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BACKGROUND AND AIM: Identifying EEG brain markers might yield better mechanistic insights into how chronic pain develops and could be treated. An existing longitudinal EEG study gave us the opportunity to determine whether the development of pain is accompanied by less alpha power-ie, a "relaxed" brain state-and vice versa. METHODS: Five-minute resting EEG with the eyes open was measured 2 times in 95 subjects at T0 (baseline) and T1 (6 months later). Based on the Short-Form Health Survey and Brief Pain Inventory questionnaire, subjects were divided into 4 groups: staying pain-free (n = 44), developing chronic pain (n = 8), becoming pain-free (n = 15), and ongoing chronic pain (n = 28). The EEG data of 14 electrodes were analyzed by multilevel regression. RESULTS: The group that developed chronic pain demonstrated less power in the lower-frequency bands over time during the resting state EEG, whereas the transition to a pain-free state had the opposite pattern. Thus, the a priori hypothesis was confirmed. CONCLUSIONS: Transitions in pain states are linked to a change in baseline EEG activity. Future research is needed to replicate these results in a larger study sample and in targeted clinical populations. Furthermore, these results might be beneficial in optimizing neurofeedback algorithms for the treatment of chronic pain.
Assuntos
Dor Crônica , Neurorretroalimentação , Humanos , Dor Crônica/terapia , Eletroencefalografia/métodos , Estudos Longitudinais , Neurorretroalimentação/métodos , EncéfaloRESUMO
BACKGROUND: Exposure is the gold standard treatment for phobic anxiety and is thought to represent the clinical application of extinction learning. Reward sensitivity might however also represent a predictive factor for exposure therapy outcome, as this therapy promotes positive experiences and involves positive comments by the therapist. We hypothesized that high reward sensitivity, as expressed by elevated reward expectancy and reward value, can be associated with better outcome to exposure therapy specifically. METHODS: Forty-four participants with a specific phobia for spiders were included in the current study. Participants were randomly assigned to exposure therapy (nâ¯=â¯25) or progressive muscle relaxation (PMR) (nâ¯=â¯19). Treatment outcome was defined as pre- versus post-therapy phobia symptoms. Before treatment, functional brain responses and behavioral responses (i.e. reaction time and accuracy) during reward anticipation and consumption were assessed with the Monetary Incentive Delay task (MID). Behavioral and neural responses in regions of interest (i.e. nucleus accumbens, ventromedial prefrontal cortex and the ventral tegmental area) as well as across the whole-brain were subsequently regressed on treatment outcomes. RESULTS: Exposure therapy was more effective in reducing phobia symptoms than PMR. Longer reaction times to reward cues and lower activation in the left posterior cingulate cortex during reward consumption were selectively associated with symptoms reductions following exposure therapy but not following PMR. Only within the exposure therapy group, greater symptom reduction was related to increased activation in the ventrolateral prefrontal cortex during reward anticipation, and decreased activation in the medial prefrontal cortex during reward consumption. CONCLUSION: Results indicate that individual differences in reward sensitivity can specifically predict exposure therapy outcome. Although activation in regions of interest were not related to therapy outcome, regions involved in attentional processing of reward cues were predictive of phobic symptom change following exposure therapy but not PMR.
Assuntos
Encéfalo/fisiologia , Terapia Implosiva , Transtornos Fóbicos/fisiopatologia , Transtornos Fóbicos/terapia , Valor Preditivo dos Testes , Córtex Pré-Frontal/fisiologia , Recompensa , Adolescente , Adulto , Método Duplo-Cego , Feminino , Neuroimagem Funcional , Humanos , Imageamento por Ressonância Magnética , Masculino , Transtornos Fóbicos/diagnóstico , Tempo de Reação , Terapia de Relaxamento , Resultado do Tratamento , Adulto JovemRESUMO
Reduced prepulse inhibition (PPI) of the acoustic startle response is thought to represent a robust biomarker in schizophrenia. Reduced PPI has been demonstrated in subjects at ultra high risk (UHR) for developing psychosis. Imaging studies report disruption of striatal dopaminergic neurotransmission in patients with schizophrenia. First, we compared the PPI of the acoustic startle response in UHR subjects versus healthy controls, to see if we could replicate previous findings of reduced PPI; secondly, we investigated our hypothesis that PPI would be negatively correlated with striatal synaptic dopamine (DA) concentration. We measured the startle reactivity and PPI of the acoustic startle response in 14 UHR subjects, and 14 age- and gender-matched healthy controls. Imaging of 11 UHR subjects and 11 healthy controls was completed by an [(123)I]-IBZM (radiotracer for dopamine D2/3 receptors) SPECT, at baseline and again after DA depletion with alpha-methyl-para-tyrosine (AMPT). The percentage change in striatal [(123)I]-IBZM radiotracer binding potential is a proxy of striatal synaptic DA concentration. UHR subjects showed reduced PPI, compared to control subjects. In both UHR and control subjects, there were no significant correlations between striatal synaptic DA concentration and PPI. We provide further evidence for the hypothesis that these two biomarkers are measuring different aspects of pathophysiology.
