Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapeutic efficacy of calcium channel blockers in stroke remains controversial, but previously used agents bind almost exclusively to L-type calcium channels. The newly-discovered N-type calcium channel is specific to neurons, and therapy involving blockade of this site has not been previously attempted. We assessed the neuroprotective effect of omega-conotoxin GVIA (CgTx), a blocker of N-type calcium channels, using both in vitro hypoxic injury to rat cortical neurons and an in vivo model of reversible spinal cord ischemia in the rabbit. In cell cultures, CgTx inhibited hypoxia-induced 45Ca accumulation and neuronal injury minimally, compared to the NMDA antagonist ketamine. In vivo, the duration of spinal cord ischemia which produced permanent paraplegia in 50% of control animals (ET50) was 24.0 +/- 2.6 min. Animals treated 2 h prior to ischemia with 0.5 nmol CgTx in the subarachnoid space had an ET50 of 26.9 +/- 1.8 min (P = 0.36). Animals treated 24 h prior to ischemia (all had persistent systemic tremor) had a ET50 of 28.9 +/- 1.8 min (P = 0.13). We conclude that pharmacologic modulation of the N-type calcium channel does not provide a significant protective effect against neuronal hypoxic-ischemic injury.
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PMID:Treatment with conotoxin, an 'N-type' calcium channel blocker, in neuronal hypoxic-ischemic injury. 208 77

We report the vasocapacitance of the cerebral circulation, as determined by cerebral blood flow reactivity to induced hypercapnia using fluoromethane positron emission tomography, in 32 patients with unilateral anterior circulation transient ischemic attacks. A hemodynamic subset of eight patients, defined based on exertional, positional, orthostatic, or cardiac dysrhythmic induction of symptomatology, is characterized by multiple (median, 4.5 attacks per patient), brief (median, 2.5 minutes per attack), continued episodes of hemispheric ischemia including focal limb shaking. Symptomatic middle cerebral artery flow territories show significantly lower (p less than 0.04) and more asymmetric (p = 0.036) vasodilatory responses in the hemodynamic subset. Although ipsilateral internal carotid artery occlusion is more prevalent in the hemodynamic subset, the features of age, mean arterial blood pressure, carbon dioxide values, serum glucose, serum hematocrit, and number or type of risk factors do not differ significantly between groups. These studies of vasocapacitance help validate clinical criteria for cerebral hemodynamic events with an objective physiologic measurement.
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PMID:Cerebral vasocapacitance and TIAs. 278 50

In order to further investigate the role of proprioceptive input from the legs for the maintenance of upright human posture ischemia was bilaterally applied at the level of the ankle or the thigh. Preservation of efferent innervation was ascertained by measurements of the maximal force of voluntary dorsi- and plantarflexion. Visual stabilization was excluded by eye closure. To test different frequency domains of postural stabilization, subjects were exposed to sudden ramp tilts or to sinusoidal low frequency (0.3 Hz) anteriorposterior displacements of the supporting platform. The results indicate that proprioceptive input from skin, pressure and joint receptors of the foot (ischemia at the ankle) is of minor importance for the compensation of rapid displacements, but plays a significant role when the platform moves at low frequencies. M1 and M2 responses in the stretched triceps surae and the late antagonistic response of the anterior tibial muscle (M3) are preserved with ischemia of the foot. Reversible ischemic paralysis or other (yet unidentified) mechanisms of destabilization must be responsible for the severe decrease of postural stability observed with ischemia at the level of the thigh and sinusoidal platform movements. Complete loss of the proprioceptive input from the legs leads to a pathognomonic 1Hz body tremor both under static and dynamic conditions.
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PMID:The significance of proprioception on postural stabilization as assessed by ischemia. 671 2

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

RheothRx Injection, an aqueous solution of a nonionic block copolymer (poloxamer 188) formulated for intravenous administration, was investigated as an inhibitor of red blood cell (RBC)-induced platelet aggregation at plasma concentrations of 0.05-5mgmL-1. Platelet aggregation was determined by measuring the fall in single platelet counts after mechanical agitation of 2mL aliquots of citrated whole blood in a 37 degrees C shaking waterbath. Inhibition of RBC-induced platelet aggregation of > 95% was observed for poloxamer 188 at a concentration of 1mgmL-1, and 41% inhibition was observed at 0.05mgmL-1. Poloxamer 188 was observed to be a more effective inhibitor of RBC-induced platelet aggregation than 2-chloradenosine (2-ClAd) or phosphoenolpyruvate/pyruvate kinase (PEP/PK). Studies using platelet rich plasma (PRP) showed that platelet aggregation could not be induced by shaking in the absence of RBC, though aggregation was induced by the addition of exogenous adenosine diphosphate (ADP). Poloxamer 188 did not inhibit ADP-induced platelet aggregation. We propose that poloxamer 188 protects RBC from mechanical trauma by non-specific adsorption of copolymer to the RBC surface (via the hydrophobic polyoxypropylene moiety), and that this effect prevents mechanical damage and hence leakage of ADP from RBC. RheothRx Injection has been shown to have value in the treatment of acute ischemic disorders such as myocardial infarction. The observation of significant inhibition of RBC-induced platelet aggregation at clinically relevant concentrations suggests that RheothRx Injection may have antithrombotic properties in vivo, and may therefore have potential not only in acute ischemia but also to prevent thrombosis within vascular prostheses or to prevent rethrombosis after angioplasty or endarterectomy.
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PMID:Inhibition of red blood cell-induced platelet aggregation in whole blood by a nonionic surfactant, poloxamer 188 (RheothRx injection). 750 70

