A Clinic Study On Sensory Gating P52 In The Bipolar Disorder And Depression

Background and ObjectiveSensory gating (SG) refers to the brain's automatic adjustment on sensoryinformation input moderately, and is one of the characteristics of brainearly-stage information processing. SG P50 suppression deficit was reported inpatients with schizophrenia and their unaffected first-degree relatives. SG P50suppression deficit is considered to be a stable phenotype of schizophrenia. Recentstudies have found that patients with bipolar disorder, especially the stable withpsychotic bipolar patients have SG P50 suppression deficits. Some reports haveproposed SG P50 deficit is a putative endophenotype for psychotic bipolar disorderand thus might reflect the impact of susceptibility genes across psychosis.In this study, patients with bipolar disorder and depression were taken as subjects.SG P50 was used to quantify the sensory gating of bipolar disorder, depression,schizophrenia patients and normal control subjects. Analysis the impact ofdifferent disease states, longitudinal history of psychosis, emotional states,drugs, smoking and other factors on SG P50 in bipolar disorder and depressionpatients, substantiating the correlation among bipolar disorder, depression andschizophrenia; and verifying whether SG P50 suppression deficit represents acandidate endophenotype associated with psychotic bipolar disorder and depressiondisorder.MethodsSubjects: The study recruited 102 patients with bipolar disorder and depression.All objects met the diagnostic criterion and the exclusion criteria of mooddisorders in CCMD-Ⅲ. 42 first-episode schizophrenia patients (Sch group) and 29normal controls (NC group) were collecting from previous studies of Changqing Wang.Organic disease of brain and mental disorders associated with physical diseases and psychoactive substances have been excluded. All had normal hearing and signedthe informed consent.Stepsteps: To met the needs of this study, we re-assessed the criterion of bipolardisorder and depression in DSM-Ⅳ. The mania only one manic episode and recurrentmania were combined into bipolar disorder group (bipolarⅠ, BP group, 55),first-episode depression and recurrent depression constituted depression group(D group, 47). Auditory evoked potential P50 of objects were recorded using theconditioning/testing paradigm presented with auditory double clicks stimuli, andPANSS, BRMS/HAMD variables were measured on the day of testing.Groups: According to the current symptoms of patients and the rating scale results(BRMS, HAMD), BP group and D group were divided into acute stage bipolar disordergroup (A-BP), remission stage bipolar disorder group (C-BP), acute stagedepression group (A-D), remission stage depression group (C-D). According to thepsychotic history and the results of PANSS rating scale, BP group and D group weredivided into psychotic bipolar disorder group (S-BP), Non- psychotic bipolardisorder group (N-BP), psychotic depression group (S-D),Non-psychotic depressiongroup (N-D).Tools: The machine for testing brain evoked potential using to record SG P50 isfully functional, digital, 40 leads, EB Neuro Sirius BB BE and made in Italy. PANSS,BRMS, HAMD of Chinese version is used to assess the clinical symptoms of patients.Statistical Methods: The SPSS 13.0 statistical package and Excel 2003 wereadopted to process the data, included the chi-square test, multiple linearregression, single factor analysis of variance (ANOVA), Kruskal-Wallis Hnon-parametric test (H test), Pearson or Spearman rank correlation analysis. P<0.05 was considered statistically significant.Results1 Comparison of SG P50 variations among different mental disorders1.1 Comparison of SG P50 variations among BP, D, Sch and NC groupsThe S2 of BP group, D group were significantly higher than NC group, S2/S1 were between NC group and Sch group, with significant difference of NC group (P<0.05),but no significant difference of Sch group (P> 0.05).1.2 Comparison of SG P50 variations among BP and D in acute or remission stage,Sch and NC groupsIn acute stage, the S2, S2/S1 of BP group, D group and Sch group were significantlyhigher than NC group (P <0.05); In remission stage, the S2 of BP group, D groupwere between NC group and Sch group, BP group was different from NC groupsignificantly (P <0.05), there were no significant differences among D group, NCgroup and Sch group (P> 0.05).1.3 Comparison of SG P50 variations among psychotic/non-psychotic BP and D, Schand NC groupsS1: N-D group was higher than NC group, Sch group, S-D group; N-BP group was higherthan Sch group, the differences were statistically significant (P <0.05).S2: S-BP group, S-D group were significantly higher than NC group (P <0.05), butnot significantly differed from Sch group (P> 0.05); N-BP group and N-D group werebetween NC group and Sch group, only BP group significantly differed from NC group(P <0.05).S2/S1: S-BP group, SD group were significantly higher