Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Substance P-like and somatostatin-like immunoreactivities (SPLI and SLI) were determined in ventricular fluid of patients with chronic pain syndromes and in a comparison group with multiple sclerosis, essential tremor, epilepsy and postanoxic myoclonus. Concentrations of SPLI and SLI were non-significantly decreased by 40% and 33% in chronic pain patients as compared with control patients without pain. There were no differences apparent between subgroups of pain patients (deafferentation pain, neoplasia-induced pain, thalamic pain). High pressure liquid chromatography combined with radioimmunoassay showed marked heterogeneity of SPLI and SLI.
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PMID:Substance P-like immunoreactivity and somatostatin-like immunoreactivity in the ventricular fluid of patients with chronic pain syndromes. 183 80

Monoamine metabolites, biopterin, acetylcholinesterase (AChE) activity, and somatostatin-like immunoreactivity (SLI) were determined in the lumbar cerebrospinal fluid (CSF) of 24 patients with dementia of the Alzheimer type (DAT) without myoclonus or extrapyramidal signs, in 8 patients with DAT and myoclonus, and in 14 age-matched healthy control subjects. In patients with DAT with myoclonus as compared with both DAT patients without myoclonus and control subjects, the concentrations of homovanillic acid and biopterin were significantly decreased. 5-Hydroxyindoleacetic acid was significantly lower in patients with myoclonic DAT as compared to patients with nonmyoclonic DAT, but not significantly lower than in control subjects. CSF AChE and SLI were significantly reduced in patients with DAT with or without myoclonus, as compared with control subjects, but AChE and SLI were not significantly different between dementia groups. These results suggest that DAT patients with myoclonus represent a distinct clinical and neurochemical DAT subtype.
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PMID:Cerebrospinal fluid neurochemistry in the myoclonic subtype of Alzheimer's disease. 246 3

The effect of the somatostatin depleting substance, cysteamine (100 mg/kg, i.p.), on cortical and amygdaloid kindled seizures was investigated. Cysteamine was tested after the establishment of amygdaloid kindling (AM group) and at two different developmental stages of cortical kindling, namely 'focal-cortical' (FC group) and 'cortico-generalized' seizures (CG group). In control, non-kindled, sham operated animals, cysteamine did not induce any spike activity or myoclonus. However, in all kindled groups clustered spike bursting appeared in the cortex within 5-15 min of the injection. The kindled bursting appeared in the cortex within 5-15 min of the injection. The kindled rats exhibited myoclonic jerks at 10 to 30 min after cysteamine injection, which coincided with the cortical spikes, and continued for about 40 min. In contrast, relatively small amounts of spiking were observed in the amygdala and this did not correlate with the myoclonus. At 4 h after cysteamine injection, the motor seizure and afterdischarge durations of the kindled seizure were prolonged in all kindled groups compared with preinjection levels. However, 24 h later the motor seizure duration and the afterdischarge duration were markedly reduced from the preinjection level in the AM and the CG groups and the tonic seizure component was suppressed in the FC group. This inhibitory effect on seizure activity lasted several days and gradually disappeared. These modifying effects of cysteamine were more marked in cortical kindled, than in amygdaloid kindled animals. The results suggest that the cortex is more sensitive to the effect of cysteamine on kindled seizures involves two phases. The first of these effect of cysteamine on kindled seizures involves two phases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myoclonus inducing and seizure modifying effect of cysteamine on cortical and amygdaloid kindled rats. 314 96

In kindled rats, the administration of cysteamine (CSH, 200 mg/kg, i.p.) 4 h prior to a kindled seizure leads to long-term (up to 10 days) inhibition of kindled seizures. CSH (200 mg/kg, i.p.) also induces myoclonic seizures in kindled rats. We suggest that the long-term inhibition of kindled seizures might be the result of the myoclonus, not the somatostatin depletion as previously suggested. Prior administration of the short-acting benzodiazepine midazolam (5 mg/kg, i.p.) eliminated the CSH-induced myoclonus and prevented the long-term inhibition of kindled seizures. These results suggest that the CSH-induced long-term inhibition of kindled seizures is the result of an interaction between the myoclonic seizure and a subsequent kindled seizure.
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PMID:Prevention of cysteamine-induced myoclonus blocks the long-term inhibition of kindled seizures. 360 50