Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Review of the neurological complications encountered in 83 patients who received cardiac homografts over a seven-year period leads to the following conclusions: (1) Neurological disorders are common in transplant recipients, occurring in over 50 per cent of patients. (2) Infection was the single most frequent cause of the neurological dysfunction, being responsible for one-third of all CNS complications. (3) The infective organisms were typically those considered to be usually of low pathogenicity: fungi, viruses, protozoa and an uncommon bacterial strain. (4) Other clinical neurological syndromes were related to vascular lesions, often apparently from cerebral ischaemia or infarction occurring during the surgical procedure, metabolic encephalopathies, cerebral microglioma, acute psychotic episodes and back pain from vertebral compression fractures. (5) The infectious complications and probably the development of neoplasms de novo, are related to immunosuppressive therapy which impairs virtually all host defence mechanisms and alters the nature of the host's response to infective agents or other foreign antigens. (6) Because neurological symptoms and signs were usually those of behavioural changes or deterioration in intellectual performance, the neurological examination was often of little value in diagnosing the nature or even the anatomical site of the neuropathological process. (7) The possibility of an infectious origin of the neurological manifestations must be aggressively pursued even in the absence of fever and a significantly abnormal spinal fluid examination. The diagnostic error made most frequently was to ascribe neurological symptoms erroneously to metabolic disturbances or to "intensive care unit psychosis" when they were in fact due to unrecognized CNS infection. (8) Maintenance of mean cardiopulmonary bypass pressures above 70 mmHg, particularly in patients with known arteriosclerosis, may reduce operative morbidity. (9) Though increased diagnostic accuracy is possible with routine use of a variety of radiological and laboratory techniques, two further requirements probably must be met before a significant reduction in the frequency of neurological complications will occur: the advent of greater immunospecificity in suppressing rejection of the grafted organ while preserving defences against infection; and a more effective armamentarium of antiviral and antifungal drugs.
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PMID:The neurological complications of cardiac transplantation. 19 13

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.
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PMID:Cerebral blood flow variations in CNS lupus. 229 89

Carbon monoxide (CO) remains the leading cause of death due to poisoning in the United States. CO produces toxicity by binding to hemoglobin, thereby reducing oxygen-carrying capacity, and by binding to myoglobin, which may impair cardiac output and result in cerebral ischemia. Severe CO poisoning results in coma or encephalopathy, but milder intoxication may occur with nonspecific symptoms suggestive of hysteria, hyperventilation, psychosis, or viral syndrome. Survivors of severe CO poisoning may have permanent neurologic or neuropsychiatric sequelae. Subtle memory deficits or personality changes may not be readily apparent to the examining physician. Administration of 100% oxygen at ambient pressure remains convenient, safe, and inexpensive. Hyperbaric oxygen can shorten the half-life of carboxyhemoglobin and can carry oxygen independent of hemoglobin. However, it is not known if either 100% oxygen or hyperbaric oxygen can actually alter mortality or improve neurologic outcome in survivors. Carefully controlled prospective studies should be carried out to assess the potential value of hyperbaric oxygen in CO poisoning.
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PMID:Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. 649 Dec 41

Thrombosis, thrombocytopenia, recurrent fetal loss and a variety of non-thrombotic neurological disorders have all been associated with antiphospholipid antibodies (aPL). Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Depression, cognitive dysfunction, depression and psychosis have all been associated with aPL. The presumed pathophysiologic mechanism underlying these manifestations is thought to be a result of cerebral ischemia in some, but not all cases. Seizures, chorea and transverse myelitis all appear to be associated with aPL. An interaction between aPL and central nervous system cellular elements rather than aPL-associated thrombosis seems to be a more plausible mechanism for these clinical manifestations. Migraine on the other hand, does not appear to be associated with aPL in either lupus or non-lupus populations. Neuroimaging studies show an increased frequency of brain abnormalities in patients with aPL, but none appear to be specific. The best treatment strategy for preventing neurological manifestations of aPL is not fully defined. For thrombotic manifestations, both antiplatelet and anticoagulant therapies have been suggested. In some patients, immunosuppressant therapy has been used. For non-thrombotic manifestations, some combination of immunosuppressant therapy and symptomatic treatment may be warranted.
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PMID:Neurological manifestations of antiphospholipid antibody syndrome. 981 77

