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A somatotopical pattern in the human lateral vestibular nucleus.
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Pick's disease. A clinical and ultrastructural study.
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Argentophilic plaques in Creutzfeldt-Jakob disease.
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Amyotrophic lateral sclerosis. Association with schizophrenic symptoms and showing Alzheimer's tangles.
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Sporadic juvenile amyotrophic lateral sclerosis. A clinicopathological study of a case with neuronal cytoplasmic inclusions containing RNA.
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Ultrastructure of neurofibrillary tangles in Steele-Richardson-Olszewski syndrome.
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Amyotrophic lateral sclerosis with diffuse neurofibrillary changes. Report of a case.
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Giant axonal neuropathy. A clinically and morphologically distinct neurological disease.
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Dementia. A brief and selective review.
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Carbon monoxide-induced neuropathy in the rat. Ultrastructural changes.
The peroneal and ventral caudal nerves of rats exposed to 2,500 ppm CO until loss of nerve conduction occurred were studied by electron microscopy. Loss of normal axonal and Schwann cell structure was seen at the node of Ranvier. This loss was more prominent in large myelinated fibers, but was also seen in small myelinated fibers at seven and ten days postexposure. At this time, ventral caudal nerve conduction velocity decreased following a transient period of recovery lasting 9 to 13 days. Repair of the node began at 14 to 21 days postexposure, when maximal nerve conduction velocity had returned to normal. Complete normalization of node structure was not seen even 60 days after exposure, in many instances.
Myoclonus in Alzheimer disease. A confusing sign.
Myoclonus in association with dementia of later adult life has been considered almost pathognomonic of Creutzfeldt-Jakob disease. However, myoclonus may also be seen with Alzheimer disease, and when the myoclonus occurs as an early manifestation of Alzheimer disease, distinction from Creutzfeldt-Jakob disease may prove difficult.
Presenile dementia with Lewy bodies and neurofibrillary tangles.
A 55-year-old man showed progressive mental deterioration over a five-year period along with a syndrome of "normal pressure hydrocephalus." At autopsy the main finding was the presence of two age-related neurocellular changes, the neurofibrillary tangle and the Lewy body, in limbic structures and in the pigmented nuclei of the brain stem. Cortical changes were mild, and senile plaques were not present. Electron microscopy occasionally showed an intimate relationship between the paired helical filaments of the neurofibrillary tangle and Lewy bodies in nerve cell processes in the hypothalamus. The findings suggest a closer relationship between Lewy bodies and neurofibrillary tangles than usually suspected. We also speculate that the presence of one type of age change in the brain may accelerate or predispose to other age changes.
Giant axonal neuropathy: combined central and peripheral nervous system disease.
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Lewy bodies in the presence of Alzheimer's disease.
Large numbers of Lewy bodies in the substantia nigra were found in a case of Alzheimer's disease. Parkinsonian symptoms were not recognized. The patient appears to be an example of an association recognized by Woodard but not yet understood. The case is discussed in the context of reported relationships between Parkinson's disease or "Lewy body disease" and dementia, on the one hand, and reports linking various forms of psychoses with an unusually high incidence of Lewy bodies, on the other.
Amyloid neuropathy and tremor in Waldenström's macroglobulinemia.
We report a case of Waldenström's macroglobulinemia with amyloid neuropathy and a parkinsonian syndrome. We describe the light and electron microscopic findings in a sural nerve biopsy specimen and discuss the possible pathogenic mechanisms in the production of the neuropathy. In contrast to a number of previous cases of neuropathy associated with Waldenström's macroglobulinemia, evidence of immunoglobulin deposition on nerve fibers was not found using immunofluorescent techniques.
Neurofibrillary change on Guam.
Distribution and occurrence of neurofibrillary change (NFC) in the brain were studied in 114 Guamanians who had neither amyotrophic lateral sclerosis (ALS) nor parkinsonism dementia (PD). Comparison was made with 28 Guamanians with ALS-PD and 53 non-Guamanians without ALS-PD. Search for NFC was made in 15 dogs and cats that lived on Guam. Most of the Guamanians without ALS-PD during and after middle age had NFC similar to that of Guamanians with ALS-PD but lesser in degree and extent of involvement. It is possible that the general population of Guam had been exposed to the unknown etiologic agent of ALS-PD during some previous period.
Bilateral symmetry of morphologic lesions in Alzheimer's disease.
We studied 16 brains of patients with Alzheimer's disease for left-right differences, or similarities, in the density of senile plaques (SPs) or neurofibrillary tangles (NFTs). Counts were made of SPs and NFTs on the left and right side of five different brain areas, which included middle frontal, superior temporal, the prosubiculum of the hippocampus (HPR), the entorhinal cortex of the hippocampus (HEN), and the basal nucleus of Meynert. The density of SPs was bilaterally symmetrical in all regions except the basal nucleus of Meynert in which technical problems may have occurred in sampling. In contrast to SPs, the density of NFTs was bilaterally symmetrical in both neocortical regions (middle frontal, superior temporal), but not in either hippocampal region (HPR, HEN). The absence of bilateral symmetry for the density of NFTs in the hippocampus, where the density of SPs was highly symmetrical, suggests that there may be a different pathogenesis for these lesions in Alzheimer's disease. The lack of a significant correlation between SP and NFT density within four of five regions, including HPR and HEN, also supports this suggestion.