MH/DF PROMEDIO ANUAL
1.5. OTRAS DISPOSICIONES QUE INCIDEN EN LA DELEGACIÓN
The study also found that in both groups P1 amplitude increased with WM load during encoding, but not retrieval. This finding replicates the pattern observed in controls from the previously reported study using the same paradigm (Haenschel et al. 2007). In the original study however, this relationship was not true for the
schizophrenia sample, as the encoding P1 amplitude did not increase with demand. The fact that the normal pattern of activation is sustained in high schizotypes could be interpreted in the following way: reduced P1 amplitude is an index of vulnerability to schizophrenia, but in non-clinical cases the visual cortex is more efficiently regulated by higher-order brain areas, resulting in activation with increased demand. In the developed condition this relationship decompensates and the top-down projections cannot modulate as effectively the primary sensory areas.
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6.4.5. Limitations
Several important limitations in regards to the currently reported finding of early visual deficits in schizotypy need to be addressed. Firstly, based on findings that P1 amplitude is dependent on spatial attention (Mangun et al. 1998), it is often argued that the observed P1 reduction could be due to differences in the level of arousal or engagement with the task. Our data argue against such criticism. Firstly, it is now well established that both P1 and N1 amplitudes are modulated by attention (Mangun et al. 1991; Luck et al. 1993; Eimer et al. 1998; Mangun et al. 1998) and in our study there was an effect of group only on the P1 but not N1. Secondly, we only analyzed the amplitude to images from successful trials. This ensured that the reported results were only from instances when the participants were actively engaged with the task.
Thirdly, the two groups did not differ in their reaction times to the task where the deficit was observed. Lastly, the two groups did not differ in their performance on the two CANTAB tasks, which both require considerable and sustained attention. Given these arguments, we believe that the effects cannot be attributed solely to difference in engagement and attention. Recent data from schizophrenia patients also argues
against an effect of attention or arousal in the P1 deficit. A study using a technique that allows the selective activation of the parvocellular pathway discovered normal P1 amplitude in patients but reduced P1 component in standard visual evoked potential technique (Lalor et al. 2008). The authors argued that it would be very unlikely that an arousal mechanism should affect only one of the two visual pathways.
A second limitation is that a recently published study did not find significant
difference between controls and patients with schizotypal personality disorder (SPD) in terms of P1 amplitude (Vohs et al. 2008). The P1 amplitude in the SPD group was lower in comparison with the controls and higher than the one in a sample of
schizophrenia patients. This pattern coincides with the results emerging from our data but the effect was not found to be significant. One possible explanation of this
discrepancy is that the SPD sample recruited for the Vohs et al. study had lower overall SPQ score compared to our sample (42.6 ± 6 vs. 49.4 ± 5) (Vohs et al. 2008). Also, the SPQ score in the Vohs et al. study was elevated mainly due to the cognitive- perceptual score (20.9±7 cognitive-perceptual; 13.0 ±7 interpersonal and 8.7 ± 5
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interpersonal and disorganized traits (19.5 ± 5 cognitive-perceptual; 19.5 ±5
interpersonal and 13.1 ± 2.6 disorganized). Previous studies have shown that negative and disorganized schizotypy tends to have greater cognitive similarities with
schizophrenia (Kendler et al. 1991). In schizophrenia itself, negative and disorganized symptoms correlate stronger with cognitive impairment than positive symptoms (O'Leary et al. 2000; Rocca et al. 2005). Also, negative schizotypy is higher among relatives of schizophrenia patients (Tsuang et al. 2002). This has led some authors to hypothesize that negative schizotypy is the one that is more closely linked to
schizophrenia (Tsuang et al. 2002). As a result the observed difference between the two studies could be regarded as further evidence for the claim that the P1 amplitude is a biomarker that reflects the level and type of psychopathology and is demonstrable in subjects with higher symptom severity.
Thirdly, it should be noted that we did not correct our results for multiple
comparisons. Therefore our results regarding P1 in schizotypy should be treated with caution and may necessitate further studies to replicate the findings. Also, the study has limited power to exclude abnormalities in the N1 and P2 components despite the confidence intervals supporting the conclusions drawn on the basis of the significance values (Tables 6.2 and 6.3).
Finally, although we have used a standard approach to ERP identification, it is nonetheless possible that slow drifts or low frequency oscillations components might have been mistaken for the peaks of interest. However, given the short duration of the peaks of interest (20 and 30 ms for P1 and N1 respectively), their well-defined
characteristics and the application of 0.3 Hz high-pass and 30 Hz low-pass filters, it is very unlikely that signal drifts or noise would have systematically obscured the ERPs of interest.
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6.4.6. Conclusion
The findings of a significantly reduced P1 amplitude in this group of healthy volunteers with elevated schizotypal traits support claims that the schizophrenia spectrum is characterized by an early sensory deficit. The abnormality also appears to contribute to higher order cognitive deficits, particularly in cases when only short stimulus encoding is possible. This provides evidence that the P1 deficit is a trait marker for the disease that could partly underlie the cognitive impairment in schizophrenia.
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