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

Benign neonatal seizures is a rare but increasingly recognized syndrome characterized by seizures in the neonatal or infantile period. Two forms are recognized: familial and nonfamilial. In both instances, the seizures may be quite severe, and status epilepticus is common. The nonfamilial form is characterized by idiopathic, self-limited seizures occurring in previously normal neonates. The seizures most commonly occur at day 5 and have been called "fifth-day fits" by some authors. Familial seizures most frequently have their onset during the first week of life, but onset may occur as late as early infancy. These seizures may recur for several months before resolving. No cause is found for the seizures, and the patient appears healthy during the interictal period. The family history reveals benign neonatal seizures in other family members. Although the prognosis is favorable in both syndromes, seizures may occasionally occur later in life in the familial form. The familial form of benign neonatal seizures is autosomal dominant, and the gene has been localized to chromosome 20.
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PMID:Benign neonatal seizures. 221 94

Benign neonatal convulsions, though rare, are seen with increasing frequency and are characterized by seizures during the neonatal period with favorable prognosis. Two distinct entities can be identified, based on whether the syndrome is familial or non-familial, with epilepsy developing in 14% of patients with the familial form. We report a retrospective study of 23 patients, 13 with benign familial neonatal seizures and 10 with benign idiopathic neonatal seizures. All except one had normal neurologic development. We observed central temporal (rolandic) EEG foci in the follow-up of a few patients in both groups, with no clinical manifestations. We consider the possibility that these entities may share common genetic factors with benign rolandic epilepsy.
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PMID:[Benign neonatal convulsions. Review of 23 cases]. 865 92

Eventually, glutamate and gamma-aminobutyric acid (GABA) are both excitatory; the first cortical synapses start to appear, some myelin is found in the cerebral hemispheres, and the long tracts are barely visible. The premature activation of N-methyl-D-aspartate (NMDA) transmission seems to generate neonatal myoclonic encephalopathy. Benign neonatal seizures and migrating partial seizures of infancy may result from an excessive or premature excitability in the deep layers. Benign rolandic epilepsy and continuous spikes and waves during slow sleep are associated with an excess of excitatory and inhibitory cortical synapses. West and Lennox-Gastaut syndromes are related to an age-dependent, diffuse cortical hyperexcitability; the clinical presentation depends on the age at onset, and spike synchronization is achieved by myelination. Idiopathic generalized epilepsy is driven by brain maturation, which induces a frontal hyperexcitability responsible for myoclonic-astatic seizures at an age comprised between that of infantile and juvenile myoclonic epilepsies. The extensive physiological time frame preceding the maturation of the hippocampal-neocortical system could explain the scarcity of cortical injuries resulting from a lesion in infants.
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PMID:[Brain maturation and epilepsy]. 2342 14

At full term, both glutamate and gamma-amino-butyric acid (GABA) are excitatory; cortical synapses are beginning to appear, there is little myelin in the cerebral hemispheres, and long tracts hardly start to develop. Neonatal myoclonic encephalopathy can result from premature activation of N-methyl-D-aspartate (NMDA) transmission. Benign neonatal seizures and migrating partial seizures in infancy could involve excessive or premature excitability of deep cortical layers. Benign rolandic epilepsy and continuous spike waves in slow sleep are consistent with an excess of both excitatory and inhibitory cortical synapses. West and Lennox-Gastaut syndromes express age-related diffuse cortical hyperexcitability, the pattern depending on the age of occurrence; synchronization of spikes is becoming possible with maturation of the myelin. Idiopathic generalized epilepsy is itself modulated by maturation that causes frontal hyperexcitability generating myoclonic-astatic seizures, between the ages of infantile and juvenile myoclonic epilepsies. Physiological delay of hippocampo-neocortical pathways maturation could account for the delayed occurrence of mesial temporal epilepsy following infantile damage, whereas premature maturation could contribute to fronto-temporal damage characteristic of fever-induced epileptic encephalopathy in school-age children, a dramatic school-age epileptic encephalopathy.
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PMID:Brain maturation and epilepsy. 2362 92