Biomedical subjects
Publications and source records attributed to G F Harding.
We report a case of an infant with cystic fibrosis in whom VEP and scotopic ERG abnormalities were found. The underlying cause of these findings, which could not be determined within the limitations of this study, may be related to dietary deficiencies.
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The aim of this study was to determine the response properties of the human visual cortex to chromatic stimuli using magnetoencephalography (MEG). Evoked responses were recorded to isoluminant red/green sinusoidal gratings for a wide range of spatial and temporal frequencies. For each condition the response was dominated by a single major component which was well modeled by an equivalent current dipole. Coregistration of MEG and MRI data provided evidence that the principal evoked cortical activity originated from visual area V1. To investigate the chromatic response properties of this area, the maximum global field power of the evoked response was plotted as a function of stimulus spatial and temporal frequency. The spatial-frequency tuning was lowpass and the temporal-frequency tuning was multimodal, with peaks at 0 and 4 Hz. The results demonstrate the use of MEG as a technique for investigating activity from discrete regions of cortex.
The aim of this study was to establish whether there is non-geniculostriate input to the extrastriate motion-sensitive area V5 in humans. Responses were measured with a SQUID neuro-magnetometer to motion stimuli presented within the blind hemifield of GY, a well-documented subject with a complete absence of the left primary visual cortical area V1. The motion stimulus was a 0.5c/deg, rapidly drifting (16Hz) achromatic sinusoidal grating. With this stimulus, the magnetic responses recorded over the temporo-parieto-occipital region in normals are well modelled by localized current sources in areas V1 and V5 (Anderson, S. J. et al., Proceedings of the Royal Society, London, Series B, 1996, 263, 423-431). As a control, evoked responses were measured to a 1.0 c/deg, stationary, photometrically isoluminant red/green sinusoidal grating. With the chromatic stimulus, the principal component of the magnetic responses recorded over the occipital pole in normals is well modelled by a current source in area V1 (Fylan, F. et al., Investigative Ophthalmology and Visual Science, 1995, 36, s1053). Both stimuli subtended 4 deg vertically by 6 deg horizontally, positioned such that the stimulus extended beyond the area of macular sparing into the lower field quadrant of the blind (or sighted) hemifield. Chromatic stimuli failed to evoked responses from GY's blind (contralateral) hemifield, consistent with there being no V1 activity in his left cortical hemisphere. However, motion stimuli did evoke responses from GY's blind hemifield, originating from a location consistent with activity in area V5. We further observed that both colour and motion stimuli evoked responses from GY's sighted (ipsilateral) hemifield. We conclude that there is non-geniculostriate input to extrastriate motion-sensitive areas in the human visual system, and that this pathway subserves the residual visual sensitivity to motion in the blind hemifield that has been demonstrated psychophysically in observer GY.
We present a Monte Carlo analysis method for evaluating MRI-MEG/EEG co-registration techniques. The method estimates the error in co-registration as a function of position within the brain. Using this analysis technique, we demonstrate the limitations of conventional head-based fiducial point methods, and propose a new strategy utilising a dental bite-bar incorporating accurately machined fiducial markers. Results presented demonstrate the improved accuracy of MEG/EEG to MRI co-registration using the bite-bar.
The principal goal of this study was to assess the development of the S-cone pathway in human infants. For comparison, development of the L-M opponent pathway was also assessed. Visual evoked responses were measured to chromatic (tritan and red-green) and luminance-modulated (yellow-black) sinusoidal gratings of 0.2 cpd, viewed binocularly at a distance of 40 cm. For each type of chromatic stimulus, responses were recorded at a range of color ratios around the adult isoluminant point, as determined using standard flicker photometry criteria. Presentation was by abrupt pattern-onset with a stimulus duration of 100 ms and an interstimulus interval of 400 ms. Responses were recorded from Oz, referred to Cz, by averaging 30 sweeps. Infants were examined between the ages of 4 weeks and 3 months. Reliable visual evoked responses were recorded to isoluminant tritan stimuli from as early as 4 weeks of age, and to red-green stimuli from 6 weeks. Responses to the luminance-modulated stimuli were evident in all infants at 4 weeks of age (the earliest age examined). Our results provide evidence that the rate of development for pathways mediating information about tritan stimuli, red-green stimuli, and luminance-modulated stimuli is similar.
