Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 48 year old woman complained of mild weakness and paresthesias of the left limbs, followed 15 days later by episodes of paroxysmal dystonia of the left limbs occurring several times daily over 10 day period. Magnetic resonance imaging (MRI) of head and neck revealed a small area of altered signal in the T2-weighted sequences in the left posterolateral quadrant of the cord at the second cervical vertebra. An MRI scan 18 months later showed no lesion. This is the second case of paroxysmal dystonia with a single MRI lesion in the cervical region on record.
Ital J Neurol Sci 1992 Sep
PMID:Paroxysmal dystonia due to a lesion of the cervical cord: case report. 836 53

Striatal 18F-Dopa uptake and glucose metabolism were studied by positron emission tomography with 6-L-[18F]fluorodopa and [18F]fluorodeoxyglucose, respectively, in 8 patients with idiopathic dystonia. Patients with abnormal findings on the brain CT and MRI were excluded from this study. The clinical diagnosis consisted of torsion dystonia in 3 patients, focal dystonia limited in the arm in 3 and cervical dystonia (spasmodic torticollis) in 2. The 18F-Dopa uptake, corrected by nonspecific retention in the cerebellum, at 120 min post-administration was evaluated, and increased 18F-Dopa uptake in the putamen and in the caudate head was observed in the patients with idiopathic dystonia compared to the normal controls. The striatal glucose metabolism in the patients with idiopathic dystonia showed no difference with the normal controls. These findings suggest that pathogenetic mechanism of idiopathic dystonia involves increased presynaptic activity of the dopaminergic system in the striatum.
J Neurol Sci 1992 Sep
PMID:Increased striatal 18F-dopa uptake and normal glucose metabolism in idiopathic dystonia syndrome. 143 86

A follow-up (1985, 1990, 1991) study revealed in female workers of hydroponic hothouses an increase of the incidence of nervous system diseases depending on the length of work (vegeto-vascular dystonia, angiodystonic syndromes, vegeto-sensory polyneuropathy). It is suggested that the main cause of nervous lesions in these cases was the complex effect of pesticides.
Lik Sprava 1992 Sep
PMID:[Nervous system lesions in the female workers of hydroponic hothouses]. 148 20

In order to assess the clinical utility of trigemino-facial reflexes in lower facial muscles, we studied perioral reflexes to mechanical and electrical stimulation in 13 patients with spasmodic dysphonia and orofacial dyskinesia and in 7 healthy subjects. Mechanical stimulation of the upper lip of all patients and electrical stimulation of the infraorbital nerve of patients with orofacial dyskinesia elicited larger perioral reflexes than in controls. In the majority of patients, hyperexcitable perioral reflexes were accompanied by increased gain of the blink reflex. In 4 patients, however, trigemino-facial reflexes were enhanced selectively in either the perioral muscles or orbicularis oculi. Our findings suggest that the quantitative assessment of perioral reflexes may provide information about the excitability of brainstem interneurons in cranial dystonia that is complementary to blink reflex studies.
Muscle Nerve 1992 Sep
PMID:Perioral reflexes in orofacial dyskinesia and spasmodic dysphonia. 151 10

The X chromosome-linked dystonia-parkinsonism syndrome (XDP) is a severe movement disorder, characterized by both dystonia and parkinsonism. XDP is a genetically homogeneous disorder. Known ancestry of all patients has been traced back to Panay, Philippines, where the disease probably originated from a single mutation (founder effect). The gene locus, DYT3, has been previously assigned to the proximal long arm of the X chromosome (Xq12-q21.1). Using four dinucleotide tandem repeat (DNTR) sequences from Xq13-derived yeast artificial chromosomes (YACs), we further delineate DYT3 within Xq13. Observation of a recombination event between DYT3 and DNTR locus 4548-7, derived from a YAC encompassing locus DXS56, establishes 4548-7 as a distal flanking marker. Assignment of DYT3 to a region in Xq13, flanked by loci 4548-7 and DXS159, is further supported by highly significant allelic association between DYT3 and a total of four DNTR loci--PY2-31, PY5-10, 4548-1, and 4548-7--located in a region defined by PGK1 and DXS56. /phi/ and /delta/ values were 0.82/0.35, 0.78/0.42, 0.65/0.34, and 0.88/0.58 for PY2-31, PY5-10, 4548-1, and 4548-7 at P less than 10(-2), P less than 10(-4), P less than 10(-3), and P less than 10(-6).
Proc Natl Acad Sci U S A 1992 Sep 01
PMID:Delineation of the dystonia-parkinsonism syndrome locus in Xq13. 151 53

