EEG and coma: is there a prognostic role for EEG?
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Biomedical subjects
Publications and source records attributed to G G Celesia.
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Several animal studies have shown an anatomical and functional separation between the ON- and OFF-pathways in the retina and in the lateral geniculate nucleus. Psychophysical studies in humans have also documented separate pathways that process increments and decrements of light. However, at the level of the visual cortex, there is electrophysiological evidence of interactions between the ON- and OFF-pathways. In addition, psychophysical studies have shown that these pathways can exhibit differential sensitivity and be differentially adapted. These findings motivated an electrophysiological study to gather further evidence of processing within the ON- and OFF-pathways in the human visual system. Using sawtooth stimulus modulation, we measured the visual evoked potential (VEP) before and after adaptation to both rapid-on and rapid-off sawtooth stimuli. The effect of adaptation was determined by comparing the VEP response in three test conditions: without adaptation, after adaptation to the same sawtooth polarity, and after adaptation to the opposite sawtooth polarity. The results reveal a selective adaptation effect, which provides physiological evidence for separate processing of increments and decrements in the human visual system. We conclude that with appropriate stimulus parameters, the VEP can serve as an objective measure of processing within the ON- and OFF-pathways in humans.
Coma, vegetative state, lock-in syndrome and akinetic mutism are defined. Vegetative state is a state with no evidence of awareness of self or environment and showing cycles of sleep and wakefulness. PVS is an operational definition including time as a variable. PVS is a vegetative state that has endured or continued for at least one month. PVS can be diagnosed with a reasonable amount of medical certainty; however, the diagnosis of PVS must be kept separate from the outcome. The patient outcome can be predicted based on etiology and age. Using outcome probabilities and etiology as criteria, patients can be subdivided in 5 groups and reasonable management guidelines can be suggested. Three levels of care can be provided to PVS patients: high technology, supportive and compassionate care. Pragmatic options for the various subgroups of patients are suggested. Management decisions will remain difficult for both the family and the health-care team. The role of the physician in these difficult cases is to share the decision-making with the family.
In a prospective study of 32 consecutive patients with homonymous visual field defects due to ischemic infarcts we found hemianopic anosognosia (HAN), defined as the unawareness of visual loss in the homonymous hemifield (or hemiquadrant), in 20 patients (62%). HAN, although occurring predominantly in right-side lesions in 16 of 26 patients (62%) was also present in four of six patients (or 67%) with left-side lesions. This group of patients has been presented in a prior report on positive spontaneous visual phenomena. HAN was associated with somatic anosognosia in nine patients and hemineglect in 17 patients. Dissociation between somatic and hemianopic anosognosia, as well as between hemineglect and HAN, was present in several patients, indicating that these phenomena may be independent of each other. Eight patients had pure homonymous hemianopia; that is, hemianopia without cognitive, motor, or somatosensory deficits. Four of these patients (Group A) had awareness of the visual deficit, whereas three patients (Group B) had HAN. Patients in these two groups had similar anatomic lesions. Patients with phosphenes, photopsias, or visual hallucinations were usually aware of their visual field loss. We suggest that HAN is most often related to failure of discovery of the deficits, occasionally to severe visual hemineglect, sometimes to generalized cognitive impairment, or to a combination of these factors. We further conclude (1) there is no specific cortical area for conscious visual perception; (2) visual awareness is processed by a distributed network including multiple visual cortices, parietal and frontal lobes, the pulvinar, and lateral geniculate bodies (lesions localized at various nodes or centers in the network may produce similar phenomena); and (3) both hemispheres are involved in visual processing and conscious awareness.
We prospectively studied 32 patients with ischemic infarction of the retrochiasmal visual pathways. Positive spontaneous visual phenomena (PSVP) in the blind hemifield were present in 13 patients (41%). The PSVP were subdivided into phosphenes, photopsias, visual hallucinations, palinopsia, and agitated delirium with hemianopia. PSVP were never associated with auditory or other sensory positive phenomena, except in patients with agitated delirium. Patients with photopsias, phosphenes, palinopsia, and visual hallucinations had similar lesions in MRI/CT, suggesting no anatomic area unique for these four phenomena. However, there was a significant difference in the severity of associated neurologic deficits between hemianopic patients with and without PSVP. Larger lesions destroying anteriorly located visual association areas precluded the development of PSVP, which may be related to release from inhibitory input of visual regions bordering the damaged area. Patients with the syndrome of agitated delirium and hemianopia had specific lesions involving the mesial aspect of the occipital lobe, the parahippocampal gyrus, and hippocampus.
