Study of P50 sensory gating deficit in schizophrenic patients with violent and aggressive behaviors / 四川精神卫生

ObjectiveTo assess the specificity of P50 auditory-evoked potential in schizophrenic patients with violent and aggressive behaviors， so as to provide objective biological markers for predicting violent behaviors of schizophrenic patients. MethodsA total of135 schizophrenic patients who met the diagnostic criteria of the International Classification of Diseases， tenth edition （ICD-10） were divided into aggressive group （n=70） and non-aggressive group （n=65） according to the assessment results of the Modified Overt Aggression Scale （MOAS）， meantime， another 60 healthy individuals matched for age and gender were set as healthy group. Then the P50 auditory-evoked potentials of all selected individuals were measured using EP/EMG system （MEB-9200， Nihon Kohden， Japan）. ResultsAmp S2 of the aggressive group was significantly higher than those of the non-aggressive group and healthy control group， with statistical differences ［（9.86±6.04）μV vs. （7.06±3.88）μV， P=0.004； （9.86±6.04）μV vs. （7.82±3.87）μV， P=0.031］. The proportion of S2/S1 ratio ≥0.5 was 72.88%， 43.86% and 30.00% in aggressive group， non-aggressive group and healthy group， which was the highest in aggressive group， with statistical differences （P<0.01）. The amplitude difference of P50 （S1-S2） of the aggressive group was lower than those of the non-aggressive group and the healthy control group， the differences were of statistical significance ［（4.35±9.39）μV vs.（9.89±8.48）μV， P=0.001； （4.35±9.39）μV vs.（13.42±9.81）μV， P<0.01］. ConclusionThe violent and aggressive behaviors in schizophrenic patients may be related to the sensory gating deficit.

Striatal and Thalamic Auditory Response During Deep Brain Stimulation for Essential Tremor: Implications for Psychosis.

INTRODUCTION: The P50, a positive auditory-evoked potential occurring 50 msec after an auditory click, has been characterized extensively with electroencephalography (EEG) to detect aberrant auditory electrophysiology in disorders like schizophrenia (SZ) where 61-74% have an auditory gating deficit. The P50 response occurs in primary auditory cortex and several thalamocortical regions. In rodents, the gated P50 response has been identified in the reticular thalamic nucleus (RT)-a deep brain structure traversed during deep brain stimulation (DBS) targeting of the ventral intermediate nucleus (VIM) of the thalamus to treat essential tremor (ET) allowing for interspecies comparison. The goal was to utilize the unique opportunity provided by DBS surgery for ET to map the P50 response in multiple deep brain structures in order to determine the utility of intraoperative P50 detection for facilitating DBS targeting of auditory responsive subterritories. MATERIALS AND METHODS: We developed a method to assess P50 response intraoperatively with local field potentials (LFP) using microelectrode recording during routine clinical electrophysiologic mapping for awake DBS surgery in seven ET patients. Recording sites were mapped into a common stereotactic space. RESULTS: Forty significant P50 responses of 155 recordings mapped to the ventral thalamus, RT and CN head/body interface at similar rates of 22.7-26.7%. P50 response exhibited anatomic specificity based on distinct positions of centroids of positive and negative responses within brain regions and the fact that P50 response was not identified in the recordings from either the internal capsule or the dorsal thalamus. CONCLUSIONS: Detection of P50 response intraoperatively may guide DBS targeting RT and subterritories within CN head/body interface-DBS targets with the potential to treat psychosis and shown to modulate schizophrenia-like aberrancies in mouse models.

Does COMT val158met polymorphism influence P50 sensory gating, eye tracking or saccadic inhibition dysfunctions in schizophrenia?

