Search PubMed⌕ Search

Biomedical subjects

W Heide

Publications and source records attributed to W Heide.

At least 37 records · Page 2Linked to original sources
PubMed1998

The effect of oral ethanol consumption on eye movements in healthy volunteers.

Horizontal and vertical eye movements were recorded and analysed with an infrared photoelectric technique in 12 healthy volunteers under various blood alcohol concentrations (0.0, 0.5, 1.0 g/kg body weight, [% per thousand]). The predictive smooth-pursuit tracking and saccadic eye movements were studied in response to unpredictable target jumps and during scanning of a classical kitchen scene and a traffic scene. Smooth-pursuit eye movement gain value decreased dose-dependently and was compensated by an increased number of catch-up saccades. With increasing blood alcohol concentrations peak velocities of horizontal and vertical visually guided reflexive saccades decreased while their latencies to the target increased. At blood alcohol concentrations of 0.5% per thousand and 1.0% per thousand healthy volunteers showed significantly longer mean fixation durations and a lower total number of exploratory saccades when scanning both the classical kitchen scene and the traffic scene. Surprisingly, in both of these scanning tasks the total fixation duration or the relative number of exploratory saccades increased in those scene sectors in which exciting situations were presented. Additionally, the time interval needed to foveate these exciting areas for the first time increased, probably due to an attention deficit. In conclusion, these findings indicate that alcohol consumption impairs the velocity and initiation of saccadic and smooth-pursuit eye movements, but that subjects can nevertheless still recognize exciting and relevant areas of visual scenes. The significant increase in fixation time, however, does not allow scanning of the entire visual scene during an adequate period of time. Therefore the reduced visual exploration caused by alcohol reflects an impaired sensorimotor processing of active visual perception.

Administration, Oral↗
PubMed1998

Lateralized human cortical activity for shifting visuospatial attention and initiating saccades.

Lateralized human cortical activity for shifting visuospatial attention and initiating saccades. J. Neurophysiol. 80: 2900-2910, 1998. The relation between shifts of visual attention and saccade preparation was investigated by studying their electrophysiological correlates in human scalp-recorded electroencephalogram (EEG). Participants had to make saccades either to a saliently colored or to a gray circle, simultaneously presented in opposite visual hemifields, under different task instructions. EEG was measured within the short interval between stimulus onset and saccade, focusing on lateralized activity, contralateral either to the side of the relevant stimulus or to the direction of the saccade. Three components of lateralization were found: 1) activity contralateral to the relevant stimulus irrespective of saccade direction, peaking 250 ms after stimulus onset, largest above lateral parietal sites, 2) activity contralateral to the relevant stimulus if the stimulus was also the target of the saccade, largest 330-480 ms after stimulus onset, widespread over the scalp but with a focus again above lateral parietal sites, and 3) activity contralateral to saccade direction, beginning about 100 ms before the saccade, largest above mesial parietal sites, with some task-dependent fronto-central contribution. Because of their sensitivity to task variables, component 1 is interpreted as the shifting of attention to the relevant stimulus, component 2 is interpreted as reflecting the enhancement of the attentional shift if the relevant stimulus is also the saccade target, and component 3 is interpreted as the triggering signal for saccade execution. Thus human neurophysiological data provided evidence both for independent and interdependent processes of saccade preparation and shifts of visual attention.

Adult↗
PubMed1997

A double-blind controlled study of gabapentin and baclofen as treatment for acquired nystagmus.

We conducted a double-blind crossover trial comparing gabapentin (up to 900 mg/day) to baclofen (up to 30 mg/day) as therapy for acquired nystagmus in 21 patients. We measured visual acuity and the nystagmus before, and at the end of, 2 weeks on each medication. For a group of 15 patients with acquired pendular nystagmus (APN), visual acuity improved significantly with gabapentin, but not with baclofen. Gabapentin significantly reduced APN median eye speed in all three planes, but baclofen did so only in the vertical plane. In 10 patients with APN, the reduction of nystagmus with gabapentin was substantial and 8 of these elected to continue taking the drug. In 6 patients with downbeat or torsional downbeat nystagmus, changes in median slow-phase eye speed were less consistent with both drugs, either increasing or decreasing, and being dependent on viewing conditions. Only 1 patient showed consistent reduction of median eye speed, and this was achieved by either drug. Our findings suggest that gabapentin may be an effective treatment for many patients with APN and that occasional patients with downbeat nystagmus will respond to gabapentin or baclofen.

