SUBSTANCE USE DISORDER EXACERBATES BRAIN ELECTROPHYSIOLOGICAL ABNORMALITIES IN A PSYCHIATRICALLY-ILL POPULATION

Objective: To assess by brain electrical activity mapping whether coca ine and alcohol abuse and dependence would exacerbate electrophysiolog ical abnormalities in a psychiatrically-ill population. Design, Settin g, and Participants: Utilizing a brain mapping system, we assessed EEG , Spectral Analysis (Quantitative EEG[QEEG]), Evoked Potentials (Audit ory and Visual), and P300 (cognitive evoked potential), in a total of 111 probands divided into three groups: controls (N = 16), psychiatric ally-ill without comorbid substance use disorder (N = 34), and psychia trically-ill with comorbid substance use disorder (cocaine and alcohol abuse and dependence) (N = 61), at an outpatient neuropsychiatric cli nic, With regard to demographic data, the group participating in this study did not differ significantly A comparison was made among the gro ups to assist in differentiating the effects of substance use disorder compared to psychiatric disease on brain electrical activity. Main Ou tcome Measures: An assessment of electrophysiological abnormalities an d their brain location in psychiatric and substance use disorder patie nts was done with a brain electrical activity mapping test. Main Resul ts: Among the non-substance use disorder, psychiatrically-iii (PI) and substance use disorder, psychiatrically-iii (PI/SD) groups, significa ntly different brain map abnormalities were observed relative to an as sessed normal population MANOVA (P = .017), Moreover, with regard to S pectral Analysis, ANOVA was significant at a P = .038, and we found a weighted linear trend of increased abnormal total spectral analysis (P = .0113), whereby substance use was significantly worse than controls , Moreover among the PI and PI/SD groups, significantly greater total evoked potential (EP) brain map abnormalities were observed when compa red with a characterized normal population (P = .0023) with increasing abnormalities as a function of substance use disorder as measured by a weighted linear trend (P = .0022). In order to determine the site of the EPS abnormalities, we evaluated these abnormalities by location, In this regard, we found all temporal abnormalities (AVBITA, see Table 2) among the PI and PI/SD groups to be significantly greater relative to an assessed normal population (P = .0026). Furthermore, we observe d a linear trend of increased temporal abnormalities with increasing s ubstance use disorder (P < .0008). in terms of bitemporal abnormalitie s (AVBIT) among the PI and PI/SD groups, we also found significantly m ore bitemporal lobe abnormalities in the PI/SD group compared to our c ontrol population (P = .009). Additionally, a weighted linear trend of increased abnormal bitemporal lobe abnormalities was observed with in creasing substance use disorder (P = .0022), In the frontal robe simil ar findings were observed, With AVBIFA the ANOVA was P < .011, with a weighted linear trend of P < .005 and the PI/SD group were significant ly more abnormal than PI or CS on a Duncan Range test. It is noteworth y that in a selected group of depressed (Major Depressive Disorder Rec urrent, 296.3) patients, we found profound abnormalities in the variou s brain map parameters tested. MANOVA and Univariate ANOVA's revealed significantly greater abnormalities in the PI and PI/SD groups compare d to assessed controls. A MANOVA for total brain abnormalities was sig nificant at P = .043 and univariate ANOVA's for composite measurements of TSA (P = .017), EPS (P = .0002), AVBITA (P = .000015), and AVBIT ( P < .00002) are also significant. With regard to EPS and AVBITA a weig hted linear trend was observed where there were increasing abnormaliti es with increasing substance use disorder, P=.0001 and P=.000003, resp ectively. Most importantly we found that in addition to increased abno rmalities with increasing substance use disorder the PI/SD group had s ignificantly more abnormalities compared to the PI group with regard t o both the TSA (P<.05) and AVBIT (P<.05) composite parameters as measu red by a Duncan Range lest. Additionally, we found increased abnormali ties in EPS in the frontal (but not occipital and parietal) lobes, AVB IF (P=.0116) and AVBIFA(P=.0116), of both the PI and PI/SD groups, whe re PI/SD groups had more abnormalities relative to PI and CS in our to tal population as well as the select depressed group, with a weighted linear trend of P=.0054 and P=.0065 respectively. Conclusion: Comorbid substance use disorder in psychiatric probands (especially in depress ed patients) significantly exacerbates a potential premorbid vulnerabi lity, and suggests a gene-environment interaction which leads psychiat rically-disturbed individuals with substance use disorder to worsen th eir brain dysfunction, particularly in the bitemporal regions of the b rain.