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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors hypothesized that patients who develop gross EEG abnormalities during clozapine treatment would have a less favorable outcome than patients who did not develop abnormal EEGs. The clinical EEGs and the Brief Psychiatric Rating Scale (BPRS) scores of 12 patients with schizophrenia and 4 patients with schizoaffective disorder were compared before and during treatment with clozapine. Eight patients developed significant EEG abnormalities on clozapine; 1 showed worsening of an abnormal pre-clozapine EEG; none of these subjects had clinical seizures. BPRS scores improved significantly in the group of patients who developed abnormal EEGs but not in the group who did not. Findings are consistent with previous reports of a high incidence of clozapine-induced EEG abnormalities and a positive association between these abnormalities and clinical improvement.
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PMID:Clozapine-induced EEG abnormalities and clinical response to clozapine. 855 49

We studied 30 patients with postictal psychosis and compared them with 33 patients with acute interictal psychosis and 25 patients with chronic psychosis. All patients had either complex partial seizures (CPS) or EEG temporal epileptogenic foci. Patients with postictal psychosis had a high incidence of psychic auras and nocturnal secondarily generalized seizures. The most striking feature that distinguished postictal psychosis from both acute interictal and chronic psychoses was phenomenological: the relatively frequent occurrence of grandiose delusions as well as religious delusions in the setting of markedly elevated moods and feeling of mystic fusion of the body with the universe. In addition, postictal psychosis exhibited few schizophreniform psychotic traits such as perceptual delusions or voices commenting. Reminiscence, mental diplopia, and a feeling of impending death were also fairly frequent complaints of patients with postictal psychosis. Interictal acute psychosis and chronic epileptic psychosis were psychopathologically similar. Although acute interictal and chronic epileptic psychoses could simulate schizophrenia, postictal psychosis results in a mental state quite different from that of schizophrenic psychosis.
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PMID:Postictal psychosis: a comparison with acute interictal and chronic psychoses. 864 Dec 32

During a 24-month period, 205 consecutive new referrals to Muhimbili psychiatric unit were studied. Their socio-demographic characteristics, sources of referral, types of treatment received before referral and the nature of their clinical problems were identified. Their neuropsychiatric disorders were classified according to ICD-10. The ratio of males to females was found to be 1.6:1. The average age was 29.3 years. 23.4% of adult patients were unemployed, two fifths of all patients were single and 70% of all subjects had less than eight years of formal education. Whereas 42.9% of all referrals were from other departments of Muhimbili hospital, the remaining were largely from parastatal dispensaries, district and regional hospitals within Dar es Salaam city. At least a fifth of all patients had consulted traditional healers prior to referral and antimalarials had been given inappropriately to 34 patients with mental problems. Mental disorders consisted of functional psychosis, 36.6% of which three quarters were schizophrenia, neurosis (19.5%), seizures (16.6%), substance abuse (8.8%), organic mental disorders (5.3%), headache (4.9%), sexual dysfunction (2.9%). The rest had conduct disorders and pseudocyesis. Seventeen percent of all cases had concomitant physical disorders. Most patients had delayed to seek medical help.
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PMID:Nature of referrals to the psychiatric unit at Muhimbili Medical Centre, Dar es Salaam. 868 72

