Cases reported "Alzheimer Disease"

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1/13. An autopsy case of Alzheimer's disease with a progressive supranuclear palsy overlap.

    A 74-year-old man developed abnormal forgetfulness, soon followed by unstable speech content and marked disorientation. At 77 years of age, the patient started to occasionally fall, an aspect of progressive supranuclear palsy. He then became bedridden. The patient eventually died of pneumonia at 79 years of age. Neuropathological examination revealed profiles of both progressive supranuclear palsy and Alzheimer's disease. Although the two conditions both belong to tauopathy, their pathologically proven combination was rare. Furthermore, the case had the possibility of being a subgroup of tauopathy.
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ranking = 1
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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2/13. Clinical and pathological study of two patients with progressive supranuclear palsy and Alzheimer's changes. Antigenic determinants that distinguish cortical and subcortical neurofibrillary tangles.

    Two cases with classical clinical manifestations of progressive supranuclear palsy (PSP) showed severe progressive dementia as an additional clinical feature. Neuropathological study demonstrated typical features of PSP in the brainstem. Additionally, histological criteria of Alzheimer's disease (AD) were observed. A topographic and immunohistological study (with neurofilament subunit and Tau and ubiquitin antibodies) of the distribution of neurofibrillary tangles (NFTs) was performed in order to compare the characteristics of NFTs from cortex and brainstem. NFTs from cortex were positive with all antibodies used and were predominantly distributed in cortical layers III and V and affected medium size neurons. Brainstem NFTs were positive only for neurofilament subunits and Tau. Cortical and brainstem NFTs showed immunohistological differences. Cortical NFTs in our two cases had a similar distribution as in control AD cases. On the basis of our observations we believe (1) that cortical tangles in our PSP cases are related to Alzheimer's disease and (2) that the cortical NFTs of PSP and AD are morphologically and immunohistologically distinct. Mechanisms concerned with the production of cortical and brainstem NFTs in PSP and AD are discussed.
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ranking = 0.84653758153654
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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3/13. Progressive supranuclear palsy with widespread cerebral lesions.

    A 51-year-old woman with no history of any familial neurological diseases initially presented with numbness in her extremities, slowing of movements, comprehension deficit, memory disturbance, dyscalculia, muscle rigidity, hyperreflexia, Parkinsonian gait, increasing disorientation, left-right disturbance, finger agnosia, alexia, acalculia, apraxia, aspontaneity, euphoria, gait disturbance, aphasia, echolalia, and in the terminal stage, mutism, contracture of lower extremities and cachexia. She died of bronchopneumonia at the age of 55. The brain showed widespread cerebral lesions, consisting of nerve cell loss and neurofibrillary tangles in the frontal, parietal and occipital cortex, demyelination and gliosis in the frontal, parietal and occipital subcortical white matter in addition to the typical pathological findings of progressive supranuclear palsy (PSP): severe neuronal loss with gliosis and neurofibrillary tangles (NFTs) in the subthalamic nucleus, globus pallidus and substantia nigra. In conclusion, we present a case of PSP with unusual clinical features (extrapyramidal signs, frontal and parietal lobe syndromes without ophthalmoplegia) and neuropathologically widespread cerebral lesions in addition to the typical pathological findings of PSP. The differential diagnosis of PSP and Alzheimer's disease and other degenerative disorders is discussed.
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ranking = 0.41441775789723
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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4/13. Diffuse lewy body disease presenting with supranuclear gaze palsy, parkinsonism, and dementia: a case report.

    A 67-year-old man with a family history of parkinsonism had visual complaints due to difficulty in convergence, which was followed 2 years later by development of bradykinesia and rigidity. The diagnosis of Steele-Richardson-Olszewski syndrome was made on the basis of a supranuclear gaze palsy, bradykinesia, rigidity, and poor response to levodopa. However, subsequent neuropathological examination revealed diffuse lewy body disease with no evidence of neurofibrillary tangles involving either subcortical or brain stem structures.
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ranking = 0.22716231276815
keywords = supranuclear, palsy
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5/13. Paired helical filaments in astrocytes: electron microscopy and immunohistochemistry in a case of atypical Alzheimer's disease.

