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Biomedical subjects

R P Lesser

Publications and source records attributed to R P Lesser.

At least 73 records · Page 4Linked to original sources
PubMed1985

Ipsilateral trigeminal sensory responses to cortical stimulation by subdural electrodes.

Twelve patients with medically intractable epilepsy had plates of chronic subdural electrodes placed over the lateral and basal cortical hemispheres during evaluations for surgical therapy. During cortical stimulation, ipsilateral sensations involving any of the branches of the trigeminal nerve were noted in the eye, face, and mouth. Some responses could have been due to dural or direct trigeminal nerve trunk stimulation, but others were probably due to electrical stimulation of trigeminal fibers accompanying the pial-arachnoidal vessels. These fibers had been demonstrated in animals, but not in humans.

Adolescent↗
PubMed1985

Pattern evoked potentials (PEPs) in Parkinson's disease.

Controversy exists in the literature concerning whether Parkinson's disease (PD) results in prolongation of pattern evoked potential (PEP) responses. PEPs were obtained in 20 patients with PD. The latencies of the first major positive potential (P2) in response to independent left and right eye stimulation were evaluated. There was no statistically significant difference (group or individual) when patients with PD were compared with age-corrected controls. There was no difference in results in comparing patients with mild, moderate, and severe PD. These results contradict previous reports of markedly abnormal PEPs.

Aged↗
PubMed1985

Preservation of voluntary saccades after intracarotid injection of barbiturate.

We studied voluntary saccades in 44 patients undergoing Wada testing before surgery for intractable epilepsy. After intracarotid injection of barbiturate, and while they were hemiplegic, patients could still make voluntary saccades toward or away from the side of injection. Sustained ipsiversive deviation of gaze was not noted. Saccades made away from the side of injection were slower than ipsilateral saccades in only 3 of 10 tests. These data support the hypothesis of parallel, independent pathways from the frontal eye fields and from the superior colliculi to the brainstem reticular nuclei that generate saccades.

Amobarbital↗
PubMed1985

Treatment of acute focal cerebral ischemia and recirculation with d-propranolol.

The purpose of the investigation was to evaluate the effects of d-propranolol upon temporary cerebral ischemia followed by a period of reperfusion, that is, a situation analogous to major cerebral artery embolization. Twenty adult cats, lightly anesthesized with nitrous oxide, underwent 4 hours of right middle cerebral artery (MCA) occlusion and 2 hours of recirculation. Ten cats were untreated and 10 cats received d-propranolol, the weak beta-blocking isomer of racemic (d,l) propranolol. The d-propranolol was infused directly into the right carotid artery at doses of 2 mg/kg, given as a bolus immediately before MCA occlusion, and 0.33 mg/kg/hour, given continuously for 6 hours beginning immediately after MCA occlusion. Systemic arterial blood pressure was similar in both groups, but heart rate was transiently reduced in the treated group immediately after the bolus injection of d-propranolol and MCA occlusion. Regional cerebral blood flow (rCBF), measured by the xenon-133 clearance technique, was not significantly different in the ischemic, right hemisphere. Electroencephalographic (EEG) activity changes in the ischemic, right hemisphere were similar in both groups, but there was significant deterioration of EEG activity in the left, nonischemic hemisphere of untreated cats after MCA reopening. Swelling of the ischemic, right hemispheres was similar in both groups and more severe than in previous studies wherein there was no recirculation phase. Carbon perfusion and blood-brain barrier changes were also similar. The results of the study failed to show a protective effect despite theoretical beneficial actions of d-propranolol. Also, the study demonstrated that d-propranolol does not have a detrimental effect upon rCBF in acute focal cerebral ischemia.

Animals↗
PubMed1984

Subcortical and cortical somatosensory potentials evoked by posterior tibial nerve stimulation: normative values.

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).

Adolescent↗
PubMed1984

Effect of stimulus intensity on subcortical and cortical somatosensory evoked potentials by posterior tibial nerve stimulation.

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.

Adolescent↗
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↗