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Previous studies examining the functional status of cortical muscarinic cholinergic M1 receptors have demonstrated an impairment in receptor-G protein coupling in Alzheimer's disease (AD) as measured by the inability of the receptor to form a high affinity agonist binding site. In order to investigate whether this alteration was a global phenomenon or a regional specific defect in signal transduction, we examined agonist binding at M1 receptors in three brain areas (superior frontal cortex, Brodmann areas 8 and 9; primary visual cortex, Brodmann area 17; and the dorsal striatum) within the same brain in controls and moderate to severe AD cases. Competition binding studies using the M1 antagonist 3H-pirenzepine (4 nM) in the presence of varying concentrations of the cholinergic agonist carbachol (50 nM to 1 mM) were performed in the presence and absence of GppNHp (100 microM), a non-hydrolyzable analog of GTP. In control membrane preparations, computer-assisted analysis of antagonist-agonist competition curves revealed that M1 receptor agonist binding fit a two site model with high and low affinity states in all three brain areas in the absence of GppNHp but only a single site in the presence of GppNHp. This is consistent with the ternary complex model of G protein-linked receptors. In contrast, curves obtained from both cortical regions from AD brains fit a single site model with low affinity in the presence or absence of GppNHp. On the other hand, agonist binding data obtained from the dorsal striatum of AD cases exhibited a two site fit, similar to that seen in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
A 72-year-old woman with epilepsia partialis continua (EPC) of the right foot is presented. Rhythmic myoclonic jerks were localized to the 1st and 2nd toes of the right foot and persisted for 72 h. EEG/video monitoring did not show any epileptiform transient in association with myoclonic jerks. MRI and MRA demonstrated an arterio-venous malformation involving the left fronto-parietal parasagittal area. Using the EMG signal from the myoclonic jerk we back-averaged the EEG 640 msec before and after the onset of the twitch. A negative-positive deflection was observed preceding the myoclonic jerks by 128-188 msec. Voltage topographic mapping showed a negative maximum in the left centro-parietal region. A multiple spatio-temporal dipole model was applied to the back-averaged deflection preceding the myoclonus. The patient's MRI was used to determine the center of the best fitting sphere, and the model was corrected accordingly. The best dipole solution consisted of 3 dipoles localized in the parasagittal frontal cortex, in the location of the motor representation for the foot. The utilization of a combined technique of back-averaging from the myoclonus and dipole source localization supported the epileptogenic etiology in this case.
This article reviews the anatomy and physiology of the visual system. The physical stimulus is coded by several separate and parallel pathways at multiple sites in the nervous system. We outline the major parallel pathways of the system, from their beginning in the retina, to the multiple cortical areas that receive visual input. Emphasis has been placed on the functional properties of the neurons of these pathways and the various cortical processing areas as they are currently known. Clinical syndromes as a result of damage to specific visual cortical areas are also described.
Steady-state pattern visual evoked potentials were recorded from the surface of the cat primary visual cortex before and after the intravenous administration of physostigmine, an agent that blocks the enzyme responsible for the breakdown of synaptically released acetylcholine. Under pentobarbital anesthesia, physostigmine increased the amplitude and changed the phase of the second response harmonic of the visual evoked potential, whereas the amplitude and phase of the fourth harmonic were not affected. These effects persisted for 15 to 45 minutes and were blocked by prior treatment with scopolamine or atropine. In addition, scopolamine or atropine administered 5 to 10 minutes after physostigmine returned the visual evoked potential to the baseline state. In comparison, when nitrous oxide was used, physostigmine caused a marked reduction in visual evoked potential amplitude, an effect that was reversed by subsequent atropine. These results indicate that the cholinergic system influences the visual evoked potential via a muscarinic pathway and that this influence is strongly affected by the anesthetic regimen used.
