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)

A 77-year-old woman underwent right fronto-temporal craniotomy for a right ruptured IC-PC aneurysm (case 1), and a 44-year-old woman underwent right fronto-temporal craniotomy for a right ruptured BA-SCA aneurysm (case 2). They were clipped completely without any troubles during surgery. But postoperative CT scan demonstrated contralateral cerebellar infarction. We recognized left-hand tremor as a neurological deficit caused by cerebellar infarction in case 1. Concerning the mechanism of contralateral cerebellar infarction after pterional craniotomy, we think that it could be; --1) changing of venous blood flow by overdrainage of cerebrospinal fluid, 2) destruction of the bridging vein because of cerebral transformation with rapid decompression, 3) ischemia caused by brain retraction and compression during operation, 4) hypertension or hypoxia during operation, 5) crossed cerebellar diaschosis, and so on. In our 2 cases, we believe that perioperative CSF overdrainage caused the contralateral cerebellar infarction or CCD. To avoid this kind of infarction, we should try to take more protective and careful procedures as well as closer perioperative management.
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PMID:[Contralateral cerebellar infarction after aneurysmal clipping with pterional craniotomy: report of two cases]. 1044 41

A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions.
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PMID:Cerebral arteriovenous malformations and movement disorders. 1046 3

New halogen atom substituted 2,3-benzodiazepine derivatives condensed with an azole ring on the seven membered part of the ring system of type 3 and 4 as well as 5 and 6 were synthesized. It was found that chloro-, dichloro- and bromo-substitutions in the benzene ring and additionally imidazole ring condensation on the diazepine ring can successfully substitute the methylenedioxy group in the well known molecules GYKI 52466 (1) and GYKI 53773 (2) and the 3-acetyl-4-methyl structural feature in 2, respectively, preserving the highly active AMPA antagonist characteristic of the original molecules. From the most active compounds (3b,i) 3b (GYKI 47261) was chosen for detailed investigations. 3b revealed an excellent, broad spectrum anticonvulsant activity against seizures evoked by electroshock and different chemoconvulsive agents indicating a possible antiepileptic efficacy. 3b was found to be highly active in a transient model of focal ischemia predictive of a therapeutic value in human stroke. 3b also reversed the dopamine depleting effect of MPTP and antagonized the oxotremorine induced tremor in mice indicating a potential antiparkinson activity.
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PMID:New non competitive AMPA antagonists. 1100 58

Between 10%-28% of patients who receive the immunosuppressant cyclosporine (CsA) experience some form of neurotoxic adverse event. Both sensorial motoric functions may be adversely affected, and thus patients present with a wide range of neurological and psychiatrical disorders. Mild symptoms are common and include tremor, neuralgia, and peripheral neuropathy. Severe symptoms affect up to 5 % of patients and include psychoses, hallucinations, blindness, seizures, cerebellar ataxia, motoric weakness, or leukoencephalopathy. Tacrolimus is associated with similar neurotoxic adverse events. Neurotoxicity may result in serious complications for some patients, particularly recipients of orthotopic liver transplants. Factors that may promote the development of serious complications include advanced liver failure, hypertension, hypocholesterolemia, elevated CsA or tacrolimus blood levels, hypomagnesemia, and methylprednisolone. Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of CsA; injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. Calcineurin inhibition by CsA and tacrolimus alters sympathetic outflow, which may play a role in the mediation of neurotoxic and hypertensive adverse events. The symptoms of CsA- and tacrolimus-associated neurotoxicity may be reversed in most patients by substantially reducing the dosage of immunosuppressant or discontinuing these drugs. However, some patients have experienced permanent or even fatal neurological damage even after dose reduction or discontinuation. CsA-sparing and tacroli-mus-sparing drug regimens that use the immunosuppressant mycophenolate mofetil, which has no neurotoxic effects, may reduce the incidence and severity of neurotoxic adverse events while maintaining an adequate level of immunoisuppression.
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PMID:Neurotoxicity of calcineurin inhibitors: impact and clinical management. 1105 66

