Summary: Purpose: Epileptiform discharges that resemble interictal spikes can be generated by slices of neocortex treated with antagonists of y-aminobutyric acid A (GABA,) receptors. These discharges can propagate horizontally for long distances. We tested the hypothesis that propagation occurs through preferred horizontal pathways that lie in a particular cortical layer.Methods: Slices were prepared from the primary somatosensory cortex of rats, maintained in vitro, and bathed with the GABA, receptor antagonist picrotoxin. Electrical stimuli were used to evoke single all-or-none paroxysmal field potentials (PFP) that were recorded with pairs or arrays of field potential electrodes.Results: To test which laminae are necessary for propagation, vertical cuts were made to force the PFF' to spread horizontally through particular layers. If slices were bathed in a high dose of picrotoxin (35 m, a bridge of cortex 350 Fm thick placed at any lamina was sufficient to support PFP propagation. However, in low picrotoxin doses (2.5 CLIK), similarly sized bridges had to include tissue from layers 415 or 516 to support propagation. When slices were cut horizontally (i.e., parallel to the pia) in strips, either upper-, middle-, or lowerlayer strips were sufficient to support PFP propagation if the picrotoxin concentration was high; however, in low picrotoxin doses, only horizontal strips that included layer 5 could support propagation. Finally, in intact picrotoxin-treated slices, focal applications of GABA were systematically applied to different laminae as the PFP propagated past; GABA was most effective at blocking or delaying propagation when it was applied to layer 5b.Conclusions: We conclude that epileptiform propagation can occur through a variety of horizontal pathways when cortical inhibition is strongly impaired. However, when inhibition is reduced only moderately, axonal pathways in layer 5 are critical for seizure spread.

Object. The diagnosis, treatment, and postoperative care of morbidly obese patients undergoing spinal surgery require modifications for body habitus. With a growing percentage of the United States population becoming morbidly obese, the surgeon may need elective or emergency treatment plans that address the special needs of these patients. The authors retrospectively reviewed the diagnosis, treatment, and postoperative care of the severely obese patient undergoing spinal surgery. Methods. To assess the associated results and complications of management that required modification for body habitus, 12 patients were included in the study (nine females); the mean age was 50 years and mean weight was 320 lb. Cases of cervical (two cases), thoracic (four cases), and lumbar surgeries (six cases) were included. The follow-up period ranged from 6 months to 2 years. Patients presented with myelopathy (five cases), radicular pain and weakness (four cases), radiculopathy (two cases), and cauda equina syndrome (one patient). Chronic progressive neurological deterioration secondary to spinal cord compression was demonstrated in nine patients and acute pain and/or weakness secondary to nerve root compression was observed in three patients. Conclusions. The authors found that although morbidly obese patients may present late in the course of their symptoms and require modifications in the use of standard neuroimaging, operative facilities, and treatment plans, open mindedness and persistence can yield satisfactory results in most cases.

Essential tremor can be suppressed with chronic, bilateral deep brain stimulation (DBS) of the ventralis intermedius nucleus (Vim), the cerebellar receiving area of the motor thalamus. The goal in this study was to correlate the location of the electrodes with the clinical efficacy of DBS in a patient with essential tremor. The authors report on a woman with essential tremor in whom chronic bilateral DBS directed to the ventral thalamus produced adequate tremor suppression until her death from unrelated causes 16 months after placement of the electrodes. Neuropathological postmortem studies of the brain in this patient demonstrated that both stimulators terminated in the Vim region of the thalamus, and that chronic DBS elicited minor reactive changes confined to the immediate vicinity of the electrode tracks. Although the authors could not identify neuropathological abnormalities specific to essential tremor, they believe that suppression of essential tremor by chronic DBS correlates with bilateral termination of the stimulators in the Vim region of the thalamus.