Glutamate is the principal excitatory neurotransmitter in brain. Our knowledge of the glutamatergic synapse has advanced enormously in the last 10 years, primarily through application of molecular biological techniques to the study of glutamate receptors and transporters. There are three families of ionotropic receptors with intrinsic cation permeable channels [N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate]. There are three groups of metabotropic, G protein-coupled glutamate receptors (mGluR) that modify neuronal and glial excitability through G protein subunits acting on membrane ion channels and second messengers such as diacylglycerol and cAMP. There are also two glial glutamate transporters and three neuronal transporters in the brain. Glutamate is the most abundant amino acid in the diet. There is no evidence for brain damage in humans resulting from dietary glutamate. A kainate analog, domoate, is sometimes ingested accidentally in blue mussels; this potent toxin causes limbic seizures, which can lead to hippocampal and related pathology and amnesia. Endogenous glutamate, by activating NMDA, AMPA or mGluR1 receptors, may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury. It may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's chorea. In animal models of cerebral ischemia and traumatic brain injury, NMDA and AMPA receptor antagonists protect against acute brain damage and delayed behavioral deficits. Such compounds are undergoing testing in humans, but therapeutic efficacy has yet to be established. Other clinical conditions that may respond to drugs acting on glutamatergic transmission include epilepsy, amnesia, anxiety, hyperalgesia and psychosis.
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PMID:Glutamate as a neurotransmitter in the brain: review of physiology and pathology. 1073 72

Antiphospholipid antibodies (aPL) have been most strongly associated with a syndrome (APS) characterized by venous and/or arterial thrombosis, thrombocytopenia, recurrent fetal losses and a variety of non-thrombotic and thrombotic neurological disorders. Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Other neurological syndromes, such as cognitive dysfunction, dementia, psychosis, depression, seizures, chorea and transverse myelopathy, have all been associated with antiphospholipid antibodies.
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PMID:Neurological involvement in antiphospholipid antibodies syndrome (APS). 1107 18

Glutamate is the major excitatory neurotransmitter of the central nervous system. Besides its importance in many physiological processes, increased glutamate release and subsequent excessive stimulation of the various glutamate receptors are thought to play critical roles in the pathophysiological mechanisms underlying many neurologic diseases. Experimental data suggest that blockade of glutamate receptors or inhibition of glutamate release has positive effects in many disease models. Glutamate antagonists are already in clinical use for the treatment of Parkinson's disease, epilepsy, spasticity, and neuropathic pain. Overall, glutamate antagonists have not been found clinically effective for neuroprotective treatment of cerebral ischemia or chronic neurodegenerative diseases, with one exception. Side effects of glutamate antagonists can be mainly attributed to central mechanisms and include psychosis, agitation, and disorientation. It is to be hoped that further development of new glutamate antagonists that block disease-relevant subtypes of glutamate receptors will lead to more effective drugs with fewer side effects.
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PMID:[Glutamate antagonists in neurology]. 1143 98