Assuntos
Gânglios da Base/metabolismo , Dopamina/metabolismo , Neurônios Dopaminérgicos/metabolismo , Inibição Pré-Pulso , Transtornos Psicóticos/etiologia , Estimulação Acústica , Adolescente , Adulto , Gânglios da Base/diagnóstico por imagem , Gânglios da Base/fisiopatologia , Benzamidas/administração & dosagem , Estudos de Casos e Controles , Meios de Contraste/administração & dosagem , Feminino , Humanos , Masculino , Transtornos Psicóticos/metabolismo , Transtornos Psicóticos/fisiopatologia , Transtornos Psicóticos/psicologia , Pirrolidinas/administração & dosagem , Receptores de Dopamina D2/metabolismo , Receptores de Dopamina D3/metabolismo , Reflexo de Sobressalto , Medição de Risco , Fatores de Risco , Tomografia Computadorizada de Emissão de Fóton Único , Adulto JovemRESUMO
Cannabis use has consistently been associated with psychotic symptoms as well as cognitive impairments. Moreover, its use may provoke subclinical psychotic symptoms and is associated with neuropsychological dysfunctions in subjects at ultra high risk (UHR) for developing psychosis. However, to our knowledge, no data are yet available on the relationship between cannabis use, UHR symptoms and information processing as assessed with event related potentials (ERP) in UHR subjects. This cross-sectional study therefore aimed to investigate N100, N200, P200 and P300 ERP components in 48 UHR subjects (19 cannabis users; UHR+C) and 50 healthy controls (21 cannabis users; HC+C). Results showed smaller P300 amplitudes in HC+C and UHR subjects compared to HC-C. Moreover, HC+C showed prolonged P300 and N200 latencies compared to HC-C and UHR-C. No significant ERP differences were found between UHR+C and UHR-C. Regarding the relationship between information processing and psychopathology, we found associations between ERP components and severity of UHR symptoms, findings being most pronounced for N100 latencies and P300 amplitudes and severity of general psychopathology and positive symptoms. We conclude that UHR subjects and healthy cannabis users demonstrate similar P300 amplitude reductions compared to non-using control subjects. In addition, the interrelation of cannabis use with prolonged ERP latencies may signify reduced information processing speed associated with cannabis use. Finally, our findings cautiously support the hypothesis that the clinical phenomena of the UHR state may be associated with abnormalities in stimulus processing.
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Estimulação Acústica/métodos , Potenciais Evocados Auditivos/fisiologia , Fumar Maconha/epidemiologia , Fumar Maconha/fisiopatologia , Transtornos Psicóticos/epidemiologia , Transtornos Psicóticos/fisiopatologia , Adolescente , Adulto , Estudos Transversais , Feminino , Humanos , Masculino , Transtornos Psicóticos/diagnóstico , Tempo de Reação/fisiologia , Fatores de Risco , Adulto JovemRESUMO
22q11 deletion syndrome (22q11DS) is a genetic disorder caused by a microdeletion on chromosome 22, which includes the gene coding for catechol-O-methyl-transferase (COMT). High dopamine (DA) levels due to COMT haplo-insufficiency may be associated with the increased risk of developing schizophrenia in adults with 22q11DS. Reduced prepulse inhibition (PPI) of the acoustic startle response has been associated with schizophrenia and with disrupted DAergic transmission in the prefrontal cortex (PFC). COMT Val(158)Met polymorphism has been shown to influence PPI. We report the first study in adults with 22q11DS to examine PPI of the acoustic startle response and its modulation by COMT Val(158)Met polymorphism. Startle reactivity (SR) and PPI of the acoustic startle response were measured in 23 adults with 22q11DS and 21 healthy controls. 22q11DS subjects were genotyped for the functional COMT Val(158)Met polymorphism. 22q11DS Met hemizygotes showed reduced SR and PPI compared with 22q11DS Val hemizygotes. The effect of COMT Val(158)Met polymorphism on PPI was no longer significant when controlling for baseline SR. Met hemizygosity in 22q11DS is associated with reduced SR and influences PPI indirectly. Decreased PFC functioning following excessive PFC DA levels may be one of the mechanisms by which the Met genotype in 22q11DS disrupts SR.
Assuntos
Síndrome da Deleção 22q11/genética , Catecol O-Metiltransferase/genética , Dopamina/metabolismo , Reflexo de Sobressalto/genética , Estimulação Acústica , Adulto , Estudos de Casos e Controles , Feminino , Genótipo , Hemizigoto , Humanos , Masculino , Polimorfismo Genético , Córtex Pré-Frontal/patologia , Adulto JovemRESUMO
The specific serotonin (5-HT) releaser, d-fenfluramine (DFEN) was used as a probe of serotonergic effects on prepulse inhibition (PPI). We wished to explore the notion that increased central serotonergic transmission was in part responsible for the psychotomimetic effects of hallucinogens using a relevant and objective physiological measure. Disruption of PPI is considered a valid pharmacological model of some aspects of the behavioural abnormalities in schizophrenia. The aim of this study was to test the hypothesis that increasing central 5-HT neurotransmission with DFEN would produce disruption of PPI. Eighteen healthy male subjects received 45mg of DFEN or placebo in a random order, within-subject, double-blind, and cross-over design. Prepulse to pulse intervals were 30ms and 120ms. The Brief Psychiatric Rating Scale (BPRS) was administered. Although mean PPI at the two prepulse intervals was not significantly different, DFEN prevented the increase in PPI usually seen at the 120ms interval and significantly increased startle magnitude, but did not alter habituation. There were no significant associations between PPI effects and behaviour.