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Sivu 1 alkaen 4959 tuloksia
Cerebral atrophy and convulsive seizures after recovery from cerebral edema and coma in a patient with fulminant hepatitis B.
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We report a 48-year-old woman who developed convulsive seizures and cerebral atrophy after recovery from fulminant hepatitis B with coma and cerebral edema at the acute stage. Neurological disturbances and cerebral signs are rare sequelae of fulminant hepatic failure (FHF); only a few cases have
Degenerate time-dependent network dynamics anticipate seizures in human epileptic brain.
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Epileptic seizures are known to follow specific changes in brain dynamics. While some algorithms can nowadays robustly detect these changes, a clear understanding of the mechanism by which these alterations occur and generate seizures is still lacking. Here, we provide crossvalidated evidence that
Hippocampal atrophy and abnormal brain development following a prolonged hyperthermic seizure in the immature rat with a focal neocortical lesion.
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In rats subjected to a focal cortical lesion soon after birth, hyperthermia at P10 induces a prolonged epileptic seizure, often followed by temporal lobe epilepsy in the adult. To determine whether brain damage and notably hippocampal atrophy occur early on in this model, whole brain as well as
Bilateral hippocampal atrophy in temporal lobe epilepsy: effect of depressive symptoms and febrile seizures.
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OBJECTIVE
Neuroimaging studies suggest a history of febrile seizures, and depression, are associated with hippocampal volume reductions in patients with temporal lobe epilepsy (TLE).
METHODS
We used radial atrophy mapping (RAM), a three-dimensional (3D) surface modeling tool, to measure hippocampal
The relation of spike foci and of clinical seizure characteristics to different patterns of mesial temporal atrophy.
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We reviewed clinical data and scalp electroencephalograms in 61 consecutive patients with temporal lobe epilepsy and mesial temporal atrophy assessed with volumetric magnetic resonance imaging: 39 patients had unilateral and 22 patients had bilateral atrophy. We attempted to determine whether any
[Mental retardation convulsions and cerebral atrophy; main neurological changes in Darier's disease].
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Darier's disease is determined by an autosomal dominant gene and is clinically characterized by confluent hyperkarotic papules. Mental retardation may appear in up to 10-20% of patients. Convulsions, spinocerebellar tract degeneration, polyneuropathy, psychiatric disorders and cerebral atrophy occur
Three-dimensional hippocampal atrophy maps distinguish two common temporal lobe seizure-onset patterns.
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OBJECTIVE
Current evidence suggests that the mechanisms underlying depth electrode-recorded seizures beginning with hypersynchronous (HYP) onset patterns are functionally distinct from those giving rise to low-voltage fast (LVF) onset seizures. However, both groups have been associated with
Absence seizures with myoclonic seizures as an early manifestation of dentato-rubro-pallido-luysian atrophy (DRPLA): a follow-up clinical course of twelve years.
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Typical absence seizures and isolated myoclonic seizures are both classified as age-related generalized seizures and are considered to be benign neurological manifestations. Concomitance of the two types of seizure is considered benign if it does not accompany other types of seizures or other
Selective ablation of alphav integrins in the central nervous system leads to cerebral hemorrhage, seizures, axonal degeneration and premature death.
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Mouse embryos genetically null for all alphav integrins develop intracerebral hemorrhage owing to defective interactions between blood vessels and brain parenchymal cells. Here, we have used conditional knockout technology to address whether the cerebral hemorrhage is due to primary defects in
Clinical and neuroimaging features of good and poor seizure control patients with mesial temporal lobe epilepsy and hippocampal atrophy.
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OBJECTIVE
Hippocampal atrophy (HA) and signal changes, detected at magnetic resonance imaging, have been associated with intractable seizures. Such a relation has been established by tertiary centers, where the prevalence of more severe cases tends to be higher. We evaluated the clinical and imaging
Intrahippocampal kainic acid, seizures and local neuronal degeneration: relationships assessed in unanesthetized rats.
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Intrahippocampal infusion of nanogram amounts of the neurotoxin kainic acid were used to investigate possible relationships between the convulsive and the local neurodegenerative properties of the amino acid. Bilateral hippocampal depth electrodes and cortical leads were employed to provide
Accumulation of zinc in degenerating hippocampal neurons of ZnT3-null mice after seizures: evidence against synaptic vesicle origin.
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In several brain injury models, zinc accumulates in degenerating neuronal somata. Suggesting that such zinc accumulation may play a causal role in neurodegeneration, zinc chelation attenuates neuronal death. Because histochemically reactive zinc is present in and released from synaptic vesicles of
[A child with choreic movement, generalized convulsion and severe neurological deterioration responded to cyclophosphamide].
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A 3-year-old girl developed right hemiplegia with acute onset, followed by generalized convulsion, choreic movement, and severe motor deterioration. She became bed-ridden a few months after the onset. Intravenous cyclophosphamide pulse therapy resulted in a remarkable improvement of her clinical
Co-induction of p75(NTR) and the associated death executor NADE in degenerating hippocampal neurons after kainate-induced seizures in the rat.
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Zinc induces in cultured cortical neurons both p75(NTR) and p75(NTR)-associated death executor (NADE), which together contribute to caspase-dependent neuronal apoptosis. Since zinc neurotoxicity may contribute to neuronal death following seizures, we examined whether p75(NTR) and NADE are co-induced
Degree of hippocampal atrophy is not related to a history of febrile seizures in patients with proved hippocampal sclerosis.
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OBJECTIVE
To examine the degree of hippocampal atrophy in patients with temporal lobe epilepsy and proved hippocampal sclerosis to determine whether or not patients with febrile seizures have more severe hippocampal atrophy. To determine whether or not there is a relation between age of seizure
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