than NC group (P <0.05);N-BP group and N-D group were between NC group and Sch group, only N-D groupsignificantly differed from Sch group (P <0.05); SD group was significantly higherthan ND group and N-BP group (P <0.05).1.4 Comparison of SG P50 variations in acute / remission stage among psychoticBP and D, Sch and NC groupThe S2, S2/S1 of S-BP group, S-D group were significantly higher than NC groupin acute / remission stage (P <0.05), but there was no significant differencebetween acute / remission stage (P> 0.05).2 Correlations between SG P50 clinical and rating scales2.1 Correlations between SG P50 and clinical rating scores in psychotic /non-psychotic BP patientsThere was no correlation between SG P50 and BRMS con-scores in S-BP group (P>0.05). The S2/S1 of N-BP group was positively correlated with BRMS con-scores (P<0.05).2.2 Correlation between SG P50 and clinical rating scores in psychotic /non-psychotic depression patientsThere were no correlation between SG P50 and HAMD con-scores,factor scores inSD group (P>0.05). The S2 and S2/S1 of SD group was positively correlated withHAMD con-scores (P<0.05), especially with the factor scores of weight change points,awareness barriers points, retardation points, sleep disturbance points andhopelessness points (P>0.05).3 The effect of drugs on SG P503.1 The effect of mood stabilizers on SG P50 of bipolar disorder patientsThe S2, S2/S1 of Lithium carbonate treatment group, valproate treatment group andthe S2 of not treated with mood stabilizers were significantly higher than NC group(P <0.05); there were no significant difference on SG P50 among the lithiumtreatment group, Valproate treatment group and not treated with mood stabilizersgroup (P> 0.05).3.2 The effect of lithium carbonate on SG P50 of bipolar disorder patientsIn acute stage, the S2 of no lithium carbonate treatment group, the S2/S1 of treatwith / without lithium carbonate group were significantly higher than NC group(P <0.05); in remission stage, the S2 of lithium carbonate treatment group wassignificantly higher compared with NC group (P <0.05); both in acute stage andremission stage, no significant difference was found on SG P50 treat with / withoutlithium carbonate (P> 0.05).3.3 The effect of valproate on SG P50 of bipolar disorder patientsIn the acute phase, the S2, S2/S1 of treat with / without valproate group weresignificantly higher than NC group (P <0.05); in remission stage, the S2 of nottreat with valproate group was significantly higher compared with NC group (P<0.05); both in acute stage and remission stage, no significant difference wasfound on SG P50 treat with / without valproate (P> 0.05).3.4 The effect of clozapine on SG P50 of bipolar disorder patientsThe S2, S2/S1 of bipolar patients treated combine with / without colzapine were significantly higher than NC group (P <0.05); in the acute stage, the S2, S2/S1of treated combine with / without colzapine group were significantly higher thanNC group (P <0.05); in remission stage, the S2, S2/S1 of treated combine with /without colzapine group were not differed from NC group (P> 0.05); the S2/S1 oftreated combine with clozapine in the acute stage was significantly higher thanin remission stage (P <0.05); both in the acute and remission stage the SG P50of treated combine with / without colzapine group showed no significant difference(P> 0.05).3.5 The effect of SSRIs and benzodiazepine on SG P50 of bipolar disorder patientsThe SG P50 in remission stage of depression patients treated with SSRIs or non-SSRIswas no significant difference(P> 0.05); there was no significant difference ofthe SG P50 between combined benzodiazepine treatment group and no benzodiazepinetreatment group (P> 0.05).4 The effect of smoking on SG P50The S2, S2/S1 of mood disorders smoked daily group (mean 20 cigarettes per day)and never smoking or had smoked group were significantly higher than NC group (P<0.05),There was no significant difference of SG P50 between two groups (P> 0.05).Conclusion1 Bipolar disorder and depression patients had SG P50 suppression deficit, mainlyfor the S2 amplitude increased, suggesting that the capacity of the brain filteringof irrelevant sensory information reduced.2 SG P50 suppression deficits in bipolar disorder and depression patients wereaffected by the disease state and psychotic symptom, since it had both trait- andstate-like components; the SG P50 was suggested to be a mediating vulnerabilityindicator.3 SG P50 suppression deficits in psychotic bipolar disorder and psychoticdepression patients were persistent, and is immune to emotional status, smoking,drug treatment and other factors, indicated that impaired P50 suppression could be an endophenotypic neurobiological marker for psychotic bipolar disorder anddepression.4 There were SG P50 deficits in psychotic bipolar disorder, psychotic depression,and schizophrenia; the non-specificity of SG P50 suppression deficit might reflectthey shared psychosis susceptibility genes.