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

A 66-year-old female suffering from HTLV-1 associated myelopathy (HAM) for more than 30 years was hospitalized because of memorial impairment, deafness, dysarthria, dysphagia, and complete paraplegia. She first noticed stiffness and weakness of the right leg at 35 years of age. Gait disturbance was slowly progressed and complete paraplegia developed 18 years later. Neurological examinations on admission revealed that she was bedridden with decubitus, mental deterioration (pre-dementia of subcortical type), bilateral optic nerve atrophy, severe sensory-neural deafness, dysarthria, complete paraplegia, and marked neurogenic bladder. Laboratory data showed mild normocytic anemia and moderate diabetes mellitus. Anti-HTLV-1 antibody titers in serum and CSF were 78,192X and 1,024X, respectively (PA method). Serum levels of soluble IL-2 receptor was markedly elevated (2,200 U/ml). Peripheral blood lymphocytes showed spontaneous proliferation when cultured for 5 days (3H-thymidine uptake; 45,285 cpm/5 X 10(4) cells). MRI examinations of the spinal cord disclosed a predominant atrophy of lower thoracic cord without any compressive lesions. Brain MRI showed diffuse high intensity lesions of the periventricular area on T2 weighted images. Such abnormalities were predominantly found in fronto-parietal region and were quite similar to those of leuko-ariosis. Single photon emission CT using 123I-iodoamphetamine showed hypoperfusion of cerebral white matter on delayed image. It has been reported that intellectual impairment and brain atrophy are not usually seen in HAM patients. The present case, however, shows that such abnormalities of the central nervous system could occur in HAM patients with a long duration of illness.
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PMID:[A case of HTLV-1 associated myelopathy progressed in course over 30 years]. 189 70

Leucoencephalopathy caused by antineoplastic drugs was reviewed. This leucoencephalopathy primarily involved the cerebral white matter, caused by various anti-neoplastic drugs such as carmofur, fluorouracil, cytarabine, cisplatin, tegafur, methotrexate, tacrolimus, and interferon alfa. The interval between the time of drug administration and the onset of leucoencephalopathy varies among the drugs, depending on the kind of the drugs, their daily dosage, duration of the administration, and presence or absence of other combined treatments. This review primarily focused on carmofur-induced leucoencephaloathy, since this drug is developed and widely used in Japan against the carcinomas of the gastrointestinal tract and breast, and has caused leucoencephalopathy at the estimated incidence of 0.026% since 1982. The common symptoms of carmofur leucoencephalopaty were gait disturbance followed by dysarthria and dementia in that order of frequency, leading to coma in the advanced stage of the encephalopathy. EEG is the most sensitive test, but cranial CT and MRI tests are more specific, and MRI T2-weighted imaging is the most useful test, revealing symmetrical bilateral diffuse high intensity areas in the cerebral white matter. Intravenous high dose MTX has a strong tendency to cause leucoencephalopathy when combined with cranial radiation therapy. Reversible posterior leucoencephalopathy proposed by Hinchey et al. in 1996 has also been caused by some antineoplastic drugs. The most important treatment of the leucoencephalopathy caused by antineoplastic drugs is the immediate cessation of the causative drugs, followed by supportive therapy which included treatment to various complications and prevention of the decubitus and contractures of the joints.
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PMID:[Leukoencephalopathy caused by antineoplastic drugs]. 1830 61

A 66-year-old man with hypertension presented with complaints of excessive daytime sleepiness (Epworth Sleepiness Score 14/24), dyspnea upon exertion, and episodes of noninjurious dream-enacting behavior. He reported tongue biting when sleeping in the right lateral decubitus position. Medications included atenolol 12.5 mg, lovastatin 20 mg, doxazosin 2 mg, amlodipine 5 mg, isosorbide mononitrate 60 mg, and aspirin 81 mg. He denied headaches, visual changes, dysarthria, dysphagia, or localized weakness. He denied use of alcohol, tobacco, or drugs.
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PMID:Positional central apnea and vascular medullary compression. 2313 63

A professional 55-year-old female experienced diver, who surfaced after the second dive, had a lucid interval before dropping Glasgow Coma Scale (GCS) to 3/15. She was admitted to intensive care unit and commenced on hyperbaric oxygen therapy. Her initial computed tomography of the head was normal but her magnetic resonance imaging of the brain at 48 hours showed extensive bilateral cortical watershed territory infarcts. She developed acute respiratory distress syndrome which resolved within a few days. Her GCS gradually improved from 3/15 to 6/15, was repatriated to United Kingdom after about 2 weeks of the insult and admitted to a tertiary care hospital where she had myoclonic seizures and was started on anti-epileptics. Then she was transferred to the Rehabilitation Medicine Ward of Leicester General Hospital, with GCS 14/15 with poor sitting balance, for her management and rehabilitation. She had weakness of right upper and lower limbs, dysarthria, neuropathic bilateral shoulder pains, pressure ulcer of left heel, bladder and bowel incontinence and cognitive issues. She improved to have significant neurological recovery within next 3 months, became ambulant independently and bladder and bowel continent. Her Barthel index (from 4 to 17), Montreal Cognitive Assessment Test, Adembrook Cognitive Examination and Berg Balance scale (from 33/56 to 44/56) improved significantly. Early diagnosis, treatment and rehabilitation can have a significant impact on the recovery of decompression illness.
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PMID:Decompression illness type II with stroke: challenging situation in acute neurorehabilitation. 3260 54

Facial lymphedema secondary to treatment by a neoplastic process is a rare and disabling pathology, causing functional and aesthetic alterations. A case report of facial and labial lymphedema describing the functional repercussion and aesthetic defect. We present a 61-years-old female patient suffered a tongue neoplasia and bilateral cervical lymphadenectomy in 2015. After several treatments, including diverse surgical interventions and adjuvant radiotherapy, developed facial and labial lymphedema. The patient was sent to our Rehabilitation Department complaining about swelling of the face and lips, dysphagia, sialorrhea, xerostomia, dysarthria and decubitus in lower lip by labia protusion. Due to the functional repercussion that it caused in the patient, rehabilitating physical treatment was planned with manual lymph drainage, facial silicone orthosis and lymphatic taping. The patient improved both subjectively as well as objectively in terms of hardness, volume and slight improvement of lip lymphedema.
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PMID:[Facial and labial lymphedema after oncological treatment. A propos of clinical case]. 3274 72