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Biomedical subjects

R P Lesser

Publications and source records attributed to R P Lesser.

At least 109 records · Page 6Linked to original sources
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

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↗
PubMedDate not supplied

Basal temporal subdural electrodes in the evaluation of patients with intractable epilepsy.

In evaluation of patients with complex partial seizures who are candidates for surgical treatment, exact definition of the epileptogenic focus is essential for a good surgical outcome. We report a new technique which permits detailed mapping of the epileptogenic activity in the basal temporal lobe and the convexity of the temporal lobe. The technique consists of placement of at least 16 basal temporal electrodes and an additional 64 electrodes covering the temporal convexity. This extensive coverage permits accurate definition of the limits of the epileptogenic focus and also of adjacent functional areas and therefore allows more significant determination than have previous techniques of the ideal extent of the surgical resection. This accuracy cannot be achieved with depth electrodes or the limited coverage provided by previously reported epidural or subdural electrode techniques.

Action Potentials↗
PubMedDate not supplied

Placebo-controlled pilot study of centromedian thalamic stimulation in treatment of intractable seizures.

Stimulation of centromedian (CM) thalamic nuclei has been proposed as a treatment for seizures. We implanted programmable subcutaneous (s.c.) stimulators into CM bilaterally in 7 patients with intractable epilepsy to test feasibility and safety. Stimulation was on or off in 3-month blocks, with a 3-month washout period in a double-blind, cross-over protocol. Stimuli were delivered as 90-microseconds pulses at 65 pulses/s, 1 min of each 5 min for 2 h/day, with voltage set to half the sensory threshold. Stimulation was safe and well-tolerated, with a mean reduction of tonic-clonic seizure frequency of 30% with respect to baseline when stimulator was on versus a decrease of 8% when the stimulator was off. There was no improvement in total number of generalized seizures with stimulation, and treatment differences were not statistically significant. Stimulation at low intensity did not alter the EEG acutely, but high-intensity stimulation induced slow waves or 2-3 Hz spike-waves with ipsilateral frontal maximum. In an open-label follow-up segment with stimulator trains continuing for 24 h/day, 3 of 6 patients reported at least a 50% decrease in seizure frequency. There were no side effects. This pilot project demonstrated the feasibility of controlled study of thalamic stimulation in epilepsy, but further study will be needed to demonstrate efficacy.

Adolescent↗
PubMedDate not supplied

Treatment of acute focal cerebral ischemia with propranolol.

Propranolol has been found to have a protective effect in experimental myocardial ischemia. Protection of ischemic kidneys was subsequently demonstrated following treatment with propranolol and its weaker beta blocking isomer, d-propranolol. The objective of the present investigation was to study the effects of propranolol (i.e., racemic d,1 mixture) and d-propranolol upon regional cerebral blood flow (rCBF) and early ischemic changes following experimental middle cerebral artery (MCA) occlusion. Thirty adult cats, lightly anesthetized with ketamine hydrochloride, underwent 3 hours or right MCA occlusion. Ten cats were untreated. Ten cats were given a continuous infusion of propranolol (1 mg/kg/hr) for 4 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion. Ten cats were given a continuous infusion of d-propranolol (0.5 mg/kg/hr) for 4 hours beginning 1 hour before MCA occlusion and a 2 mg/kg bolus immediately before occlusion. The therapeutic agents were injected directly into the right carotid artery. The rCBF in the right Sylvian region was not significantly different in the 3 groups. EEG changes also were similar. Carbon filling defects were found to be smallest in the d-propranolol-treated group. Light microscopic studies demonstrated a reduction in infarct size in the propranolol and d-propranolol groups. The findings of the investigation indicated that propranolol and d-propranolol do not have a deleterious effect on rCBF after MCA occlusion and suggested that these agents have a protective effect upon ischemic cerebral tissue.

Animals↗