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K M Perryman

Publications and source records attributed to K M Perryman.

29 records · Page 2Linked to original sources
PubMed1987

Differential effects of inferior temporal cortex lesions upon visual and auditory-evoked potentials in the amygdala of the squirrel monkey (Saimiri sciureus).

Visual-evoked potentials (VEPs) and auditory-evoked potentials (AEPs) were elicited from amygdala nuclei and inferior temporal (IT) cortex in chaired, alert squirrel monkeys to diffuse flash and click stimuli. VEPs were recorded from electrodes placed in basalis lateralis amygdalae (BLA) and basalis medialis amygdalae (BMA) while AEPs could also be obtained from additional electrode sites in basalis accessorius medialis (BAM), centralis amygdalae (CeA), and lateralis amygdalae (LA). The amygdala-evoked potentials resulting from stimulation of the two modalities were similar in terms of component configuration. AEPs recorded from the IT cortex had shorter latencies than the amygdala VEPs that were recorded. Both modalities of stimulation elicited potentials with shorter onset latencies in the amygdala than those recorded from the surface of IT cortex. Bilateral ablation of the IT cortex eliminated VEPs recorded from the BMA but not the BLA amygdala region. AEPs recorded from BMA as well as other amygdala areas were not consistently affected by these IT cortical ablations.

Amygdala↗
PubMed1986

Neuronal responses in rostral trigeminal brain-stem nuclei of macaque monkeys after chronic trigeminal tractotomy.

Unilateral trigeminal tractotomy was carried out at the level of the obex, just rostral to the subnucleus caudalis, in five young adult Macaca fascicularis monkeys. The animals had been trained previously to perform a behavioral shock avoidance task in response to electrical stimulation of dental pulp and facial skin. Tractotomy produced an elevation in the stimulus strength which elicited escape behavior when facial skin was stimulated but not when the tooth pulp was stimulated. Unit activity, evoked by electrical stimulation of the tooth pulp and facial skin as well as innocuous and noxious mechanical stimulation of orofacial regions, was recorded from neurons in the trigeminal main sensory nucleus and the subnuclei oralis and interpolaris of the spinal nucleus 8 to 12 weeks after tractotomy. Primary afferent input to these nuclei is unaffected by the tractotomy which is located more caudally. The tractotomy interrupts primary afferent input into the trigeminal nucleus caudalis and also intranuclear connections between caudalis and the more rostral nuclei. Forty-one units contralateral and 47 ipsilateral to the tractotomy were studied. Thirty-six of the units responded only to low-threshold mechanical or electrical stimulation of orofacial zones, 46 were responsive to innocuous mechanical and electrical stimulation of orofacial zones and also to electrical stimulation of the dental pulp. Six units responded only to dental pulp stimulation. No statistically significant differences between the populations of neurons ipsilateral and contralateral to the tractotomies were found relating to the size or location of the peripheral receptive fields, latencies, thresholds, mean firing densities, or responsiveness to the various forms of stimulation. The behavioral results suggest that trigeminal relay neurons rostral to the obex are able to signal dental pain sensation, and the physiological studies confirm that the firing of such neurons is unaffected by tractotomy. The physiological studies demonstrate that the firing patterns of relay neurons activated by natural and electrical cutaneous facial stimuli and which are located in trigeminal brain-stem nuclei rostral to the obex are also not affected by tractotomy. The cutaneous facial analgesia observed after tractotomy thus appears to be due to deafferentation of relay neurons in trigeminal nucleus caudalis rather than to alterations in coding patterns in rostrally located trigeminal neurons due to interruption of the intratrigeminal pathway between the caudal and rostral nuclear groups.

Animals↗
PubMed1984

Pathways for orofacial pain sensation in the trigeminal brain-stem nuclear complex of the Macaque monkey.