Acetates↗
PubMed1997

Slow saccades and other eye movement disorders in spinocerebellar atrophy type 1.

In order to study the relation between genotype and phenotype, a detailed study of the course of oculomotor deficits was performed in three patients with autosomal-dominant cerebellar ataxia, subtype spinocerebellar atrophy type 1 (SCA 1) using clinical testing and electrooculography. DNA analysis revealed a CAG repeat expansion of 65 in the SCA 1 gene on chromosome 6p in all patients. A progressive disorder of the saccadic system became obvious, leading to a marked slowing of saccadic eye movements and loss of pathological and physiological nystagmus. An upward gaze palsy developed early, followed by horizontal and downward gaze palsy at a later state of the disease. Smooth pursuit eye movements were disturbed to a lesser extent; the vestibulo-ocular reflex was reduced. As an additional feature, severe loss of visual acuity developed due to progressive optic nerve atrophy. The oculomotor deficits can be explained by progressive damage to the brain stem rather than to the cerebellum. Each combination of oculomotor deficits with or without optic atrophy may occur irrespective of the gene locus of the disease, making a correlation between clinical signs and genetic findings difficult.

Adult↗
PubMed1997

Autosomal dominant vitreoretinochoroidopathy.

BACKGROUND: Autosomal dominant vitreoretinochoroidopathy recently has been described as a condition characterized by peripheral chorioretinal atrophy and areas of hypopigmentation and hyperpigmentation between the equator and the ora serrata circumferentially in the ocular fundus. We describe the clinical features of a family, some members of which have this disorder. This is the first such report of a family outside the United States. METHODS: We examined a family of 15 individuals, seven of whom were affected. RESULTS: The main clinical findings were peripheral pigmentary changes for 360 degrees, with a discrete boundary near the equator. In one patient, a partial vitreous detachment was found that was creating increasing traction to the macula and to the peripheral retina. Vitreous surgery successfully relieved the traction, and vision recovered from 20/100 to 20/25. One patient lost visual acuity at the age of 10 years when complete rhegmatogenous detachment occurred. In two women, a horizontal nystagmus was present showing typical signs of a congenital nystagmus. Results of electrooculography demonstrated a marked reduction of light rise and a clear reduced Arden ratio in one patient. CONCLUSIONS: Autosomal dominant vitreoretinochoroidopathy appears clinically as mainly a peripheral tapetoretinal disease; patients with this disease have been reported in and outside the United States. In addition to the typical peripheral features, significant vitreous traction maculopathy and congenital nystagmus associated with the disease were found.

Adult↗
PubMed1996

On-line brain potential correlates of right parietal patients' attentional deficit.

EEG potentials evoked by cues and targets were recorded in Posner's visual cueing task from 10 patients with lesions of the right parietal cortex and from age-matched healthy subjects. The patients' N1 component evoked by left-side cues was reduced at the right-parietal recording site, suggesting a general impairment in processing left-side visual input. As usual, patients' keypress responses were delayed when left targets were preceded by right cues. There were two correlates of this delay in the patients' EEG potentials evoked by the critical combination of right cue/left target: their mean amplitude 160-280 ms after target onset ('Nd') was less negative than with other combinations of cue and target, and the following frontal P300 was enhanced. The Nd reduction seems to be an on-line measure of patients' momentary decrease of attention for the left hemifield, while the frontal P300 might reflect the patients' attempts at reorienting. In conclusion, different components were sensitive to different aspects of the patients' disorder, suggesting the utility of this approach for developing detailed hypotheses on the mechanisms of attentional deficits involved in visual extinction and neglect.

Aged↗
PubMed1996

Deficits of smooth pursuit eye movements after frontal and parietal lesions.

