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

Two initially healthy infants developed acute encephalopathic illnesses characterized by stupor, seizures, cerebrospinal fluid (CSF) erythrocytic and monocytic pleocytosis, increased CSF protein, and decreased CSF glucose and progression to chronic decerebration. In one case, herpes simplex virus was recovered from cutaneous lesions. The initial computed tomography (CT) scan revealed widespread subcortical increased attenuation with further increase after contrast medium injection and patchy areas of decreased attenuation in the deep cerebral white matter. Subsequent CT scans demonstrated progressive cortical calcifications and persistence of low attenuation areas. Autopsy revealed multiple cystic encephalomalacia. The second infant had similar clinical, CSF, and CT findings but remains in a chronic decerebrate state at 14 months of age. The CT abnormalities seen in these patients have not been encountered in any of 13 other infants with the clinical diagnosis of meningitis or encephalitis. Multiple cystic encephalomalacia of infancy is a rare condition with a uniformly bleak prognosis. Computed tomography may prove useful in the early diagnosis, thereby aiding clinicians in counseling and in the acute and long-term management of patients with this lesion.
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PMID:Multiple cystic encephalomalacia of infancy: computed tomographic findings in two cases with associated intracerebral calcification. 42 99

Thirteen infants with neonatal seizures showed paroxysmal monorhythmic electrographic activity, predominantly in the alpha range (8 to 13 Hz) and localized to the rolandic cortical areas. This rhythmic discharge, which is commonly lateralized, represents an electrical seizure discharge. Such discharges may exist as the only electrographic seizure activity, but in the majority of cases (8/13) independent epileptiform discharges are observed in other cortical areas. All infants with paroxysmal monorhythmic alpha activity had clinically observed seizures. Computerized tomography performed six or more weeks after observing the electrographic abnormality demonstrated diffuse as well as localized cortical atrophy in a distribution similar to the monorhythmic alpha activity. In other cases, localized monorhythmic alpha activity was correlated on subsequent evaluations with focal neurological abnormalities (eg, hemiparesis and hemiatrophy) and a high incidence of microcephaly (83%). On the basis of these findings, we suggest that encephalomalacia may be important in the pathogenesis of paroxysmal monorhythmic alpha seizures in the neonate.
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PMID:Neonatal paroxysmal monorhythmic alpha activity. 62 27

We studied a 24-year-old man who had reading epilepsy after removal of a left frontal arteriovenous malformation. Lesion analysis by means of a neuroanatomic template placed a 2-cm region of encephalomalacia anterior to the left central sulcus in premotor cortex (Brodmann's area 6). Lexical and nonlexical reading activation tests demonstrated seizures during reading and increased discharge rates when the patient was reading aloud or silently articulating. Seizures (perceived or actual jaw clicking) were electrographically characterized by brief left frontocentral epileptiform transients. Grapheme to phoneme transformation, not linguistic complexity, appears to be the critical stimulus in some reading epilepsies. The case adds anatomic relevance to the phonologic component of reading and supports the putative role of dominant premotor cortex in activation of precise sequences of motor linguistic output in reading and writing. Reading epilepsy may be a reflex or action myoclonus syndrome localized to Brodmann's area 6 (Exner's area).
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PMID:The role of dominant premotor cortex and grapheme to phoneme transformation in reading epilepsy. A neuroanatomic, neurophysiologic, and neuropsychological study. 152 84

One hundred neonates determined prospectively to be at risk for neurologic handicap underwent magnetic resonance imaging with a high-field (1.5 T) imager. Thirty-three demonstrated a total of 37 lesions consistent with hypoxic-ischemic encephalopathy, including periventricular leukomalacia (n = 12), basal ganglia hemorrhage (n = 5), multicystic encephalomalacia (n = 5), and focal parenchymal hemorrhage (n = 15). Diagnoses by ultrasonography and computed tomography were compared with those by magnetic resonance imaging in 29 and 17 infants, respectively. Ultrasonography agreed more frequently with magnetic resonance imaging than did computed tomography. Ultrasonography detected 79% of lesions demonstrated by magnetic resonance imaging whereas computed tomography detected only 41%. Periventricular leukomalacia was seen most often in preterm infants, basal ganglia hemorrhage and multicystic encephalomalacia primarily occurred in term infants, and focal parenchymal hemorrhage occurred at all gestational ages. Basal ganglia hemorrhage and multicystic encephalomalacia were strongly associated with histories of perinatal asphyxia, seizures, and early abnormal neurological status. All infants with basal ganglia hemorrhage (5/5) and multicystic encephalomalacia (5/5) and the majority with periventricular leukomalacia (9/12) and focal parenchymal hemorrhages (9/15) had developmental abnormalities at discharge.
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PMID:Prospective observations of 100 high-risk neonates by high-field (1.5 Tesla) magnetic resonance imaging of the central nervous system. II. Lesions associated with hypoxic-ischemic encephalopathy. 201 18