The goal of this paper is to draw conclusions about the usefulness of the standard EEG in psychiatry. In general, two thirds of psychiatric referrals for an EEG are expected to provide useful information. The emphasis in schizophrenia is placed on left-sided abnormalities, especially on the left temporal area. In mood disorders the emphasis is on right-sided foci, in addition to the controversial 6/sec spike and wave complexes, small sharp spikes and positive spikes. In the acute stage of alcoholism, a relationship is seen between the degree of intoxication and the amount of slow activity, while in the chronic stage an increase in slow activity is seen, but another change is fast activity on the temporal areas. During withdrawal a low seizure threshold can be seen as irregular bilateral spike and wave complexes. During abstinence 2-4 yr may be required before slow wave sleep is normal in all regards. Among the organic mental syndromes, delirium shows slow activity, except in delirium tremens, which often is associated with a normal record with fast activity. In dementia the prevalence of EEG abnormalities is related to the degree of impairment. After five sessions of ECT diffuse slow waves are often seen. In other conditions, among developmental disorders about one half of autistic children show abnormalities and epileptiform activity is not uncommon. Mild nonspecific abnormalities are seen in about 40% of dyslexics and also in behavior disorders. Anxiety disorders include anorexia nervosa, showing abnormal background activity related to the effect of starvation on cerebral metabolism. In panic attacks paroxysmal activity can be seen. In borderline personality positive spikes have been (again) associated with impulsivity and 6/sec spike and wave complexes with interpersonal problems. Of the drugs of abuse psilocybin and phencyclidine are often associated with generalized epileptiform patterns and with marijuana the alpha shows a decreased frequency with increased amplitude. Typically, an increase in slow activity is seen with psychotropic drugs if there is a change in the level of awareness. Finally, distinctive personality traits are, at times, seen in temporal lobe epilepsy and the phenomenon of "forced normalization" may appear when seizures stop and psychotic symptoms appear.
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PMID:A review of the usefulness of the standard EEG in psychiatry. 871

Epilepsy is a well-documented consequence of about 150 rare genetic syndromes and malformations of the central nervous system. These syndromes are generally associated with fairly gross defects within the central nervous system and they were thought to be responsible for a small minority of cases. However, improved methods of neuropathological investigations and extensive magnetic resonance imaging studies have revealed a range of disturbances in cortical cytoarchitecture in patients with epileptic seizures previously considered as idiopathic (up to 70% of epilepsy). Structural abnormalities have also been demonstrated in the brain in schizophrenia. These consist of disturbed cortical cytoarchitecture (best described in the temporal lobe) and a diffuse loss of grey matter. The absence of the pathological stigma characteristic of degenerative processes indicates that these structural changes are the result of an abnormal pattern of brain development. The relationship between the type and location of developmental abnormality and the subsequent clinical syndrome (e.g. generalized or localized epilepsy) and the effects of aberrant cortical development on the functional integrity of the adult brain require definition.
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PMID:Pathology of cortical development and neuropsychiatric disorders. 872 98

Excitatory amino acids (EAA) became known as neurotransmitters of the central nervous system (CNS) in the last decade. The most studied EAA are glutamate and aspartate. Both are synthetized by the same mechanism as gamaaminobutyric acid. (Fig. 1). Glutamate is widely distributed in the CNS and the spinal cord, being the areas of higher concentration the cerebral cortex, the hypocampus and the cerebellum. There have been identified two type of receptors for glutamate: ionotropic and metabotropic. The former includes three different types: NMDA, AMPA and KA. NMDA receptor is coupled to a Na+ and Ca2+ channel being the second ion the most important one. This receptor has several sites of binding for various substances. Along with the site for N-methyl-D-aspartate, which binds glutamate and/or aspartate, there have been identified a site for the binding of glycine (which is different from the strychnine sensitive one), a site for poliamines such as spermine and spermidine, and a site for the binding of Zn2+ (Table 1). AMPA receptor is associated to a Ca(2+)-Na+ channel, being in this case the Na+ the most important ion. There are two metabotropic type receptors: L-AP4 and trans-ACPD. Both are coupled to a G protein and agonists exert their action increasing phospholipase C activity which in turn induces an increment of IP3 and diacyl-glicerol, and a consecutive releasing of Ca2+ from intracellular stores. EAA play a role in some physiological processes. One of them is long-term potentiation (LTP), an electrochemical phenomenon involved in memory consolidation. Antagonists of NMDA and AMPA receptor prevent the development of LTP, and conversely, the agonist of glycine site of NMDA receptor--D-cycloserine--facilitates memory consolidation. Since 1957, EAA are considered neurotoxic substances and there are many indirect evidences to support this statement. Pathogenesis of neuronal damage elicited by EAA involves the events shown in Fig. 3. Prevention of the cascade of events that provokes neurotoxicity may be achieved by NMDA antagonists, but once it has begun it may be only aborted subtracting the Ca2+ from the medium, using nifedipine or blocking AMPA receptor with an antagonist (CNQX). EAA have been shown to play a toxic role in neuronal damage induced by ischemia. Research using various experimental models demonstrated that NMDA receptor antagonists (i.e. MK 801) blocks postischemic damage. Interventions at various levels of the pathogenic cascade shown in Fig. 4 provoke the same results. There is enough evidence to suspect that NMDA and AMPA receptors are altered in epilepsy. NMDA antagonists (i.e. MK801 or AP5) prevent the development of epileptic seizures induced by kindling; CNQX, an AMPA antagonist, blocks the increase in electrical activity induced by K+ in slices of hypocampus; felbamate, an antiepileptic drug, blocks the glycine site (not strychnine sensitive) decreasing NMDA receptor activity. Several neurodegenerative disorders have been associated with exogenous administration or accidental intake of EAA. (i.e. neurolatirism, Guam disease). Similarities between these diseases and lateral aminotrophic sclerosis indicate that in the latter EAA may play a pathogenic role. Finally, the psychotomimetic effect of phencyclidine (an antagonist of NMDA receptor) suggests that in schizophrenia, together with dopaminergic neurotransmission impairment, some dysfunction of glutamate pathways may be present.
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PMID:[Role of excitatory amino acids in neuropathology]. 872 78

