Correlation of symptom clusters of schizophrenia with absolute powers of main frequency bands in quantitative EEG.

BACKGROUND: Research of QEEG activity power spectra has shown intriguing results in patients with schizophrenia. Different symptom clusters have been correlated to QEEG frequency bands. The findings have been to some extent inconsistent. Replication of the findings of previous research is thus an important task. In the current study we investigated the correlations between the absolute powers of delta, theta, alpha, and beta frequency bands over the fronto-central scalp area (FC) with the PANSS subscales and the Liddle's factors in 16 patients with schizophrenia.The authors hypothesised a priori the correlations reported by Harris et al (1999) of PANSS negative subscale with delta power, Liddle's psychomotor poverty with delta and beta powers, disorganisation with delta power and reality distortion with alpha power on the midline FC. METHODS: The sample consisted of 16 patients with chronic schizophrenia considered as having insufficient clinical response to conventional antipsychotic treatment and evidencing a relapse. The correlations between quantitative electroencephalography (QEEG) absolute powers of delta (1.5-3.0 Hz), theta (3.0-7.5 Hz), alpha (7.5-12.5 Hz), and beta (12.5-20.0 Hz) frequency bands over the fronto-central scalp area (FC) with PANSS subscales and Liddle's factors (reality distortion, disorganisation, psychomotor poverty) were investigated. RESULTS: Significant positive correlations were found between the beta and psychomotor poverty (p < 0.05). Trends towards positive correlations (p < 0.1) were observed between delta and PANSS negative subscale and psychomotor poverty. Alpha did not correlate with reality distortion and delta did not correlate with disorganisation.Post hoc analysis revealed correlations of the same magnitude between beta and psychopathology generally over FC. CONCLUSION: The a priori hypothesis was partly supported by the correlation of the beta and psychomotor poverty. Liddle's factors showed correlations of the same magnitude with PANSS subscales. Supplementary analysis showed beta frequency correlating non-specifically over FC with a wide range of psychiatric symptomatology in patients with schizophrenia having a relapse.

ADHD and sleep in homicidal men with antisocial personality disorder.

A history of attention deficit hyperactivity disorder (ADHD) is commonly found in subjects with antisocial personality disorder (ASP). Besides ASP, childhood ADHD also predicts drug abuse disorders and criminal activity in adulthood. Childhood ADHD and ASP appear to be the only psychiatric disorders reported to be associated with an increase in deep sleep. The aims of the present study were to retrospectively measure the childhood ADHD of habitually violent men with ASP and Cloninger type 2 alcoholism, and to characterize the possible relationship between childhood ADHD and sleep architecture in these men. The subjects of the study consisted of 14 homicidal offenders recruited from a forensic psychiatric examination. Ten age- and gender-matched healthy volunteers served as controls. Childhood ADHD symptoms were measured using the Wender-Utah Rating Scale (WURS). The main findings were that violent offenders with ASP had significantly higher mean WURS scores compared with controls, and both the absolute and percentage amount of stage 4 sleep as well as delta and theta powers in this sleep stage were positively correlated with the WURS scores. The present study supports the idea that childhood ADHD is associated with the abnormal sleep architecture in habitually violent men with ASP. These two disorders seem to share, at least partly, the same central nervous system deficit.

Clozapine-induced QEEG changes correlate with clinical response in schizophrenic patients: a prospective, longitudinal study.

BACKGROUND: The changes of theta activity (3.5-7 Hz) in the quantitative electroencephalography (QEEG) and serum clozapine levels and their correlation with clinical response, measured by the Positive and Negative Syndrome Rating Scale (PANSS) for schizophrenia, were examined prospectively in 16 patients suffering from schizophrenia during 18 weeks of clozapine (CLO) treatment. METHODS: Evaluations were performed on five occasions: before the initiation of CLO treatment at baseline and after 1, 3, 10, and 18 weeks of treatment. Doses of CLO starting from 50 mg/day were determined on the basis of clinical response. In the PANSS subscales for positive and negative symptoms, a significant (P < 0.05) improvement was observed after the first week, and in the subscale for general symptoms, improvement was seen after three weeks of treatment with CLO. A significant increase in theta power (P < 0.01) was found after three weeks of CLO treatment in the electrodes over the fronto-central scalp area, most distinctly in the midline. RESULTS: After three weeks we observed significant inverse correlations between the theta power increase and the changes in PANSS subscales for negative (P < 0.01) and positive (P < 0.05) symptoms, and after 10 weeks, between the theta power increase and the change in PANSS subscales for general (P < 0.05) and positive (P < 0.05) symptoms. After 18 weeks a trend of inverse correlation between the PANSS subscales for general and negative symptoms and the right and midline theta power increase was observed, but not with regard to positive symptoms. There were trends, but no significant correlations, between CLO treatment response and serum CLO levels. CONCLUSIONS: These findings indicate that the change in the theta frequency in QEEG and particularly in the midline electrodes over the fronto-central scalp area might be a more sensitive indicator for the evaluation of CLO treatment adequacy than the serum CLO level.