A 38-year old male patient with no history of psychiatric illness developed a progressive psychotic disorder after bilateral (predominantly left) mesencephalo-thalamic cerebral ischaemia. The reason of the emergency hospitalization was the sudden onset of a confusional state, culminating in a fluctuating comatose status. The neurological examination found mild right hemiparesia, praxic disorders and reactive left mydriasis with paresia of the downward vertical stare, leading to the hospitalisation in the neurology department for suspicion of a cerebral vascular ischaemic accident. The psychiatric symptoms started with acoustic-verbal hallucinations, poorly structured paranoid delusions, progressively developed over two weeks, followed by behavioural disorders with psychomotor agitation and heteroaggressivity. The patient was transferred to the psychiatric department, because of the heteroaggressive risk and lack of morbid consciousness, in spite of recovering from the confusional status. An intensive psychiatric management was proposed, combining a psychotherapeutic approach with 4 mg of risperidone and adjustable doses of benzodiazepine according to the psychomotor agitation. During the next days, there was a net recovery of the behavioural disorders, in spite of the persistence of the ideas of persecution. All the neurological symptoms also decreased. An anomaly of the polygon of Willis was found on a cerebral arteriography (the posterior cerebral arteries had a foetal origin, dependent on carotidal axes and not on the vertebro-basilar system). The main emboligen risk factor was the presence of a permeable foramen ovale, discovered during a transoesophageal echography. The patient underwent a surgical correction of the permeable foramen ovale. The psychiatric hospitalization for three months was continued by ambulatory follow-up. The initial positive symptoms (delusions, acoustic-verbal hallucinations) progressively diminished while negative symptoms became predominant after few months. One year after the first hospitalization the patient presented a second psychotic decompensation, with delusions of persecution, jealousy and behavioural disorders with heteroaggressivity, that required an emergency psychiatric hospitalization. The wife of the patient decided to divorce, because she was "frightened by the threats of death" from her husband. A neurological assessment during the second hospitalization in psychiatry did not find new ischaemic lesions after the cardiac surgery for the permeable foramen ovale, nor relevant changes in cerebral perfusion. The final diagnosis after the psychiatric follow-up of 14 months was: psychotic disorder with delusional ideas, due to cerebral ischaemia (DSM IV). There are relatively few data in the literature regarding persistent psychotic disorders in the context of ischaemic mesencephalo-thalamic lesions. However, several authors support the hypothesis of a possible disconnection of the thalamic nuclei, the frontal lobes and limbic system as a risk factor or a triggering factor for psychotic disorders in cerebral ischaemia. Observations concerning the occurrence of psychotic disorders following cerebral--especially localised--ischaemia may help to better understand the neuro-physiological mechanisms triggering or accompanying the psychiatric symptomatology. The role of functional cerebral imagery in the detection of possible structural lesions related to clinical observations must be emphasised. The slow progression (over a year) to psychotic disorder with predominantly negative symptoms emphasized the importance for long-term prospective studies. Isolated clinical observations arouse the interest for a specific scale for psychotic disorders occurring after cerebral ischaemia, similar to existing specific scale for post-ischaemic depressive disorders. The necessity of systematic psychiatric examination and re-evaluations in thalamic cerebral ischaemia is to be highlighted, both for the differential diagnosis and for the early psychiatric care.
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PMID:[Persistent psychotic disorder following bilateral mesencephalo-thalamic ischaemia: case report]. 1553 16

Dehydroepiandrosterone is the precursor of sex hormone, and can be synthesized in the brain de novo, which means it is a kind of neurosteroid. Animal experiments and clinical researches have proved that DHEA exhibits a variety of functional activities in the nervous system, including neurotrophic, neuroprotective effects and enhancement' of learning and memory, which suggests that it may be useful in preventing and treating some neural diseases such as neurodegenerative diseases, cerebral ischemia, trauma, psychosis and so on. The mechanisms of the effect of DHEA on protection against oxidative stress, excitotoxicity, apoptosis etc. were found to be through both genomic and nongenomic way. These effects and mechanisms in nervous system were summarized in the present paper.
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PMID:[Functions and mechanisms of dehydroepiandrosterone in nervous system]. 1726 68

Agmatine is a polyamine that is produced via decarboxylation of l-arginine by the enzyme arginine decarboxylase. It binds to various receptors and has been accepted as a novel neurotransmitter in brain. In experimental studies, agmatine exhibited anticonvulsant, antinociceptive, anxiolytic and antidepressant-like actions. Furthermore, it has some beneficial effects on cerebral ischemia models in animals. Agmatine interacts with the mechanisms of withdrawal syndromes for several addictive agents. It also modulates some processes involved in learning and memory. Thus, agmatine seems to be a valuable agent for the treatment of behavioral and neurodegenerative disorders. However, the aberrant release and transmission of agmatine in the central nervous system (CNS) may be associated with mechanisms of several CNS disorders, such as psychosis. Interactions between agmatine and other central neurotransmitter systems, such as the glutamatergic and nitrergic systems, are also very important. In light of the current literature on agmatine, we can anticipate that the central agmatinergic system may be an important target in development of novel strategies and approaches for understanding the etiopathogenesis of some important central disorders and their pharmacological treatments. The main objective of this review is to investigate and update the information on effects of agmatine in CNS and highlight its pharmacological importance in central disorders.
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PMID:The pharmacological importance of agmatine in the brain. 2189 93


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