Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients suffering from presenile dementia and two patients suffering from senile dementia were treated with phthalazinol. A limited but definite improvement in attentiveness, vocabulary reception and psychologic attainment and also a limited but definite improvement in range of motion, gait and endurance were noted shortly after the treatment with phthalazinol and the progression of their dementia seemed to be temporarily retarded by phthalazinol. Seven patients suffering from parenchymatous cerebellar degeneration (late cortico-cerebellar atrophy) and four patients suffering from olivopontocerebellar atrophy were treated with phthalazinol. A relatively rapid, limited and sustained improvement of cerebellar functions, including those of speaking, writing and walking, was noted in almost all patients. Also, rigidity, akinetic tendency and abnormal posture seen in olivopontocerebellar atrophy fairly well responded to the treatment. Dysphagia, disturbance of micturition, and hypersecretion of saliva have also rapidly and completely disappeared in all cases. The cases with a long history responded relatively poorly, but the cases with a relatively short history responded quite strikingly to the therapy. No side effects were noted.
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PMID:Treatment of senile dementia and cerebellar disorders with phthalazinol. Cyclic AMP-increasing agent, phthalazinol, in therapeutic trials in hitherto incurable morbid conditions (I). 18 66

An autosomal dominant presenile dementia affecting 39 individuals in a seven-generation, 383-member pedigree has been studied at Indiana University. In the affected members of this family, clinical symptoms occurred early in life, with an average age at onset of 48.8 years. The presenting clinical features include disequilibrium, neck stiffness, dysphagia, and memory loss. As the disease progresses, further cognitive decline, superior-gaze palsy, and dystaxia also are observed. The average duration from onset of symptoms to death is approximately 10 years. Neuropathologic studies of nine affected individuals showed neuronal loss in several areas of the CNS, as well as argentophilic tau-immunopositive inclusions in neurons and in oligodendroglia. A limited genomic screen by use of DNA samples from 28 family members localized the gene for this disorder to a 3-cM region on chromosome 17, between the markers THRA1 and D17S791. The gene for tau also was analyzed, through samples from the family.
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PMID:Familial multiple-system tauopathy with presenile dementia is localized to chromosome 17. 934 89

A 58-year-old man developed dysarthria followed by a personality change. Subsequently, he developed muscle weakness and atrophy of the left upper and lower limbs, leading to repeated falls when he tried to walk. Neurological examination showed mild dementia, dysarthria, dysphagia, atrophy and fasciculation of the tongue, and muscle weakness and atrophy of all four extremities, particularly on the left side. Deep tendon reflexes were slightly diminished in the upper limbs and slightly exaggerated in the lower limbs without Babinski's sign. Cranial MRI revealed marked atrophy of the medial portions of the temporal lobes, more striking on the right, and T2-weighted imaging revealed symmetrical high-intensity signals from the posterior limbs of the internal capsules to the cerebral peduncles in the midbrain, extending to the pons on the left. 125I-IMP SPECT showed diffuse reduction of RI uptake in the frontal and temporal lobes, which was more marked on the right. We diagnosed this is a case of motor neuron disease with presenile dementia, which Mitsuyama et al. proposed as a new clinical entity, as well as a rare example of bilateral degeneration of the pyramidal tract on cranial MRI.
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PMID:[A case of motor neuron disease with presenile dementia showing bilateral degeneration of the pyramidal tract on cranial MRI]. 1143 70