Biomedical subjects
Publications and source records attributed to R P Lesser.
Auditory evoked potentials (AEPs) were determined in 16 patients with near-miss sudden infant death syndrome. The AEPs were normal in all patients except one with prolonged 1 to V interpeak latency (bilaterally) and another with an asymmetry of interear 1 to V interpeak latency difference. These results indicate that AEPs do not permit detection of infants at high risk for crib death.
Cortical somatosensory evoked potentials to posterior tibial nerve stimulation were obtained in 29 normal controls varying in age and body height. In obtaining these potentials we varied recording derivations and frequency settings. Our recordings demonstrated the following points: N20 (dorsal cord potential) and the early cortical components (P2, N2) were the only potentials that were consistently recorded. All other subcortical components (N18, N24, P27, N30) were of relatively low amplitude and not infrequently absent even in normals. All absolute latencies other than N2 were correlated with body height. However, interpeak latency differences were independent of body height. Below the age of 20, subcortical but not cortical peak latencies correlated with age, but this appeared to be due to changes in body height in this age group. Absolute amplitudes and amplitude ratios (left/right and uni/bilateral) showed marked interindividual variability and have very limited value in defining abnormality. The use of restricted filter windows facilitated the selective recording of postsynaptic potentials (30-250 Hz) and action potentials (150-1500 Hz).
The effects of stimulus intensity on subcortical and cortical somatosensory evoked potentials (SEPs) to posterior tibial nerve (PTN) stimulation were studied in 16 normal controls. Stimulus intensity was evaluated as a function of sensory threshold (S). Motor threshold (M) varied between 1 S and 2 S. The amplitude of N18 (afferent volley immediately before it enters the spinal canal) increased approximately linearly up to at least 4.5 S. N20 (dorsal cord potential) also demonstrated a linear increase up to at least 4 S but the rate of increase was significantly smaller. All central components (subcortical brain-stem components P27 and N30, and cortical components N1 and P2) showed an even smaller rate of increase which was non-linear and reached a plateau at 3 S. The relatively higher rate of increase of N18 as compared with N20 was most probably due to the recording of sensory impulses plus antidromic impulses in motor fibers. The smaller rate of increase and early saturation of all the central components compared with N20 suggests that of all the afferent fibers generating N20 only the low threshold fibers participate in the generation of more central components. Stimulus intensities of 3 S are recommended for clinical studies of the central SEPs to PTN stimulation.
With the aid of chronic subdural electrodes we have been able to record from the posterior banks of the sylvian fissure, auditory evoked potentials (AEPs) that had morphologies and peak latencies compatible with the primary AEPs described by Celesia and Puletti (1969). These AEPs had amplitudes that were not only affected by the side of stimulus presentation but were maximal in an area close to the primary auditory cortex. The AEPs also displayed an extremely steep spatial gradient and were not altered by pentobarbitone sodium and nitrous oxide anaesthesia. Together, these properties suggest that these subdurally recorded potentials are near-field evoked potentials from the primary auditory cortex. The focal nature of these potentials also allows them to be used as effective electrophysiological tools for localization of the primary auditory cortex in patients.
In three patients stimulation of the frontal speech area resulted in one or more of the following symptoms: speech arrest, writing arrest, or impaired rapid alternating movements of the tongue, fingers or toes. Speech arrest could be altered at individual points either with or without impairment of rapid movements or writing, but writing was not impaired without concomitant difficulties with either speech or rapid finger movements. Our data suggest that the frontal speech area may function to integrate complex motor functions, some speech related and others not. We also confirm previous conclusions that Exner's writing centre is not separate from Broca's area and that the writing defect in Broca's aphasia can occur without involvement of the motor strip.
We have evaluated the afterdischarge thresholds and functional response thresholds in 21 patients with chronically implanted arrays of subdural electrodes. Afterdischarge thresholds varied from 2 to greater than 15 mA over the tested cortex, by as much as 12 mA in individual patients, and by as much as 12 mA between adjacent electrodes. Thresholds for functional alteration varied from 2 to 15 mA in tested cortex, by as much as 9.5 mA in individually tested patients, and by as much as 6.5 mA between adjacent electrodes. We conclude that the optimal localization of functional cortical areas requires different stimulation intensities at different points. The use of too high an intensity would produce afterdischarges at some positions. The use of too low an intensity would falsely make others appear functionally "silent."
A patient with Crohn's disease and generalized seizures who lacked the distal small bowel and ascending colon required 600 mg of intravenous phenytoin daily (11 mg/kg/24 h) to maintain her plasma phenytoin levels in the 12-24 micrograms/ml range. She received no oral phenytoin. Stool volumes ranged from 1,125 to 1,875 ml/24 h, and stool fraction phenytoin levels from 15 to 41 micrograms/ml. Urinary 5-(p-hydroxyphenyl)-5-phenylhydantoin and phenytoin levels in three 24-h samples were sufficient to account for 26, 46, and 57% of the administered drug, compared with the expected 70-90%. This was most likely due to an alteration of the normal cycle of absorption and reexcretion between the intestinal lumen and the blood resulting in net excretion of phenytoin into the bowel.
