A. López Aguerri

Figure 6.4. F1 (top) and F2 (bottom) form and motion VEP amplitudes (µV) taken from a region of interest (ROI). Amplitudes were averaged across electrodes within the ROI for each participant and group means were then calculated. Error bars represent the standard error of the mean.

The preceding analysis of correlations across topographies does not address the issue of overall amplitude of response, as patterns of activation can be correlated but have a lower base level in one group. To determine whether amplitudes were different, mean amplitudes

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were taken from a cluster of electrodes identified as most active in the control group in mesopic conditions. These regions of interest (ROIs) are shown above the form and motion plots in Figure 6.4.

As can be seen in Figure 6.4, F1 VEP amplitudes were reduced in the stationary group compared to controls for both form and motion. A repeated measures ANOVA comparing controls and stationary patients found a main effect of test (F(1,27) = 4.391, p = 0.046), with responses higher for motion than for form; light (F(1,27) = 20.540, p <0.001), with responses higher at mesopic than scotopic levels; and group (F(1,27) = 12.225, p = 0.002) with

responses higher in the control group. There was also a significant light x group interaction (F(1,27) = 5.476, p = 0.027) indicating the stationary patients and controls were differentially affected by light levels. As Figure 6.4 shows, for both form and motion, F1 amplitudes were more reduced in scotopic (as compared with mesopic) conditions for controls than for stationary patients.

Patient and control F2 amplitudes showed a main effect of light (F(1,24) = 24.540, p<0.001) with responses higher at mesopic than scotopic levels, but no main effect of test (F(1,24) = 2.818, p = 0.106) or light x group interaction (F(1,24) = 0.260, p = 0.146) indicating the stationary patients and controls were similarly affected by light levels. Unlike F1 amplitudes, there was no significant effect of group (F(1,24) = 1.139, p = 0.297) which suggests that stationary patients and controls were similarly affected across tests and light levels.

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6.4 D

Coherent form and motion SSVEP tests were carried out with stationary (ACHM) patients to assess whether they had different patterns or amplitudes of cortical activation relative to controls. Topographic plots showed that F1 responses, sensitive to stimulus coherence, varied between patients and controls with patient responses generally weaker and less clear. F2 responses, sensitive to local changes were comparable between the two groups.

For the form stimulus these F2 responses were localised to the occipital midline. Motion F2 responses were also located over the occipital midline in mesopic conditions but minimal responses were seen for both groups in the scotopic condition.

Correlational analyses of F1 amplitudes taken from all scalp electrodes revealed further consistencies and discrepancies between the two groups. Responses to coherent form stimuli were significantly correlated between patient and control groups in both mesopic and scotopic conditions. Responses to coherent motion, however, were not significantly

correlated between groups in mesopic conditions and were negatively correlated in scotopic conditions. The result that form responses but not motion responses showed similarities in topography between patients and controls suggests there may be different neural substrates for coherent motion (but not form) processing in the patients. It may be that form processing uses the same network in patients as in controls while for motion processing a different network is used. Lack of correlation in motion topographies was not explained simply by a weak response in the patient group. Importantly, the correlated topography for form in patients and controls does not imply “normal” cortical processing of coherent form, as the subsequent analysis of amplitudes showed these to be reduced in the patient group.

Mean amplitudes of responses to coherent form and motion stimuli at the two light levels were analysed in specific regions of interest. Patients had reduced F1 form and motion amplitudes relative to controls but comparable F2 amplitudes. These reductions in amplitude

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are consistent with behavioural results of reduced mean perceptual sensitivity to coherence for both kinds of stimuli (chapter 5). F1 amplitudes also showed a different effect of light in controls and patients, with controls showing a greater reduction in amplitude from mesopic to scotopic levels than the patients. This is also in line with behavioural results (chapter 5), in which controls’ performance deteriorated more markedly at lower light levels, consistent with loss of the additional cone signal at low light in controls, but not patients. SSVEP results did not show significant differential impairments across the two tests, form and motion (i.e. any interactions involving group and test). However, the stimulus which showed most striking dissociations from the others behaviourally, biological motion, was not included here as it did not provide measurable SSVEP responses in controls or patients.

The results suggest that similar neural substrates may be underlying form perception in the controls and patients but not motion perception. Patients’ processing of these stimuli is not at normal levels, however, as amplitudes of responses to both are reduced. Exactly what underlies differences between patients and controls in coherent motion F1 topographies remains unclear. Most striking is the significant negative correlation in patient vs. control motion topographies in scotopic light, where controls show a mid-right occipital peak (Fig. 1, bottom row, first plot), while patients show very little activation in the same region but some more frontal activation (Fig. 1, bottom row, second plot) that is absent in controls.

It is of interest that patients showed greater impairments on form tests than motion tests in the behavioural chapter (chapter 5). It may be that the shift in activation seen in patients’

motion topography represents a developmental specialisation that allows for better motion perception when vision is impaired. While no other imaging studies investigating coherent motion perception in ACHM have been carried out, related work has been carried out with amblyopia. Interestingly, an fMRI study demonstrated atypical neural activation when

patients viewed coherent motion through their amblyopic eye compared to controls, an effect which was not seen when patients viewed the stimulus through their non-amblyopic eye

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(Thompson, Villeneuve, Casanova, & Hess, 2012). Amblyopic patients had previously demonstrated normal coherent motion perception on behavioural tasks when tested using their amblyopic eye (Thompson, Aaen-Stockdale, Mansouri, & Hess, 2008). As with our findings, these results suggest that when vision is impaired, there is a change in neural activation which is associated with a relative preservation of coherent motion perception.

The correlational analysis also revealed that form responses remained consistent in

topography across mesopic and scotopic conditions for both groups. Motion results, however did not correlate with each other across mesopic and scotopic conditions in patients or controls. This suggests that the form VEP responses were generated by similar brain

regions in mesopic and scotopic conditions while motion VEP responses were generated by different regions. Patients and controls were consistent in this finding and both therefore appear to be shifting their pattern of activation to motion responses in low light. As with the finding that patients show different motion responses to controls, the shift in motion

topography in low light may be further evidence that different brain regions are activated in response to coherent motion when vision is limited. As with the amblyopic patients described previously (Thompson et al., 2012), low light presents a situation in which visual input is impaired relative to brighter conditions.

The finding that F2 amplitudes were not significantly different between patients and controls suggests that processing of local elements of coherent form and motion stimuli may be similar between the two groups. This is also reflected in the topographic plots which show similar regions and intensities of activation. These results therefore suggest specific changes in global processing (F1) rather than local processing (F2). One reason the F1 amplitudes may have shown differences between patients and controls may lie in the ROIs used. These were selected based on the control group data, however the topographic plots and

correlational analyses suggest that in some cases patient topography differed from controls.

The ROIs may not therefore represent the areas of peak activation in the patients. Given the

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small group size, it was not possible to select a clear peak ROI in the patient group.

However, these results indicate interesting differences between the patients and controls in both form and motion processing.

The brain regions underlying coherent form and motion perception in ACHM patients remains elusive. Further work using imaging techniques with better spatial resolution such as source localisation or fMRI would allow for a greater understanding of how neural activity may differ from normal in ACHM. These results provide important insight into the fact that the neural activation in ACHM differs from controls, especially in the case of coherent motion perception.

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C HAPTER 7. D ISCUSSION