Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 6-year-old boy developed a flaccid hemiplegia and dysarthria following several transient episodes of nausea, vomiting, and ataxia. An anomly of the dens was discovered, permitting subluxation of C-1 on C-2. A segmental occlusion of the right vertebral artery and an aneurysm of the left vertebral artery were found at the C-2 level, as well as a thromboembolic occlusion of the rostral end of the basilar artery. It appeared that the repeated cervical subluxation produced occlusive, aneurysmal, and embolic vascular disease, and that clinical symptoms were the result of ischemia in the territory perfused by the vertebrobasilar arteries.
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PMID:Occlusive vertebrobasilar artery disease associated with cervical spine anomaly. 113 Mar 56

BMY-14802, a selective sigma ligand currently under investigation as an atypical antipsychotic agent, was tested for potential anti-ischemic activity. BMY-14802 (10, 30 and 50 mg/kg) did not produce any stereotyped behavior, ataxia or seizures. When gerbils were pretreated with 10, 30 or 50 mg/kg of BMY-14802 30 min prior to bilateral occlusion of carotid arteries for 5 min, BMY-14802 significantly protected against ischemia-induced neuronal loss in the hippocampus. Thus, BMY-14802 may also be useful as an anti-ischemic agent that does not produce psychotomimetic effects.
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PMID:BMY-14802 protects against ischemia-induced neuronal damage in the gerbil. 151 77

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
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PMID:Transient ischemic attack-related syncope. 204 43

We examined the effect of dilazep dihydrochloride (dilazep) on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats (SHRs). Ataxia and loss of the righting reflex were noted in some SHR after 4 hr occlusion of the bilateral common carotid arteries; and 11 of 15 animals died within 72 hr after reperfusion. One hour after reperfusion, the cerebral water content increased significantly. The chemiluminescence value in the brain homogenate increased slightly during occlusion; and following reperfusion, there was a transient but marked further increase, indicating the acceleration of lipid peroxidation that resulted from free radical reactions. The i.v. infusion of dilazep (0.3-3 mg/kg/hr for 4 hr) during occlusion dose-dependently reduced the appearances of neurological symptoms and mortality during occlusion and after reperfusion. The increase in cerebral water content and chemiluminescence value were clearly prevented by dilazep (3 mg/kg/hr). It is concluded that dilazep possesses the ability to prevent the appearances of neurological symptoms and brain edema induced by ischemia and reperfusion. The suppression of lipid peroxidation may be involved in the mechanism of the preventive effect of dilazep on cerebral injury.
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PMID:[Effect of dilazep dihydrochloride on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats]. 235 33

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

Three patients with transient cerebellar dysfunction following head injury are described. Acute cerebellar signs, such as ataxia, nystagmus, and dysarthria, occurred just after trauma and resolved gradually, disappearing in every patient. Cerebrospinal fluid and computed tomography examinations were normal but magnetic resonance imaging and single photon emission computed tomography revealed cerebellar lesions. These findings distinguish cerebellar concussion from cerebellar contusion and suggest that the synergistic effect of trauma and ischemia may be the pathophysiological basis of this unusual syndrome.
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PMID:Cerebellar concussion--three case reports. 752 52

We report the clinical findings and stroke mechanisms of 63 patients with cerebellar infarcts. We divided the intracranial vertebrobasilar circulation into the proximal territory (P), fed by the intracranial vertebral arteries and their branches; the middle territory (M), fed by the proximal and middle basilar artery and its branches; and the distal territory (D), fed by the rostral basilar artery and its branches. Cerebellar infarcts were classified by vascular territories P, M, D, P&D, and middle-plus (P&M, M&D, and P&M&D). Patients with P infarcts (11 patients) frequently had vertigo, gait instability, limb ataxia, and headache, whereas patients with D infarcts (15 patients) most often had limb ataxia, gait instability, and dysarthria. Patients with P&D infarcts (17 patients) had signs and symptoms of both groups combined. Infarcts in which the middle territory was involved, either alone (three patients) or combined with other territories (17 patients) were dominated by brainstem signs and symptoms. The predominant stroke mechanisms in the P, D, and P&D groups were embolic due to intra-arterial or cardiac embolism. When the M territory was involved, either alone or with P, D, or P&D territories, stroke mechanisms were more varied, and there was often large-artery occlusion with hemodynamic ischemia.
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PMID:Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. 805 34

A nuclear oculomotor nerve syndrome is rarely caused by mesencephalic lesions. We describe 5 patients, 4 with unilateral syndrome (3 due to ischemia and 1 to mesencephalic hemorrhage) and 1 with bilateral nuclear ischemia of the third cranial nerve. These patients represent 0.2% of those admitted with cerebral vascular pathology over the last 12 years. Symptoms are consistent with descriptions of the anatomic organization of this nucleus, with peripheral paralysis of the contralateral superior rectus and possible bilateral involvement of the eyelid elevator and the pupillary constrictor muscles. A noteworthy symptom seen in these cases is supranuclear paralysis of the upward gaze on the side of the lesion, with ocular elevation achieved in response to oculocephalic stimuli in 2 cases and with Bell's synkinesis in 4. We analyze the nature of 22 published cases of unilateral nuclear damage and of 14 published cases of bilateral nuclear damage. Unilateral damage may or may not lead to ipsilateral pupillary involvement, uni- or bilateral eyelid ptosis, contralateral ocular hypotropia, and possible horizontal paresis of the contralateral gaze. Associated deficits are hemiparesis or crossed hemiataxia. Unresponsive pupils and bilateral ptosis associated with tetraparesis, bilateral ataxia and altered states of consciousness were seen with bilateral nuclear lesions. Infarction is the main cause (in 32 out of 41) and recovery of full ocular movement is uncommon.
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PMID:[Nuclear oculomotor nerve syndrome due to mesencephalic infarction or hemorrhage. Five cases and a review of literature]. 808 84

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94

The activation of glutamate receptors by endogenuous glutamate has been implicated in the processes that underlie cell loss associated with ischemia and trauma and in the development of some neurodegenerative diseases. The antagonism of NMDA-sensitive glutamate receptors may therefore have therapeutic applications. The present study compared the side effects and neuroprotective potency of 1-aminoadamantane hydrochloride (amantadine), 1-amino-3,5-dimethyladamantane hydrochloride (memantine), and (+)-5-methyl-10,11-dihydro-5H-debenzocyclhepten-5,10-imine maleate ((+)-MK-801) against NMDA injected directly into the nucleus basalis magnocellularis of rats. Each drug significantly attenuated the loss of nucleus basalis magnocellularis cholinergic cells. The ED50s were respectively 0.077, 2.81 and 43.5 mg/kg for (+)-MK-801, memantine and amantadine, giving a relative potency ratio of 1:36:565. The ratio of the ED50 for the side effects observed, including ataxia, myorelaxation and stereotypy, and the ED50 for neuroprotective ability, was highest for memantine and the lowest for (+)-MK-801. The results suggest that a potential neuroprotective action of NMDA receptor antagonists, memantine and amantadine in particular, can be seen at low doses lacking side effects.
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PMID:MK-801, memantine and amantadine show neuroprotective activity in the nucleus basalis magnocellularis. 866 45


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