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Biomedical subjects

R P Lesser

Publications and source records attributed to R P Lesser.

157 records · Page 9Linked to original sources
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↗
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

Electroencephalographic changes during simple partial seizures.

We analyzed retrospectively the clinical and EEG data in 13 patients with simple partial seizures (SPS). All EEGs were recorded with surface electrodes with the standard 10-20 system and additional closely spaced scalp and subfrontotemporal skin electrodes. Seventy-seven seizures were recorded. We detected electrographic correlates with SPS in 10 of 13 patients (77%) and in 47 of 77 seizures (61%). The most common ictal correlates were rhythmic theta waves or spikes. Of the SPS with EEG changes, 58% were motor, 14% were sensory, and 28% were psychic seizures. Use of additional electrodes and recording channels may account for the higher incidence of EEG changes in this study than has been reported previously in the literature.

Adolescent↗
PubMedDate not supplied

Clinical and electroencephalographic evidence for sites of origin of seizures with diffuse electrodecremental pattern.

A diffuse electrodecremental ictal pattern (DEP) has been associated with tonic seizures and, less often, with other forms of epilepsy and has been considered to reflect a generalized seizure disorder of diffuse cortical or subcortical (brainstem) origin. In some seizures associated with DEP, however, focal ictal manifestations have been observed. We reviewed the records of all patients admitted to our seizure monitoring unit for 3 years and detected 39 patients with seizures associated with DEP. In 23 of 39 patients, clinical ictal behaviors resembled seizures of unilateral supero/mesiofrontal lobe origin and interictal EEG showed a prominent unilateral frontal component. Nine of 39 had complex absences (CA)/complex partial seizures (CPS); 4 of them were of unilateral frontal lobe origin. Seven of 39 patients had tonic or atonic seizures. Seven patients were studied further with subdural electrodes. Ictal onsets showed a high-frequency frontal lobe discharge. We conclude that in a subgroup of patients a generalized electrodecremental pattern on scalp EEG results from a regional cortical high-frequency ictal discharge originating in a single frontal lobe.

Adult↗
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↗
PubMedDate not supplied

Treatment of acute focal cerebral ischemia with prostacyclin.

The object of this investigation was to study the effects of prostacyclin (PGI2) upon the evolution of acute focal cerebral ischemia in the cat. Twenty-five fasted adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion. Eleven cats received an intracarotid infusion of PGI2 in buffered saline pH 10.5 (100 ng/kg/min at 0.01 ml/kg/min), and 11 cats received intracarotid buffered saline pH 10.5 (0.01 ml/kg/min) without therapeutic agents. Treatment with PGI2 was started upon MCA occlusion and continued for 6 hours. Thirty minutes prior to perfusion, the animals were given fluorescein and Evans blue by intravenous injection. The cats were perfused-fixed in vivo with carbon and buffered formalin 6 hours after MCA occlusion. Another 3 cats received tritium labeled intracarotid PGI2, and peripheral venous samples were collected and assayed for PGI2 plasma levels. Mean arterial pressure was stable in PGI2 treated animals during 6 hours of MCA occlusion, while untreated cats had significant progressive hypertension during that period. The rCBF (measured by the intracarotid 133Xe method) decreased markedly in all animals immediately upon MCA occlusion. However, untreated animals had a significant progressive improvement in rCBF during the occlusion period, while PGI2 treated animals had no such improvement. Quantitative EEG changes, gross edema, areas of fluorescein extravasation, patterns of carbon perfusion, and infarct size were not significantly different in the two groups. While most untreated animals had marked Evans blue extravasation after 6 hours of MCA occlusion, most PGI2 treated animals had no such extravasation, indicating some protection of the blood-brain barrier in these animals.

Acute Disease↗
PubMedDate not supplied

Treatment of acute focal cerebral ischemia with propranolol.

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.

Animals↗
PubMedDate not supplied

Clinical diagnoses and EEG interpretation.

A sample of 62 electroencephalographers in the United States evaluated 10-second samples of eight electroencephalograms. The evaluations were performed with and without knowledge of the clinical history. Evaluations consisted of multiple choice questions related to electroencephalographic observations, clinical diagnosis, and requests for additional tests such as computerized tomography and cerebrospinal fluid studies. The results indicate that clinical history influences interpretation, with considerable variation among readers in the number and type of additional tests requested.

Brain Diseases↗