Biomedical subjects
Publications and source records attributed to R P Lesser.
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.
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The objectives of this study were to evaluate the use of brain stem auditory evoked potentials (BAEPs) in 10 adult patients with vascular disorders of the posterior circulation that were treated surgically and to compare the BAEPs with the neurological findings. The vascular lesions included basilar artery stenosis in 3 patients, vertebral artery stenosis in 1 patient, brain stem/cerebellar arteriovenous malformation in 2 patients, and basilar artery aneurysm in 4 patients. Measurement of BAEPs were carried out during operation in all cases. Eight patients had BAEPs measured before operation, and 9 patients had BAEPs measured after operation. Repeat postoperative studies were performed in patients with changes in neurological status. In general, BAEP abnormalities correlated with the neurological findings before and after operation. Six patients had normal intraoperative studies. None of them had clinical findings of pontomesencephalic dysfunction after operation. Three patients with significant BAEP abnormalities during operation had neurological findings of pontomedullary ischemia after operation. Transient BAEP changes in 1 patient were thought to be the result of brain stem retraction. The BAEPs were lost in 3 patients who died. The use of BAEP measurement did not lengthen the operative procedures. However, the technique used in this study required 4 to 8 minutes for the accumulation and interpretation of each average, thereby delaying feedback to the surgeon. The results of this study suggest a potential role for BAEP monitoring in identifying brain stem injury during posterior circulation surgery.
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Somatosensory evoked potentials were recorded from chronically implanted subdural electrodes in six patients with intractable seizures. The following conclusions were reached: 1) The initial cortical negativity-positivity (N1 with a latency of about 20 msec and P2 with a latency of about 24 msec) recorded in the postcentral area was an expression of the classical primary surface positivity, but N1 was generated by the posterior pole of an early horizontal dipole in area 3b, and P2 was generated by the positive pole of a slightly delayed vertical dipole in area 1 and 2.2) P2 permitted the most accurate localization of the primary somatosensory area. 3) No potentials were elicited in the primary somatosensory area by stimulation of the ipsilateral hand. 4) No cortical potentials were seen at stimulation intensities below the sensory threshold. The cortical distribution of evoked potentials evoked by weak and strong intensities had significantly different distribution. 5) The recovery function of cortical evoked potentials showed a U-curve with an early period of facilitation (10 to 30 msec) followed by a prolonged period of subnormality which peaked at about 50 msec. The recovery curve at different cortical loci differed.
To study the distribution of the early (first 80 ms) human cortical potentials evoked by stimulation of the posterior tibial nerve at the ankle, scalp electrodes were placed within a 12-cm radius from the vertex and were separated by approximately 3 cm. With unilateral stimulation the response at the hemisphere ipsilateral to the stimulus was consistently of substantially higher amplitude and at times opposite in polarity to the contralateral response. An explanation of this paradoxical lateralization is that the cortical generators of the evoked potentials to posterior tibial nerve stimulation are located in the mesial surface of the cortex, adjacent to the the interhemispheric tissue, and therefore project transversely or parallel (not perpendicular) to the scalp surface. A similar paradoxical lateralization with similar paradoxical lateralization with similar cause has been reported concerning occipital evoked potentials in response to half-field pattern stimulation.
We present a patient with epilepsia partialis continua involving the right leg who demonstrated sharp waves paradoxically distributed over the vertex and right hemisphere. Posterior tibial nerve evoked potentials also showed a similar paradoxical lateralization. We postulate that generators situated on the mesial surface of the left hemisphere projected their activity obliquely, leading to paradoxical lateralization of the recorded electrical activity.
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We identified the sites of origin of the somatosensory evoked potentials to median nerve stimulation by recording directly from the cervical cord in the course of intraoperative monitoring. The N9 potential occurred before any potentials recorded from the cord or dorsal roots. Potentials with latencies corresponding to N11 were recorded at the median nerve root entry zone of the lower cervical cord. High-amplitude potentials were recorded at the level of the foramen magnum, with latencies approximating or following P13, suggesting that this potential is generated at the cervicomedullary junction.