Three electrophysiological endophenotypes are routinely studied in schizophrenia (SCZ): smooth pursuit eye movement (SPEM) dysfunction, deficits in P50 auditory-evoked potential inhibition, and saccadic inhibition deficits. The current study aimed to investigate the relationship between the COMT val158met polymorphism and these three endophenotypes. One hundred four SCZ patients (DSM-IV-R criteria) and 89 healthy controls were included in this study. P50 auditory-evoked potential inhibition, antisaccade paradigm and SPEM were analyzed. All individuals were genotyped for the COMT val158met. SCZ patients showed a higher rate of deficits measured by the SPEM, antisaccade and P50 inhibition paradigms without association with COMT val158met. However, in our control group, we have found an association between the Val polymorphism and the smoking status. More importantly, we have found a higher accuracy of saccades during the predictive pursuit task associated to the Met polymorphism in controls but not in SCZ patients who were receiving antidopaminergic medications. This result is in line with the hypothesis of the relationship between the Met polymorphism of the COMT gene, a higher level of dopamine in the prefrontal cortex and the role of the fronto-cerebellar loop in smooth predictive pursuit.

Pattern of P50 suppression deficit in patients with epilepsy and individuals with schizophrenia / Padrão do déficit de supressão do P50 em pacientes com epilepsia e em indivíduos com esquizofrenia

OBJECTIVE: To identify P50 suppression in patients with epilepsy, to investigate the effect of seizure control on P50 suppression, and to compare epilepsy patients with individuals with schizophrenia and healthy volunteers. METHOD: P50 evoked potential parameters and P50 suppression were studied crossectionally in patients with uncontrolled or controlled epilepsy, in individuals with schizophrenia and in healthy volunteers. RESULTS: Individuals with schizophrenia had significantly smaller conditioning stimulus (S1) amplitude, and patients with epilepsy had larger test stimulus (S2) amplitude. Mean S2/S1 ratio was 0.71±0.33 for patients with uncontrolled epilepsy; 0.68±0.36 for patients with controlled epilepsy; 0.96±0.47 for individuals with schizophrenia, and 0.42±0.24 for healthy volunteers. CONCLUSION: The sensory filter of patients with epilepsy is altered, and this alteration is not associated with seizure control. Also, it works differently from the sensory filter of individuals with schizophrenia.

OBJETIVO: Identificar se existe déficit de supressão do P50 em pacientes com epilepsia, verificar a influência do controle das crises nesse déficit, comparando com pacientes com esquizofrenia e com voluntários saudáveis. MÉTODO: Os parâmetros do potencial evocado P50 e sua supressão foram estudados, com um corte transversal, em pacientes com epilepsia controlada ou não, esquizofrenia e em voluntários saudáveis. RESULTADOS: Indivíduos com esquizofrenia apresentam uma amplitude de S1 significativamente menor que os demais, sendo que os pacientes com epilepsia apresentavam uma resposta S2 de maior amplitude. A média da razão S2/S1 foi de 0,71±0,33 nos pacientes com epilepsia não controlada; 0,68±0,36 naqueles com epilepsia controlada; 0,96±0,47 nos com esquizofrenia e 0,42±0,24 nos controles normais. CONCLUSÃO: O filtro sensitivo de pacientes com epilepsia é alterado, e essa alteração não está associada com o controle das crises. Além disso, ele funciona de forma diferente do filtro sensitivo dos indivíduos com esquizofrenia.

Study on the P50 Auditory Evoked Potential in Mood Disorder Subjects / 신경정신의학

OBJECTIVES: Diminished suppression of the P50 response, a consistent finding in schizophrenia, has also been reported in patients with bipolar disorder. It is a promising endophenotype for schizophrenia, but its relationship to genetic liability in mood disorder is controversial. The present study investigated event-related brain potential (ERP) indices of auditory processing and sensory gating in mood disorder and subgroups of patients with bipolar disorder with or without a history of psychosis using the P50 dual-click procedure. METHODS: The P50 auditory evoked potential response to paired stimuli was measured in 77 subjects with mood disorder (58 with bipolar disorder and 19 with major depressive disorder) and 28 healthy controls. P50 parameters were compared between groups. RESULTS: P50 suppression in patients with mood disorder did not differ from that in the healthy subjects. Except for S1 latency, there were no significant differences in P50 parameters between the diagnosis groups. In patients with bipolar disorder, a history of psychosis made no difference to P50 parameters. CONCLUSION: P50 was not significantly impaired in patients with mood disorder. There has been much debate on the meaning of P50, and more studies including longitudinal within-subjects studies are warranted to clarify the meaning and mechanisms of P50.