Deficit in P50 sensory gating has repeatedly been shown in schizophrenia. In order to determine the contribution of trait and/or state features to P50 gating deficit in schizophrenia we evaluated the P50 gating in patients with first-episode schizophrenia (FES) at acute and post-acute phases. Subject groups comprised 16 patients with FES and 24 healthy controls. Patients were tested at the acute phase of the illness and retested at the post-acute phase when their positive symptoms improved. During the testing at the acute phase five patients were neuroleptic-naive and the others were taking atypical antipsychotics which were started recently in order to control the acute excitation. Patients were receiving risperidone, olanzapine or quetiapine treatment at the post-acute phase. P50 gating was impaired in patients at the acute phase compared to controls. However, at the post-acute phase P50 gating was increased compared to the acute phase, reaching to the gating values of controls. P50 gating improvement might be emerged from atypical antipsychotic medication, although this can only be definitively determined by randomized studies including different antipsychotics.
"Patterson et al8 concluded that their meta-analysis confirms the existence of event-related potential deficits in schizophrenia, with significance similar to the most robust findings reported in neuroimaging and neuropsychology in schizophrenia. Similar conclusions found also several others meta-analytic or detailed review studies which show sensory gating impairments in early stages of schizophrenia that become more prominent in chronic stages of schizophrenia.8,11,13,15,114 Further meta-analytical data by Chang et al115 confirm that the sensory gating deficit in patients with schizophrenia is well documented; nevertheless, certain findings raise doubts about the validity and utility of the S2/S1 ratio as a measure of sensory gating. "
[Show abstract][Hide abstract] ABSTRACT: Sensory gating disturbances in schizophrenia are often described as an inability to filter redundant sensory stimuli that typically manifest as inability to gate neuronal responses related to the P50 wave, characterizing a decreased ability of the brain to inhibit various responses to insignificant stimuli. It implicates various deficits of perceptual and attentional functions, and this inability to inhibit, or "gate", irrelevant sensory inputs leads to sensory and information overload that also may result in neuronal hyperexcitability related to disturbances of habituation mechanisms. These findings seem to be particularly important in the context of modern electrophysiological and neuroimaging data suggesting that the filtering deficits in schizophrenia are likely related to deficits in the integrity of connections between various brain areas. As a consequence, this brain disintegration produces disconnection of information, disrupted binding, and disintegration of consciousness that in terms of modern neuroscience could connect original Bleuler's concept of "split mind" with research of neural information integration.
[Show abstract][Hide abstract] ABSTRACT: Tinnitus is a frequent disorder and very difficult to treat. Both animal studies and clinical observations suggest that dopaminergic substances might have potential for the treatment of tinnitus. Here, we investigated the dopamine agonist piribedil for the treatment of chronic tinnitus. In all participants, we performed audiometry, electrocochleography (ECoG), and otoacoustic emissions before treatment began.
To assess the efficacy and safety of the dopaminergic drug piribedil for the treatment of tinnitus and to evaluate whether ECoG and acoustic otoemissions might be useful for predicting treatment response.
Prospective randomized double-blind crossover study.
One hundred patients with tinnitus were randomized into a double-blind, placebo-controlled, prospective crossover study. All patients underwent distortion product acoustic otoemissions with and without contralateral suppression and ECoG. Patients received 50 mg piribedil and placebo for 90 days each, separated by a 30-day washout period. Treatment effects were assessed by using the Tinnitus Handicap Inventory and a visual analog scale. Fifty-six patients completed the trial.
There was no significant improvement of Tinnitus Handicap Inventory and visual analog scale score after piribedil treatment as compared with placebo. However, results were characterized by high interindividual variability. Post hoc analysis of piribedil effects revealed that piribedil treatment responders differed from nonresponders by the occurrence of a double peak in the ECoG. In addition, normal distortion product acoustic otoemission suppression patterns indicated better treatment response with piribedil. The incidence of side effects during piribedil treatment was 23.3%, leading to interruption of treatment in all cases.
Piribedil is not superior to placebo in the treatment of tinnitus. Piribedil treatment responders differed from nonresponders by specific findings in the ECoG and in the distortion product acoustic otoacoustic emissions, suggesting a beneficial effect of piribedil in an electrophysiologically characterized tinnitus subgroup.
Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 08/2009; 30(5):676-80. DOI:10.1097/MAO.0b013e3181ab8fd5 · 1.79 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Diminished suppression of the P50 auditory evoked potential is a widely used sensory gating phenotype in the molecular genetic studies of schizophrenia. The aim of this study was to explore the relationship between this phenotype and neuregulin 1-related intracellular signaling processes.
The P50 evoked potential was recorded in 30 first-episode, never-medicated patients with schizophrenia and in 30 healthy comparison volunteers. Neuregulin 1-induced activation of the phosphoinositide 3'-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3beta system was characterized by the measurement of the phosphorylated AKT to total AKT ratio in peripheral B lymphoblasts.
Relative to comparison subjects, patients with first-episode schizophrenia displayed diminished P50 suppression and decreased neuregulin 1-induced AKT phosphorylation. There was a significant relationship between P50 suppression and AKT phosphorylation.
Decreased neuregulin 1-induced activation of the PI3K/AKT system is associated with impaired sensory gating in first-episode schizophrenia.
American Journal of Psychiatry 04/2010; 167(4):444-50. DOI:10.1176/appi.ajp.2009.09050723 · 12.30 Impact Factor
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