PURPOSE: Seizures provoked by television viewing may be triggered by patterns in the television image or by flicker from the display itself. We examined the incidence of EEG abnormalities elicited by patterns displayed on television sets with two different frame rates to evaluate the likely contribution of photosensitive and pattern-sensitive mechanisms to television- and video-game epilepsy. METHODS: Televisions with frame rates of 50 and 100 Hz were used to present 35 patients who were photosensitive or pattern-sensitive with grating patterns. These patterns comprised vertical square-wave and sine-wave gratings of 90% contrast, and the spatial frequency was varied between 0.25-7 cycles/degree. EEGs were analysed for laboratory sensitivity to patterned and unpatterned intermittent photic stimulation (IPS). RESULTS: Significantly fewer EEG abnormalities were elicited by patterns displayed on the 100 Hz frame-rate television than on the 50-Hz frame-rate television. No abnormalities were observed in response to the blank screens of either television. Thirty-three patients showed abnormalities in response to patterned IPS but only 15 in response to diffuse flash. Two patients showed no laboratory evidence of photosensitivity. Patients who were sensitive to patterned IPS at 50 Hz were significantly more likely to demonstrate abnormalities to patterns displayed on the 100-Hz frame-rate television than were patients who were not sensitive to 50-Hz patterned IPS. CONCLUSIONS: We suggest that for many patients, the combination of high-contrast patterns and screen flicker may elicit the observed EEG abnormalities. For patients with sensitivity to screen flicker, the use of a high frame-rate television may be beneficial in reducing the risk of seizures.
PURPOSE: One hundred patients with photosensitive epilepsy were investigated as part of an ongoing follow-up study. Average duration of follow-up was 14 years; mean age at follow-up was 27 years. METHODS: All patients were EEG investigated using a standard technique of intermittent photic stimulation (IPS). The presence of a photoparoxysmal response (PPR) or a degraded PPR indicated the presence of photosensitivity. RESULTS: Seventy-seven patients became seizure free. Of the untreated patients, photosensitivity disappeared in 14 patients but was present in 32 patients. Of the patients who were treated, 31 showed evidence of PPRs or degraded PPRs, but 23 patients no longer showed evidence of photosensitivity. Thirty-two mothers had 67 children during the follow-up period. Thirteen have so far proved to be sensitive to IPS in the laboratory and four have also had photosensitive seizures induced in the outside environment. Nine of the children have been found not to be photosensitive nor have they had seizures. CONCLUSIONS: This study suggests that photosensitivity persists in at least two thirds of patients with photosensitive epilepsy and that valproate is effective in controlling this photosensitivity.
Using a multi-channel SQUID-based neuromagnetometer, we have determined the location, temporal dynamics and functional response properties of the human homologue of the primate cortical area V5 (MT). We provide evidence that area V5 in humans is located near the occipito-temporal border in a minor sulcus immediately below the superior temporal sulcus. this area is selective for low spatial frequencies ( < or = 4.0 c/deg), responds to a wide range of temporal frequencies ( < or = 35 Hz) and shows response saturation for stimulus contrasts greater than 10%. In addition, we find that this area is not responsive to purely chromatic patterns but is responsive to motion-contrast stimuli. Our results are consistent with the hypothesis that area V5 in humans represents a stage of processing within the magnocellular pathway. We discuss our results in relation to the widespread belief that area V5 in humans is specifically concerned with motion perception.
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We describe cortical potentials evoked by balloon distension of the proximal and distal oesophagus in 8 healthy right handed volunteers. Oesophageal stimulation was performed using a pump which rapidly inflated a 2 cm silicone balloon positioned either 3 cm distal to the upper oesophageal sphincter or 5 cm proximal to the lower oesophageal sphincter, at a frequency of 0.2 Hz, using inflation volumes which produced a definite but not painful sensation. Oesophageal evoked cortical potentials were recorded in all subjects with an initial negative and positive component (N1 and P1), followed by a second negative and positive component (N2 and P2) in 6 subjects. The morphology and the scalp topography of the N1 component elicited by proximal and distal oesophageal stimulation suggests activation of the primary somatosensory cortex and/or the insular. There was also evidence for hemispheric dominance for the N1 potential which was independent of handedness. The frontal emphasis of the proximal oesophageal N1 component, in contrast to the central emphasis of the distal oesophageal N1 component, suggests that different neuronal populations were activated by stimulation of the two sites. The frontal emphasis of the ensuing P1 component from both oesophageal sites suggests that it originates in a separate precentral source. The topography of the N2 components obtained by stimulation of either oesophageal site was similar to that of the N1 component, suggesting that they originate in similar areas of the cortex. The P2 component evoked by stimulation of both oesophageal sites was localised at the vertex. The inter- and intra-subject variation in the morphology of the N2 and P2 components suggests that secondary cortical processes related to cognition may be involved in their generation.
The incidence of 'telephillic syndrome' (impulsive attraction to television), in three photosensitive epileptic patients who were referred to our neurophysiology clinic because they were having seizures is reported. Two were females, aged fourteen and eight respectively, one was a male aged twenty-five years. All the patients had a family history of epilepsy. The age range of onset of photosensitivity was 3.5-12 years and the most common seizure inducing factor was flickering light from the television (TV) viewing. They were all 'telephillic'. The predominant seizure type found in these patients was tonic-clonic seizure. Comprehensive electroencephalographic (EEG) investigation was carried out including hyperventilation. The basic EEG showed abnormal spike and wave activity on eye opening and eye closure in all the patients. Intermittent photic stimulation (IPS) evoked occipital spikes and photoparoxysmal response (PPRs) at a photosensitivity range of 758 flashes per second (fps). Pattern sensitivity test using a Gratings pattern revealed a sensitivity range of 1.03-3.5 cycles per second (cpd). And the predominant area of brain activity was the right mid-post temporal regions. Binocular stimulation offered no protection in one patient.
