[Neurological or interdisciplinary outpatient pain treatment: comparison of treatment success and satisfaction]. / Neurologische oder interdisziplinäre Schmerzambulanz: Vergleich des Behandlungserfolges und der Zufriedenheit.

The aim of this study was to compare the satisfaction and success of treatment for pain patients who were interdisciplinary (anaesthesiological, psychosomatic, neurological, orthopedic) treated or underwent neurological care alone. Methods We selected 183 patients who were treated in our neurological clinic and in our interdisciplinary pain management center (IST). Of these, 142 patients having polyneuropathy, headache or muskuloskelettal pain were included in the final analysis. 39 patients (27.5 %) were treated in the IST and 103 patients were treated exclusively by a neurologist. These patients were asked to complete a questionnaire, and were queried about the satisfaction and pain parameters. Results The neurological and multidisciplinary pain treatment led to a similar improvement in pain (p < 0.001). This effect was independent of the underlying disease. The interdisciplinary outpatient treatment resulted not primarily in an increased patient satisfaction. Conclusions The reduction of pain and patient satisfaction of neurological outpatient pain treatment were comparable with those of a multidisciplinary outpatient therapy. The only significant advantage of the interdisciplinary treatment was lower hospitalization rate after therapy. This result cannot evaluate the efficiency of inpatient or day hospital pain management, but suggests that in many cases a neurological outpatient pain therapy is sufficient, so that neurological outpatient care should be promoted.

Active pain coping is associated with the response in real-time fMRI neurofeedback during pain.

Real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback is used as a tool to gain voluntary control of activity in various brain regions. Little emphasis has been put on the influence of cognitive and personality traits on neurofeedback efficacy and baseline activity. Here, we assessed the effect of individual pain coping on rt-fMRI neurofeedback during heat-induced pain. Twenty-eight healthy subjects completed the Coping Strategies Questionnaire (CSQ) prior to scanning. The first part of the fMRI experiment identified target regions using painful heat stimulation. Then, subjects were asked to down-regulate the pain target brain region during four neurofeedback runs with painful heat stimulation. Functional MRI analysis included correlation analysis between fMRI activation and pain ratings as well as CSQ ratings. At the behavioral level, the active pain coping (first principal component of CSQ) was correlated with pain ratings during neurofeedback. Concerning neuroimaging, pain sensitive regions were negatively correlated with pain coping. During neurofeedback, the pain coping was positively correlated with activation in the anterior cingulate cortex, prefrontal cortex, hippocampus and visual cortex. Thermode temperature was negatively correlated with anterior insula and dorsolateral prefrontal cortex activation. In conclusion, self-reported pain coping mechanisms and pain sensitivity are a source of variance during rt-fMRI neurofeedback possibly explaining variations in regulation success. In particular, active coping seems to be associated with successful pain regulation.

Detection of central circuits implicated in the formation of novel pain memories.

Being able to remember physically and emotionally painful events in one's own past may shape behavior, and can create an aversion to a variety of situations. Pain imagination is a related process that may include recall of past experiences, in addition to production of sensory and emotional percepts without external stimuli. This study aimed to understand 1) the central nervous system processes that underlie pain imagination, 2) the retrieval of pain memories, and 3) to compare the latter with visual object memory. These goals were achieved by longitudinally investigating brain function with functional magnetic resonance imaging in a unique group of healthy volunteers who had never experienced tooth pain. In these subjects, we compared brain responses elicited during three experimental conditions in the following order: imagination of tooth pain (pain imagination), remembering one's own house (object memory), and remembrance of tooth pain following an episode of induced acute tooth pain (pain memory). Key observations stemming from group-level conjunction analyses revealed common activation in the posterior parietal cortex for both pain imagination and pain memory, while object and pain memory each had strong activation predominantly within the middle frontal gyrus. When contrasting pain imagination and memory, significant activation differences were observed in subcortical structures (ie, parahippocampus - pain imagination > pain memory; midbrain - pain memory > pain imagination). Importantly, these findings were observed in the presence of consistent and reproducible psychophysical and behavioral measures that informed on the subjects' ability to imagine novel and familiar thoughts, as well as the subjects' pain perception.

Meta-analysis of real-time fMRI neurofeedback studies using individual participant data: How is brain regulation mediated?

