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

Although human aggression is frequently inferred to parallel aggression based on testosterone in nonprimate mammals, there is little concrete support for this position. High- and low-aggression individuals do not consistently differ in serum testosterone. Aggression does not change at puberty when testosterone levels increase. Aggression does not increase in hypogonadal males (or females) when exogenous testosterone is administered to support sexual activity. Similarly, there are no reports that aggression increases in hirsute females even though testosterone levels may rise to 200% above normal. Conversely, castration or antiandrogen administration to human males is not associated with a consistent decrease in aggression. Finally, changes in human aggression associated with neuropathology are not consistent with current knowledge of the neural basis of testosterone-dependent aggression. In contrast, human aggression does have a substantial number of features in common with defensive aggression seen in nonprimate mammals. It is present at all age levels, is displayed by both males and females, is directed at both males and females, and is not dependent on seasonal changes in hormone levels or experiential events such as sexual activity. As would be expected from current knowledge of the neural system controlling defensive aggression, aggression in humans increases with tumors in the medial hypothalamus and septal region, and with seizure activity in the amygdala. It decreases with lesions in the amygdala. The inference that human aggression has its roots in the defensive aggression of nonprimate mammals is in general agreement with evidence on the consistency of human aggressiveness over age, with similarities in male and female aggressiveness in laboratory studies, and with observations that some neurological disturbances contribute to criminal violence. This evidence suggests that human aggression has its biological roots in the defensive aggression of nonprimate mammals and not in hormone-dependent aggression based on testosterone.
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PMID:Aggression in humans: what is its biological foundation? 830 50

We report the results of 34 patients who underwent corpus callosotomy between 1986 and 1989 with 28-65 months of postoperative follow-up (mean 42 months). Thirty-two patients had mental retardation and 26 had significant behavioral problems. Thirteen patients had total section, 8 had subtotal section with preservation of the posterior half of the splenium, and 13 had section of the anterior two thirds of the callosum. Satisfactory seizure control was achieved in 25 patients (73.5%) Atonic seizures, followed by tonic seizures, generalized tonic-clonic seizures (GTCs), and atypical absence seizures were most improved. Myoclonic and complex partial seizures (CPS) did not improve significantly. No deterioration in seizure status was observed postoperatively. Two patients developed previously unobserved simple seizures and CPS postoperatively, but they were not as disabling as the preoperative seizures. Among the patients with behavioral problems, 81% had significant decrease in aggressiveness, hyperactivity, and/or attention deficit. Patients who underwent total section had interhemispheric disconnection symptoms that improved progressively and did not interfere with daily life. Decreased speech output, dysarthria, and gait dyspraxia occurred after total callosal section and persisted in 5 of the 13 patients. Patients who underwent anterior two thirds or subtotal sections did not have such symptoms. Early postoperative complications consisted of aseptic ventriculitis (5), subdural hematoma (1), and wound infection (4) and resolved without sequelae.
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PMID:Corpus callosotomy in treatment of medically resistant epilepsy: preliminary results in a pediatric population. 840 46

Intracranial cavernous malformations are vascular anomalies consisting of endothelium-lined caverns filled with blood at various stages of thrombosis and organization and separated by a collagenous stroma devoid of mature vessel wall elements. They occur in an estimated 0.45 to 0.9% of the population, with male and female patients equally affected and all ages represented. They commonly manifest as seizures, gross intracranial hemorrhage, and focal neurological deficits. Lesions are frequently multiple in the same patient, and 10 to 30% are associated with familial clustering. Several reports have documented a dynamic clinical-radiological lesion behavior with de novo lesion genesis, intralesional and perilesional hemorrhage, and corresponding fluctuations in lesion size. Hemorrhagic risk and neurological disability seem to be related to multiple factors, including lesion location, age, gender, state of reproductive cycle, and previous hemorrhage. Lesions may behave aggressively with repetitive hemorrhages and cumulative disability or may remain quiescent for many years. Management strategies include expectant follow-up in patients with asymptomatic or inaccessible lesions, excision of symptomatic and accessible lesions, and radiosurgery of progressively symptomatic lesions in inoperable locations. Relevant disease-specific outcome parameters are proposed to guide clinical decisions and future research. Prospective, stratified, hypothesis-driven studies using rigorous epidemiological methods must be undertaken to delineate patient and lesion factors influencing clinical aggressiveness. Biological studies are essential to uncover strategies to predict and modify lesion behavior.
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PMID:Intracranial cavernous malformations: lesion behavior and management strategies. 855 86

