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Biomedical subjects

R T Knight

Publications and source records attributed to R T Knight.

At least 91 records · Page 5Linked to original sources
PubMed1988

The effects of lesions of superior temporal gyrus and inferior parietal lobe on temporal and vertex components of the human AEP.

We recorded auditory evoked potentials (AEPs) to 1 kHz tone bursts in controls and patients with unilateral lesions centered in posterior superior temporal gyrus and adjacent caudal inferior parietal lobule (STG) or in rostral inferior parietal lobule (IPL). Controls generated a vertex maximal N94 (N1b) and P200 (P2) and additional P45, N78 and N127 temporal AEP components (P45, N1a, N1c). Similar to prior reports, in controls the N1a was most prominent over the left temporal lobe and the P45 was largest over the right temporal lobe consistent with behavioral and anatomical data indicating differential organization of left and right human temporal lobe. The N1c was recorded equally from both T3 and T4 electrodes and was enhanced in the temporal site contralateral to the ear of stimulation. The patient groups had differential effects on AEPs. Unilateral STG lesions resulted in bilateral reductions of the N1b and P45 and marked unilateral reductions of the N1a and N1c over lesioned hemisphere. IPL lesions resulted in bilateral but non-significant reductions of the N1b and N1c. The scalp topography results in normal subjects combined with the effects of unilateral STG lesions provide supportive evidence that the temporal maximal components of the human AEP (P45, N1a, N1c) are generated by radially oriented neuronal dipole sources located in STG. The bilateral reduction of the N1b vertex response by unilateral STG lesions is compatible with a unilateral disruption of a vertically oriented dipole situated in the posterior superior temporal plane. The results emphasize the critical role of the superior temporal plane and lateral superior temporal gyrus in generation of human long latency AEPs.

Brain Diseases↗
PubMed1988

Effects of lesions of temporal-parietal junction on perceptual and attentional processing in humans.

When stimuli with larger forms (global) containing smaller forms (local) are presented to subjects with large lesions in the right hemisphere, they are more likely to miss the global form than the local form, whereas subjects with large lesions in the left are more likely to miss the local than the global form. The present study tested whether the global/local impairment in subjects with posterior lesions was due to deficits in controlled attentional processes, passive perceptual processes, or both. Attentional control was examined by measuring reaction time changes when the probability of a target appearing at either the global or local level was varied. Patients with unilateral right or left lesions centered in temporal-parietal regions and age-matched controls served as subjects. Because neurophysiological and neuropsychological evidence have implicated temporal regions in visual discrimination and inferior parietal regions in the allocation of attention to locations in the visual field, patients with left hemisphere lesions were further subdivided into those with lesions centered in the superior temporal gyrus (LSTG) or rostral inferior parietal lobule (LIPL). Patients with right hemisphere injury could not be analogously subdivided. The results revealed that the LSTG group was able to control the allocation of attention to global and local levels normally, while the LIPL group was not. In contrast, the LSTG group showed a strong baseline reaction time advantage toward global targets, while normals and the LIPL group showed no advantage toward one level or the other. Finally, the perceptual component was affected differentially by lesions in the right hemisphere and LSTG, with lesions in the left favoring global targets and lesions in the right favoring local targets. These findings indicate that the hemispheric global/local asymmetry is due to a perceptual mechanism with a critical anatomical locus centered in the STG.

Adult↗
PubMed1987

Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions.

We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39-72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.

Adult↗
PubMed1986

Phenytoin increases the severity of cortical hemiplegia in rats.

The effects of systemic phenytoin administration on the motor deficit resulting from a cortical lesion were studied in rats trained to walk coordinately on a narrow beam. The somatomotor cortex lesion was produced by an indwelling cannula through which saline or GABA were infused chronically via an osmotic minipump. Phenytoin (50 mg/kg i.p.) administered between days 3 and 5 after the intracortical catheter implantation produced a significant increase in the severity of the resulting hemiplegic syndrome. This DPH effect was more noticeable in those animals also receiving intracortical GABA infusions. The anticonvulsant at the dose used had no effect on motor performance when administered preoperatively or when given to the animals 14 days after surgical intervention when their hemiplegic syndrome had cleared. These findings suggest that phenytoin administration to brain-damaged individuals in the initial postlesion stage may be deleterious.

Animals↗
PubMed1986

gamma-Aminobutyric acid-induced potentiation of cortical hemiplegia.