An increasing number of studies using real-time fMRI neurofeedback have demonstrated that successful regulation of neural activity is possible in various brain regions. Since these studies focused on the regulated region(s), little is known about the target-independent mechanisms associated with neurofeedback-guided control of brain activation, i.e. the regulating network. While the specificity of the activation during self-regulation is an important factor, no study has effectively determined the network involved in self-regulation in general. In an effort to detect regions that are responsible for the act of brain regulation, we performed a post-hoc analysis of data involving different target regions based on studies from different research groups. We included twelve suitable studies that examined nine different target regions amounting to a total of 175 subjects and 899 neurofeedback runs. Data analysis included a standard first- (single subject, extracting main paradigm) and second-level (single subject, all runs) general linear model (GLM) analysis of all participants taking into account the individual timing. Subsequently, at the third level, a random effects model GLM included all subjects of all studies, resulting in an overall mixed effects model. Since four of the twelve studies had a reduced field of view (FoV), we repeated the same analysis in a subsample of eight studies that had a well-overlapping FoV to obtain a more global picture of self-regulation. The GLM analysis revealed that the anterior insula as well as the basal ganglia, notably the striatum, were consistently active during the regulation of brain activation across the studies. The anterior insula has been implicated in interoceptive awareness of the body and cognitive control. Basal ganglia are involved in procedural learning, visuomotor integration and other higher cognitive processes including motivation. The larger FoV analysis yielded additional activations in the anterior cingulate cortex, the dorsolateral and ventrolateral prefrontal cortex, the temporo-parietal area and the visual association areas including the temporo-occipital junction. In conclusion, we demonstrate that several key regions, such as the anterior insula and the basal ganglia, are consistently activated during self-regulation in real-time fMRI neurofeedback independent of the targeted region-of-interest. Our results imply that if the real-time fMRI neurofeedback studies target regions of this regulation network, such as the anterior insula, care should be given whether activation changes are related to successful regulation, or related to the regulation process per se. Furthermore, future research is needed to determine how activation within this regulation network is related to neurofeedback success.

Reduced D2/D3 Receptor Binding of Extrastriatal and Striatal Regions in Temporal Lobe Epilepsy.

OBJECTIVE: Dopamine is an endogenous neuromodulator in cortical circuits and the basal ganglia. In animal models of temporal lobe epilepsy (TLE), seizure threshold is modulated to some extent by dopamine, with D1-receptors having a pro- and D2-receptors an anticonvulsant effect. We aimed to extend our previously reported results on decreased D2/D3 receptor binding in the lateral epileptogenic temporal lobe and to correlate them with demographic and seizure variables to gain a more comprehensive understanding of the underlying involvement of the dopaminergic system in the epileptogenesis of TLE. METHODS: To quantify D2/D3 receptor binding, we studied 21 patients with TLE and hippocampal sclerosis (13 left- and eight right-sided) and 18 controls using PET with the high-affinity dopamine D2/D3-receptor ligand 18F-Fallypride to image striatal and extrastriatal binding. TLE was defined by interictal and ictal video-EEG, MRI and 18F-Fluorodeoxyglucose PET. Voxel-based statistical and regions-of-interest analyses were performed. RESULTS: 18F-Fallypride binding potential was significantly reduced in the affected temporal lobe and bilateral putamen. A positive correlation between age at onset of epilepsy and [18F]FP BPnd (binding potential non-displaceable) in temporal regions on the epileptogenic side was found, as well as a negative correlation between epilepsy duration and [18F]FP BPnd in the temporal pole on the epileptogenic side and a positive correlation between the estimated number of lifetime GTCS and [18F]FP BPnd in the hippocampus on the epileptogenic side. SIGNIFICANCE: The areas of reduced D2/D3 receptor availability correspond to "the irritative zone" surrounding the epileptogenic area. Moreover, reduced D2/D3 receptor availability was detectable in the basal ganglia, which are suspected to be involved in a control circuit for epileptic seizures. The correlational analysis additionally suggests that increased epilepsy duration leads to increasing impairment of the dopaminergic system.

Latency of interictal epileptiform discharges in long-term EEG recordings in epilepsy patients.

