Year : 2011 | Volume : 6 | Issue : 26 | Page : 2037-2041
Ling Ge1, Xiuchun Ge2, Yong Xu3, Kerang Zhang3, Jing Zhao4, Xin Kong4 1 Department of Medical Psychology, Shanxi Medical College for Continuing Education, Taiyuan 030012, Shanxi Province, China
2 Shanxi Cardiovascular Hospital, Taiyuan 030024, Shanxi Province, China
3 Department of Psychiatry, First Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
4 College of Humanities and Social Science, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
LINK TO ABSTACT
The results of the current investigation of ERPs in individuals suffering from IAD were in accordance with the findings of previous studies of other addictions[17-20]. Specifically, we found reduced P300 amplitude and longer P300 latency in individuals exhibiting addictive behaviors compared with healthy controls. These results support the hypothesis that similar pathological mechanisms are involved in different addiction behaviors.
FROM THE CONCLUSION
The results of the current investigation of ERPs in individuals suffering from IAD were in accordance with the findings of previous studies of other addictions[17-20]. Specifically, we found reduced P300 amplitude and longer P300 latency in individuals exhibiting addictive behaviors compared with healthy controls. These results support the hypothesis that similar pathological mechanisms are involved in different addiction behaviors.
Several previous studies have focused on the association between IAD and the P300, reporting reduced P300 amplitudes[11, 20]. In contrast, we did not observe a significant P300 amplitude reduction in the present study. However, we found that prolonged P300 latency was associated with IAD, consistent with one previous study[20]. Although clear conclusions cannot be drawn regarding the P300 amplitude discrepancy, sample size and statistical power may have played a major role. The current study examined a relatively large sample size (n = 38), systematic recruitment and strict exclusion criteria for diagnosing IAD. The present findings may thus be more statistically reliable than those of previous studies, but should still be interpreted with caution. On the other hand, the age of participants may have also affected the results. All of the individuals in our sample were middle-aged men (mean age of IAD participants: 32.5 ± 3.2 years; mean age of controls: 31.3 ± 10.5 years), whereas a younger sample population was examined in the previous study by Yu et al [11] (mean age of IAD subjects: 22.0 ± 0.9 years; mean age of controls: 22.0 ± 0.7 years). It is possible that attentional resource allocation of cognitive processing is of greater importance in the development of IAD in older people compared with younger people.
Another major finding of the present study was that the initially prolonged P300 latency in people with IAD decreased significantly after CBT. Considering the scarcity of studies on IAD including treatment and follow-up measures, the association between P300 latency and IAD treatment in our sample should be interpreted with caution. Further research should be conducted to replicate this finding, using larger sample sizes and other treatment types. P300 latency is considered to provide a measure of attentional resource allocation[21], and prolongation of this ERP component has been discussed as an index of neurodegenerative processes affecting callosal size and the efficiency of interhemispheric transmission[22-23]. The present findings suggest that people with IAD may have problems with the speed of perception and cognitive processing of auditory stimuli. Because of the limited knowledge about cognitive function in IAD, it is currently difficult to identify the potential mechanisms underlying the effect of P300 latency.
Previous studies have reported that the P3 represents a family of related but dissociable components including the “Novelty” P3a and the “Target” P3b [24-25]. The P3a represents an automatic orienting response to novel or otherwise salient stimuli [24, 26]. The P3b is commonly associated with voluntary attention and the updating of working memory[27]. In the present study, correlations were found not only between the P3a and P3b latency and IAD, but also with the effect of CBT. In contrast, no associations were found with the N1 and P2 components. While the N2 component was not correlated with the effects of CBT, it was associated with IAD. Taken together, these findings indicated that deficits in cognitive function associated with IAD are not related to selection and attention to novel stimuli (N1 and P2). Rather, IAD appears to involve responses to novel stimuli (P3a), working memory (P3b) and conscious recognition (N2). Moreover, part of the cognitive function could improve through short-term psychological intervention. These preliminary findings are clearly speculative at present and require further confirmation in future studies.
In summary, a prolonged P300 latency was found to be associated with IAD. This prolonged P300 latency decreased to normal levels after a three-month CBT program. These findings indicate that deficits in cognitive function may be involved in IAD, and that these can be improved by clinical psychological treatment. Further studies examining this association are needed to replicate this finding in different age samples, and with a larger sample size.
;