To assess the contribution of the human frontal and parietal cortices to smooth pursuit (SP) eye movements, we recorded ocular motor responses to predictable (periodic) and unpredictable (step-ramp) foveal pursuit stimuli and to constant-velocity optokinetic full-field motion in 31 patients with chronic focal unilateral hemispheric lesions and in 50 age-related healthy adults, using infrared reflection oculography. Lesions were located either in the posterior parietal cortex (PPC), leaving the visual fields largely intact, or in the region of the frontal eye fields (FEF), the dorsolateral prefrontal cortex (PFC) or the supplementary motor area (SMA). We found (i) directional deficits in terms of lower pursuit velocities with ipsiversive target motion, more pronounced with predictable than with step-ramp stimuli, in patients with FEF lesions more frequently (in each of the four cases) than in patients with PPC lesions (in four out of 13 cases with foveal and in eight out of 13 cases with optokinetic stimulation); (ii) a relatively prolonged latency of direction reversal with periodic constant-velocity stimuli after SMA lesions (three cases), implying impaired anticipation of the target trajectory; (iii) no SP deficits following selective prefrontal lesions (eight cases); (iv) in some patients with PPC lesions (four out of 13) retinotopic deficits of SP initiation in both horizontal directions when step-ramp stimuli started in the contralesional hemifield, including prolonged pursuit latencies, which were independent of contralateral visual hemineglect. Directional and retinotopic SP deficits in patients with PPC lesions corresponded to SP deficits after unilateral lesions of middle temporal (MT) and medial superior temporal (MST) cortex in the monkey, and occurred only when lesions included the junction of Brodmann areas 19, 37 and 39, where the human homologues of MT and MST are assumed to lie. In conclusion, human SP eye movements are controlled, as in non-human primates, by a network of frontal and posterior cortical areas. Selective damage to each of these areas impairs specific SP subfunctions, reflecting subsequent stages of cortical processing from visual motion input to SP-related motor output.

Adult↗
PubMed1996

[See-saw nystagmus. Clinical aspects, diagnosis, pathophysiology: observations in 2 patients].

See-saw nystagmus is an uncommon but characteristic kind of nystagmus. Typically there is intorsion and elevation of one eye and simultaneous extorsion and depression of the other eye. The nystagmus can be of pendular-waveform or jerk-waveform. The pendular-waveform see-saw nystagmus is commonly due to a midline meso-diencephalic, bilaterally compressing mass. The jerk-waveform see-saw nystagmus is mostly due to a unilateral lesion in the meso-diencephalic junction. For explanation, a current theory assumes a unilateral lesion of the interstitial nucleus of Cajal sparing the rostral interstitial nucleus of the medial longitudinal fascicle. Another concept suggests a lesion of the vertical vestibulo-ocular-reflex. We report two patients with jerk-waveform see-saw nystagmus. In both patients an internuclear ophthalmoplegia was found additionally. The origin was a unilateral brainstem infarction in both cases. We explain the symptomatology of see-saw nystagmus and discuss the actual theories of its origin.

Brain Mapping↗
PubMed1995

Cortical control of double-step saccades: implications for spatial orientation.

To accurately localize a visual target in space despite eye movement-induced shifts of its retinal image, the brain must take into account both its retinal location and information about current eye position or at least the preceding eye displacement. We examined this ability with respect to saccadic eye movements by applying "double-step" stimuli, where the locations of two sequentially flashed target lights have to be fixated by two successive saccades performed after their disappearance. As the 2nd saccade will not start at the spatial location from which the 2nd target was seen, a dissonance arises between its retinal coordinates and the motor coordinates of the required 2nd saccade. Nevertheless, these saccades were performed quite accurately by 32 healthy human adults. To investigate the contribution of the cerebral cortex, we recorded horizontal double-step saccades in 35 patients with focal unilateral hemispheric lesions. Whereas frontal lesions impaired temporal properties, posterior parietal lesions caused spatial dysmetria or failure of even ipsiversive 2nd saccades following contraversive 1st saccades. This reflects an inability to compensate for retinospatial dissonance by using nonretinal information (corollary discharge) about eye displacement associated with a previous saccade into the contralesional hemifield. In conclusion, the parietal cortex is crucial for spatial constancy across saccades.