Visual processing of sinusoidally modulated gratings was studied in a group of patients (n = 11) with Alzheimer's disease (AD) and an elderly normal control group (n = 9). Spatial square wave gratings (1.47 c/d) were reversed at a temporal frequency of 4 or 8 Hz. EEG recordings at rest and during visual stimulation were obtained from 20 channels using the 10/20 international system. The power spectrum of the 2nd and 4th harmonic of the stimulation frequency was calculated by Fast Fourier Transform (FFT) at a resolution of 0.25 Hz. Association of activity between occipital, temporal, parietal and central regions was measured by intra- and inter-hemispheric coherence and phase at harmonics of the stimulation frequency. A significant difference (P < 0.01) in evoked activity of the 4th harmonic at O1 and O2 was found between the two groups with less activity in the AD patients. In the AD group there was a significant correlation (P < 0.05) between evoked activity at the 2nd harmonic of the 8 Hz visual stimulation and Mini-Mental State (MMS) score. This correlation was independent of the age effect on MMS. Response phase between O1 and O2 for both 4 and 8 Hz stimuli was close to 0 degree C and coherence had similar values in both groups. Occipital and central regions showed a phase reversal for all harmonic responses to both visual stimuli. The AD patients showed statistically significant (P < 0.05) phase dispersion at O1-P3 and O2-P4 not seen in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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Topographic amplitude distribution of the hemifield pattern visual evoked potential (PVEP) shows substantial intersubject variability. Many subjects have larger P100 amplitudes paradoxically over the hemisphere ipsilateral to the stimulated field, whereas others show larger responses over the stimulated hemisphere. The present study was designed to determine whether a single equivalent dipole model could correctly identify the field of stimulation, and therefore the hemisphere activated, under conditions in which the surface distribution is variable. Under conditions used in the present study, visual examination of the surface amplitude distribution of the P100 peak could not be reliably used to identify the hemifield that was stimulated. Of 28 hemifield PVEPs, obtained from 14 normal subjects, only 13 showed higher amplitude ipsilateral to the field of stimulation. Thus, neither examination of EP wave forms nor topographic maps provided an accurate means for determination of which hemifield was stimulated or which hemisphere was activated. The single equivalent dipole model correctly identified the stimulated hemisphere for 25/28 hemifield PVEPs. Orientation of the equivalent dipole accounted for much of the variability in surface amplitude distribution, with tangential orientations obtained in subjects with ipsilaterally predominant P100 surface topography. Although the dipole model improved identification of the stimulated hemisphere, dipoles were located anterior or inferior to the occipital lobe in some subjects. Results suggest that dipole modeling can provide useful information regarding the source of surface recorded potentials.
We obtained steady-state visual evoked potentials (VEPs) to sinusoidal gratings alternating at 4 Hz with spatial frequencies varying from 0.5 to 8 cpd in 21 normal controls and 21 patients with multiple sclerosis (MS), and analyzed responses by fast Fourier transform. Amplitude- and phase-spatial frequency functions were obtained and referred to as amplitude and phase "visuograms." We observed two types of abnormalities in the phase visuograms of MS patients: (1) abnormal responses at all spatial frequencies tested (37%), and (2) abnormal responses only at selective spatial frequencies (52%). Some patients had phase lag limited to low, middle, or high spatial frequencies. Steady-state and transient VEPs to 2 and 4 cpd showed a similar percent of abnormalities. The use of more than one spatial frequency stimulus increased the diagnostic yield by 17%. Our data confirm that MS may selectively affect specific neuronal channels within the visual pathways.
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Event-related potentials (ERPs) are scalp recorded electrophysiological responses that are related to an internal cognitive event. This review summarizes recent findings on the effects of neurologic disease and the origin of ERPs obtained in expectancy, attention, memory, and linguistic tasks. Cognitive ERPs allow the physiologic activity of the brain to be analyzed with exquisite temporal resolution. Our understanding of these potentials is incomplete at present. Advances in cognitive psychology and source localization of these surface potentials, however, may result in an increased understanding of both the organization of cognitive processing in the brain and cognitive deficits that result from neurologic disease.