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)

The potential causes of neurogenic oropharyngeal dysphagia in cases in which the underlying neurologic disorder is not readily apparent are discussed. The most common basis for unexplained neurogenic dysphagia may be cerebrovascular disease in the form of either confluent periventricular infarcts or small, discrete brainstem stroke, which may be invisible by magnetic resonance imaging. The diagnosis of occult stroke causing pharyngeal dysphagia should not be overlooked, because this diagnosis carries important treatment implications. Motor neuron disease producing bulbar palsy, pseudobulbar palsy, or a combination of the two can present as gradually progressive dysphagia and dysarthria with little if any limb involvement. Myopathies, especially polymyositis, and myasthenia gravis are potentially treatable disorders that must be considered. A variety of medications may cause or exacerbate neurogenic dysphagia. Psychiatric disorders can masquerade as swallowing apraxia. The basis for unexplained neurogenic dysphagia can best be elucidated by methodical evaluation including careful history, neurologic examination, videofluoroscopy of swallowing, blood studies (CBC, chemistry panel, creatine kinase, B12, thyroid screening, and anti-acetylcholine receptor antibodies), electromyography, and magnetic resonance imaging (MRI) of the brain, plus additional procedures such as lumbar puncture and muscle biopsy as indicated. Little is known about aging and neurogenic dysphagia, specifically the relative contributions of natural age-related changes in the oropharynx and of diseases of the elderly, including periventricular MRI abnormalities, in producing dysphagia symptoms and videofluoroscopic abnormalities in this population.
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PMID:Neurogenic dysphagia: what is the cause when the cause is not obvious? 780 24

The patient was a 72-year-old man who had a history of subtotal gastrectomy for gastric ulcer at age of 37 years. He had no familial history of hereditary disorders. In 1980 he noticed mild ataxic gait which exaggerated while he closed eyes. The symptoms increased gradually, and four years later he noticed hypoesthesia of his soles. In 1983 he was admitted to the National Center Hospital for Mental, Nervous and Muscular Disorders for the first time. Neurological examination revealed dysarthria, ataxic gait, disturbance of coordination to a slight degree, and muscle strength of the upper and lower limbs were in normal range. Mild hypoesthesia of pain and temperature sensation, and marked decrease of deep sensation and vibration of the lower extremities were demonstrated. Romberg sign was positive. EMG studies revealed low amplitude of action potential and normal motor nerve conduction velocity. Biopsy of the sural nerve showed marked decrease of both large and small myelinated fibers. In 1998 he was admitted second time for the further examination. Laboratory examination including routine blood examination, blood chemistry including CRP, TPHA, vitamin B1, B2, B12, A, E, K, hexosaminidase A in leucocyte were in normal range. CSF was normal. Genetic studies including SCA 1, 2, 3, 6, DRPLA, CMT1A, CMTX 1 were all negative. MCV of lower limbs was in normal range, though SCV was not evoked in the upper and lower limbs. MRI studies showed mild atrophy of the bilateral lobulus of the cerebellum which was not so much changed in the last 5 years. The clinical symptoms revealed dominant posterior column disturbance, ataxia and sensory neuropathy. These combination was not described in the previous literature, and this case may be a new variant of the spinocerebellar degeneration.
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PMID:[A case with posterior column ataxia associated with cerebellar ataxia and sensory neuropathy]. 1061 59

Chronic ethyl alcohol abuse is associated with different types of neurological involvement. We report a 51-year-old woman with alcoholic encephalopathy, neuropathy and autonomic dysfunction. After the alcohol abuse of about thirty years, gait disturbance, dysphagia and dysarthria progressively worsened. We thought that the disease was caused by poor nutrition due to chronic alcohol abuse and vitamin B1, B12 deficiency. Her neurological symptoms and signs improved after discontinuation of alcohol and nutritional treatment.
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PMID:[A case of alcoholic multiple nervous system degeneration]. 1079 21

Severe methylenetetrahydrofolate reductase deficiency is an autosomal recessive metabolic disorder of folate metabolism causing elevated plasma homocysteine levels and homocystinuria (MIM 236250). A developmentally delayed 10-year-old girl presented with symptoms of progressive ataxia, dysarthria, tremor, mental status changes, and white-matter changes on magnetic resonance imaging. These changes occurred during a 3- to 4-month time period, with an acceleration of symptoms during 2 to 3 weeks. The patient was found to have extremely high serum homocysteine and low-normal serum methionine. She received treatment with vitamin B12, folate, betaine, multivitamins, and aspirin, with subsequent improvement of her symptoms and reduction in her serum homocysteine level. This case emphasizes the need to include homocystinuria in the differential diagnosis of children with acute/subacute neurological changes, particularly in the context of developmental delay.
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PMID:Severe methylenetetrahydrofolate reductase (MTHFR) deficiency: a case report of nonclassical homocystinuria. 1865 82

We report a rare case of multiple cranial nerve palsy associated with pregnancy, the cause of which remained to be clarified despite of extensive inspections. A 28-year-old woman with type 1 diabetes on insulin therapy developed left oculomotor nerve palsy in the fourth month of pregnancy. Her symptoms improved after one month's administration of vitamins B1 and B12. Numbness appeared in the left side of the face in the 8th month of pregnancy, and then moved to the right side in two weeks. Dysarthria and dysphagia occurred one month later. Bulbar symptoms were worsened, and she became unable to eat or drink. Neurological examination revealed disturbance of sensation in the right side of the face, soft palate paresis, and bilateral atrophy and fasciculation of the tongue. Extensive laboratory examinations including immunological and endocrinological studies, cerebrospinal fluid examination and brain magnetic resonance imaging were unremarkable. These symptoms remitted spontaneously after delivery, and the methylprednisolone pulse therapy accelerated the improvement. Neurological examination done one year after delivery showed complete recovery of the symptoms except for persistent tongue atrophy.
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PMID:[Recurrent multiple cranial nerve palsy in a gravida with type 1 diabetes, that remitted after delivery and with steroid therapy]. 1893 78