A double mutation in the alpha-secretase site in the betaA4 region of mouse amyloid precursor protein (APP) reduced its secretion from COS cells, polarized MDCK cells and rat primary neurons. Expression of this mutant in the brain of mice, using the neuron-specific elements of the mouse Thy-1 gene promoter, resulted in transgenic mice that became progressively hyperactive, displayed seizures and died prematurely. In three different transgenic lines the severity of the phenotype was related directly to the expression levels of the transgene, estimated by both mRNA and protein levels. In addition, homozygous mice derived from each transgenic strain showed more severe symptoms which also occurred earlier in life than in heterozygotes. The observed symptoms were, however, not essentially different in the different lines. Increased aggressiveness, disturbed responses to kainic acid and N-methyl-D-aspartate, neophobia and deficiency in exploratory behavior were demonstrated in these mice. In the brain, the observed neuropathological changes included necrosis, apoptosis and astrogliosis in the hippocampus, cortex and other areas. The data demonstrate that incomplete or incorrect alpha-secretase processing of APP results in severe neurotoxicity and that this effect is expressed in a dominant manner.
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PMID:Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice. 863 59

The authors analysed the correlation between different clinical, radiological, and pathological variables and the presence and intensity of brain oedema associated to intracranial meningioma in 400 consecutive patients studied by computerized tomography (CT). The following factors did not show significant correlation with brain oedema development: the age and sex of the patient, the occurrence of focal deficits, the presence of skull changes (endostosis, exostosis, osteolysis), the occurrence of tumour calcification, the density of the tumour on plain CT scan, the presence of a cystic component, the pathological subtype of meningioma (both conventional and non-conventional), and the presence of histological features of tumour aggressiveness, such as an increased vascularization, high cellularity, high mitotic index, pleomorphism, necrosis, and brain infiltration. Factors showing a statistically significant correlation with the presence and intensity of brain oedema at the bivariate analysis were: the presence of symptoms (p < 0.001), the duration of the clinical history (p < 0.05), the location and size of the tumour (p < 0.001), the type (heterogeneous vs homogeneous), and intensity of tumour contrast enhancement (p < 0.001), the presence of irregular tumour margins (p < 0.001), and the existence of focal low density intratumoural areas (p < 0.001). The multivariate analysis using only clinical parameters showed that the group of variables with the highest power for predicting the presence of brain oedema (concordance level of 76.8%) included: the presence of symptoms, the occurrence of seizures (focal or generalized), the presence of an intracranial hypertension syndrome, and the age of the patient. The multivariate analysis using only anatomico-radiological parameters showed that the model which included the size of the tumour, the intensity of contrast enhancement, the tumour margins, and meningioma location, predicted the presence of brain oedema in 80.8% of the cases. Though the results of the present study do not definitively support any of the major physiopathological theories proposed to explain brain oedema formation in patients with intracranial meningioma, some findings could favour the so-called hydrodynamic theory.
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PMID:Brain oedema in patients with intracranial meningioma. Correlation between clinical, radiological, and histological factors and the presence and intensity of oedema. 880 Mar 22

The authors report a long-term follow-up of 11 new subjects with benign myoclonic epilepsy. There were some unusual clinical features such as the need for dual therapy in 45.5% of subjects, and the presence of non-epileptic myoclonus in 54.5%, neither of which influenced the prognosis. Neuropsychological and behavioral evolution was less favorable in 45.5% of patients (mental retardation, school learning problems, attention deficit disorder, hyperkinesia, aggressiveness, irritability, negativism). The less favorable neuropsychological outcome might be related to additional interacting factors such as personal antecedents, seizure onset and antiepileptic treatment.
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PMID:Benign myoclonic epilepsy: long-term follow-up of 11 new cases. 940 94

Pervasive developmental disorder (PDD) is occasionally associated with medically intractable complex partial seizures. The outcome of PDD was explored in three males and two females who underwent epilepsy surgery at 32 months to 8 years of age (mean = 4 years) after onset of epilepsy at 1 week to 21 months of age (mean = 11 months). Four children had temporal lobe resections (three right, one left; two for focal cortical dysplasia, and two for tumors), and one had a right temporoparieto-occipital resection (for focal cortical dysplasia). Each child underwent repeated evaluations by a pediatric neuropsychologist and psychiatrist. Fourteen to 47 months (mean = 23 months) after operation, one child with persistent seizures had moderate developmental and behavioral improvement, three children (two seizure free, one with rare staring spells) had mild developmental and behavioral improvement, and the remaining child (seizure free) experienced a worsening of her PDD. The four children with mild-to-moderate improvement in postoperative cognitive and behavioral development still demonstrated persistent delay. Cognitive gains were confirmed by neuropsychologic testing in the oldest patient but were not reflected in test results from the three younger children, who had more modest improvement. The child with worsening of her PDD had cognitive and emotional deterioration to babbling, echolalia, aggressiveness, decreased social interaction, and increased mouthing of objects beginning several months postoperatively. These results suggest that families should be counseled that PDD symptoms in children with focal epileptogenic lesions may or may not improve after epilepsy surgery, even if the surgery is successful with respect to seizure control.
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PMID:Epilepsy surgery in children with pervasive developmental disorder. 1037 79

