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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.



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obtained with the telescope. Long, narrow telescopes have the smallest maximum apparent fields of view; short, fat ones have the widest maximum fields.





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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.

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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.

of the accessory nerves or the motor nuclei (progressive bulbar palsy). The supranuclear innervation of the spinal accessory nuclei is apparently mainly ipsilateral as evidenced by contraversive turning of the head during a seizure, the result of contraction of the ipsilateral sternocleidomastoid muscle. Whether this is attributable to a direct ipsilateral tract, or to double crossing, is not known.

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.

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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-.

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