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Biomedical subjects

R P Lesser

Publications and source records attributed to R P Lesser.

At least 145 records · Page 8Linked to original sources
PubMed1983

Cortical somatosensory evoked potentials in response to hand stimulation.

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.

Cerebral Cortex↗
PubMed1982

Paradoxical lateralization of cortical potentials evoked by stimulation of posterior tibial nerve.

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.

Adolescent↗
PubMed1982

Paradoxical lateralization of parasagittal sharp waves in a patient with epilepsia partialis continua.

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.

Adult↗
PubMed1981

Early somatosensory potentials evoked by median nerve stimulation: intraoperative monitoring.

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.

Electric Stimulation↗
PubMed1981

Treatment of acute focal cerebral ischemia with dimethyl sulfoxide.

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.

Acute Disease↗
PubMed1981

Treatment of acute focal cerebral ischemia with concentrated albumin.

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.

Animals↗
PubMed1979

Acute generalized polyneuropathy accompanying lithium poisoning.

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.

Adolescent↗
PubMed1979

Effect of stimulus intensity on short latency somatosensory evoked potentials.

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.

Adult↗
PubMed1979

Analysis of the clinical problems in parkinsonism and the complications of long-term levodopa therapy.

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.

Adolescent↗
PubMed1978

Dystonia: a disorder often misdiagnosed as a conversion reaction.

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.

Adolescent↗
PubMedDate not supplied

The effects of sleep on median nerve short latency somatosensory evoked potentials.

The effects of sleep on median nerve short latency somatosensory evoked potentials were studied in 7 subjects made up of 6 patients being evaluated for seizure disorders by all-night electroencephalograms and 1 normal healthy volunteer. The median nerve was stimulated at the wrist, and the peripheral (N9), subcortical (P13) and early cortical (N1, P2) evoked potentials were recorded during full wakefulness and natural night-time sleep. Sleep-wake state was monitored by the simultaneously obtained polysomnogram. The latencies of the cortical responses were prolonged during non-rapid eye movement (NREM) sleep. In 3 of the subjects P2 was consistently bifid during NREM sleep only. The second component of the bifid potential, 3-4 msec longer in latency than the first, appeared to be selectively enhanced during NREM sleep whereas the first component tended to become less prominent or even disappear. This suggests that the 2 peaks have different generators that are affected differently by NREM sleep. These are clinically relevant findings for interpretation of routine clinical studies.

Adult↗
PubMedDate not supplied

Short latency somatosensory evoked potentials recorded around the human upper brain-stem.

We analyzed the intracranial spatiotemporal distributions of the N18 component of short latency median nerve somatosensory evoked potentials (SSEPs) in 3 patients with epilepsy. In these patients, depth electrodes were implanted bilaterally into the frontal and temporal lobes, with targets including the amygdala and hippocampus; the latter two targets are close to the upper pons and midbrain. In this study N18 was divided into the initial negative peak (N18a) and the following prolonged negativity (N18b). Mapping around the upper pons and midbrain showed that: (1) the amplitude of the first negativity, which coincided with scalp N18a, was larger contralateral to the side of stimulation, but showed no polarity change around the upper brain-stem; and (2) the second negativity, which was similar to scalp N18b, did show an amplitude difference or a polarity change. This wave appeared to reflect a positive-negative dipole directed in a dorso-ventral as well as dorso-lateral direction from the midbrain, where positivity arises from the dorsum of the midbrain, contralateral to the side of the stimulation. Recordings from depth electrode derivations oriented in a caudo-rostral direction suggest that N18a and N18b may in part reflect neural activity originating from the upper pons to midbrain region which projects to the rostral subcortical white matter of the frontal lobe as stationary peaks.

Adult↗
PubMedDate not supplied

Epileptic seizures due to thrombotic and embolic cerebrovascular disease in older patients.

Thromboembolic vascular disease is a frequent precipitant of seizures, and is the most common etiology in older patients. The occurrence of seizures shortly after a stroke, however, does not necessarily indicate that the patient will continue to have seizures following initial recovery. This is true even when patients present in epileptic status. This may be because early and late seizures are produced by different pathophysiologic mechanisms.

Adult↗
PubMedDate not supplied

Transient focal abnormalities of neuroimaging studies during focal status epilepticus.

We report transient changes in computed tomography (CT) and magnetic resonance imaging (MRI) scans in a patient with focal status epilepticus, referred to us with a tentative diagnosis of neoplasm based on CT and angiographic findings. EEG seizures originated independently from each temporal-occipital area, predominantly from the right. Previous EEGs had shown almost exclusively right temporo-occipital epileptogenic activity. MRI showed increased signal intensity, and CT showed decreased right hemisphere attenuation without enhancement. One month later, there was resolution of the radiological and clinical abnormalities. The transient CT and MRI changes probably represented focal cerebral edema, developing during focal status epilepticus. Lack of change in the left hemisphere probably reflected the quantitative difference in epileptic activity. Clues to the diagnosis of focal edema due to status include: (1) changes on electrical and imaging studies that correlate anatomically with the clinical status, and (2) resolution of abnormalities with appropriate seizure control. In patients with suspected seizure disorders, electrical and clinical data should be correlated before interpretation is made of focal lesions seen by neuroimaging techniques.

Adult↗