Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrocephalus associated with aqueductal stenosis is not uncommon after the 2nd year of life. In some patients, stenosis is due to slow-growing periaqueductal tumors that can only be revealed by magnetic resonance examination. We reviewed 31 cases of children with aqueductal stenosis and hydrocephalus diagnosed after the second year of life, and operated on in the Section of Paediatric Neurosurgery of UCSC between 1982 and 1993. Eighteen cases (Group I) had nonneoplastic aqueductal stenosis, while in 13 cases (Group II) it was demonstrated a periaqueductal tumor by NMR. Intracranial hypertension was the most frequent symptom at diagnosis in both groups. In Group I mental and growth retardation were frequent, while cerebellar signs were quite common in Group II. The treatment of choice for hydrocephalus was a V-P shunt. Tumors in Group II were not directly treated, because of their benign behaviour. Subdural hematoma was a relatively common shunt complication in these patients. In 2 cases we observed an atypic complication: patients developed an altered level of consciousness, upsight paresis and distony, without any sign of increased intracranial pressure, or cerebro-spinal fluid infection. One of these patients died; we treated the second patient with L-Dopa (Sinemet 150 mg/die); he progressively improved and had a complete remission of symptoms. Surgical mortality was nil; long-term mortality was 12.5%. In 76.1% of Group II patients we have not observed any tumor growth; 50% of Group I patients has still a complete remission of preoperative symptoms (follow-up 2-12 years).
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PMID:[Late clinical manifestations of hydrocephalus associated with aqueductal stenosis]. 890 May 60

We reported a 74-year-old male case of progressive supranuclear palsy (PSP) who responded to tandospirone citrate, a serotonin receptor (5-HT1A) agonist. The patient manifested postural instability and gait disturbance at 71 years. Additionally, he showed vertical gaze paresis, regidity of the neck, extremities and trunk, bradykinesia and mild cognitive impairment. A brain MRI revealed moderate atrophy of bilateral frontal/temporal lobes and of midbrain tegmentum one year after the onset. The patient had been diagnosed as PSP and treated with L-DOPA. However, L-DOPA therapy showed only transient response for a few months. His symptoms deteriorated gradually, and he became unable to sit, stand up or walk by himself. Tandospirone citrate was additionally administered at 30 mg/day. Rigidity and bradykinesia were remarkably improved in two weeks after the start of tandospirone treatment. He became able to stand up and walk a short distance with supports in four weeks. Cognitive disturbance was also slightly improved. Tandospirone citrate was effective on our case of PSP, especially on rigidity. Our findings suggest that combination of levodopa and tandospirone citrate is a useful therapy for PSP.
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PMID:[A case of progressive supranuclear palsy improved with tandospirone citrate]. 1148 61