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)

Both ictal nystagmus and cortical blindness may occur transiently in acute cerebral disorders and therefore escape clinical detection, particularly in confused, agitated patients. The following case report describes a young woman with chronic myelogenous leukemia who became progressively ill following bone marrow transplantation. During the course of her illness, acute ictal nystagmus developed from focal right occipital ischemia; postictally she remained cortically blind with possible visual hallucinations for 48 hours.
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PMID:Cortical blindness following ictal nystagmus. 397 48

A 30-year-old woman had an arachnoid cyst in the trigone of the right lateral ventricle 5 years before she developed episodic auditory and visual hallucinations as well as delusions of persecution. The psychotic episodes tended to occur after the patient had lain in bed for 1 to 2 hours. After craniotomy and wide excision of the cystic membrane, draining the cystic fluid to the lateral ventricle, the psychotic episodes subsided in a follow-up period of 6 months. We believe that when the patient was recumbent, the trigone cyst blocked the temporal horn further, caused local ischemia, and triggered the psychosis, which was a form of partial complex psychomotor seizure.
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PMID:Arachnoid cyst of the lateral ventricle manifesting positional psychosis. 849 62

Unilateral auditory hallucinations are a rare lateralization phenomenon experienced in one ear or from one direction. We recently encountered a 63-year-old right-handed man who developed transient unilateral auditory hallucinations associated with pure word deafness. The patient had a past history of myocardial infarction, lung cancer and aortic aneurysm, but no previous psychiatric or convulsive disorders. About six months before admission, he developed right hemiparesis and motor aphasia caused by a hemorrhagic left parietal infarct. These symptoms gradually improved over three weeks. Two days before admission, he suddenly lost the ability to understand spoken words. He concurrently experienced auditory hallucinations arising from the right anterior direction. On admission, he was very embarrassed to simple verbal commands. He was unable to comprehend spoken words and repeat speech, although he could fairly follow written commands. Confrontation naming, reading aloud, comprehension, spontaneous writing remained relatively unaffected, although he occasionally made paraphasic errors. He could distinguish environmental sounds such as a telephone ringing or running water. After gradual improvement of his auditory incomprehension, he began to describe auditory hallucinations of verbal, musical and elementary types. He was fully aware of the hallucinatory nature of his experience, and took some notes. Two days before admission, from the right anterior side of his head he heard a familiar radio announcer reporting news about the earthquake in Osaka Prefecture and the recommended places of refuge. After similar experiences over several days, he repetitively heard a familiar Japanese traditional song from the right side, which was followed by elementary auditory hallucinations such as a car engine and a siren. These symptoms spontaneously disappeared after nine days. Besides his auditory hallucinations, visual hallucinations and illusional emotion were temporarily present. The Wechsler adult intelligence scale revealed a verbal IQ of 91 and a performance IQ of 100. Pure tone audiometry revealed bilateral, mild peripheral sensorineural hearing loss. Brainstem auditory evoked potentials were unrevealing. The EEG showed slow activities in the left temporoparietal region. Magnetic resonance imaging of the brain failed to reveal any relevant abnormalities except for an old hemorrhagic parietal infarct. The SPECT with Tc99m-HMPAO, however, showed reduced blood flow in the left temporal lobe including the first temporal convolution as well as in the left parietal lobe. Based on the SPECT findings, unilateral auditory hallucinations in our patient are considered to have resulted from the left temporal lobe ischemia. Our case indicates that unilateral auditory hallucinations may have a clinicoanatomical correlation with contralateral temporal lobe lesions.
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PMID:[Unilateral auditory hallucinations due to left temporal lobe ischemia: a case report]. 882 99

Recent clinical trials with non-competitive and competitive N-methyl-D-aspartate (NMDA) receptor antagonists in patients with stroke have shown that these patients develop more adverse effects, particularly psychomimetic effects such as hallucinations and agitation, than normal volunteers at equivalent doses. We therefore examined whether such increased adverse effect potential of NMDA antagonists also occurs in a rat model of permanent focal ischemia. For this purpose, the right middle cerebral artery was occluded under halothane anesthesia, and behavioral alterations in response to the non-competitive NMDA antagonist, MK-801 (dizocilpine), were recorded after recovery from anesthesia. Behavioral alterations in ischemic rats were compared with those in sham-lesioned rats in a blinded fashion. MK-801 (0.4 mg/kg) induced psychomimetic-like stereotyped behaviors which were about twice as intense in ischemic than in non-ischemic rats. A similar trend for enhanced adverse effects was seen with the competitive NMDA antagonist CGS 19755 (Selfotel). Although more NMDA antagonists have to be tested to draw definite conclusions, the present data may indicate that enhanced sensitivity of stroke patients to adverse effects of NMDA antagonists can be predicted by use of a focal ischemia model in rats, thus allowing use of this model for developing novel cytoprotective strategies targeted to minimize glutamatergic excitotoxicity with reduced adverse effect potential.
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PMID:Focal ischemia enhances the adverse effect potential of N-methyl-D-aspartate receptor antagonists in rats. 948 68

