Journal of neurotherapy最新文献

INTRODUCTION: It has been reported that individuals with Autism Spectrum Disorder (ASD) have abnormal reactions to the sensory environment and visuo-perceptual abnormalities. Electrophysiological research has provided evidence that gamma band activity (30-80 Hz) is a physiological indicator of the co-activation of cortical cells engaged in processing visual stimuli and integrating different features of a stimulus. A number of studies have found augmented and indiscriminative gamma band power at early stages of visual processing in ASD; this may be related to decreased inhibitory processing and an increase in the ratio of cortical excitation to inhibition. Low frequency or 'slow' (≤1HZ) repetitive transcranial magnetic stimulation (rTMS) has been shown to increase inhibition of stimulated cortex by the activation of inhibitory circuits. METHODS: We wanted to test the hypothesis of gamma band abnormalities at early stages of visual processing in ASD by investigating relative evoked (i.e. ~ 100 ms) gamma power in 25 subjects with ASD and 20 age-matched controls using Kanizsa illusory figures. Additionally, we wanted to assess the effects of 12 sessions of bilateral 'slow' rTMS to the dorsolateral prefrontal cortex (DLPFC) on evoked gamma activity using a randomized controlled design. RESULTS: In individuals with ASD evoked gamma activity was not discriminative of stimulus type, whereas in controls early gamma power differences between target and non-target stimuli were highly significant. Following rTMS individuals with ASD showed significant improvement in discriminatory gamma activity between relevant and irrelevant visual stimuli. We also found significant improvement in the responses on behavioral questionnaires (i.e., irritability, repetitive behavior) as a result of rTMS. CONCLUSION: We proposed that 'slow' rTMS may have increased cortical inhibitory tone which improved discriminatory gamma activity at early stages of visual processing. rTMS has the potential to become an important therapeutic tool in ASD treatment and has shown significant benefits in treating core symptoms of ASD with few, if any side effects.

INTRODUCTION: Preoccupation with drug and drug-related items is a typical characteristic of cocaine addicted individuals. It has been shown in multiple accounts that prolonged drug use has a profound effect on the EEG recordings of drug addicts when compared to controls during cue reactivity tests. Cue reactivity refers to a phenomenon in which individuals with a history of drug abuse exhibit excessive psychophysiological responses to cues associated with their drug of choice. One of the aims of this pilot study was to determine the presence of an attentional bias to preferentially process drug-related cues using evoked and induced gamma reactivity measures in cocaine addicts before and after biobehavioral treatment based on neurofeedback. Another aim was to show that central SMR amplitude increase and frontal theta control is possible in an experimental outpatient drug users group over 12 neurofeedback sessions. METHOD: Ten current cocaine abusers participated in this pilot research study using neurofeedback combined with Motivational Interviewing sessions. Eight of them completed all planned pre- and post -neurofeedback cue reactivity tests with event-related EEG recording and clinical evaluations. Cue reactivity test represented a visual oddball task with images from the International Affective Picture System and drug-related pictures. Evoked and induced gamma responses to target and non-target drug cues were analyzed using wavelet analysis. RESULTS: Outpatient subjects with cocaine addiction completed the biobehavioral intervention and successfully increased SMR while keeping theta practically unchanged in 12 sessions of neurofeedback training. The addition of Motivational Interviewing helped retain patients in the study. Clinical evaluations immediately after completion of the treatment showed decreased self-reports on depression and stress scores, and urine tests collaborated reports of decreased use of cocaine and marijuana. Effects of neurofeedback resulted in a lower EEG gamma reactivity to drug-related images in a post-neurofeedback cue reactivity test. In particular, evoked gamma showed decreases in power to non-target and to a lesser extent target drug-related cues at all topographies (left, right, frontal, parietal, medial, inferior); while induced gamma power decreased globally to both target and non-target drug cues. Our findings supported our hypothesis that gamma band cue reactivity measures are sufficiently sensitive functional outcomes of neurofeedback treatment. Both evoked and induced gamma measures were found capable to detect changes in responsiveness to both target and non-target drug cues. CONCLUSION: Our study emphasizes the utility of cognitive neuroscience methods based on EEG gamma band measures for the assessment of the functional outcomes of neurofeedback-based biobehavioral interventions for cocaine use disorders. This approach may have significant potential for identifying both physiological and clinical

INTRODUCTION: Error monitoring and correction is one of the executive functions and is important for effective goal directed behavior. Deficient executive functioning, including reduced error monitoring ability, is one of the typical features of such neurodevelopmental disorders as autism, probably related to perseverative responding, stereotyped repetitive behaviors, and an inability to accurately monitor ongoing behavior. Our prior studies of behavioral and event-related potential (ERP) measures during performance on visual oddball tasks in high-functioning autistic (HFA) children showed that despite only minor differences in reaction times HFA children committed significantly more errors. METHODS: This study investigated error monitoring in children with autism spectrum disorder (ASD) with response-locked event-related potentials - the Error-related Negativity (ERN) and Error-related Positivity (Pe) recorded at fronto-central sites. The ERN reflects early error detection processes, while the Pe has been associated with later conscious error evaluation and attention re-allocation. Reaction times (RT) in correct trials and post-error slowing in reaction times were measured. In this study fourteen subjects with ASD and 14 age- and IQ- matched controls received a three-category visual oddball task with novel distracters. RESULTS: ERN had a lower amplitude and longer latency in the ASD group but was localized in the caudal part of anterior cingulate cortex (ACC) in both groups. The Pe component was significantly prolonged in the ASD group but did not reach significance in amplitude differences compared to controls. We found significant post-error slowing in RTs in controls, and post-error acceleration in RTs in the ASD group. CONCLUSIONS: The reduced ERN and altered Pe along with a lack of post-error RT slowing in autism might be interpreted as insensitivity in the detection and monitoring of response errors and a reduced ability of execute corrective actions. This might result in reduced error awareness and failure in adjustment when dealing with situations where erroneous responses may occur. This deficit might be manifested in the perseverative behaviors often seen in individuals with ASD. The results are discussed in terms of a general impairment in self-monitoring and other executive functions underlying behavioral and social disturbances in ASD.