The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 +/- 10 ml/100 g/minute in the untreated group and 45 +/- 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled erythrocytes in the right sylvian region. The period of erythrocyte transit before occlusion was 10 +/- 1 seconds in the untreated group and 10 +/- 2 seconds in the treated group. After 6 hours of occlusion, the erythrocyte transit time was 18 +/- 3 seconds in the untreated group and 19 +/- 3 seconds in the treated group. Increasing delay in erythrocyte transit during the 6-hour occlusion period was seen in 5 untreated cats and 6 treated cats and was thought to represent a progressive increase in microvascular resistance. The complete washout of erythrocytes indicated the absence of microcirculatory obstruction. Electroencephalography (EEG) showed a reduced amplitude of activity in the right cerebral hemisphere after occlusion in cats with an rCBF consistently below 18 ml/100 g/minute. No significant EEG differences were found between the untreated and treated groups. Treatment with DMSO failed to modify the developing ischemia edema, neuronal alterations, or the changes in blood-brain barrier permeability to Evans blue dye and fluorescein. In this study DMSO was ineffective in preventing ischemic damage or acted when irreversible injury had already taken place.
The object of the investigation was to study the effects of concentrated albumin upon the evolution of cerebral infarction. 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 concentrated (i.e., 25 g/100 ml) human serum albumin (5 ml/kg i.v.) at the time of MCA occlusion. The blood volume increased 30 to 40% in the cats receiving concentrated albumin. The hematocrit fell for 32 +/- 5% (SD) before occlusion to 23 +/- 6% at 2.5 hours after occlusion in treated cats, whereas the hematocrit in untreated cats remained stable at 35 +/- 5. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 42 +/- 11 ml/100 g/minute in the untreated cats and 44 +/- 8 ml/100 g/minute in the treated cats. Untreated and treated cats had similar reductions of rCBF in the right sylvian region to less than or equal to 18 ml/100 g/minute at some point after occlusion. An index of erythrocyte flow and microcirculatory resistance was determined by measuring the transit of 99Tc-labeled erythrocytes in the right sylvian region. The erythrocyte transit time before occlusion was 10 +/- 2 seconds in the untreated group and 9 +/- 1 seconds in the treated group. After 6 hours, the erythrocyte transit was 19 +/- 3 seconds in the untreated group and 15 +/- 3 seconds in the treated group (p less than or equal to 0.1), suggesting that less microcirculatory impairment occurred in some treated cats. Electroencephalographic changes during the initial 3 hours of occlusion were less severe in the treated cats than in the untreated cats, suggesting that the collateral flow in the border zone of the MCA territory initially may have been improved by treatment. Impairment of carbon perfusion, ischemic edema, and neuronal alterations after 6 hours of occlusion were the same in both groups. Increased permeability of the blood-brain barrier to Evans blue dye, however, was more marked in the treated group. The findings of the study indicate that concentrated albumin does not substantially modify the evolution of cerebral infarction.
A woman with typical symptoms of lithium toxicity had, in addition, severe generalized sensorimotor peripheral neuropathy, which cleared completely as the recovered. Electrodiagnostic studies suggested axonal lesions; autopsy ten months later revealed no residual abnormalities. Previous studies have shown that lithium can affect peripheral nerve function, but this is the first reported case of peripheral neuropathy in association with lithium toxicity.
The peripheral and central potentials evoked by percutaneous electrical stimulation of the median nerve were investigated in a group of neurologically normal subjects. We found: (1) Motor threshold stimulation gave consistently submaximal responses and probably does not represent an optimal intensity for routine use. (2) The sum of motor plus sensory threshold gave potentials which were consistently at, or close to, maximal in amplitude. This intensity was comfortable for all subjects. (3) When stimulating at intensities above motor threshold, the increase in amplitude of peripheral potentials markedly exceeded that of the central potentials. There was evidence suggesting that amplitudes would decline at very high stimulus intensities. (4) The P13 peak latency and the P13--N9 interpeak latency declined and the N17--P13 interpeak latency increased with increasing intensities of stimulation. The N9 and N18 peak latencies remained stable.
We evaluated the current status of 131 patients with idiopathic parkinsonism who were receiving levodopa therapy. The residual parkinsonian symptoms and signs were tabulated, as were the adverse effects from medication. Response to therapy was correlated with duration of the disease and with duration of treatment. Patients with on-off or wearing-off effects were likely to have been treated for 4 years or longer. Patients treated with levodopa for 4 to 8 years were significantly more impaired with parkinsonism than patients treated for 0 to 3 years, even when patients were matched for total duration of disease. These data suggest that the deterioration of responsiveness after several years of levodopa therapy may be due to the therapy itself. Our findings support the concept that utilization of levodopa therapy should be delayed until a patient becomes significantly impaired in occupational or social situations.
The authors studied the records of 84 patients who had idiopathic torsion dystonia. Thirty-seven cases had originally been misdiagnosed as primarily psychiatric illness. Only 1 patient presented with dystonic movements that were clearly part of a more general psychiatric disorder. The authors believe her to be the first reported patient whose dystonia is undeniably of psychogenic origin.
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