PURPOSE: To assess the latency of interictal epileptiform discharges (IED) and seizures in long-term EEG recordings of patients with epilepsy. METHOD: IED latency was measured in 210 consecutive patients (mean (SD) age 38.6 ± 13.9 years) with active epilepsy and the relationship to clinical variables was analyzed retrospectively. Median duration of EEG recording was 101.5h (95% confidence interval [CI] 92 to 117 h). RESULTS: IEDs were absent in 45 (21.4%) and present in 165 (78.6%) patients who had a longer duration (p < 0.001) and early onset (p < 0.01) of epilepsy and more often had IEDs in prior standard EEGs (p < 0.01), a structural etiology (OR 2.4, CI: 2.1-2.7), or temporal lobe epilepsy (OR 9.6, CI: 9.0-10.2). IED latency did not correlate with other clinical variables. Median latency to the emergence of the first IED was 9.3h (CI: 7.5-11.4) occurring in 7.3%, 9.7%, 74.6%, 87.9%, and 96.4% within 20 min, 30 min, 24h, 48 h, and 72 h, respectively. Seizure frequency was higher in patients with (n = 165) than without IEDs (n = 45) (72.1% vs. 46.6%, p < 0.01) and seizure latency (median 21.6h, CI: 16.8-27.3) was influenced by the presence of IEDs, whereas the presence of seizures did not influence the latency and frequency of IEDs. CONCLUSION: If present, in the majority of epilepsy patients IEDs occurred during the first 72 h of long-term video-EEG recording. Repeated video-EEG or video recordings of habitual seizures are needed to minimize false negative studies.

Comparison of anterior cingulate vs. insular cortex as targets for real-time fMRI regulation during pain stimulation.

Real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback allows learning voluntary control over specific brain areas by means of operant conditioning and has been shown to decrease pain perception. To further increase the effect of rt-fMRI neurofeedback on pain, we directly compared two different target regions of the pain network, notably the anterior insular cortex (AIC) and the anterior cingulate cortex (ACC). Participants for this prospective study were randomly assigned to two age-matched groups of 14 participants each (7 females per group) for AIC and ACC feedback. First, a functional localizer using block-design heat pain stimulation was performed to define the pain-sensitive target region within the AIC or ACC. Second, subjects were asked to down-regulate the BOLD activation in four neurofeedback runs during identical pain stimulation. Data analysis included task-related and functional connectivity analysis. At the behavioral level, pain ratings significantly decreased during feedback vs. localizer runs, but there was no difference between AIC and ACC groups. Concerning neuroimaging, ACC and AIC showed consistent involvement of the caudate nucleus for subjects that learned down-regulation (17/28) in both task-related and functional connectivity analysis. The functional connectivity toward the caudate nucleus is stronger for the ACC while the AIC is more heavily connected to the ventrolateral prefrontal cortex. Consequently, the ACC and AIC are suitable targets for real-time fMRI neurofeedback during pain perception as they both affect the caudate nucleus, although functional connectivity indicates that the direct connection seems to be stronger with the ACC. Additionally, the caudate, an important area involved in pain perception and suppression, could be a good rt-fMRI target itself. Future studies are needed to identify parameters characterizing successful regulators and to assess the effect of repeated rt-fMRI neurofeedback on pain perception.

Central correlation of muscle sympathetic nerve activation during baroreflex unloading - a microneurography-positron emission tomography study.

The baroreceptor reflex controls spontaneous fluctuations in blood pressure. One major control variable of the baroreflex is the sympathetic vasoconstrictor activity to muscles [MSNA; burst frequency (BF) and burst incidence (BI)], which can be quantitatively assessed by microneurography. We aimed to investigate the central regions involved in baroreflex regulation of MSNA. Healthy men (mean age 25 years) participated in three experimental sessions. (i) Microneurography recordings of MSNA from the left peroneal nerve during rest and baroreflex unloading, induced by lower body negative pressure (LBNP; -40 mmHg). If MSNA could be reliably recorded throughout this procedure (n = 15), the subjects entered the positron emission tomography (PET) experiments. The two PET sessions took place in a randomised order. Cerebral glucose metabolism (18-fluorodeoxyglucose) was analysed after: (ii) baroreflex unloading (LBNP); and (iii) control condition (lying in the LBNP chamber without suction). The PET data were analysed employing SPM8. LBNP elicited a significant increase in MSNA in all successfully recorded subjects (BI: P = 0.001; F = 5.54; BF: P < 0.001; F = 36.59). As compared with the control condition, LBNP was associated with increased PET regional glucose metabolism bilaterally in the orbitofrontal cortex (OFC; BA 11, 47). Related to the rise of BF, there was increased activation of the left OFC (BA 11); related to the rise of BI there was increased activation of the brainstem corresponding to the rostral ventrolateral medulla. Our data support a role for the ventrolateral medulla and the OFC in baroreflex-mediated control of MSNA in humans.

