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and they considered them to be related In the variant described by Tandan and colleagues, an autosomal dominant syndrome of Charcot-Marie-Tooth polyneuropathy was combined with ptosis, parkinsonism, and dementia, again without Lewy bodies or senile plaques Other variants have been described by Schmitt and coworkers and by Mata and colleagues Hudson has reviewed 42 sporadic cases in which ALS-parkinsonism-dementia were combined (see References) Under the title Spastic Pseudosclerosis, Jakob, in 1921, described a chronic disease of middle to late adult life, characterized by abnormalities of behavior and intellect; weakness, ataxia, and spasticity of the limbs (chie y the legs); extrapyramidal symptoms such as rigidity, slowness of movement, tremors, athetotic postures, and hesitant, dysarthric speech; and normal spinal uid The pathologic changes were diffuse and consisted mainly of an outfall of neurons in the frontal, temporal, and central motor gyri, corpus striatum, ventromedial thalamus, and bulbar motor nuclei In one of Jakob s cases, there were also prominent changes in the anterior horn cells and corticospinal tracts in the spinal cord like those of ALS The latter nding gave rise to Wilson s concept of the disease as a corticostriatospinal degeneration A degenerative and probably familial disorder that had been described earlier by Creutzfeldt was considered by Spielmeyer to be suf ciently similar to the one of Jakob to warrant the designation Creutzfeldt-Jakob disease As discussed in Chap 33, the disorder described by Creutzfeldt and Jakob has been a source of endless controversy because of its indeterminate character On the one hand, it has been confused with the subacutely evolving myoclonic dementia, or subacute spongiform encephalopathy, which is now known to be an infection due to an unconventional transmissible prion agent The authors believe that the latter disease, which is described on page 653, bears at best only a super cial resemblance to the one described by Creutzfeldt and Jakob and that the two disorders should be clearly separated Unfortunately, the use of the eponym for the prion-related disease is so entrenched in medical usage that any attempt to delete it stands little chance of success On the other hand, sporadic and familial cases that are not transmissible and lack a prominent spongiform change merge with a rather heterogeneous but overlapping group of degenerative disorders, all rare, including progressive dementia and spastic paraplegia, progressive frontotemporal dementia and ALS, the Parkinson-dementia-ALS complex of Guam, and the corticopallidospinal degeneration of Davison One is tempted to conclude that the spastic pseudosclerosis of Jakob may not constitute a disease type, and certainly everyone agrees that the term pseudosclerosis (also used for the WestphalStrumpell form of hepatolenticular degeneration) is meaningless The Guamanian Parkinson-dementia-ALS complex deserves separate comment because it has been well de ned in a large number of carefully studied cases with almost uniform clinical and pathologic features The disease occurs in the indigenous Chamorro peoples of Guam and the Mariana islands, predominantly in men between ages 50 and 60 Progressive parkinsonism and dementia are combined with upper or lower motor neuron disease (ALS is also common among the Chamorro), leading to death in 5 years The pathologic changes, described by Hirano and others, consist of severe cortical atrophy with neuro brillary tangles but, notably, no detectable amyloid plaques, even with sensitive neurochemical staining As in Parkinson disease, the substantia nigra and to a lesser extent other pigmented nuclei are depopulated of nerve cells but contain no Lewy bodies Cases with amyotrophy show the typ-.

ical loss of anterior horn cells The cause of the Guamanian multisystem degeneration is not known, although several studies have incriminated one or more adverse environmental in uences, including putative neurotoxins in the food supply

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From time to time the authors have encountered families in which several members developed a spastic paraparesis and a gradual failure of intellectual function during the middle adult years The patient s mental horizon narrowed gradually, and the capacity for high-level thinking diminished; in addition, the examination showed appropriately exaggerated tendon re exes, clonus, and Babinski signs In one such family the illness had occurred in two generations; in another, three brothers in a single generation were af icted Skre described two recessive types of hereditary spastic paraplegia in Norway, one with onset in childhood, the other in adult life In contrast to the dominant form (see further on), the recessive types displayed evidence of more widespread involvement of the nervous system, including dementia, cerebellar ataxia, and epilepsy Also, Cross and McKusick have observed a recessive type of paraplegia accompanied by dementia beginning in adolescence They named it the Mast syndrome, after the af icted family Worster-Drought and others have reported the pathologic ndings in two cases of this type In addition to senile plaques and neuro brillary changes, there was demyelination of the subcortical white matter and corpus callosum and a patchy but gross swelling of the arterioles, which gave the staining reactions for amyloid ( Scholz s perivascular plaques ) Van Bogaert and associates published an account of similar cases that showed the characteristic pathologic features of Alzheimer disease Adult forms of metachromatic leukodystrophy and adrenoleukodystrophy may present with a similar clinical picture (Chap 37) Quite rare instances of the same syndrome with adult onset have turned out to be due to phenylketonuria or other aminoacidopathies (see Chap 37) Another interesting association of familial spastic paraplegia is with progressive cerebellar ataxia Fully one-third of the cases that we have seen with such a spastic weakness were also ataxic and would fall into the category of spinocerebellar degenerations Yet another variant of this group of diseases has been described by Farmer and colleagues; the inheritance in their cases was autosomal dominant, and the main clinical features were deafness and dizziness, ataxia, chorea, seizures, and dementia, evolving in that order Postmortem examinations of two patients disclosed calci cation in the globus pallidus, neuronal loss in the dentate nuclei, and destruction of myelinated bers in the centrum semiovale.

Under this title, Robitaille and colleagues have described a distinct type of progressive neurologic disease in adults characterized clinically by spasticity, chorea, dementia, and a predominantly sensory polyneuropathy Structures that closely resembled Lafora bodies and corpora amylaceae were found in large numbers in both central and peripheral neural processes (mainly in axons) and also in astrocytes These basophilic PAS-positive structures (up to 40 m in size) were composed of glucose polymers (polyglucosans) and were readily demonstrated in sural nerve biopsies Some were also found in the heart and liver

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