    A 54-year-old man who had cerebellar ataxia and pseudobulbar palsy at the age of 29 years, and soon developed dementia, myoclonus and convulsions, died after about 20 years in a vegetative state. Histological examination of the extensively atrophic and devastated brain (680 g) revealed the almost total loss of cerebral cortical neurons associated with numerous beta-protein amyloid plaques, many extracellular tangles and a large number of hypertrophic astrocytes, and prominent amyloid angiopathy. The astrocytes were frequently immunopositive for anti-human tau antibody (anti-htau) and anti-ubiquitin antibody (anti-ubi). Double immunostaining with anti-htau and anti-glial fibrillary acidic protein (GFAP) antibody clearly demonstrated htau-positive domains within the GFAP-positive perikarya/and processes of several astrocytes. Electron microscopy of the hippocampal CA1, which was completely devoid of pyramidal neurons, revealed, in astrocytes, abnormal filaments indistinguishable from the paired helical filaments (PHFs) seen in neurons. On immunoelectron microscopy, the filaments were observed to be labeled with anti-htau and anti-ubi, exhibiting the same immunohistochemical features as neuronal PHFs. This is the first demonstration of clearly constricted and both tau- and ubiquitin-positive PHFs in astrocytes, indicating that, in some special conditions like in our case, processes similar to those that attack neurons also affect astrocytes and ultimately make the latter form PHFs.
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ranking = 6.6759231438933E-6
keywords = palsy
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6/13. Visual facial grasp.

    Some patients with degenerative neurological diseases have a release of the vestibular-ocular reflex (VOR), as detected by passive head movement during visual fixation on a moving target ("doll's eyes"maneuver). However, a positive doll's eyes sign might be induced by other defects and the purpose of this article is to describe a new ocular sign of cortical dysfunction, the visual facial grasp. We observed three patients, one with progressive supranuclear palsy (PSP), another with probable Alzheimer's disease (AD) and a third with cortico-basal degeneration (CBD) all of whom appeared to demonstrate a release of the vestibulo-ocular reflex (VOR) with passive head movements. Whereas the patient with PSP, who was unable to inhibit the VOR regardless of the visual target used probably had a true release of the VOR, the patients with AD and CBD were able to inhibit this reflex when the visual target was the examiner's moving face. These two patients also exhibited spontaneous preference for visual fixation on the examiner's face and improvement in smooth pursuit when the examiner's face was the visual target. This clinical observation suggests that the deficits in these two patients with AD and CBD were related to the emergence of a primitive stimulus-bound behavior, the visual facial grasp.
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ranking = 0.16930751630731
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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7/13. Late-onset frontotemporal dementia associated with progressive supranuclear palsy/argyrophilic grain disease/Alzheimer's disease pathology.

    Progressive supranuclear palsy (PSP) is typically manifested by vertical supranuclear gaze palsy, frequent falls early in the disease course, axial rigidity and poor response to levodopa. Prominent anterograde memory dysfunction with subsequent impairment in other cognitive domains is characteristic of Alzheimer's disease (AD). No clear clinical syndrome has been identified in argyrophilic grain disease (AGD). frontotemporal dementia (FTD) is characterized by apathy, emotional blunting, disinhibition, and impairment in executive functioning despite relatively preserved memory and visuospatial abilities. Cognitive deficits are known to occur in PSP; however, overt clinical FTD without parkinsonism or supranuclear gaze palsy associated with PSP pathology has rarely been documented. We report an elderly patient with the typical clinical, neuropsychometric, and neuroimaging features of FTD who had autopsy findings most consistent with PSP plus AGD and AD in limbic structures. We suggest that PSP with or without coexisting AD and AGD be included in the differential diagnosis of patients presenting with FTD.
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ranking = 0.82937255073398
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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8/13. Pick's disease with Pick bodies combined with progressive supranuclear palsy without tuft-shaped astrocytes: a clinical, neuroradiologic and pathological study of an autopsied case.