One-hundred-eight EEGs from 47 newborn infants were compared with the postmortem neuropathological findings. The degree of EEG background abnormality had good correlation with the severity of the brain lesion; the more severe the EEG background abnormality, the more extensive and intensive the morphological change. Widespread encephalomalacia was demonstrated in six infants who manifested isoelectric tracings. In particular, cerebral cortex, corpus striatum, thalamus, midbrain, and pons were affected in all patients with this abnormal EEG pattern. Burst-suppression patterns, which were seen in seven infants, also correlated with multifocal severe brain damage, but there was no common structure that was consistently affected for all patients with this pattern. Positive rolandic sharp-wave transients (PRS) appeared highly specific for white matter lesions. All eight infants with PRS had white matter lesions. However, the sensitivity of PRS for white matter lesions was not high (32%), and the white matter lesions of PRS-positive patients were not necessarily composed of periventricular leukomalacia. The sensitivity of EEG asymmetry was also low (40%) for the focality of morphological change, although the specificity was relatively high (85%). The origin of seizure discharges, on the other hand, had poor correlation with the site of the brain lesion.
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PMID:Neonatal electroencephalography and neuropathology. 270 14

Recent investigations at several institutes have demonstrated extensive acute brain pathology in experimental animals exposed to single subcutaneous doses of the chemical warfare nerve agents soman or sarin. Lesions include neuronal and neurophil degeneration, necrosis, and in animals that survive for several weeks, a degenerative encephalopathy characterized by mineralization, encephalomalacia, atrophy, and hydrocephalus. The cerebral cortex, amygdaloid complex, hippocampus, and multiple thalamic nuclei are consistently affected. This pattern of injury resembles that described for epilepsy and ischemic brain injury. Some animals have cardiac lesions characterized by acute necrosis with subsequent mild inflammation and fibrosis. Anticonvulsants protect experimental animals from lesion development. In rats, this encephalopathy causes long-range behavioral changes characterized by hyperactivity during routine handling and variances in traditional behavioral tests. The histopathologic features and distribution of lesions in nerve agent-poisoned animals support the hypothesis that epileptiform seizure activity is a major factor in nerve agent pathology. Other localized insults such as ischemia and hypoxia probably contribute to the pathogenesis.
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PMID:Pathology of nerve agents: perspectives on medical management. 409 82

The medical records of 89 children followed at a multidisciplinary Meningomyelocele Clinic at the Children's Clinics for Rehabilitative Services were reviewed. Almost all children in southern Arizona with meningomyelocele are followed at this clinic. Eight children (foreign nationals) were excluded because they were not eligible for neurosurgery/neurology services at the clinic. The remaining 81 children have been followed at the clinic from 0.25 to 21 years. Seventeen children (21%; age: 1.3-17 years, mean: 9.1 +/- 4.4 years; follow-up: 1.3-16 years) manifested seizures at some time during their course. All children with seizures had shunted hydrocephalus. Neonatal seizures occurred in 2 children currently not receiving medication. An additional 3 children had an acute symptomatic seizure associated with an intraventricular hemorrhage during ventriculoperitoneal shunt revision, 2 of whom later developed epilepsy. Fourteen children (17.3%) had epilepsy; 12 were taking antiepileptic drugs. Seizures were controlled on medication in 5 children. EEG abnormalities were present in 12 children (focal slowing 4, focal spikes 8, diffuse slowing 3, generalized or bilaterally synchronous spike-wave 4). Most of these children (12/14) had evidence of additional central nervous system (CNS) pathology (i.e., areas of encephalomalacia or past stroke 7, cerebral malformations 2, CNS calcifications 1, and frequent apneic spells/cardiac arrest 2). We conclude that epilepsy occurs in approximately 17% of children with meningomyelocele, and most have other CNS pathology to account for their seizures.
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PMID:Epilepsy in children with meningomyelocele. 757 45