A 78-year-old right-handed man with idiopathic orthostatic hypotension and a history of Hashimoto's thyroiditis presented over 2 years with recurrent, stereotyped attacks of bilateral limb shaking and metamorphopsia, which were precipitated by standing more than 3 or 4 minutes, or walking a few meters. These symptoms would resolve upon squatting or lying down and did not occur spontaneously at rest. He did not lose consciousness during the attacks. Speech, power, and sensation were preserved during these attacks. He had no history of seizures or habit of smoking. On examination, his supine blood pressure was 110/60 mmHg, and 62/27 mmHg on standing, with the pulse rate being 61/min and 66/min, respectively. Although he showed orthostatic hypotension, he did not complain of fainting or lightheadedness on standing alone. Magnetic resonance imaging of the brain revealed mild periventricular white matter changes and multiple small ischemic lesions bilaterally in the cerebral deep white matter. An electroencephalogram (EEG) showed mild, generalized slowing of nonspecific feature. EEG monitoring during a limb shaking episode showed no epileptiform abnormalities. Cerebral angiogram revealed a moderate degree of stenosis of the left internal carotid and a mild degree of stenosis of the right internal carotid, the right vertebral arteries and the left vertebral arteries. A single-photon emission computed tomography (SPECT) showed a moderate compromise of perfusion of the left internal carotid territory. After managing both hypotension and orthostatic hypotension with antihypotensive medication and levothyroxine sodium, his symptoms dramatically disappeared. Thus, we diagnosed that transient hemodynamic insufficiency due to combination of vascular stenosis and hypotension was the cause of these symptoms. Limb shaking is a well-described presentation of carotid artery occlusive disease and is usually unilateral. Bilateral limb shaking is rare and only 2 cases have been reported. Metamorphopsia is also a rare symptom of vertebrobasilar ischemia. We suggest that bilateral limb shaking correlates with hypoperfusion in the anterior border zones and metamorphopsia with that in the posterior border zones of both hemispheres. Hemodynamic TIA should be considered as a cause of movement disorders affecting four limbs.
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PMID:[Orthostatic hypotension with repeated bilateral limb shaking and metamorphopsia. A case of hemodynamic transient ischemic attacks]. 1108 97

A quantitative analysis of two rat syndromes of myoclonus are presented, modeling myoclonic epilepsy and postanoxic myoclonus. Like the human conditions, both of the models benefit therapeutically from drugs that act on the serotonin system. The rat model of myoclonic epilepsy is associated with a profound loss of serotonin throughout the brain (except in the striatum) and is generated by an oscillator that is synchronized around the midline. The rat model of posthypoxic myoclonus does not demonstrate a significant reduction in serotonin in any location of its brain and is generated by a non-oscillating circuit in the medulla. Although some forms of myoclonic epilepsy may benefit from serotonin drugs because they are caused by a decrease in brain serotonin, our data indicate that posthypoxic myoclonus is not caused by a decrease in the serotonergic innervation of any region of the brain. That the raphe nuclei do not degenerate after global brain ischemia was noted by C. David Marsden in a discussion of the histologic findings of three of his human cases of posthypoxic myoclonus (page 117 of reference 10) and led him to question the hypothesis that posthypoxic myoclonus was due to a loss of serotonin neurons. Our data confirm his observation in the rat, but also indicate that density of serotonin fibers and terminals throughout the brain is not reduced by the brain ischemia that produces posthypoxic myoclonus. It remains to be determined whether the physiologic responsiveness of serotonin neurons is altered by global brain ischemia and whether changes in serotonin release or serotonin receptor properties are associated with posthypoxic myoclonus. The stability of the serotonin system in posthypoxic myoclonic rats is remarkable when one considers the wide range of disorders that is produced by the prolonged brain ischemia. The inability of the most severely posthypoxic myoclonic rats to perform 7-Hz tongue protrusions indicates substantial physiologic disruption of brainstem motor function. Moreover, the posthypoxic myoclonic rat suffers from ataxia, seizures, retrograde amnesia, and impaired ability to learn. The wide spectrum of these deficits is sharply constrasted by its apparently intact serotonin system. We have identified the inferior olive as a locus that may generate the rhythmic components of tremor and myoclonus in syndromes that are truly associated with a dramatic loss of brainstem serotonin. Serotonin acts within the inferior olive to constrain its rhythmic firing. Without intraolivary serotonin, olivary neurons are predisposed to oscillate continuously, providing a substrate upon which sustained rhythmic spiking may be superimposed. It is clear that such unconstrained rhythmicity produces synchronized whole-body tremor at 10 Hz (33, 41-43). The effects of serotonin to suppress olivocerebellar rhythmicity are mediated by postsynaptic 5-HT2 receptors that reduce the magnitude of the low-threshold calcium conductance, IT. It is notable that dysregulation of this conductance has been associated with hyper-rhythmic states in the thalamus underlying cognitive disorders ranging from depression to tinnitus (49), indicating a common mechanism underlying a variety of neurologic conditions. The identification of a specific brainstem locus (inferior olive), serotonin receptor 5-HT2, and ionic current IT involved in a form of rhythmic myoclonus may provide multiple clues toward which future pharmacotherapies can be directed.
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PMID:The serotonin hypothesis of myoclonus from the perspective of neuronal rhythmicity. 1196 57

A case of parkinsonian syndrome caused by normal pressure hydrocephalus (NPH) accompanied by cauda equina neurinoma is reported. A 69-year-old woman presented with typical symptoms of parkinsonism, including akinesia, resting and postual tremor, and cog-wheel rigidity. CT scan of the brain revealed dilatation of ventricles, but she did not present dementia and urinary incontinence that are common symptoms in NPH. Her cerebrospinal fluid (CSF) pressure was normal, and her protein level was high at 2,970 mg/dl. An electroencephalogram (EEG) showed diffuse slow waves. An IMP-SPECT images of the brain showed diffuse reduction of radioisotope uptake. Levodopa was not effective in treating her parkinsonism. Removal of the tumor caused dramatic improvement in her parkinsonism. Her CSF protein level was normalized and EEG and SPECT images were improved after the operation. However, ventricular size on brain CT showed no change. It was considered that the causal mechanism of NPH was due to high protein levels in the CSF. The parkinsonism in this case was caused by dysfunction of the circuits linking the cortex, basal ganglia, and thalamus associated with metabolic disorder due to periventricular ischemia. Typical parkinsonism caused by NPH associated with spinal cord tumor has not been reported. When we examine a patient with parkinsonian syndrome caused by NPH, we should check the CSF protein level. And if that level is high, the possibility of spinal cord tumor should be considered.
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PMID:[A case of parkinsonian syndrome caused by normal pressure hydrocephalus accompanied by the cauda equina neurinoma]. 1242 62

