The distribution of the mossy fiber synaptic terminals was examined using the Timm histochemical method in surgically excised hippocampus and dentate gyrus from patients who underwent lobectomy of the anterior part of the temporal lobe for refractory partial complex epilepsy. The dentate gyrus of epileptic patients demonstrated intense Timm granules and abundant mossy fiber synaptic terminals in the supragranular region and the inner molecular layer. In contrast, the dentate gyrus of presenescent nonepileptic primates demonstrated no Timm granules in the supragranular region. In nonepileptic senescent primates, occasional very sparse supragranular Timm granules were results are morphological evidence of mossy fiber synaptic reorganization in the temporal lobe of epileptic humans, and suggest the intriguing possibility that mossy fiber sprouting and synaptic reorganization induced by repeated partial complex seizures may play a role in human epilepsy.

Abnormal functional activity induces long-lasting physiological alterations in neural pathways that may play a role in the development of epilepsy. The cellular mechanisms of these alterations are not well understood. One hypothesis is that abnormal activity causes structural reorganization of neural pathways and promotes epileptogenesis. This report provides morphological evidence that synchronous perforant path activation and kindling of limbic pathways induce axonal growth and synaptic reorganization in the hippocampus, in the absence of overt morphological damage. The results show a previously unrecognized anatomic plasticity associated with synchronous activity and development of epileptic seizures in neural pathways.

Objective: To address the need for brief, reliable, valid, and standardized quality of life (QOL) assessment applicable across neurologic conditions. Methods:Drawing from larger calibrated item banks, we developed short measures (8-9 items each) of 13 different QOL domains across physical, mental, and social health and evaluated their validity and reliability. Three samples were utilized during short form development: general population (Internet-based, n ϭ 2,113); clinical panel (Internet-based, n ϭ 553); and clinical outpatient (clinic-based, n ϭ 581). All short forms are expressed as T scores with a mean of 50 and SD of 10.

Magnetic resonance imaging (MRI) was performed after complex febrile convulsions (CFCs) in 27 infants. Definite MRI abnormalities were seen in 6 of the 15 infants with focal or lateralized CFCs and in none of the 12 infants with generalized CFCs. In 2 of the 6 infants with lateralized CFCs and abnormal MRIs, the MR images showed preexisting bilateral hippocampal atrophy consistent with the history of perinatal insults in these infants. However, the remaining 4 infants with MRI abnormalities and lateralized CFCs had significantly longer seizures than other infants and had MRI changes suggesting acute edema with increased hippocampal T2-weighted signal intensity and increased volume predominantly in the hippocampus in the hemisphere of seizure origin. Of those with acute edema, 1 had electrographical seizure activity recorded in the temporal region and another had a choroid fissure cyst displacing the affected hippocampus; both infants had follow-up MRIs showing that hippocampal atrophy had developed. These patients demonstrate that prolonged and focal CFCs can occasionally produce acute hippocampal injury that evolves to hippocampal atrophy. Finally, evidence of preexisting hippocampal abnormalities in several infants and electrographical temporal lobe seizure activity in 1 suggests the possibility that CFCs actually originated in the temporal lobes in some patients.

No abstract