Osteoprotegerin: a new biomarker for impaired bone metabolism in complex regional pain syndrome?

Osteoprotegerin (OPG) is important for bone remodeling and may contribute to complex regional pain syndrome (CRPS) pathophysiology. We aimed to assess the value of OPG as a biomarker for CRPS and a possible correlation with radiotracer uptake in 3-phase bone scintigraphy (TPBS). OPG levels were analyzed in 23 CRPS patients (17 women; mean age 50±9.0 years; disease duration: 12 weeks [IQR 8-24]), 10 controls (6 women; mean age 58±9.6 years) and 21 patients after uncomplicated fractures (12 women; mean age: 43±15 years; time after fracture: 15 weeks [IQR: 6-22]). The CRPS and control patients also underwent TPBS. OPG in CRPS patients was significantly increased by comparison with both control groups (P=0.001; Kruskal-Wallis test; CRPS patients: 74.1 pg/mL [IQR: 47.1-100.7]; controls: 46.7 pg/mL [IQR: 35.5-55.0]; P=0.004; fracture patients: 45.9 pg/mL [IQR: 37.5-56.7]; P=0.001). As a diagnostic test for CRPS, OPG had a sensitivity of 0.74, specificity of 0.80, positive predictive value of 68% and negative predictive value of 84%. Receiver operating characteristic curve analysis showed an area under the curve of 0.80 (CI: 0.68-0.91). For the CRPS-affected hand, a significant correlation between OPG and TPBS region of interest analysis in phase III was detected (carpal bones; r=0.391; P=0.03). The persistent OPG increase in CRPS indicates enhanced osteoblastic activity shown by increased radiotracer uptake in TPBS phase III. A contribution of bone turnover to CRPS pathophysiology is likely. OPG might be useful as a biomarker for CRPS.

Pain in chemotherapy-induced neuropathy--more than neuropathic?

Chemotherapy-induced neuropathy (CIN) is an adverse effect of chemotherapy. Pain in CIN might comprise neuropathic and nonneuropathic (ie, musculoskeletal) pain components, which might be characterized by pain patterns, electrophysiology, and somatosensory profiling. Included were 146 patients (100 female, 46 male; aged 56 ± 0.8 years) with CIN arising from different chemotherapy regimens. Patients were characterized clinically through nerve conduction studies (NCS) and quantitative sensory testing (QST). Questionnaires for pain (McGill) and anxiety/depression (Hospital Anxiety and Depression Scale) were supplied. Patients were followed-up after 17 days. Large- (61%) and mixed- (35%) fibre neuropathies were more frequent than small-fibre neuropathy (1.4%). The 5 major chemotherapeutic regimens impacted differently on large- but not on small-fibre function and did not predict painfulness. Chronic pain associated with CIN was reported in 41.7%. Painless and painful CIN did not differ in QST profiles or electrophysiological findings, but different somatosensory patterns were found in CIN subgroups (pain at rest [RestP], n = 25; movement-associated pain [MovP], n = 15; both pain characteristics [MovP+RestP], n = 21; or no pain [NonP], n = 85): small-fibre function (cold-detection threshold, CDT: z score: -1.46 ± 0.21, P < 0.01) was most impaired in RestP; mechanical hyperalgesia was exclusively found in MovP (z score: +0.81 ± 0.30, P < 0.05). "Anxiety" discriminated between painful and painless CIN; "CDT" and "anxiety" discriminated between patients with ongoing (RestP) and movement-associated pain (MovP) or pain components (MovP+RestP). The detrimental effect of chemotherapy on large fibres failed to differentiate painful from painless CIN. Patients stratified for musculoskeletal or neuropathic pain, however, differed in psychological and somatosensory parameters. This stratification might allow for the application of a more specific therapy.

Inhibition of neuropeptide degradation suppresses sweating but increases the area of the axon reflex flare.

The neuropeptides CGRP (calcitonin gene-elated peptide) and substance P (SP) mediate neurogenic inflammation. Both are degraded by the neutral endopeptidase (NEP) which can be blocked by phosphoramidon. The aim was to evaluate the effect of NEP inhibition on sweating and vasodilatation. Dermal microdialysis was performed on the skin of 39 subjects. Two fibres were perfused with phosphoramidon (0.01%, 0.02% or 0.2%), two with saline. Acetylcholine (ACh) was either added to the microdialysis perfusate (n = 30, 10(-2)  m) or thermoregulatory sweating was induced (n = 9). Co-application of phosphoramidon reduced cholinergic and thermoregulatory sweating. However, the flare size - a localized increase in superficial blood flow after ACh-application - was significantly increased. The increase in flare size is most probably due to increased CGRP levels. The inhibition of sweating by phosphoramidon may involve an increase in SP, a reduction in CGRP-degradation fragments or a direct inhibitory action of phosphoramidon.

