Seizure induction and magnetic brain stimulation after stroke.
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Biomedical subjects
Publications and source records attributed to J Zihl.
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Measurements of binocular depth inversion using a stereoscopic slide projection with polarized light were performed in healthy volunteers before and after cannabis intake. Since binocular depth inversion represents an illusion occurring in the perception of semantically meaningful objects projected in a 3-D inverted fashion, the hypothesis can be tested that cannabis-induced "psychedelic states" represent a condition in which the human CNS is unable to correct implausible perceptual hypotheses. The data demonstrate a strong cannabis-induced impairment of binocular depth inversion.
Threshold elevation in the periphery of the visual field as a consequence of repetitive stimulation can be abolished by stimulating a mirror-symmetric position in the contralateral visual half-field. A patient suffering from a congenital malformation of the right superior colliculus did not exhibit threshold elevation when stimulated repeatedly in the left visual field. Stimulation in the right visual half-field resulted in the usually observed threshold elevation, but stimulating a mirror-symmetric position in the left visual half-field did not abolish threshold elevation in the right half-field. These observations suggest that: (a) threshold elevation probably occurs as a consequence of collicular adaptation and (b) the mirror-symmetrically organized interhemispheric interaction is mediated at the collicular level.
Typical roving eye movements (pendular deviations of the bulbi) were observed in a 41-year-old patient with bilateral symmetrical softenings in the anterior thalamic region. They constantly appeared after lid closure with a mean latency of 7.3 sec. The mean frequency was 0.25 cps, the mean amplitude 30 degrees. The phenomenon of roving eye movement is discussed with regard to the supranuclear structures regulating binocular eye movements.
The visual functions of a patient suffering from a brain lesion incorporating the left n. pulvinar was examined in order to assess the contribution of this structure to human vision. With the exception of the following abnormalities visual functions were normal. First, there was a decrease in the critical flicker frequency in the periphery (but not in the parafoveal region) of the right visual hemifield, that is, that contralateral to the pulvinar lesion. However, the second and most striking characteristic was--as shown by presenting visual stimuli bilaterally and simultaneously-a 'neglect' for the periphery of this contralateral visual half-field. This 'neglect' was a function of (a) position in the visual field (eccentricity), (b) stimulus properties (size and luminance), (c) temporal properties (length of presentation and interstimulus interval). In addition to this reduced capacity to detect stimuli appearing in the periphery of the right visual hemifield, there was also prolonged latency of visually evoked saccadic eye movements and a paucity of spontaneous eye movements directed towards the right visual hemifield. These results are interpreted in terms of a contribution of the n. pulvinar to the detection of light stimuli presented in the periphery of the visual field, and support the view that the tectopulvinar extrastriate visual pathway plays an important role in the control of visual attention.
Patients with postchiasmatic visual field defects were trained at the border of their visual field. Using a psychophysical method, light-difference thresholds were determined repeatedly in this visual field area. Improvement in contrast sensitivity and increase in size of the visual field could be obtained by this training procedure. The improvement was confined to the trained visual field area and showed interocular transfer indicating its central nature. Althoughh only contrast sensitivity was trained, the observed improvement was not limited to this visual function. Visual acutity, critical flicker fusion, and colour perception also showed and improvement suggesting an association of these functions. The improvement was restricted to the training period-no spontaneous recovery was observed between or after the periods of training. It is suggested that a lesion in the central visual system does not always result in a complete and permanent loss of function. The critical level of function that normally has to be reached for sufficient neuronal sensitivity may be obtained by systematic visual stimulation in the area between the intact and blind parts of the visual field. This increase in neuronal sensitivity leads to an improvement in visual performance.
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On the basis of a clinical and electrooculographic observation the phenomenon of periodic alternating eye deviation is discussed. The few cases in the literature are reviewed and the topography of the lesions causing eye deviation is considered.
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Electrooculographic (EOG) records were studied in 10 neurological patients with disturbances of activation according to clinical assessment and in 12 normal subjects. Rapid horizontal eye movements (saccades) and movements of the eyelids (blinks) were measured. It was concluded that the frequency distribution of blinks and saccades indicates activation deficits in a sensitive and reliable way. The continuous decrease of activation from orthological to pathological states could be shown by counting the frequencies of blinks and saccades. The relationship between the two variables is interpreted with regard to its functional significance.
Perimetry at various times of day in patients with large visual field defects due to postretinal lesions showed significant variations of visual field size. The largest visual fields were observed at noon, the smallest in the evening. Such systematic variations were observed only in patients who showed a gradual increase of increment threshold between the intact parts of the visual field and the scotoma. In two patients who showed an abrupt transition between intact and blind areas of the visual field, no obvious diurnal variation was observed. It is suggested that an endogenous modulation of neuronal sensitivity coupled to a hypothetical circadian oscillator is the basis of the diurnal variation.
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