It has previously been shown that 0.6 mg of scopolamine produces a delay in the flash visual evoked potential of young normal volunteers, while the pattern-reversal response does not change in latency. Recent work has shown that this drug differentially affects parvocellular and magnocellular systems. To investigate this effect, two studies were performed. In the first study, 0.4 mg of scopolamine was injected intramuscularly into 11 young, healthy male volunteers who had fasted overnight. The visual evoked potential was recorded to both binocular flash stimulation and monocular pattern-reversal stimulation by means of a checker-board consisting of 56' checks in a 28 degrees field. Responses were recorded before administration of the drug and then 1, 2, 4 and 6 hours after administration. The scopolamine produced a slowing of the flash P2 latency of approximately 6 ms (p < 0.05) two hours after drug administration. There was no effect on the latency of the flash N2 or pattern-reversal N75 or P100. There was an increase in amplitude of the flash N2-P2 component 6 hours after drug administration and an increase in the amplitude of the N75 and P100 2, 4 and 6 hours after the drug. Further subjects were investigated with the use of topical administration of 0.125% scopolamine applied monocularly. In all studies the other eye acted as a control. The subjects were again young healthy volunteers. The visual evoked potential was recorded to both flash and pattern-reversal stimulation with a checkerboard consisting of 60' checks counterphasing at 2 Hz within a 5 degrees field. Results suggest that systemic scopolamine affects the tectal pathway but has no peripheral effect.
Visual evoked magnetic responses to pattern onset/offset stimuli were recorded in 5 normal subjects. The outgoing and ingoing magnetic currents were seen maximally over the contralateral visual cortex to the half field stimulated in the majority of subjects. The distribution of magnetic currents with half field stimulation would be consistent with a dipole on the midline with the positive end pointing laterally. Quadrantic stimuli produced dipoles which would be consistent with a vector sum of dipoles situated, in the case of upper quarter field stimulation, in the lingual gyri on the floor of the calcarine fissure. Lower quadrantic stimulation produced a vector consistent with dipoles on the cuneal gyrus and on the ceiling of the calcarine fissure producing a resultant vector. The use of paired octant stimuli to improve localisation was demonstrated on both right left and upper and lower half fields.
We have previously reported on the development of black/white pattern reversal VEPs in premature babies of more than 30 weeks post-menstrual age (PMA). Unlike the flash VEP, the pattern reversal VEP shows a similar morphology to that of the full term infant and the major positive component (P1) decreased in latency with increasing PMA. The N1 and N2 components were more likely to be present with increasing maturity. In our present study we are examining the development of the transient chromatic pattern VEP. In order to produce a purely chromatic stimulus it is necessary to remove luminance cues. Based on forced choice preferential looking we developed a method of determining the isoluminant point for infants. Preference was tested for a flickering sinusoidal red and green grating over the uniform field. As sensitivity for chromatic flicker is much poorer than for luminance flicker, sensitivity is expected to be least when the residual luminance variation in the stimulus is at a minimum. The red/green luminance ratio at which this occurs represents the isoluminant point. From this method we found the subjective isoluminant point for infants of 2-3 months of age to be very close to the objective measure of isoluminance. Using this information, pattern reversal VEPs to 20 chromatic red/green and achromatic checks were studied and it would appear that pattern reversal VEPs cannot be obtained to isoluminant stimuli before 7 weeks chronological age.
Visual evoked potentials were measured on patients with Parkinson's disease and Alzheimer's disease and normal controls to assess the function of dopamine and acetylcholine in the visual system. Dopamine is a neurotransmitter known to be present in the retina of primates and is found to be severely depleted in the substantia nigra of patients with Parkinson's disease. Acetylcholine is also known to be present in the retina, visual cortex, and superior colliculus and is found to be grossly reduced in patients with Alzheimer's disease. Stimuli were designed to preferentially activate functionally separate pathways in the visual system described as magnocellular and parvocellular. The four stimuli were a diffuse flash; an achromatic, 73' check counterphasing at 6 Hz at a contrast of 30%; an achromatic 10' check counterphasing at 2 Hz at a contrast of 85%; and an isoluminant red/green grating of 4 cpd presented using an on and off cosine ramp of 200 ms. The results indicate that an acetylcholine deficit produces a delay to the flash P2 component of the visual evoked potential. No change was detected when other stimuli were used.