akinetic mutism/protease

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An autopsied case of V180I Creutzfeldt-Jakob disease presenting with panencephalopathic-type pathology and a characteristic prion protein type.

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A 73-year-old Japanese woman showed slowly progressive aphasia, apraxia and dementia. She had no family history of prion disease or dementia. One year later she showed parkinsonism and corticobasal degeneration was initially suspected. On MRI, the left temporal neocortex seemed swollen on

[A case of MM1+2 Creutzfeldt-Jakob disease with a longitudinal study of EEG and MRI].

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We report a case of definite MM1 + 2 sporadic Creutzfeldt-Jakob disease (sCJD). A 66-year-old woman was admitted to our hospital with memory disturbance and disorientation for three months. On admission she presented a progressive cognitive insufficiency. Electroencephalography (EEG) revealed a

Familial Creutzfeldt-Jakob disease with an R208H-129V haplotype and Kuru plaques.

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OBJECTIVE To report the clinical and neuropathological features in the first patient seen, to our knowledge, with familial Creutzfeldt-Jakob disease and an R208H mutation associated with a Val/Val homozygosity at codon 129 in the prion protein gene (PRNP) and a type 2 protease-resistant prion

An autopsy case of MM2-cortical + thalamic-type sporadic Creutzfeldt-Jakob disease.

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A 59-year-old Japanese man presented with depressed mood, insomnia, abnormal behavior and dementia. Visual and gait disturbance with ataxia also developed. Diffusion-weighted MRI showed widespread regions of hyperintensity in the bilateral cerebral cortex. The patient died at 62 after a progressive

MM1-type sporadic Creutzfeldt-Jakob disease with unusually prolonged disease duration presenting with panencephalopathic-type pathology.

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We report an autopsy case of MM1-type sporadic Creutzfeldt-Jakob disease (sCJD) with an unusually prolonged disease duration of 58 months. The initial symptom was progressive mental disorder followed by advanced cognitive impairment. Clinical progression was generally slow; myoclonus appeared at 17

Creutzfeldt-Jakob disease with an M232R substitution: report of a patient showing slowly progressive disease with abundant plaque-like PrP deposits in the cerebellum.

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Patients with genetic Creutzfeldt-Jakob disease in which arginine is substituted for methionine at codon 232 (M232R) of the prion protein gene (CJD232) have been described in Japan, and a recent study has revealed the presence of two clinical phenotypes: a rapidly progressive type (rapid-type) and a

An autopsied case of Creutzfeldt-Jakob disease with mutation in the prion protein gene codon 232 and type 1+2 prion protein.

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A 68-year-old Japanese man gradually showed abnormal behavior and gait disturbance with bradykinesia. Slowly progressive dementia, including memory disturbance and disorientation, was also observed. Cerebral cortical hyperintensity on diffusion-weighted MRI was observed 6 months after onset. The

An autopsied case of MM1 + MM2-cortical with thalamic-type sporadic Creutzfeldt-Jakob disease presenting with hyperintensities on diffusion-weighted MRI before clinical onset.

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A 78-year-old Japanese man presented with rapidly progressive dementia and gait disturbances. Eight months before the onset of clinical symptoms, diffusion-weighted magnetic resonance imaging (DWI) demonstrated hyperintensities in the right temporal, right parietal and left medial occipital

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