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)

Using a novel in vivo model for cerebral ischemia produced by short-lasting compression of a well-defined brain area of sensorimotor cortex we studied neuroprotective effects of the NMDA NR2B subunit selective antagonist, CP-101,606, in Sprague-Dawley rats. Cortical compression for 30 min produced a consistent and highly reproducible functional impairment, that is paresis of contralateral hind and fore limbs. The neurological deficit was accompanied by marked brain damage in cerebral cortex, hippocampus and thalamus as identified by Fluoro-Jade, a marker of general neuronal cell death. Using a daily performed beam walking test it was shown that untreated animals recovered from their functional impairment within 5-7 days following surgery. Intravenous administration of increasing doses (1, 5, 10, 20 mg/kg) of the NMDA NR2B subunit receptor specific antagonist, CP-101,606, dose-dependently improved the rate of functional recovery and protected against the ischemic brain damage in cerebral cortex, hippocampus, and thalamus as identified 2 days after the ischemic insult. Based upon these results, we conclude that NMDA NR2B receptor subunits represent potential targets to reduce not only the functional deficits, but also neuronal death in cortex and several midbrain regions produced by moderate, transient, cerebral ischemia.
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PMID:The NMDA NR2B subunit-selective receptor antagonist, CP-101,606, enhances the functional recovery the NMDA NR2B subunit-selective receptor and reduces brain damage after cortical compression-induced brain ischemia. 1498 68

Cerebral ischemia was produced by moderate compression for 30 min of a specific brain area in the sensorimotor cortex of Sprague-Dawley rats. On day 1, that is 24 h after the transient sensorimotor compression, ischemia-exposed animals displayed a marked focal neurological deficit documented as impaired beam walking performance. This functional disturbance was mainly due to contralateral fore- and hind-limb paresis. As assessed by daily beam walking tests it was shown that there was a spontaneous recovery of motor functions over a period of five to seven days after the ischemic event. Using histopathological analysis (Nissl staining) we have previously reported that the present experimental paradigm does not produce pannecrosis (tissue cavitation) despite the highly reproducible focal neurological deficit. We now show how staining with fluorescent markers for neuronal death, that is Fluoro-Jade and TUNEL, respectively, identifies regional patterns of selective neuronal death. These observations add further support to the working hypothesis that the brain damage caused by cortical compression-induced ischemia consists of scattered, degenerating neurons in specific brain regions. Postsurgical administration of the AMPA receptor specific antagonist, LY326325 (30 mg/kg; i.p., 70 min after compression), not only improved beam walking performance on day 1 to 3, respectively but also significantly reduced the number of Fluoro-Jade stained neurons on day 5. These results suggest that enhanced AMPA/glutamate receptor activity is at least partially responsible for the ischemia-produced brain damage detected by the fluorescent marker Fluoro-Jade.
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PMID:Fluoro-Jade and TUNEL staining as useful tools to identify ischemic brain damage following moderate extradural compression of sensorimotor cortex. 1536 48

After acute injury of the central nervous system extracellular adenosine 5'-triphosphate (ATP) can reach high concentrations as a result of cell damage and subsequent increase in membrane permeability. Released ATP may act as a toxic agent, which causes cellular degeneration and death, mediated through P2X and P2Y receptors. Mechanisms underlying the various effects of purinoceptor modulators in models of cerebral damage are still uncertain. In the present study the effect of P2 receptor inhibition after permanent middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats was investigated. Rats received either the non-selective P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) or artificial cerebrospinal fluid (ACSF) as control by the intracerebroventricular route. First, these treatments were administered 10 min before MCAO and subsequently twice daily for 1 or 7 days after MCAO. The functional recovery of motor and cognitive deficits was tested at an elevated T-labyrinth. The PPADS-treated group showed a significant reduction of paresis-induced sideslips compared with ACSF-treated animals. Infarct volume was reduced in the PPADS group in comparison with the ACSF group. A significant decrease in intermediately and profoundly injured cells in favour of intact cells in the PPADS group was revealed by quantification of celestine blue/acid fuchsin-stained cells in the peri-infarct area. The data provide further evidence for the involvement of P2 receptors in the pathophysiology of cerebral ischaemia in vivo. The inhibition of P2 receptors at least partially reduces functional and morphological deficits after an acute cerebral ischaemic event.
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PMID:Neuroprotective effects of the P2 receptor antagonist PPADS on focal cerebral ischaemia-induced injury in rats. 1681 87

35-year old patient was admitted to the Department of Neurology, Medical University of Bialystok because of paresis of his left upper limb, progressing over last 10 months and right facial nerve paresis, which started a month ago. During neurological examination he presented with right facial and arm paresis, dysarthric speech, obesity and hypertension. The patient was previously hospitalized in regional hospital, where a lumbar puncture was done revealing normal composition of cerebrospinal fluid. His brain CT revealed bilateral hypodensive areas in frontal and parietal regions of vasogenic character. Doppler ultrasound showed significant slowing of blood flow velocity in both internal carotid arteries. Brain angiography presented with very weak contrast filling of intracranial branches of carotid and vertebral arteries and showed stenosis at the terminal portion of the internal carotid arteries and at the proximal portion of the anterior and middle cerebral arteries. The patient had transthoracic and transesophageal echocardiography, Holter ECG, lab tests (routine lab tests plus coagulation system evaluation with C protein resistance test, anticardiolipne antibodies, antinuclear antibodies, anticytoplasmatic antibodies and thyroid hormones) checked--all tests were within normal range. Based on cerebral angiography and clinical symptoms, after excluding any other reasons of cerebral ischemia, the patient was diagnosed with moyamoya disease and arterial hypertension. The patient was treated pharmacologically with improvement--regression of face assymetry and dysarthria and diminishing of his right arm paresis. The authors of this paper pay attention to moyamoya disease as a rare reason of ischemic strokes in the young in our geographic region. They remind moyamoya disease diagnostic criteria, its etiology and treatment.
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PMID:[Moyamoya disease as a cause of ischemic cerebral stroke in young people]. 1744 85

A 72-year-old man with an obliteration of the brachial artery received a vertical infraclavicular block (VIP) for vascular surgery but 20 h after the operation a complete paresis of the affected extremity occurred. A new vascular obliteration could be excluded. During the diagnostic examination the patient noticed a snapping noise in the cervical column when moving his head and an abrupt recovery of the neurological deficits occurred. The radiological diagnostic provided no indication of cerebral ischemia or lesions of the brachial plexus. An additional diagnostic finding was a profound herniated vertebral disc with compression of the myelon. Fortunately, the neurological deficits completely returned to normal.
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PMID:[Neurological complication after a vertical infraclavicular brachial plexus block. Case report of possible differential diagnoses of a neurological deficit]. 2008 53


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