Ultra-marathon runners are different: investigations into pain tolerance and personality traits of participants of the TransEurope FootRace 2009.

INTRODUCTION: Susceptibility to pain varies among individuals and may predispose to a higher risk for pain disorders. Thus, it is of interest to investigate subjects who exhibit higher resistance to pain. We therefore tested pain tolerance and assessed personality traits of ultra-marathon athletes who are able to run 4487 km (2789 mi) over 64 days without resting days and compare the results to controls. METHODS: After approval of the local ethics committee and with informed consent, 11 participants of the TransEurope FootRace (TEFR09 participants) and 11 matched (age, sex, and ethnicity) controls without marathon experience in the last 5 years were enrolled. They were tested for cold pain tolerance (cold pressor [CP] test), and the 240 item trait and character inventory (TCI) as well as the general self-efficacy (GSE) test were obtained. RESULTS: TransEurope FootRace participants had a highly significant greater cold pain tolerance in the CP test than controls (P = 0.0002). While the GSE test showed no differences, the TCI test provided TEFR09 participants to be less cooperative and reward dependent but more spiritually transcendent than the controls. Significant positive correlations were found between the CP test pain score at 180 seconds and several TCI subscales showing that higher pain scores correlate with higher reward dependence, dependence, cooperativeness, empathy, and pure-hearted conscience. CONCLUSIONS: Personality profiles as well as pain tolerance of our sample of TEFR09 participants differ from normal controls and-as obtained in previous studies-probably also from chronic pain patients. Low pain perception may predispose a person to become a long-distance runner. It remains unclear, however, whether low pain perception is cause or consequence of continuous extreme training.

The efficacy of acupuncture in human pain models: a randomized, controlled, double-blinded study.

Acupuncture is frequently used to treat pain, although data supporting the analgesic efficacy from placebo-controlled studies is sparse. In order to get evidence for acupuncture analgesia we performed a study with 2 well-recognized experimental human pain models - the cold-pressor (CP) test and intradermal capsaicin injection. Fifty healthy men were included. Our study compared Traditional Chinese Medicine-based acupuncture to sham acupuncture with Streitberger placebo needles in a randomized, controlled, double-blinded trial. The primary endpoint was the reduction of mean pain intensity during 3minutes of CP test or of mean pain intensity within 10minutes after capsaicin injection. Secondary parameters were defined to substantiate the findings. To ensure comparability, somatosensory (measured by quantitative sensory testing) and psychological parameters were investigated and found to be the same in both groups. Analyses (repeated-measures analyses of variance) showed a significant (P=0.009) but clinically questionable pain reduction in the verum group for capsaicin-induced pain, which was mainly driven by an effect of Traditional Chinese Medicine acupuncture on small pain ratings (max. reduction from 7/100 rating at baseline to 2.5/100 at intervention). Neither pin-prick hyperalgesia, nor allodynia, nor neurogenic flare associated with capsaicin injection, nor pain ratings during the CP test, were significantly different between groups. In addition, there was no placebo response. Attitude towards acupuncture and partial unblinding did not affect the results. We conclude that acupuncture on predefined points has a minor effect on experimental pain in healthy subjects.

Expectations modulate long-term heat pain habituation.

Habituation to pain was shown to be a complex mechanism involving the pain encoding regions and the antinociceptive system in the brain. Pain perception can be modulated by cognitive factors; however it is unclear whether cognitive factors also influence habituation to pain. We used an established experimental design with repetitive moderate painful heat stimulation over eight consecutive days. Thirty-seven healthy subjects were recruited and assigned to four different groups: The first group (n=10) was instructed that pain perception over time will habituate; the second group (n=9) that pain will increase; the third group (n=8) was instructed that pain will remain stable over the 8 days of pain stimulation and the fourth group (n=10) was not given any specific information and served as a control group. We found that the control group habituated as described before. However, it was abolished in the second (sensitize) and third (stable) group, but was very strongly demonstrated in the first (habituation) group. In this group, habituation tended to be increased as compared to the control group. In conclusion, our findings highlight the importance of context information in pain studies and contribute to our knowledge about pain processing and behaviour.

