MR imaging volumetry of subcortical structures and cerebellar hemispheres in temporal lobe epilepsy.

BACKGROUND AND PURPOSE: There is mounting evidence of extratemporal volume changes associated with medically refractory temporal lobe epilepsy (TLE). This MR imaging study aimed to characterize volume changes in subcortical structures and cerebellar hemispheres with respect to lateralization of the seizure focus, onset and duration of epilepsy, and frequency of generalized tonic-clonic seizures (GTCS). METHODS: Amygdalar, hippocampal, thalamic, caudate head, and cerebellar volume measurements were obtained in the preoperative MR images of 40 patients with TLE (20 right, 20 left), who underwent temporal lobe resection with good outcome, and in 20 right-handed control participants. All 3D MR images were spatially aligned and normalized before measurements were obtained. Standardized volumes and right-to-left volume ratios (VRs) were compared between control participants and right and left TLE groups. Multiple regression analyses were performed to study the effects of epilepsy onset and duration and GTCS frequency on ipsilateral-to-contralateral VRs with respect to the resected seizure focus. RESULTS: Thalamic volumes were smaller bilaterally in patients with TLE. Hippocampal volumes were smaller ipsilateral to the seizure focus, but there was no significant volume loss involving the amygdala, caudate, or cerebellum. Hippocampal and amygdalar right-to-left VRs differed significantly between right and left TLE groups and controls, whereas thalamic right-to-left VRs differed only between the TLE groups. Thalamic ipsilateral-to-contralateral VRs were correlated positively with epilepsy onset and negatively with epilepsy duration. Caudate ipsilateral-to-contralateral VRs were positively, whereas amygdalar and cerebellar VRs were negatively, correlated with GTCS frequency. CONCLUSIONS: Unilateral amygdalar and bilateral thalamic volume loss, in the absence of caudate head atrophy, is likely to reflect seizure-induced injury due to TLE. Correlations of VRs affecting the amygdala, caudate, and cerebellum with GTCS frequency may also reflect injury or a prediposition for secondary generalization. Potential effects of complex partial seizures, febrile seizures, or antiepileptic medications on subcortical structures need to be evaluated in future studies.

Steady growth cone currents revealed by a novel circularly vibrating probe: a possible mechanism underlying neurite growth.

The rate and direction of neurite growth have been shown in a number of studies to be determined by the distribution of adhesive sites on the growth cone. Recent evidence showing that the application of extrinsic electric fields can redistribute membrane molecules and alter both the rate and direction of neurite growth have raised the question whether endogenous electric fields might be produced by steady currents in growth cones. To investigate this question, we have devised a novel circularly vibrating microprobe capable of measuring current densities in the range of 5 nA/cm2 (near the theorectical limit of sensitivity), with a spatial resolution of 2 micron. The design of this device and the development of a novel algorithm for computing current vectors on-line is described. Using this probe we have found that cultured goldfish retinal ganglion cell growth cones generate steady inward currents at their tips. The measured currents, in the range of 10-100 nA/cm2, appear to flow into the filopodia at their tips and back outward near the junctures of the filopodia and the growth cone. The currents appear to be produced only during active growth. Ion substitution experiments support the conclusion that the majority of this current is carried by Ca2+ ions, which we postulate flow through a population of activated voltage-sensitive Ca2+ channels located on the filopodial tips. Calculation of the transmembrane current density (4 X 10(-6) nA/cm2) leads to an estimate of channel density (10 channels/micron2) in close agreement with the measured density of Ca2+ channels in other systems. The assumption that calcium channel proteins are conveyed to nerve terminals by active transport, whereas sodium channel proteins are conveyed passively by a slower somatofugal diffusion process [Strichartz et al, 1984], would explain why developing neurons tend to display Ca2+-sensitive electrogenesis at their growing tips, and Na+-sensitive action potentials later in development. In order to gain some insight into the possible role of these steady growth currents, we estimated the membrane depolarization and axial voltage gradient they produce. It is likely that the currents produce sufficient membrane depolarization (approximately equal to 4 mV) to cause autogenous activation of ion channel permeabilities. Similarly, the axial voltage gradient (approximately equal to 4 mV/cm) would be expected to move intracytoplasmic vesicles by electrophoresis at a rate (20-40 microns/hr) very close to that at which the filopodia are observed to grow.(ABSTRACT TRUNCATED AT 400 WORDS)