In temporal lobe epilepsy (TLE) lesion patients the pathology, location of intracranial ictal EEG onsets, and hippocampal neuron losses were compared. Patients (n = 63) were classified into: (1) Tumors (n = 26, e.g. astrocytomas, gangliogliomas); (2) vascular (n = 9, e.g. cavernous and venous angiomas); (3) developmental (n = 17, e.g. cortical dysplasia, heterotopias); or (4) atrophic (n = 11, e.g. cortical or white matter encephalomalacia). Other variables were; (1) the location of the temporal lesion in the mesial to lateral, and anterior to posterior plane, (2) a clinical history of an initial precipitating injury (IPI) prior to the onset of TLE (e.g. prolonged first seizure, head trauma), (3) hippocampal neuron densities, (4) focal or regional location by intracranial depth EEG of ictal onsets, and (5) seizure outcomes. Results showed that severe hippocampal neuron losses were associated with two statistically significant findings. First, patients with mesial lesions in or adjacent to the body of the hippocampus had greater neuron losses compared to mesial lesions anterior or posterior to the hippocampus (P = 0.04). Second, lesion patients with an IPI history had greater Ammon's horn (AH) neuron losses compared to those without IPI histories (P = 0.0005), and the profile of loss was similar to hippocampal sclerosis (HS). Granule cell losses correlated in a complex manner in that; 1) by regression analysis densities decreased with longer intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs (P = 0.05), and (3) developmental patients with IPIs had greater granule cell loss than patients without IPIs (P = 0.009). Mesial-temporal depth EEG electrodes were the first areas of ictal activity in 15 of 16 patients (94%), and greater hippocampal neuron losses were not associated with focal mesial-temporal EEG onsets. Seizure outcomes were worse in tumor patients compared to HS patients (P = 0.01), and patients with post-resection seizures had incomplete resections of their lesions and/or hippocampi. These results indicate that in TLE lesion patients the amount and pattern of hippocampal neuron loss depends on the location of the lesion, the pathologic classification, and a history of an IPI. Further, despite variable neuron losses, in temporal lesion patients the hippocampus was nearly always involved in the genesis or propagation of the chronic seizures.
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PMID:The pathophysiologic relationships between lesion pathology, intracranial ictal EEG onsets, and hippocampal neuron losses in temporal lobe epilepsy. 758 88

The use of the supratentorial-infraoccipital approach is reported in seven patients with posteromedial temporal lobe lesions. No patient had permanent morbidity. Gross total resection of three low-grade gliomas and two gangliogliomas was achieved in five patients; one patient had subtotal resection of a low-grade glioma with adjacent gliosis, and one was initially thought to have a glioma but proved to have encephalomalacia on final pathological analysis. The patients ranged in age from 5 to 34 years. All seven patients presented with seizures, and four had uncontrolled seizures preoperatively. Six have been seizure-free since surgery (mean follow-up period 15 months), and one is well controlled on anticonvulsant medication. An anatomical study was performed to delineate the microsurgical anatomy relevant to operating on the medial temporal lobe through this posterior approach. A viewing wand intraoperative navigational system was utilized with this approach and proved helpful in gaining access as far anterior as the uncus through this occipital craniotomy. This approach is favorable in selected patients with posterior, medial, temporal lobe tumors because resection of otherwise difficult lesions may be accomplished without sacrificing lateral temporal lobe cortex or transecting the optic radiations.
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PMID:Supratentorial-infraoccipital approach for posteromedial temporal lobe lesions. 776 Jan 95

A patient with a remote infarct, seizures, mild hemiparesis, and dysphasia became obtunded over four months and died. Computerized tomography (CT) over 5 years showed a consistent, large, wedge-shaped left hemisphere hypodensity with a central calcification, but without signs of mass effect. This was interpreted as an infarct of the left middle cerebral artery territory. Post-mortem examination of the brain revealed the entire area appearing as infarct on CT was a gliosarcoma. We suspect that the unusual CT appearance of the lesion was likely caused by multiple pathologies: a low grade glioma transforming into a gliosarcoma that was able to spread throughout the area of infarct encephalomalacia without revealing a typical CT appearance of mass effect. The patient's brief period of deterioration probably coincided with transformation of the tumor into a gliosarcoma. The variable CT characteristics of gliosarcomas are reviewed.
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PMID:Unusual evolution and computerized tomographic appearance of a gliosarcoma. 808 41


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