Do intensity ratings and skin conductance responses reliably discriminate between different stimulus intensities in experimentally induced pain?

UNLABELLED: The present study addresses the question whether pain-intensity ratings and skin conductance responses (SCRs) are able to detect different intensities of phasic painful stimuli and to determine the reliability of this discrimination. For this purpose, 42 healthy participants of both genders were assigned to either electrical, mechanical, or laser heat-pain stimulation (each n = 14). A whole range of single brief painful stimuli were delivered on the right volar forearm of the dominant hand in a randomized order. Pain-intensity ratings and SCRs were analyzed. Using generalizability theory, individual and gender differences were the main contributors to the variability of both intensity ratings and SCRs. Most importantly, we showed that pain-intensity ratings are a reliable measure for the discrimination of different pain stimulus intensities in the applied modalities. The reliability of SCR was adequate when mechanical and heat stimuli were tested but failed for the discrimination of electrical stimuli. Further studies are needed to reveal the reason for this lack of accuracy for SCRs when applying electrical pain stimuli. PERSPECTIVE: Our study could help researchers to better understand the relationship between pain and activation of the sympathetic nervous system. Pain researchers are furthermore encouraged to consider individual and gender differences when measuring pain intensity and the concomitant SCRs in experimental settings.

Insular cortex activity is associated with effects of negative expectation on nociceptive long-term habituation.

It is generally accepted that acute painful experience is influenced by context information shaping expectation and modulating attention, arousal, stress, and mood. However, little is known about the nature, duration, and extent of this effect, particularly regarding the negative expectation. We used a standardized longitudinal pain paradigm and painful heat test stimuli in healthy participants over a time course of 8 consecutive days, inducing nociceptive habituation over time. Thirty-eight healthy volunteers were randomly assigned to two different groups. One group received the information that the investigators expected the pain intensity to increase over time (context group). The other group was not given any information (control group). All participants rated the pain intensity of the daily standardized pain paradigm on a visual analog scale. In agreement with previous studies the pain ratings in the control group habituated over time. However, the context group reported no change of pain ratings over time. Functional imaging data showed a difference between the two groups in the right parietal operculum. These data suggest that a negative context not only has an effect on immediate pain but can modulate perception of pain in the future even without experience/conditioning. Neuronally, this process is mediated by the right opercular region.

Blink rate during tests of executive performance after nocturnal traffic noise.

This analysis is on the hypothesis that nocturnal traffic noise affects sleep quality whereas performance decrement is avoided by increased effort expressed by a decrease in blink rates (BRs) during a visual task. Twenty-four persons (12 women, 12 men; 19-28 years, 23.56+/-2.49 years) slept during three consecutive weeks in the laboratory while exposed to road, rail, or aircraft noise with weekly permuted changes. Each week consisted of a random sequence of a quiet night (32 dBA) and three nights with equivalent noise levels of 39, 44 and 50 dBA respectively. The polysomnogram was recorded during all nights. Every morning the participants rated their sleep quality and then completed two executive tasks (Go/Nogo-, Switch-task). Neither of the two performance tests was affected by nocturnal noise. Sleep efficiency and subjective sleep quality decreased with increasing noise levels but were not associated with the type of noise. In contrast, BRs were associated with the type of noise, not with noise levels. The results do not support the hypothesis concerning the BR. The possible reasons are discussed. However, the results do not exclude that other physiological parameters such as heart rate or brain potentials measured during the tests might have revealed alterations associated with nocturnal noise exposure.

The relationship between poor sleep and inhibitory functions indicated by event-related potentials.

The present study focused on the relationship between normal variations of sleep and inhibitory functions as reflected in event-related potentials. For this reason one night of 21 healthy participants was analysed. After waking up all participants completed a visual Go/Nogo task. On the basis of a sleep disturbance index (SDI) the participants were separated into 8 SDI-good and 13 SDI-poor sleepers using a cluster analysis. The results showed that Nogo-N2 amplitude was smaller and Nogo-P3 latency longer in SDI-poor sleepers. Moreover, Go-P3 amplitude was smaller in SDI-poor sleepers. Performance parameters were not influenced by poor sleep. We concluded that poor sleep specifically affects the intensity of pre-motor inhibitory processes (Nogo-N2 amplitude), the speed to inhibit a motor response (Nogo-P3 latency) and the intensity of task-relevant information processing (Go-P3 amplitude). In further studies, it should be explored under which conditions such subliminal deficits also become relevant for overt behaviour.