Eleven Macaque monkeys underwent a variety of lesions in the trigeminal afferent system; namely, tractotomy, rhizotomy, and radiofrequency destruction of various components of the bulbospinal trigeminal nuclear complex. Behavioral responses were evaluated before and after the lesions using a quantitative paradigm which measured lever-pressing in response to electrical stimulation of the dental pulp or facial skin, and by assessing adversive responses to facial cutaneous and intraoral pin-scratch. Thresholds for lever-pressing in response to cutaneous facial stimulation were elevated by tractotomy, elevated further by a combination of tractotomy and rhizotomy of the seventh, ninth, and 10th cranial nerves and cervical dorsal roots C1-3, and maximally elevated by complete radiofrequency destruction of the trigeminal nucleus caudalis. These lesions also abolished adversive responses to cutaneous facial pin-scratch. None of these lesion combinations, however, altered lever-pressing responses to dental pulp stimulation. Radiofrequency destruction of the trigeminal nuclei principalis, oralis, and interpolaris caused elevations of lever-pressing thresholds in response to dental pulp stimulation, and also smaller but statistically significant elevations on cutaneous electrical stimulation. Mild reductions in adversive responses to cutaneous pin-scratch were also produced by these rostral nuclear lesions, suggesting analgesia. The experiments suggest that primary afferent fibers for dental pain perception travel only in the trigeminal nerve and that these fibers relay via the trigeminal brain-stem nuclei principalis, oralis, and interpolaris. Primary afferent fibers for cutaneous facial pain perception travel in the trigeminal, facial, glossopharyngeal, and vagus nerves, and the upper cervical dorsal and ventral roots, and these afferents relay mainly in the trigeminal nucleus caudalis.

Animals↗
PubMed1981

Effect of trigeminal tractotomy on behavioral response to dental pulp stimulation in the monkey.

Trigeminal tractotomy near the level of the obex was carried out in 10 macaque monkeys. Behavioral responses were evaluated by a quantitative paradigm measuring lever-press responses to electrical stimulation of the dental pulp or facial skin, and by assessing facial response to cutaneous pin-scratch before and after the tractotomy. Two pharmacological agents, strychnine and L-dopa, were administered and their effect on behavioral responses to these stimuli was studied. Tractotomy did not produce dental analgesia. Thresholds for escape from cutaneous electrical stimulation of facial skin, however, were elevated, consistent with marked hypalgesia to pin-scratch. The adversive responses to pin-scratch were absent in peripheral portions of the face, but near the midline and inside the oral cavity they were usually decreased or normal. Pharmacological agents caused a reduction in escape thresholds to cutaneous electrical stimulation and a shrinkage or abolition of the zone of analgesia to pin-scratch. The results imply that trigeminal nucleus caudalis, which undergoes deafferentation by tractotomy, may not be essential for processing of nociceptive information from the teeth, oral cavity, and midline facial zones. This findings is contrary to long-held hypotheses concerning facial pain mechanisms. The ability of strychnine and L-dopa to alter nociceptive escape thresholds is consistent with the idea, suggested by Denny-Brown, that facial nociception depends on central summation in the entire spinal trigeminal nucleus from overlapping afferent inputs contained in the trigeminal nerve, other cranial nerves, and the upper cervical nerve roots.

Afferent Pathways↗
PubMed1980

Pulvinar neuron responses to spontaneous and trained eye movements and to light flashes in squirrel monkeys.

Single unit responses were recorded in the pulvinar nucleus of the squirrel monkey (Saimiri sciureus) while awake and alert, with the head fixed but free to make eye movements. Peri-saccadic time histograms revealed only post-saccadic responses to eye movements made spontaneously in the dark or in a uniformly illuminated field (Ganzfeld), or to trained eye movements made in response to a spot of light in the periphery. Of 120 pulvinar neurons that responded to eye movements in the light, approximately one-quarter was responsive to eye movements in the dark. In one group of monkeys about half of the eye movement-responsive cells in the light were responsive to light flash in the dark; in another group approximately half of the eye movement-responsive cells in the light were also responsive to trained eye movements. Of particular interest is the fact that pulvinar neurons responsive to eye movements were located within a restricted region oriented vertically and cutting across lateral and inferior pulvinar, rostrally, and lateral and medial pulvinar, caudally. The results have been interpreted as supporting the concept of convergence and integration of visual and oculomotor input in the pulvinar and also its potential role in the mediation of visual attention.

Animals↗
PubMed1980

Effects of long-term raphe nucleus stimulation on chronic limbic seizures in monkeys.