The first indication that histamine might be important in the functioning of the brain was the finding that the centrally penetrating histamine H1 antagonists had marked sedative properties. Subsequently with the development of more specific compounds and drugs for the H1, H2 and H3 receptors a greater understanding of the neurotransmitter/modulator role of histamine in the CNS has been possible. Histamine is now associated with wakefulness, suppression of seizures, hypothermia and emesis. The histamine H1 antagonists have been shown to potentiate opioid-induced analgesia, and modify eating and drinking patterns as well as endocrine secretions from the pituitary gland. Additionally, clinically useful antidepressants have been shown to inhibit histamine-sensitive adenylate cyclase from the mammalian brain. Recently, a possible role for both histamine H1 and H2 receptors in schizophrenia has been reported. As more specific and centrally-penetrating histaminergic compounds are developed, so the roles of histamine as a neurotransmitter/modulator in the brain will be better understood.
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PMID:Histaminergic drugs as modulators of CNS function. 873 45

Clozapine (Clozaril) represents the first major advance in the pharmacological treatment of schizophrenia since the introduction of antipsychotics into clinical practice in the 1950s. Studies consistently support its efficacy for reducing positive symptoms in acutely psychotic patients and in treatment-resistant patients, for preventing positive symptom exacerbations as a maintenance treatment, and for reducing symptoms of hostility and violence. There is evidence to suggest that clozapine may improve social and occupational functioning and quality of life and may reduce affective symptoms, hospitalizations, secondary negative symptoms, and tardive dyskinesia. Its most significant side effects include agranulocytosis, seizures, weight gain, hypotension and tachycardia, sedation, and perhaps rebound psychosis (with abrupt discontinuation of medication).
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PMID:Clozapine: efficacy and safety. 874 86

This study examines communication characteristics and specific language deficits in 47 children and adolescents diagnosed with early-onset schizophrenia using DSM-III-R criteria. All had been referred for speech and language services because of apparent communication problems. Standardized tests and formal measures were used to identify impairment in discrete areas of communication, including pragmatics, receptive and expressive vocabulary and syntax, abstract language, auditory processing, and speech production. Results showed that these discrete areas were variably involved, with pragmatics, prosody, auditory processing, and abstract language having the greatest involvement. The communication deficits identified in the early-onset group closely resembled the phenomenology reported in studies of the communication characteristics of adults with schizophrenia. This comparison thus lends further support to the presence of the same disorder as seen in adults. The roles of gender, mental retardation, and seizure disorders are also discussed as additional risk factors in the development of communication problems and schizophrenia.
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PMID:Speech and language disorders in children and adolescents with schizophrenia. 874 94

The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine-epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism).
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PMID:The role of dopamine in epilepsy. 878 31


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