Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 69-year-old woman was admitted due to gradual progression of daytime sleepiness and forgetfulness over a period of approximately 1 month. Bradycardia and hypothermia were observed on admission, and neurological examination revealed memory disturbance, mild dysarthria, and bradykinesia. Fluid-attenuated inversion recovery (FLAIR) images of the brain magnetic resonance imaging (MRI) indicated signal hyperintensity in the region bordering the lateral and third ventricles. Serum anti-aquaporin 4 (AQP4) antibody was detected. The patient had no history or findings of optic neuritis or myelitis, and she was diagnosed as anti-AQP4 antibody-associated disorder. Diencephalon lesion and/or symptoms are rarely observed at the onset of neuromyelitis optica. Differential diagnosis of this disorder is necessary in cases manifesting diencephalon symptoms or involving lesions bordering the third ventricle without evidence of previous optic neuritis or myelitis.
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PMID:[Hypothermia and memory disturbance as initial manifestations associated with lesions of the diencephalon in a patient with anti-aquaporin 4 antibody-associated disorder: a case report]. 2514 37

A 52-year old woman first noted dysphagia four months before admission followed by dysarthria two months later. She then developed weakness of all limbs and became unable to walk. All these symptoms, associated with tongue atrophy, slowly progressed, leading to the initial clinical impression of a motor neuron disease, although her nerve conduction study and electromyography showed no abnormalities. Her brain MRI with T2 weighted/diffusion weighted image (DWI)/fluid attenuated inversion recovery (FLAIR) revealed a high signal lesion located at dorsal medulla oblongata. She proved positive for anti-aquaporin 4 antibody, which confirmed the diagnosis of neuromyelitis optica spectrum disorders (NMOSD). We conclude that NMOSD may initially present with progressive bulbar palsy and pyramidal tract disorder over a few months, mimicking a motor neuron disease. Awareness of this atypical presentation helps establish an early diagnosis of this treatable entity.
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PMID:[A case of neuromyelitis optica spectrum disorders, with slowly progressive bulbar palsy, mimicking a motor neuron disease]. 3081 45

We herein report the case of a 54-year-old man who abused toluene for 25 years and gradually developed gait disturbance. Neurological findings showed mild cognitive impairment, hearing impairment, dysarthria, marked hyperreflexia of the limbs, spastic paraplegia, slight impairment of deep sensation, and urinary disturbance; however, there was no muscular atrophy. Serum antibodies against human T-lymphocytic virus 1 and aquaporin 4 were negative. Biochemical analysis did not show an increase in very-long-chain fatty acids. The cerebrospinal fluid was normal for the cell number and protein level but positive for oligoclonal IgG band, with a mildly increased IgG index. Brain MRI showed marked high intensity in the bilateral periventricular, deep cerebral and subcortical white matter as well as atrophy of the cerebrum, cerebellum and brainstem, and thinning of the corpus callosum. Spinal MRI showed marked atrophy of the lower cervical spinal cord, thoracic spinal cord, and conus medullaris. Spinal cord lesions are extremely rare in chronic toluene intoxications, and there are no reports of spinal cord atrophy. Lateral and ventral columns of the spinal cord are responsible for pyramidal tract signs, and insidious ongoing inflammation related to chronic toluene intoxication in the central nervous system is predicted to underlie the pathogenesis.
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PMID:[Generalized spinal cord atrophy and oligoclonal IgG band in the cerebrospinal fluid due to chronic toluene intoxication: a case report]. 3223 42