Visual disorders are an important symptom in the migraine of developing age. Different kinds of visual disturbances can precede, accompany or follow a migraine attack. These visual disturbances can be grouped into negative (hemianopsia, quadrantopsia, scotoma) and positive (phosphene, teicopsia, metamorphopsia, macropsia, micropsia, teleopsia, diplopia, dischromatopsia, hallucination disturbances) disorders. The pathogenetic mechanism of the visual phenomena of migraine has not yet been clarified. Various hypotheses have been proposed: vasospasm with consequent ischemia of some cerebral areas, the opening of arteriovenous shunts between the intra and extra cerebral circulation, the formation of microthrombi in arterioles and dopaminergic hypersensitivity of some nervous centers. We have studied 1787 children, affected by migraine with (13%) or without (87%) aura. Among the patients, 211 (12%) referred visual disorders, especially scotoma and phosphene. These data let us hypothesize that a relationship between migraine and visual disorders is present also in pediatric age. However this relationship is less important than in adults.
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PMID:Migraine with visual aura in developing age: visual disorders. 1082 7

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

This paper reviews our recent studies of the role of cortical spreading depression (CSD) in the pathogenesis of brain disorders. Our investigation is a computational one, involving the development and utilization of a complex neuro-metabolic model of the interactions assumed to occur in the cortex during the passage of multiple CSD waves. Incorporating these neuro-metabolic changes of CSD within a neural network model of normoxic cortex produces cortical activation patterns during the passage of a CSD wave that, projected onto the visual fields, resemble the visual hallucinations observed during the migraine aura. When focal ischemia is simulated with the model, the evoked CSD waves are found to affect the expansion of the infarction into the ischemic penumbra. Our findings support the hypothesis that CSD does play an important pathogenic role in these and other neurological disorders, and suggest additional experimental studies that may further substantiate it.
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PMID:Cortical spreading depression and the pathogenesis of brain disorders: a computational and neural network-based investigation. 1147

Proper management of chemotoxicity in transplant patients requires detailed knowledge of the biochemical mechanisms underlying immunosuppressant toxicity. Neurotoxicity is one of the most significant clinical side effects of the immunosuppressive undecapeptide cyclosporine, occurring at some degree in up to 60% of transplant patients. The clinical symptoms of cyclosporine-mediated neurotoxicity consist of decreased responsiveness, hallucinations, delusions, seizures, cortical blindness, and stroke-like episodes that mimic those clinical symptoms of mitochondrial encephalopathy. Clinical computed tomography (CT) and magnetic resonance imaging (MRI) studies have revealed a correlation between clinical symptoms of cyclosporine-mediated neurotoxicity and morphological changes in the brain, such as hypodensity of white matter, cerebral edema, metabolic encephalopathy, and hypoxic damages. Paradoxically, in animal models cyclosporine protects the brain from ischemia-reperfusion (I/R) injury. Interestingly, cyclosporine appears to mediate both neurotoxicity (under normoxic conditions) and I/R protection across the same range of drug concentration. Both toxicity and protection might arise from the intersection of cyclosporine with mitochondrial energy metabolism. This review addresses basic biochemical mechanisms of: 1) cyclosporine toxicity in normoxic brain, and 2) its protective effects in the same organ during I/R. The marked and unparallel potential of magnetic resonance spectroscopy (MRS) as a novel quantitative approach to evaluate metabolic drug toxicity is described.
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PMID:Biochemical mechanisms of cyclosporine neurotoxicity. 1508 83

Higher visual disorders as discussed in this paper comprise visual hallucinations, palinopsy, hemineglect, Balint Holmes syndrome, prosopagnosia, visual objectagnosia, alexia without agraphia and cerebral achromatopsia. Such disorders are frequently caused by ischemia, but tumors, trauma and intoxication are possible as well. As a rule, higher visual disorders are a transient phenomenon. It is important to inform the patient and his family about the nature of the disorder and consider persisting disorders during rehabilitation.
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PMID:[Higher visual disorders]. 1928 Jan 96

Hearing disturbances are not commonly reported in stroke or transient ischemic attack. We describe a case of a 60-year-old man with fluctuating brainstem ischemia with basilar artery thrombosis where the patient has consistently described hearing "white noise," bilaterally becoming progressively louder over 10 minutes that prevented him from hearing surrounding noise including the radio. These episodes were transient and preceded episodes of hemiparesis or reduced conscious level. We correlate this to the sequential imaging findings from the patient. We discuss how this case provides in vivo evidence for localization of auditory hallucinations in the context of the auditory pathways and their blood supply, and review 25 previous cases of auditory hallucinations and possible mechanisms.
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PMID:Localization of bilateral auditory hallucinations and correlation to imaging in posterior circulation stroke. 2311 81


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