A novel model of hemiplegia in young and aged rats is described. Osmotic minipumps were used to deliver a chronic (7 days), localized application of gamma-aminobutyric acid (GABA) (100 micrograms/microliter/h), to the somatomotor cortex of unrestrained rats. This resulted in an easily quantifiable, contralateral and reversible motor syndrome in both young and aged animals. In the young group, the motor deficit cleared over 5-day period, while in the aged animals it persisted for at least a 2-week period. Control animals treated with saline-filled minipumps did not develop a long-lasting motor deficit. The GABA-induced facilitation of hemiplegia due to small motor cortex lesions and the age effects on behavioral recovery of function are discussed. Cortical inhibitory mechanisms may play a role in debilitating syndromes such as stroke or post-epileptic paralysis.

Animals↗
PubMed1986

Electrophysiologic evidence of increased distractibility after dorsolateral prefrontal lesions.

Patients with left prefrontal lesions and control subjects showed enhanced event-related potentials (ERPs) to attended tone sequences presented in a dichotic attention task. ERP enhancements were comparable at short and long interstimulus intervals (ISIs), and did not depend upon whether attended stimuli were preceded by other attended stimuli or by distracting stimuli in the opposite ear. In contrast, patients with right prefrontal lesions showed absent ERP attention effects to contralateral (left ear) tones at all ISIs, and reduced attention effects to ipsilateral tones at long ISIs and when these were preceded by distracting sounds. The results are consistent with an asymmetric organization of dorsolateral prefrontal cortex, and indicate that increased distractibility may contribute to the attention disorders that follow prefrontal lesions.

Attention↗
PubMed1985

Altered peripheral and brainstem auditory function in aged rats.

A technique for conducting free-field brainstem auditory evoked potential (BAEP) audiometry in unanesthetized, unrestrained rats revealed a non-recruiting 18 dB elevation of click threshold in aged rats. BAEPs were first recorded in young and aged rats to clicks of equal intensity (80 dB SPL). Compared to the young group, aged animals exhibited longer wave I and wave IV latencies with no difference seen in the I-IV central conduction time. The prominent negative wave (No) following wave IV was also delayed and the I-No and IV-No conduction times increased in the aged group. When BAEPs were recorded to clicks with intensities adjusted to 35 dB above individual threshold, no differences in wave I or wave IV latencies or in the I-IV central conduction time were found between groups. However, the No component was delayed and the I-No and IV-No conduction times remained prolonged in the aged group. The results suggest that in addition to changes in peripheral auditory structures, changes in the rostral auditory brainstem accompany age-related hearing loss in rats.

Aging↗
PubMed1985

Surface auditory evoked potentials in the unrestrained rat: component definition.

Auditory evoked potentials (AEPs) to click and pure tone stimuli were recorded in unrestrained, unanesthetized rats. The middle latency rat AEPs (N17, P23, N38) had midline scalp distributions similar to human MAEPs and were recorded to within 15 dB above BAEP threshold. In contrast to human MAEPs, rat MAEPs were decreased in amplitude at high stimulation rates and only the N17 component was unaltered by slow wave sleep. The longer latency N50, N80 and P130 components had several response properties comparable to human N100-P200 vertex potentials. These included restricted midline fronto-central scalp distributions, progressive increases in amplitude at ISIs up to 4-8 sec and marked attenuation during slow wave sleep. The frequency sensitivity of the rat AEP revealed a decreased response to pure tones below 4 kHz but robust responses for stimuli up to at least 45 kHz. There was a notch in the rat audiogram with decremented component amplitudes to pure tone stimuli centered at 35 kHz. When equated for intensity, click and pure tone stimuli in the range of the rats maximal audiometric sensitivity (8-20 kHz) generated comparable AEP components. These results provide normative data on rat surface recorded AEPs. It is suggested that these surface recorded rat AEPs are generated by subcortical neural systems involved in the detection of auditory transients.

Animals↗
PubMed1984

Inhibitory modulation of cat somatosensory cortex: a pharmacological study.

In anesthetized preparations, GABA and taurine produced rapid, reversible inhibition of the negative component (N20) of the primary somatosensory evoked potential (SEP) without effect on the earlier positivity (P11). This effect was also produced by low doses of 4-aminopyridine. Neither bicuculline or picrotoxin antagonized these drug effects. A predominance of type B GABA receptors in the superficial layers of the somatosensory cortex is proposed.

4-Aminopyridine↗
PubMed1984

Chewing oscillopsia. A case of voluntary visual illusions of movement.

A 60-year-old man had a history of frontal headaches and chewing-related oscillopsia. Examination disclosed a retro-orbital epidermoid cyst that had eroded through the lateral orbital wall and under the temporalis muscle. The illusion of movement was due to mechanical displacement of the tumor mass and eye by contraction of the temporalis muscle. Removal of the cyst produced complete remission of the oscillopsia.

Epidermal Cyst↗
PubMed1984

Bitemporal lesions dissociate auditory evoked potentials and perception.