Long-term electrical stimulation of the raphe nuclei was performed in two monkeys with chronic psychomotor seizures. The daily seizure rate was significantly reduced in one monkey when a stimulus charge of 0.1 microC was used, but not during a subsequent experiment using a 0.4 microC charge. A charge of 0.4 microC also failed to alter the frequency of limbic seizures in a second monkey. The raphe stimulation caused neural damage to the brain stems of both animals. The possible effect this damage may have had on the repeatability of the results suggests that long-term raphe stimulation, like some other neural prostheses, may have diminishing effectiveness over time.

Aluminum Hydroxide↗
PubMed1979

Procaine-induced seizures in epileptic monkeys with bilateral hippocampal foci.

Intravenous procaine HCl given at low doses (0.5-2.5 mg/kg) to two monkeys with bilateral alumina hippocampal foci depressed interictal spiking or had little effect. At 5.0 mg/kg unilateral limbic activation occurred. At 10.0 mg/kg unilateral or bilateral limbic activation and generalized seizures could be evoked within 3-10 min. At higher doses (15 and 20 mg/kg) bilateral limbic activation or brief (one min) generalized seizures occurred. The unilateral-onset psychomotor seizures were not identical to spontaneous psychomotor seizures, and the generalized seizures never occurred spontaneously in these monkeys. However, these results do indicate that procaine challenges may selectively activate limbic epileptogenic areas without activation of debilitating generalized tonic-clonic seizures.

Animals↗
PubMed1979

Effects of chronic cerebellar stimulation on chronic limbic seizures in monkeys.

No influences of chronic cerebellar stimulation were found in 10 different controlled experiments in 5 different monkeys with chronic alumina-induced psychomotor seizures. The stimulation parameters used were comparable to those used in human epileptics, and continuous daily EEG and behavioral monitoring allowed all seizures to be measured for daily frequency and duration over the several weeks of the experiments. Nocturnal seizures were similarly quantified in 3 monkeys to verify that cerebellar stimulation did not affect them. Motor cortex potentials evoked by cerebellar pulses confirmed that the stimulations were activating the cerebellum throughout the experiments, and measures of electrode access resistance and impedance verified that the electrodes remained in contact with the cerebellum. In one monkey given phenobarbital medication, interictal morbid behavior appeared to be improved by chronic stimulation of either cerebellum or dorsolateral frontal cortex, thus indicating an arousal influence of brain stimulation not due to cerebellum per se.

Aluminum Hydroxide↗
PubMedDate not supplied

Dementia with leukoaraiosis: clinical differentiation by temporoparietal hypometabolism on (18)FDG-PET imaging.

Patients with dementia and leukoaraiosis may have either Alzheimer's disease (AD) with cerebrovascular changes or a form of vascular dementia (VaD). The presence or absence of the characteristic AD pattern of bilateral temporoparietal hypometabolism on (18)FDG-PET was used to differentiate 30 patients with progressive dementia and severe leukoaraiosis. Compared to 18 patients with the typical AD pattern (group I), the remaining 12 (group II) had better recognition memory, and greater difficulty with sustained attention and serial reversals. Better recognition memory, confluent periventricular leukoaraiosis, and poorer sustained attention distinguished all group II patients from group I. Dementia patients with severe leukoaraiosis and bilateral temporoparietal hypometabolism may have predominant AD; those who lack this pattern and have confluent leukoaraiosis may have a greater contribution from VaD. Copyrightz1999S.KargerAG,Basel

Aged↗
PubMedDate not supplied

Quantitative EEG during a double-blind trial of THA and lecithin in patients with Alzheimer's disease.

Quantitative electroencephalography (EEG) was performed on eight of ten Alzheimer patients in a double-blind, inpatient-outpatient tetrahydroaminoacridine (THA) and lecithin trial. Neuropsychological measures were related to EEG activity. Patient baseline dominant parietal rhythms (DPRs) and power spectral distributions differed significantly from controls. Severity of cognitive impairment was related to the degree of parietal slowing. Inpatient THA treatment resulted in increased DPR frequency in six of eight patients. Four of eight inpatients demonstrated reduced power in the delta and theta bands. During the outpatient long-term treatment phase, six of the patients were able to continue. Three of these improved significantly on tests of cognition. Two of these improved patients demonstrated DPRs with increased frequency. One of these patients also showed a decrease in slow-wave activity. Thus, THA may accelerate DPRs while reducing power in the slower EEG bands. However, there appears to be only a tentative coupling between individual quantitative EEG measures and cognitive performance associated with THA administration.

Aged↗