Several mouse models for Huntington's disease (HD) have been produced to date. Based on differences in strain, promoter, construct, and number of glutamines, these models have provided a broad spectrum of neurological symptoms, ranging from simple increases in aggressiveness with no signs of neuropathology, to tremors and seizures in absence of degeneration, to neurological symptoms in the presence of gliosis and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) positivity, and finally to selective striatal damage associated with electrophysiological and behavioral abnormalities. We decided to analyze the morphology of striatum and hippocampus from a mouse transgenic line obtained by microinjection of exon 1 from the HD gene after introduction of a very high number of CAG repeat units. We found a massive darkening and compacting of striatal and hippocampal neurons in affected mice, associated with a lower degree of more classical apoptotic cell condensation. We then explored whether this morphology could be explained with alterations in gene expression by hybridizing normal and affected total brain RNA to a panel of 588 known mouse cDNAs. We show that some genes are significantly and consistently up-regulated and that others are down-regulated in the affected brains. Here we discuss the possible significance of these alterations in neuronal morphology and gene expression.
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PMID:Early alterations in gene expression and cell morphology in a mouse model of Huntington's disease. 1089 61

The anticonvulsant action and the long-term effects on learning, memory and behavior of the new generation antiepileptic drug gabapentin (GBP) were investigated in immature animals. Kainic acid (KA) was administered to rats on postnatal day (P) 35. Animals were treated with GBP or saline from P36 to P75 and spontaneous seizure frequency was monitored. After tapering the drug, the rats were tested in the water maze and open field test. Brains were then analyzed for histological lesions. Animals treated with GBP following KA-induced status epilepticus had a reduced incidence of spontaneous recurrent seizures, a better pathology score, and less aggressiveness compared to saline-treated controls. Effectiveness of GBP on seizure threshold was tested using flurothyl inhalation in 10 separate age groups of animals ranging from the newborn period to adulthood. Furthermore, GBP plasma concentration peaks were determined in all age groups. At all ages, GBP pre-treated animals demonstrated a higher seizure threshold. Plasma GBP concentrations did not significantly change with age. These data suggest that acute administration of a single therapeutic dose of GBP increases the seizure threshold at all ages studied, while chronic treatment following the status reduces spontaneous seizure frequency and cell damage and has no long-term adverse consequences on cognitive processes during development.
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PMID:Anticonvulsant action and long-term effects of gabapentin in the immature brain. 1107 80

Since the dorsal and ventral hippocampus in the rat may act differently from one another in limbic seizures, we studied effects of orthogonal transection between the dorsal and ventral hippocampus upon kainic acid-induced amygdalar seizures. A total of 26 rats were divided into three groups. Ten rats underwent transection using a modified wire knife (transection group); 16 others were untransection group (n=10) and controls (n=6). All the rats then underwent stereotactic implantation of electrodes in the left amygdala (LA), left dorsal hippocampus (LdH), left ventral hippocampus (LvH), and the left sensorimotor cortex (LCx). A stainless steel cannula also was introduced into the LA. Rats except controls later received 1.0 microg of kainic acid (KA) via the cannula. Controls received phosphate buffer solution alone. In the untransection group, multiple spike discharges in the LA immediately propagated concurrently to the LvH and LdH. Propagation involved the LCx to become status epilepticus 1 to 2 h after KA injection. Seizures, characterized by mastication, salivation, facial twitching, forelimb clonus, and sometimes rearing and falling, lasted 1 to 2 days. Microscopic examination revealed severe neuronal cell damage in the LA, LvH, and LdH. In the transection group, multiple spike discharges initiated from the LA and were propagated to LvH, but LdH as well as LCx involvement was slight. Status epilepticus involved only the LA and LvH 1 to 2 h following KA injection. Seizures subsided within 24 h, showing no ictal manifestations except for aggressiveness. Overall, seizures were weak and transient compared with those in controls. Histologically, hippocampal neuronal damage was slight, but damage to amygdalar neurons was similar to that in untransection group. No electroclinical and histological changes were seen in controls. These results indicated that connections between the dorsal and ventral hippocampus are important for full development of KA-induced amygdalar seizures.
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PMID:Hippocampal transection attenuates kainic acid-induced amygdalar seizures in rats. 1128 62


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