The concentration of iron was determined in the serum of 35 patients; 10 with akathisia, 8 with dystonia and 17 without akathisia or dystonia. The patients exhibiting akathisia or dystonia had significantly lower serum concentration of iron than the patients without akathisia or dystonia. Neuroleptic-induced akathisia or dystonia may be facilitated by the low serum iron.
Acta Psychiatr Scand 1991 Sep
PMID:Low serum iron in patients with neuroleptic-induced akathisia and dystonia under antipsychotic drug treatment. 168 97

A nocturnal polygraphic study was performed on 10 patients with cranial dystonia (blepharospasm (BS) and oromandibular dystonia (OMD)). All patients showed impaired sleep efficiency and reduced slow and REM sleep, more marked in subjects with severe dystonia. Abnormal muscular activity decreased progressively with deeper sleep and during the first hours of the night, without disappearing. A disordered hypnic++ pattern and impaired motor control even during sleep are typical features in cranial dystonia.
Electroencephalogr Clin Neurophysiol 1991 Sep
PMID:Sleep and cranial dystonia. 171 8

We re-examined 371 infants with birth weights less than 1501 g at a corrected age of 18-20 months. This sample amounted to 91% of such infants admitted to one of the six neonatal intensive care units in Hamburg between July 1983 and 1986. The neurological examination and a developmental evaluation using the Griffith Developmental Scale revealed higher rates of abnormalities than in most other studies. Fifty-five children (14.8%) suffered from cerebral palsy, classified in 45 as spastic diplegia, in 5 as spastic tetraplegia, in 1 as spastic hemiplegia and in 4 as dystonia. Of the children, 41 (11%) showed minor neurological deviations (hyperactivity, clumsiness, intention tremor). The development of 30 children (8%) without neurological abnormalities was moderately retarded (DQ 80-89, corrected for gestational age [GA]). Nineteen children (5%) were severely retarded (DQ less than 80, corrected for GA) and four children (1.5%) were blind due to retrolental fibroplasia. An isolated delay of speech development was found in 5 children. Seventy children (18.9%) had a major and 87 children (23.5%) a minor handicap.
Eur J Pediatr 1991 Sep
PMID:Development of very low birth weight infants: a regional study of 371 survivors. 172 Mar 87

Ten advanced Parkinson pts (mean 8 years since diagnosis), 6 male and 4 female, 57 to 69 years old, mean 5.9 years on L-Dopa therapy, were put on Madopar HBS to assess the efficacy of the drug. All the pts had levodopa end-of-dose wearing-off type secondary motor fluctuations, 9 of them with dyskinesia and dystonia. Clinical evaluation was performed in basal conditions (pts on standard L-Dopa therapy) 1.6 and 12 months on Madopar HBS therapy. Parkinson signology was quantified with the modified Columbia scale (0 to 44), and motor fluctuations and dyskinesia with a scale 0 to 4 according to intensity and frequency. Pts received mean 1.150 mg. HBS daily dose plus 100 to 200 mg standard L-Dopa added to the early morning dose for a faster effect. At 12 months, a 60% decrease in "off" periods, a 50% decrease in feet dystonia, with no change in orofacial dystonia were observed. Dyskinesia decreased in intensity but not in frequency. There was a 50% decrease of Parkinson signology in "on" periods. In conclusion, Madopar HBS reduces the signology of the long-term Levodopa therapy syndrome and therefore is commendable in pts with advanced Parkinsonism.
Rev Med Chil 1991 Sep
PMID:[Levodopa and controlled release benserazide in the handling of motor fluctuations in Parkinson's disease]. 184 94

Focal dystonia and hemifacial spasms are difficult to treat. Medication and surgery may suppress the dystonic movements but the improvement is not satisfactory. The present article reviews use of Botulinum toxin in cases of focal dystonia. Injections of very small doses of Botulinum A toxin into the affected muscles is a new and efficient therapy for patients with focal dystonia. The toxin acts by inhibiting the release of acetylcholine from the nerve terminal, leading to a localized paralysis of the treated muscle. The effect is temporary and gradually diminishes, but the treatment can be repeated. The use of Botulinum toxin must be applied on the basis of a thorough knowledge of its effect and possible side effects.
Tidsskr Nor Laegeforen 1991 Sep 10
PMID:[Treatment of focal dystonia with botulinum toxin]. 194 48


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