Nō to shinkei = Brain and nerve
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We reported a 62-year-old man of late-onset familial amyloid polyneuropathy type I(transthyretin Met 30-associated familial amyloid polyneuropathy) from Ehime Prefecture. There was no family history related to endemic Japanese foci (Nagano and Kumamoto foci). He demonstrated paraesthesia in the legs and mild autonomic symptoms at the age of 52. ⋯ These symptoms of this patient was slowly progressive. He hoped liver transplantation (brain death or living-related) treatment if possible. Now he became 68-year-old and bed-ridden.
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We report a 72-year-old woman who died of respitory failure. History included onset of diabetes mellitus at the age of 67 years and hypertension at the age of 72 years. The patient had been in good health otherwise until 2000, when she had onset of numbness or tingling of the bilateral lower limbs. ⋯ There were relatively older lesions with demyelinating features in the spinal roots that were particularly dominant in the anterior roots. No demyelinated plaques in the optic chiasm, tracts and nerves, or in the cerebero-cerebellar white matter were found. Systemic pathological diagnosis was lung edema with fresh hemorrhage, pancreatic atrophy consistent with diabetes mellitus and choleductlithiasis.
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We report a 68-year-old right-handed Japanese woman who had a history of progressive difficulty in understanding speech and naming. Neuropsychological examination presented Gogi (word meaning) aphasia and impairment of semantic memory for some common objects. She also presented acalculia and mild constructional impairment. ⋯ Magnetic resonance (MR) imaging showed atrophy in the left temporal lobe and the left parietal lobe. Single photon emission computed tomography (SPECT) scans demonstrated a decrease of regional cerebral blood flow in the atrophic sites and the left frontal lobe. We pointed out that the atrophy of the parietal lobe was atypical in the early stage of cortical degenerative disease presenting Gogi aphasia, in addition to in the light of classification of Fronto-Temporal Lobar Degeneration (FTLD).
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Case Reports
[Generalized muscle weakness mimicking periodic paralysis in a patient with toluene abuse].
A 23-year-old Japanese man was admitted to our hospital because of acute generalized muscle weakness and frequent vomiting. He had been diagnosed as having hypokalemic periodic paralysis, since he had recurrent episodes of transient generalized muscle weakness with a hypokalemia. Laboratory studies have revealed a severe hypokalemic hyperchloremic metabolic acidosis, elevated serum levels of creatine phosphokinase and ammonia. ⋯ With intravenous supplement of potasium, his muscle strength improved. Chronic exposure to toluene induces various neurological disorders, such as encephalopathy, cerebellar and pyramidal signs, peripheral neuropathy. In addition, it should be kept in mind that hypokalemic muscle weakness can be induced by the renal tubular acidosis resulting from chronic toluene exposure, and that it is by no means easy to distinguish hypokalemic periodic paralysis if it occurs recurrently.