Adult↗
PubMed1995

[Congenital nystagmus in the ophthalmologic automobile driving fitness verdict].

BACKGROUND: A driver with congenital nystagmus (CN) is supposed to have a certain minimum visual acuity and a minimum velocity of reading, with the head directed straight ahead or 10 degrees laterally. The ability to perform different oculomotor tasks depends, however, on individual properties of nystagmus and compensatory mechanisms, as is demonstrated in 4 cases. METHODS: Detailed electrooculographic (EOG) recordings were performed in 4 CN patients, in addition to the examination of visual functions. RESULTS: The visual acuity of patient 1 is sufficient (0.6 on both eyes), yet his retinal image is intermittently destabilized by a periodic alternating nystagmus. Case 2 with high myopic astigmatism and severely reduced visual acuity (right eye: finger counting; left eye: 0.2) compensates for his vertical pendular nystagmus by head nodding and for his manifest-latent horizontal nystagmus by a head turn. The optimal visual acuity of patient 3 (horizontal pendular nystagmus) is 0.3, with an oblique head position and convergence. In other head and gaze positions he has a coarse jerk nystagmus beating in the direction of gaze. Patient 4, with a high myopic astigmatism, microstrabism and manifest-latent fixational nystagmus, has a visual acuity between 0.2 and 0.3 in both eyes. He had been a licensed professional car driver, in spite of contradicting national and international criteria: but his license was refused later. CONCLUSIONS: In patients with CN, the influence of head and gaze position, monocular fixation, convergence and self or object motion on nystagmus intensity and wave forms could be important for driving, because it might influence visual acuity and motion perception. The latter hypothesis still has to be proven in further studies, performed under conditions relevant for traffic.

Adult↗
PubMed1994

The presaccadic cortical negativity prior to self-paced saccades with and without visual guidance.

The presaccadic negativity (PSN) of the scalp EEG potential prior to self-initiated saccades aimed either at a visual target or at the remembered position of that target in total darkness was analysed in 10 normal subjects. Under both conditions a PSN with a negligible EOG contamination was found, showing 4 characteristics: (1) In both conditions, the PSN maximum is localized at the vertex, probably containing the activity of the supplementary motor area. (2) At an electrode placed over the frontal eye field (FEF) contralateral to the saccade direction, there is a temporary, circumscribed maximum prior to saccades to the visual target, thus probably reflecting activity of the FEF. (3) Prior to saccades to the visual target, there is a statistically significant interhemispheric difference of the PSN over the parietal cortex with a larger amplitude over the hemisphere contralateral to the saccade direction; this might be attributed to directed visual attention. (4) Prior to saccades without visual guidance in darkness there is a statistically significant interhemispheric difference of the PSN over the frontal cortex with a larger amplitude over the hemisphere contralateral to the saccade direction. The amplitude of the PSN decreased in the course of the experiment, probably due to psychological factors such as attention and motivation. Our results suggest that the PSN is a readiness potential preceding voluntary saccades, containing activity related both to unspecific psychological processes and to specific movement preparation in the frontal and parietal ocular motor areas.

Adult↗
PubMed1994

Reduction of P3b in patients with temporo-parietal lesions.

By recording event-related EEG potentials from patients with frontal, parietal, or temporo-parietal lesions, we wanted to determine the cortical area that is relevant to the P3b component, replicating the approach used by Knight and associates who found reduced P3bs in patients with temporo-parietal lesions. They used auditory and somatosensory stimuli. We wanted to replicate their findings in auditory and visual oddball tasks and analysed potentials evoked by targets and by standard stimuli. Temporo-parietal patients' P3bs were reduced with auditory targets and lacked a distinct Pz maximum with visual targets. Further, auditory N1 was reduced both with targets and standards, P3 to visual standards and P2 to auditory standards were reduced. Parietal patients' P3bs differed only slightly from the control group, being somewhat reduced over the lesioned hemisphere with visual stimuli. Their P3 to visual standards was, however, reduced to the same extent as was the temporo-parietal patients'. Frontal patients did not differ from the control group both in their P3b and in their P3 to standards but had a number of conspicuous features in modality-specific components. In sum, our results on P3b (as well as on N1) replicate Knight's findings, confirming his conclusion that integrity of the temporo-parietal junction is critical for P3b. Implications for hypotheses on P3 are discussed.