    We report clinical, neuroradiologic features, and neuropathologic findings of a 76-year-old man with coexistent Pick's disease and progressive supranuclear palsy. The patient presented with loss of recent memory, abnormal behavior and change in personality at the age of 60. The symptoms were progressive. Three years later, repetitive or compulsive behavior became prominent. About 9 years after onset, he had difficulty moving and became bedridden because of a fracture of his left leg. His condition gradually deteriorated and he developed mutism and became vegetative. The patient died from pneumonia 16 years after the onset of symptoms. Serial MRI scans showed progressive cortex atrophy, especially in the bilateral frontal and temporal lobes. Macroscopic inspection showed severe atrophy of the whole brain, including cerebrum, brainstem and cerebellum. Microscopic observations showed extensive superficial spongiosis and severe neuronal loss with gliosis in the second and third cortical layers in the frontal, temporal and parietal cortex. There were Pick cells and argyrophilic Pick bodies, which were tau- and ubiquitin-positive in neurons of layers II-III of the above-mentioned cortex. Numerous argyrophilic Pick bodies were observed in the hippocampus, especially in the dentate fascia. In addition, moderate to severe loss of neurons was found with gliosis and a lot of Gallyas/tau-positive globus neurofibrillary tangles in the caudate nucleus, globus pallidus, thalamus, substantia nigra, locus coeruleus and dentate nucleus. Numerous thorned-astrocytes and coiled bodies but no-tuft shaped astrocytes were noted in the basal ganglion, brainstem and cerebellar white matter. In conclusion, these histopathological features were compatible with classical Pick's disease and coexistence with progressive supranuclear palsy without tuft-shaped astrocytes.
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ranking = 1.0158450978439
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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9/13. Neuropathological findings in a case of coexistent progressive supranuclear palsy and Alzheimer's disease.

    A 66-year-old man was investigated for increasing forgetfulness and frequent falls. Following appropriate investigations, the cause was presumed to be senile dementia of the Alzheimer type. He was reviewed one year later and found to have impaired vertical gaze and a hoarse voice. Progressive dementia, nuchal rigidity, anarthria, and sphincteric incontinence developed subsequently. A diagnosis of progressive supranuclear palsy was made. He died four years after the initial assessment. Neuropathological examination revealed changes characteristic of progressive supranuclear palsy, and suggestive of Alzheimer's disease. Globose tangles, granulovacuolar bodies and gliosis were present in the midbrain, the pons, the dentate nucleus of the cerebellum, and the globus pallidus. Senile plaques and occasional neurofibrillary tangles and granulovacuolar bodies were found in the hippocampus, amygdala, and temporal cortex. The coexistence of two disease processes resulting in dementia is discussed.
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ranking = 1.0158450978439
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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10/13. Frequency of Alzheimer's neurofibrillary tangle in the brains of progressive supranuclear palsy, postencephalitic parkinsonism, Alzheimer's disease, senile dementia and non-demented elderly person.

    The frequency and the distribution of Alzheimer's neurofibrillary tangles were examined in those cases of progressive supranuclear palsy (one case), postencephalitic parkinsonism (one case), Alzheimer's disease (two cases), senile dementia (two cases) and non-demented elderly person (three cases). The light microscopic pattern of Alzheimer's neurofibrillary tangles seen in progressive supranuclear palsy was similar to those in postencephalitic parkinsonism, Alzheimer's disease, senile dementia and non-demented elderly person. Some differences in the frequency and the distribution of Alzheimer's neurofibrillary tangles were demonstrated.
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ranking = 1.0158450978439
keywords = progressive supranuclear, supranuclear, supranuclear palsy, palsy
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