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)

The Syndrome of Transient Global Amnesia is clinically characterized by a disorder of the ability to form memory engrams, appearing suddenly and lasting for several hours. Since the first papers on this syndrome by Bender (1956) and Fisher and Adams (1964) approximately one hundred cases of transient global amnesia have been described. Symptomatology, course, somatic findings and differential diagnosis are discussed with consideration of the literatur and three own observations. Regarding the etiology most authors discuss a transitory localized ischemia in the circulatory area of the vertebral-basilar artery system. Relapsing episodes occur less frequently than single episodes. In connection with this disorder characterized by the paroxysmal occurence and the episodic course, possible ways of genesis of amnesic syndromes are discussed. Theoretically three types of amnestic syndromes of organic origin may be differentiated: (1) amnesia in the frame of "function psychosis", i.e. of global mental deterioration caused by various diffuse brain function disorders; (2) amnesia caused by a combination of diffuse (function psychosis) and local brain function disorder; (3) purely local type of amnesia without function psychosis. In the combined type of amnesia a dissociation between the severity of memory disorders and relatively mild function psychosis is to be found. The importance of psychopathometric investigations, i.e. of quantitative determination of other mental dysfunctions besides memory disorder, for the interpretation of an amnesic syndrome is emphasized. Unfortunately these have not been possible in the cases described in this paper.
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PMID:[Transient global amnesia - a paroxysmal amnestic syndrome (author's transl)]. 104 11

Genes that predispose to psychosis may act by making individuals more vulnerable to the disruptive effects of various prenatal insults. Fetal organogenesis is mostly completed in the first prenatal trimester. The second trimester is a critical period of massive neuronal migration from the periventricular germinal matrix to the cortex. A peripheral appendage developing simultaneously with this neural migration to the cortex is the distal upper limb. The ectodermal cells of the fetal upper limb migrate to form the hand skin during the fourth and fifth months of gestation (first two-thirds of the second prenatal trimester). Discrepancies in hand morphology between two identical (monozygotic [MZ]) co-twins may be temporal markers, that is, the "fossilized" evidence of various ischemic and other nongenetic insults that may have affected one fetus more than his MZ co-twin during that early part of the second trimester. In twins, prenatal insults (e.g., ischemia) frequently do not affect both co-twins to the same extent, so we examined seven putative markers of prenatal injury to the hand in 24 MZ twin pairs discordant for schizophrenia or delusional disorder. Compared with well co-twins, the affected co-twins had significantly higher total scores of fourth- and fifth-month dysmorphological hand anomalies.
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PMID:Subtle signs of prenatal maldevelopment of the hand ectoderm in schizophrenia: a preliminary monozygotic twin study. 195 69

The most important premise for a successful surgical treatment of epilepsy lies in an accurate diagnosis of the focus location. The hitherto employed methods for this purpose are meticulous analysis of seizure contents and scalp EEGs, but spatial localization of the focus sites is far beyond the capacity of these diagnostic measures. With the advent of positron emission tomography (PET), in vivo observation of human brain metabolism has become possible. The indices of brain metabolism such as cerebral blood flow (rCBF), cerebral metabolic rate of glucose or oxygen (CMRG, CMRO2) are noninvasively measured by PET offering priceless information for diagnosing brain dysfunction such as ischemia, degeneration, psychosis, or epilepsy. Kuhl et al. first employed PET in assessment of epileptic foci, in which interictal foci were beautifully detected as discrete "hypometabolic zones". Many researchers have confirmed this invaluable finding, and nowadays PET seems to have acquired the citizenship as one of the most capable diagnostic measures in focus localization. We have hitherto applied PET study in 72 epileptic patients. The main contents of their seizures consists of complex partial in 32, elementary partial in 32, generalized in 6, and others in 3 cases. We administered perorally 10 mCi glucose labeled with C11 produced in the JSW Baby Cyclotron for the study of CMRG. The continuous inhalation method of CO2 and O2 labeled with O15 produced in the same cyclotron was also employed for measurement of rCBF and CMRO2. In both studies, epileptic foci were shown as well demarcated hypometabolic zones with decreased CMRG, rCBF or CMRO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of convexity focal epilepsy--based on diagnosis of PET and subdural EEG]. 310 88