We studied auditory evoked potentials (AEPs) in an 82-year-old female patient who became suddenly deaf following the second of two strokes. The patient showed markedly elevated pure tone thresholds, was unable to discriminate sounds and could not understand speech. Brain-stem auditory evoked potentials (BAEPs) were normal. CT scans revealed bilateral lesions of the superior temporal plane which included auditory cortex. Two experiments were performed. In the first, tones, complex sounds and speech stimuli were presented at intensities above and below the patient's perceptual threshold. P1, N1 and P2 components were elicited by each of the stimuli--whether or not they were perceived. In particular, stimuli presented below threshold evoked large amplitude, short latency responses comparable to those produced in a control subject. In a second experiment, the refractory properties of the N1-P2 were examined using trains of tones. They were also found to be similar to those of normal subjects. Shifts in the pitch of the tones near the end of the train (when refractory effects were maximal) evoked N1-P2s with enhanced amplitudes, although the change in pitch was not perceived by the patient. In both experiments AEP scalp topographies were normal. The results suggest that bitemporal lesions of auditory cortex can dissociate auditory perception and long-latency auditory evoked potentials. A review of evoked potential studies of cortical deafness suggests that the neural circuits responsible for N1-P2 generation lie in close proximity to those necessary for auditory perception.

Aged↗
PubMed1984

Decreased response to novel stimuli after prefrontal lesions in man.

Experiments were conducted to study the contribution of prefrontal cortex to the generation and modulation of two varieties of P300 activity. Control subjects generated typical parietal maximal P300 responses to detected target stimuli. Unexpected, novel auditory stimuli presented to controls generated an earlier latency, fronto-centrally distributed P300 response. A similar earlier latency, fronto-central P300 is generated to unexpected, novel visual stimuli. The occurrence of this phenomenon in both the auditory and visual modalities suggests that it may reflect neural activity of a common CNS system involved in the orienting response. Subjects with unilateral prefrontal damage generated P300 complexes to target stimuli that did not differ from the control responses. Prefrontal damage, however, resulted in a specific defect in the P300 response to the unexpected novel stimulus. Prefrontal patients showed neither N200 enhancement nor the fronto-central P300 response to the novel stimulus that was found in control subjects. These findings indicate that prefrontal regions are critical for the organism's response to unexpected novel stimuli. Abnormalities in prefrontal control of sensory-limbic integration may be a critical element in the decreased P300 to novel stimuli found in these unilateral prefrontal lesioned patients. It is suggested that major features of the human frontal lobe syndrome may be explained by a physiological inability to control attention and orientation systems after prefrontal damage.

Acoustic Stimulation↗
PubMed1984

Alcohol and the central nervous system.

Acute Wernicke-Korsakoff syndrome is an underdiagnosed cause of reversible coma in the alcoholic patient. Chronic toxic effects of ethanol include nutritional polyneuropathy, cerebellar degeneration, and diffuse cortical damage with resultant alcoholic dementia. The rapid correction of hyponatremia can result in the iatrogenic syndrome of central pontine myelinolysis.

Adult↗
PubMed1983

Autosomal dominant motor system degeneration in a black family.

Autosomal dominant motor system degeneration has been described primarily in Portuguese families from the Azorean Islands. The symptoms include various combinations of ataxia, pyramidal and extrapyramidal signs, appendicular dystonias, tics, ophthalmoplegias, and peripheral neuropathies with amyotrophy. One non-Portuguese, non-Azorean black family has been described previously; this report describes a second such family affected by autosomal dominant motor system degeneration.

Adult↗
PubMed1983

Solitary metastasis of systemic malignant lymphoma to the cerebellopontine angle.

Systemic malignant lymphoma rarely produces solitary metastasis to the brain. We report such a case in the cerebellopontine (CP) angle mimicking an acoustic neurinoma. CT scan showed a large, round mass in the CP angle which enhanced homogeneously following contrast infusion. The internal auditory meatus appeared to be eroded. The clinical, radiological, and pathological findings are presented.

Cerebellar Neoplasms↗
PubMed1983

Reversed hemispheric organization in a lefthander.

For left-handers, cognitive functions are organized in the brain similarly to right-handers or they are more diffusely represented. In this study, we report a left-handed patient with a focal right temporal-parietal lesion who evidenced a lasting Wernicke's aphasia and visual-spatial functioning typical of a right-hander with left-hemisphere in involvement. The patient's performance on other tasks (e.g. praxis, singing) as well as observed behavioral changes also resembled those of a right-hander with left-hemisphere compromise. This case suggests that it is possible for cognitive functions to be inversely represented in the two hemispheres.

Aged↗