We evaluated the therapeutic efficacy and toxicity of high-dose monotherapy, using carbamazepine or phenytoin, in patients with previously uncontrolled seizures. Treatment with a single drug was equal to or better than polypharmacy, but only a few patients became free of seizures. Toxicity was mild and associated with higher total plasma levels after polypharmacy. Free fractions ranged from 0.14 to 0.30 for carbamazepine and from 0.60 to 0.13 for phenytoin. Toxicity was associated with free phenytoin levels above 3 micrograms/ml; there was no clear relationship between free carbamazepine level and toxicity.
A patient with intractable partial seizures was intensively studied before surgical removal of the epileptogenic focus. A subdural electrode array was surgically placed over the left temporoparietal cortex to better localize the epileptogenic focus and localize cortical function. In addition to speech and sensory findings, acalculia, agraphia, right-left confusion, and finger agnosia were transiently produced by electrical stimulation in the perisylvian area. These findings and their relationship to the controversy surrounding Gerstmann's syndrome are discussed.
The purpose of this investigation was to study the effects of a selective thromboxane A2 (TXA2) synthetase inhibitor (TSI) upon the evolution of cerebral infarction in the cat. Adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion for 4 hours followed by a 2-hour period of reperfusion before sacrifice. Ten cats received 3 mg/kg TSI intravenously immediately before, and 10 cats received 3 mg/kg TSI intravenously immediately after MCA occlusion. Ten cats were used as controls receiving no treatment. The bleeding time was determined at baseline and at the end of each experiment. Electroencephalographic (EEG) recordings were obtained before and after MCA clipping and MCA release, and at hourly intervals thereafter. Regional cerebral blood flow (rCBF) was measured using the xenon-133 (133Xe) clearance technique before and after MCA occlusion, after MCA reopening, and before terminating each experiment. Thirty minutes before each cat was sacrificed, Evans blue dye and sodium fluorescein were given intravenously. The animals were then perfused with colloidal carbon and the brains removed and evaluated for midline shift. Evans blue dye and sodium fluorescein extravasation, carbon staining, and infarct size. The bleeding time, arterial blood pressure, rCBF changes, brain swelling, and vital dye extravasation were not statistically different between the three treatment groups. The EEG changes, carbon staining, and infarct size differences between the three groups also failed to reach statistical significance, but there was a suggestion that these parameters were adversely affected in the cats pretreated with TSI. Ten additional cats undergoing MCA occlusion and reperfusion were used for pharmacological studies. Five of them received 3 mg/kg TSI intravenously immediately after MCA occlusion, and serial drug and thromboxane B2 (TXB2) levels (a stable metabolite of TXA2) were determined. Another five cats were not treated and serial TXB2 levels were obtained. Production of TXA2 was inhibited by 95% in cats receiving TSI. In conclusion, thromboxane synthetase inhibition failed to modify favorably the evolution of cerebral infarction. When TSI was given before MCA occlusion, cerebral infarction tended to be more extensive.
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Posterior tibial nerve (PTN) evoked potentials (EPs) at the lumbar-low thoracic level have waveforms similar to median nerve (MN) EPs at the cervical level. They consist of a short-duration negativity (N18 and N10, respectively), which reflects the afferent volley before it enters the spinal canal, and a longer-duration, later negativity (N20 and N12, respectively), which consists mainly of slow frequencies and most probably is a postsynaptic dorsal cord potential. At the neck-scalp derivation the MN EP consists of two near-field negativities (N10 and N12) that are recorded from the neck electrode and two far-field positivities (P11 and P13) that are recorded from the scalp electrode. The neck-scalp response to PTN stimulation consists of a near field potential N24 that is followed by a far-field potential P27.
A beneficial effect of dimethyl sulfoxide (DMSO) in the treatment of acute focal cerebral ischemia has not been proven. In the present study, two established experimental models of acute focal cerebral ischemia were treated with DMSO. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. No improvement of EEG findings, erythrocyte transit, regional cerebral blood flow (rCBF), blood-brain barrier permeability, or morphological findings were demonstrated in the DMSO-treated cats. In a second study, 15 conscious adult baboons underwent temporary left MCA occlusion (6 or 12 hours) using an implanted occluding device. Seven baboons were not treated and 8 baboons received continuous intravenous infusions of DMSO for 10 hours beginning 30 minutes after occlusion. Four of the baboons that were treated with DMSO also were treated with pentobarbital coma for 96 hours starting 4 hours after occlusion. Analysis of the neurological scores after 1 week survival indicated that treatment with DMSO alone and DMSO and pentobarbital coma did not improve the outcome. Morphological changes were similar in the 3 groups. The findings of our investigation indicate that DMSO is ineffective in treating acute focal cerebral ischemia.
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A patient had episodes of bilateral paresthesias with retained consciousness. The attacks were clinically considered to be psychogenic seizures. Electroencephalography indicated that the attacks were epileptic, perhaps originating from the second sensory area. Electroencephalographic recording of a seizure is essential in differentiating epileptic from psychogenic episodes.