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

In this article a case of schizophrenic-like symptoms in a patient with thrombo-angiitis obliterans (TAO) is presented. His CT and MRI findings indicated a diffuse ischemia in the white matter, suggestive of TAO, not of focal lesions. The patient, except for age, did not have other risk factors for other cerebrovascular diseases. Psychotic symptoms may be the result of cerebral TAO, via deep and periventricular white matter lesions.
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PMID:Schizophrenic-like symptoms in a patient with thrombo-angiitis obliterans (Winiwarter-Buerger's disease). 1184 Nov 31

Antiphospholipid syndrome can be associated with several neurological manifestations. The most common symptom is headache. It has also been associated with cognitive dysfunction, probably due to ischemia. A high prevalence of antiphospholipid antibodies has been found in patients with epilepsy and in transverse myelitis. The most common thrombotic manifestation is stroke. Venous thrombosis can also be found, yet it is less frequent. A stroke in a young person obliges to rule out the antiphospholipid syndrome. The neurological manifestations can mimic multiple sclerosis. Thus, determination of antiphospholipid antibodies is recommended in the study of patients with atypical manifestations of multiple sclerosis. Other manifestations associated with antiphospholipid antibodies include chorea, neurosensorial deafness, Guillain-Barre syndrome, and psychotic disorders.
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PMID:[Neurological manifestations of the antiphospholipid syndrome]. 1587 82

Excitotoxicity is thought to be a major mechanism in many human disease states such as ischemia, trauma, epilepsy and chronic neurodegenerative disorders. Briefly, synaptic overactivity leads to the excessive release of glutamate that activates postsynaptic cell membrane receptors, which upon activation open their associated ion channel pore to produce ion influx. To date, although molecular basis of glutamate toxicity remain uncertain, there is general agreement that N-methyl-d-aspartate (NMDA) subtype of ionotropic glutamate receptors plays a key role in mediating at least some aspects of glutamate neurotoxicity. On this view, research has focused in the discovery of new compounds able to either reduce glutamate release or activation of postsynaptic NMDA receptors. Although NMDA receptor antagonists prevent excitotoxicity in cellular and animal models, these drugs have limited usefulness clinically. Side effects such as psychosis, nausea, vomiting, memory impairment, and neuronal cell death accompany complete NMDA receptor blockade, dramatizing the crucial role of the NMDA receptor in normal neuronal processes. Recently, however, well-tolerated compounds such as memantine has been shown to be able to block excitotoxic cell death in a clinically tolerated manner. Understanding the biochemical properties of the multitude of NMDA receptor subtypes offers the possibility of developing more effective and clinically useful drugs. The increasing knowledge of the structure and function of this postsynaptic NMDA complex may improve the identification of specific molecular targets whose pharmacological or genetic manipulation might lead to innovative therapies for brain disorders.
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PMID:New targets for pharmacological intervention in the glutamatergic synapse. 1683 14