Histochemical analysis of NADPH-diaphorase (NADPH-d) activity was performed on segments of the lumbar spinal cord in rabbit after 7 days pretreatment with the Ginkgo biloba extract Tanakan, and 30 min of ischemia followed by 24 h of reperfusion. In sections of the L5 segment of the spinal cord of untreated controls, NADPH-d-positive neurons were identified in the dorsal horns, in the pericentral region and occasionally in the ventral horns. The rabbits were completely paraplegic after 30 min of ischemia and 24 h of reperfusion. High NADPH-d activity was found in the wall of blood vessels in sections of the L5 segment and the numbers of NADPH-d-positive neurons in all sites was moderately elevated. After 7 days of Tanakan pretreatment, 30 min of ischemia and 24 h of reperfusion, the animals did not show paraplegia. Only a light tremor of the hind limbs was observed. NADPH-d activity in blood vessels and neurons was similar to that in controls. In the dorsal horns, NADPH-d positivity in neurons and fibres was increased. Our results indicate that Tanakan can scavenge free radicals produced during ischemia/reperfusion and may reduce reperfusion damage.
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PMID:NADPH-diaphorase activity in the spinal cord after ischemic injury and the effects of pretreatment with Ginkgo biloba extract (EGb 761). 1255 15

The aim of present study was to evaluate the effects of immunophilin ligands (cyclosporin A, FK506 and rapamycin) on the simulated ischemia-induced release of pro-inflammatory cytokines (IL-1beta, TNF-alpha and IL-2) in rat primary astrocyte cell cultures. Astrocytes were exposed to cyclosporin A (CsA) (0.25, 0.5, 1, 10, 20 and 50 microM), FK506 (1, 10, 100, 1000 nM) and rapamycin (10, 100, 500 and 1000 nM). In vitro simulated ischemia significantly increased secretion of IL-1beta, TNF-alpha and IL-2 by astrocyte cultures deprived of microglia (by shaking and incubating with L-leucine methyl ester). CsA (at concentrations of 10-50 microM), FK506 (at all used concentrations) and rapamycin (in dose-dependent manner) significantly attenuated IL-1beta release after 24 h exposure to ischemic conditions. Immunophilin ligands at all used concentrations significantly decreased TNF-alpha levels in culture media after 24 h exposure to ischemia. Moreover, significant decrease in IL-2 secretion at 0.25, 0.5, 1 and 50 microM CsA and FK506 at concentrations of 100 and 1000 nM were observed. The results suggest that immunophilin ligands may regulate glial activity during ischemia by affecting the release of pro-inflammatory cytokines.
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PMID:Immunophilin ligands decrease release of pro-inflammatory cytokines (IL-1beta, TNF-alpha and IL-2 in rat astrocyte cultures exposed to simulated ischemia in vitro. 1504 87

A neuropathic-like pain syndrome was produced in rats following prolonged hindpaw ischemia and reperfusion, creating an animal model of complex regional pain syndrome-Type I (CRPS-I; reflex sympathetic dystrophy) that we call chronic post-ischemia pain (CPIP). The method involves placing a tourniquet (a tight fitting O-ring) on one hindlimb of an anesthetized rat just proximal to the ankle joint for 3 h, and removing it to allow reperfusion prior to termination of the anesthesia. Rats exhibit hyperemia and edema/plasma extravasation of the ischemic hindpaw for a period of 2-4 h after reperfusion. Hyperalgesia to noxious mechanical stimulation (pin prick) and cold (acetone exposure), as well as mechanical allodynia to innocuous mechanical stimulation (von Frey hairs), are evident in the affected hindpaw as early as 8 h after reperfusion, and extend for at least 4 weeks in approximately 70% of the rats. The rats also exhibit spontaneous pain behaviors (hindpaw shaking, licking and favoring), and spread of hyperalgesia/allodynia to the uninjured contralateral hindpaw. Light-microscopic examination of the tibial nerve taken from the region just proximal to the tourniquet reveals no signs of nerve damage. Consistent with the hypothesis that the generation of free radicals may be partly responsible for CRPS-I and CPIP, two free radical scavengers, N-acetyl-L-cysteine (NAC) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl (Tempol), were able to reduce signs of mechanical allodynia in this model.
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PMID:Chronic post-ischemia pain (CPIP): a novel animal model of complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) produced by prolonged hindpaw ischemia and reperfusion in the rat. 1549 78


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