Acoustic Stimulation↗
PubMed1990

Impairment of vertical motion detection and downgaze palsy due to rostral midbrain infarction.

We present two cases with acute onset of vertical gaze palsy, mainly consisting of impaired downgaze and apraxia of downward head movements, together with neuropsychological deficits (hypersomnia, impaired attention and disorders of memory and affective control). CT and MRI revealed bilateral post-ischaemic lesions in the dorsomedial thalamus and the mesodiencephalic junction, dorsomedial to the red nucleus, thus being restricted to the territory of the posterior thalamosubthalamic paramedian artery, which includes the region of the rostral interstitial nucleus of the medial longitudinal fascicle as the main premotor nucleus for the generation of vertical saccades. In our patients, oculographic examination with electro-oculography and magnetic search coil recording showed severe impairment of downward more than upward saccades and only minor deficits of vertical pursuit and the vestibulo-ocular reflex. Visual functions were normal, with one exception: a psychophysical test of motion perception revealed a significant deficit in the detection of vertical movements. This could be due to a central adaptive mechanism which, in order to minimize oscillopsia, might elevate thresholds for vertical motion perception in cases of vertical gaze palsy. As an alternative explanation, lesions within the midbrain tegmentum could have damaged subcortical visual pathways involved in motion perception.

Cerebral Infarction↗
PubMed1990

Epidural blood patch reduces the incidence of post lumbar puncture headache.

In 50 patients, aged 16 to 58, an autologous blood patch was injected into the epidural space immediately after diagnostic lumbar puncture. The incidence of postpuncture headache was 22%, which was significantly lower than in a control group (40 patients, aged 17 to 54), where it amounted to 45%. Compared to the control group, the patients with epidural blood patch had significantly less postpuncture complaints between the 1st and 3rd day following lumbar puncture. Lower back pain as the only side effect was experienced by 30 to 40% of the patients in each of the 2 groups. We conclude that the epidural blood patch is practicable and effective in the prophylaxis of postpuncture headache, but cannot prevent its occurrence in all cases.

Adolescent↗
PubMed1987

Representation of edges of variable blur by neuronal responses in the lateral geniculate body and the visual cortex of cats: limits of linear prediction.

We have measured the responses of cells in the cats lateral geniculate body and the visual cortex to edges which were blurred to various degrees (cosinusoidal blur). For the same cells also the responses were determined to sinusoidal gratings of various fundamental frequency and to slits of various blur and width. All stimuli were moved across the receptive fields at various speeds. The responses of most cells increased with increasing edge sharpness, but usually reached a maximum at a blur corresponding to a high frequency cutoff at 0.6-1.2 c/deg. The responses to the sharpest edges were usually smaller than those to a blurred edge (up to -50% in individual cells and -15% in the average). After normalization, the responses predicted from the spatial frequency tuning curves and the Fourier transform of the edge stimuli corresponded well to the measured blur functions up to the maximum of the edge response which varied considerably between cells, however. At edge sharpness beyond that maximum, the predicted curves rose up to edge sharpness with high frequency cutoff 1.6-1.8 times above that which produced the experimental neuronal response maximum. On the other hand, responses could increase with edge sharpening in spatial frequency regions, in which no or only small responses were seen with sinusoidal gratings (e.g. at lower spatial frequencies in "band pass neurons"). Geniculate X- and cortical simple cells as well as those geniculate Y-cells which showed phase locked grating responses behaved similarly in all respects. We concluded that edge sharpness is not represented by response amplitude of individual neurons but by the spatial distribution of excitatory peaks across the representation of the retinotopic cortical map. Our findings further indicate that spatial models of receptive fields assuming linear signal summation have only a limited value for predicting edge sharpness.

Animals↗