to dementing illness in young adulthood (page 829) Personality change or dementia is one constellation, the other being myoclonic seizures with subsequent dementia and even later pyramidal and extrapyramidal signs As the disease progresses, cerebellar ataxia, spasticity and rigidity or athetosis, or mixtures thereof, are combined with dementia As a measure of the variability of the clinical presentation, a recent patient of ours had vague visual dif culties at age 51 and evolved a spastic quadriparesis with disinhibited behavior over 5 years Further comments regarding the unusual presentations of this disease can be found further on, under Adult Forms of Inherited Metabolic Disease van Bogaert pointed out to our colleague R D Adams that relatives of these patients may have retinal changes without neurologic accompaniments The genetic defect for the adult form has been partially analyzed (see below) Of all the lipidoses, these cerebroretinal degenerations had for decades de ed unifying biochemical de nition Our understanding of these diseases is dif cult because they embody both enzymatic defects and structural protein dysfunctions In a few of the early childhood types, mutations of one of several lysosomal enzymes have been identi ed, as summarized by Mole and by Wisniewski and colleagues As mentioned earlier, Zeman and coworkers have shown that the cytoplasmic inclusions are auto uorescent and give a positive histochemical reaction for both ceroid and lipofuscin, but this material is not different biochemically from the lipid substance that accumulates in aging cells In addition to the presence of curvilinear bodies in the cytoplasm of neurons and other tissues, some in a ngerprint pattern, there is a reduction in type II synapses.

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