Elevated levels of endogenous glucocorticoids (GCs) or prolonged treatment with high doses of dexamethasone (DEX) or other GCs preparations are frequently associated with psychosis as well as cognitive deficits, such as the impairment of memory and learning. GCs potentiate stress or ischemia-induced accumulation of excitatory amino acids in the extracellular space of hippocampus. The antagonism of glutamate receptors may potentially improve safety profile of therapy with GCs. The purpose of the present study was to investigate the effect of dizocilpine maleate (MK-801), non-competitive NMDA glutamate receptor antagonist, on neurotoxic effect of the prolonged treatment with the high dose of DEX. The results showed that DEX (120 mg/kg/day for 7 days) impaired the long-term memory and the motor coordination, reduced the body weight and induced the lethality of mice. The morphological and ultrastructural study have confirmed damage to hippocampal neurons especially in the CA3 region after the prolonged treatment with DEX alone. Damaged pyramidal neurons showed robust changes in the shape of the nucleus and cytoplasm condensation. MK-801 alone (at non-toxic dose of 0.3 mg/kg/day), changed neither the behavior of mice nor morphology of the hippocampal neurons. However, it did not prevent the neurotoxic effects of DEX. On the contrary, it intensified DEX-induced neurotoxicity.
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PMID:Influence of dizocilpine (MK-801) on neurotoxic effect of dexamethasone: behavioral and histological studies. 1713 53

To a large extend schizophrenia has been shown to be heritable, with neuregulin-1 (NRG1) one of the candidate genes considered to play a role in the pathophysiology of the disorder. While several polymorphisms within this gene have been reported to be associated with schizophrenia, the impact of NRG1 risk genotypes on disturbed brain function and symptoms of the disease is unknown and might be elucidated using post-mortem studies. Neuregulins are signalling proteins and the NRG1 family encodes at least 15 different splice variants, classified into four isoforms. They play an important role in cell differentiation, migration, myelination and proliferation of oligodendrocytes and neurons. Dysfunction in these processes may be related to neurodevelopmental disturbances in schizophrenia. NRG1 isoforms are differentially expressed in relevant brain regions of schizophrenia patients such as the prefrontal cortex and hippocampus and may contribute to pathophysiological processes. Different NRG1 genotypes have been shown to influence gene expression of isoforms and the risk-associated variants are in primarily non-coding and promoter regions, probably operating by altering gene expression or splicing. In addition, NRG1 regulates the expression of the nicotinic acetylcholine receptor, and expression of the gamma-aminobutyric acid (GABA(A)) and N-methyl-D: -aspartate receptor in the brain. However, the contribution of NRG1 risk genotypes to expression of isoforms and cognitive or psychotic symptoms in patients remain to be investigated in prospective post-mortem studies. In animal models of ischemia/hypoxia, NRG1 has been shown to act as a therapeutic, neuroprotective agent and should be investigated in more detail in transgenic animal models.
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PMID:Impact of neuregulin-1 on the pathophysiology of schizophrenia in human post-mortem studies. 1898 92

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used, but have risks associated with their use, including significant upper gastrointestinal tract bleeding. Older persons, persons taking anticoagulants, and persons with a history of upper gastrointestinal tract bleeding associated with NSAIDs are at especially high risk. Although aspirin is cardioprotective, other NSAIDs can worsen congestive heart failure, can increase blood pressure, and are related to adverse cardiovascular events, such as myocardial infarction and ischemia. Cyclooxygenase-2 inhibitors have been associated with increased risk of myocardial infarction; however, the only cyclooxygenase-2 inhibitor still available in the United States, celecoxib, seems to be safer in this regard. Hepatic damage from NSAIDs is rare, but these medications should not be used in persons with cirrhotic liver diseases because bleeding problems and renal failure are more likely. Care should be used when prescribing NSAIDs in persons taking anticoagulants and in those with platelet dysfunction, as well as immediately before surgery. Potential central nervous system effects include aseptic meningitis, psychosis, and tinnitus. Asthma may be induced or exacerbated by NSAIDs. Although most NSAIDs are likely safe in pregnancy, they should be avoided in the last six to eight weeks of pregnancy to prevent prolonged gestation from inhibition of prostaglandin synthesis, premature closure of the ductus arteriosus, and maternal and fetal complications from antiplatelet activity. Ibuprofen, indomethacin, and naproxen are safe in breastfeeding women. Care should be taken to prevent accidental NSAID overdose in children by educating parents about correct dosing and storage in childproof containers.
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PMID:NSAID prescribing precautions. 2000 Feb 99


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