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

We hypothesize that apnea induced by shaking or by shaking combined with impact plays a major role in the pathophysiology of nonaccidental head trauma and accounts for the poor outcome in this subgroup of patients. In a retrospective study of 28 children who suffered significant nonaccidental head injury, 57% had a history of apnea prior to hospitalization, 82% were intubated upon admission, and 71% had early seizures. For further evidence of ischemia and hypoxia, the first recorded blood pressure was < 80 in 50% and the arterial pH < 7.3 in 54%. Seventy-one percent had diffuse brain swelling which is characteristic of cerebral hypoxia and/or ischemia on the first CT scan. None of the children who had clinical evidence of cerebral hypoxia or ischemia had a good outcome. We conclude that trauma-induced apnea causes cerebral hypoxia and/or ischemia which is more fundamental to outcome than the mechanism of injury (shaken vs. shaken with impact), subdural hemorrhage, subarachnoid hemorrhage, diffuse axonal injury, parenchymal shear, or brain contusion.
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PMID:Role of apnea in nonaccidental head injury. 874 99

Arbutamine is a new catecholamine designed for use as a pharmacologic stress agent. This study compared the sensitivity of arbutamine with symptom-limited exercise to induce echocardiographic signs of ischemia. Arbutamine was administered by a computerized closed-loop delivery system that controls the infusion rate of arbutamine toward a predefined rate of heart rate increase and maximum heart rate limit. Beta blockers were stopped > or = 48 hours before both tests. Stress was stopped for intolerable symptoms, or clinical, electrocardiographic or echocardiographic signs of ischemia (new or worsening wall motion abnormality), target heart rate (> or = 85% age predicted maximum heart rate), or plateau of heart rate response. Thirty-seven patients were entered into the study (35 arbutamine and exercise, 1 arbutamine only, 1 exercise only), of which 30 had angiographic evidence of coronary artery disease (> or = 50% lumen diameter narrowing). Rate-pressure product increased significantly in response to both stress modalities (p < 0.001) and was significantly greater with exercise (11,308 +/- 2,443) than with arbutamine (9,486 +/- 2,479, p < 0.001). The time to maximum heart rate was longer during arbutamine stress echocardiography than during exercise testing (17.3 +/- 9.4 versus 9.3 +/- 4.2 minutes, respectively, p < 0.001). There were more patients with interpretable echo data for arbutamine (82%) than for exercise (67%). Sensitivity for recognition of myocardial ischemia was 94% (95% confidence interval 70% to 100%) and 88% (95% confidence interval 62% to 98%), respectively. The most frequent adverse events during arbutamine (n = 36) were dyspnea (5.6%) and tremor (5.6%). Two arbutamine stress tests were discontinued due to arrhythmias: 1 patient had premature atrial and ventricular beats, and the other had premature atrial contractions and atrial fibrillation. Arrhythmias were well tolerated and resolved without sequelae. In conclusion, the sensitivity of arbutamine to induce echocardiographic signs of ischemia was similar to that of exercise despite a lower rate-pressure product. Arbutamine was well tolerated and provides a reliable alternative to exercise echocardiography.
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PMID:Comparison of arbutamine and exercise echocardiography in diagnosing myocardial ischemia. 907 May 46

Sensory abnormalities and changes in spontaneous behavior were examined after a photochemically induced ischemic lesion of the rat sciatic nerve. Male adult rats were anesthetized and the sciatic nerve was exposed. After the intravenous injection of a photosensitizing dye, erythrosin B, the exposed nerve was irradiated just proximal to the nerve trifurcation with light from an argon laser. Three different irradiation times were used, 30 s, 1 and 2 min. In sham-operated rats, the exposed sciatic nerve was irradiated for 2 min without prior injection of the erythrosin B. Rats were tested for the presence of mechanical, cold and heat allodynia or hyperalgesia. All the animals in the 1- and 2-min irradiation groups developed mechanical, cold and heat allodynia after nerve irradiation. A significant dose-dependent effect of laser exposure time was observed for all modalities tested (2 min > 1 min > 30 s = sham). The maximum effects were observed at 3 and 7 days postirradiation and remained present for up to 10 weeks. No significant contralateral effects were observed in any of the groups. In three separate groups of rats (1, 2 and 4 min of laser exposure), the presence of possible signs of spontaneous pain (paw shaking, paw elevation and freezing behavior) was tested. A significant and exposure time-dependent increase in spontaneous paw elevation and paw shaking was observed which was maximal at week 1, but resolved at 4 weeks (4 min > 2 min > 1 min > sham). In addition, animals in all ischemic groups, but not in the sham group, showed a significant increase in freezing behavior up to 4 weeks after nerve irradiation. Light microscopic evaluation of nerves removed 7 days post-irradiation, i.e. when maximal allodynia was observed, showed clear evidence of demyelination of large myelinated fibers. These data indicate that photochemically-induced peripheral nerve ischemia is associated with abnormal pain-related behaviors, including mechanical, thermal and cold allodynia and signs of spontaneous pain. The incidence and severity of the behavioral changes are clearly dependent on the exposure time and are probably due to, at least in part, a demyelinaton. These results partly confirm previous data using a similar technique and suggest that this may represent a new animal model for peripheral neuropathy of ischemic origin. The advantages of the present model are its good reproducibility and the fact that the nerve injury can be easily quantified and graded.
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PMID:Photochemically-induced ischemia of the rat sciatic nerve produces a dose-dependent and highly reproducible mechanical, heat and cold allodynia, and signs of spontaneous pain. 969 58


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