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1/4. arm levitation in progressive supranuclear palsy.

    Spontaneous arm levitation (SAL) is well-recognized in cortical-basal ganglionic degeneration, but not in other neurodegenerative diseases. We report six cases of progressive supranuclear palsy (PSP) with SAL. Pathologic examination in four revealed the classic features of PSP with additional areas of focal cortical degeneration. We conclude that SAL can occur in PSP and its occurrence may be a marker of cortical degeneration.
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2/4. A differential diagnosis of Parkinsonism.

    Parkinsonism is a common, age-related syndrome, characterized by resting tremor, bradykinesias, rigidity, and postural reflex impairment. Though Parkinsonism is not very difficult to recognize, all Parkinsonism is not created equal and it is important to distinguish among the most common identifiable syndromes. This review discusses the key clinical features of these various syndromes, including Parkinson's disease, progressive supranuclear palsy, multiple system atrophy, corticobasal ganglionic degeneration, lewy body disease, vascular Parkinsonism, and Parkinsonism with no clear etiology. Symptomatology and diagnostic testing for each syndrome are discussed and 4 typical cases are analyzed to offer clinicians guidance in making a differential diagnosis for Parkinsonism.
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3/4. 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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4/4. Cortical degeneration in progressive supranuclear palsy. A comparison with cortical-basal ganglionic degeneration.

    We report 3 patients with progressive supranuclear palsy (PSP) who developed limb apraxia, focal dystonia, and arm levitation late in the course of the disease. Neuropathological examination revealed cortical degeneration in addition to the characteristic pathological findings of PSP. Semiquantitative comparative histological and immunohistological studies of the neocortex of these patients as well as 5 cases of classical PSP and 4 cases of cortical-basal ganglionic degeneration (CBGD) revealed a distinctive form of cortical degeneration in PSP. The cortical degeneration was often circumscribed and confined to premotor and motor cortex. It was characterized by neuronal loss and gliosis. Swollen neurons were only rarely observed in neocortex of PSP cases in contrast with CBGD, where they were abundant. Neuronal and glial tau as well as tau immunoreactive threads were seen in both PSP and CBGD, but were more abundant in CBGD. The appearance of tau reactive astrocytes also differed in both disorders; tufted astrocytes were seen exclusively in PSP, while typical annular astrocytic plaques were confined to CBGD. These observations indicate that cortical degeneration occurs in PSP and may be associated with atypical clinical manifestations that lead to diagnostic difficulties.
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