Asperger syndrome, alexithymia and perception of sleep.

Two research traditions, the one on Asperger syndrome (AS) and the other on alexithymia, have produced similar findings independently of each other indicating a possible association between these two phenomena. Both conditions are also associated with impaired initiation and continuity of sleep. Twenty AS adults were compared with 10 healthy controls using the Toronto Alexithymia Scale and the Basic Nordic Sleep Questionnaire. AS subjects were significantly more alexithymic and reported lower sleep quality as compared with controls. AS and alexithymia are associated although the mediating factors are unknown. It is possible that alexithymic traits predispose to anxiety, which in turn lowers the sleep quality in AS adults. Alternatively, low sleep quality might be due to AS itself.

Sleep among habitually violent offenders with antisocial personality disorder.

The aim of the present study was to characterize the subjective and objective sleep and sleep quality in habitually violent offenders with DSM-IV diagnosis of antisocial personality disorder using a sleep questionnaire, actigraphy, polysomnography and power spectral analysis. Subjects for the study were 19 drug-free males (mean age +/- SEM 30.7 +/- 2.58 years) recruited from a forensic psychiatric examination in a special ward of a university psychiatric hospital. The most striking finding was the high amount of slow-wave sleep, particularly the deepest S4 stage (17% as compared with 6% in healthy controls), in males with antisocial personality disorder. Moreover, in the spectral power analysis, both the delta and the theta power were significantly elevated. Whether this increase in persons with antisocial personality disorder reflects a specific brain pathology, or a delay in the normal development of sleep patterns in the course of ageing needs to be clarified with further experiments.

Human impulsive aggression: a sleep research perspective.

Impulsive aggression is commonly associated with personality disorders, in particular antisocial and borderline personality disorders as well as with conduct disorder and intermittent explosive disorder. The relationship between impulsive aggression and testosterone is well established in many studies. One of the aims of this study was to characterize the relationship between earlier-mentioned different categorical psychiatric diagnosis describing human impulsive aggression and sleep using polysomnography and spectral power analysis. Another aim was to study the relationship between serum testosterone and sleep in persons with severe aggressive behaviour. Subjects for the study were 16 males charged with highly violent offences and ordered for a pretrial forensic psychiatric examination. The antisocials with borderline personality disorder comorbidity had significantly more awakenings and lower sleep efficiency compared with the subjects with only antisocial personality disorder. The subjects with severe conduct disorder in childhood anamnesis had higher amount of S4 sleep and higher relative theta and delta power in this sleep stage compared with males with only mild or moderate conduct disorder. The same kind of sleep architecture was associated with intermittent explosive disorder. In subgroups with higher serum testosterone levels also the amount of S4 sleep and the relative theta and delta power in this sleep stage were increased. The study gives further support to the growing evidence of brain dysfunction predisposing to severe aggressive behaviour and strengthens the view that there are different subpopulations of individuals with antisocial personality varying in impulsiveness. The differences in impulsiveness are reflected in sleep architecture as well.

Antisocial violent offenders with attention deficit hyperactivity disorder demonstrate akathisia-like hyperactivity in three-channel actometry.

Actometry enables quantitative and qualitative analysis of various hyperactivity disorders. Antisocial violent offenders have demonstrated diurnal increases in motor activity that may be related to attention deficit hyperactivity disorder (ADHD) that often precedes antisocial development. Motor restlessness in ADHD has common features with neuroleptic-induced akathisia. In this study, three-channel actometry was used to compare 15 antisocial violent offenders who had a history of ADHD with 15 healthy control subjects and 10 akathisia patients. The Barnes Akathisia Rating Scale (BARS) was used for clinical evaluation of akathisia symptoms. Ankle movement indices and the ankle-waist ratio differentiated the antisocial patients from the healthy controls significantly, with no overlap, and the same parameters expectedly differentiated the akathisia patients from the healthy controls. The repetitive, rhythmic pattern of akathisia was found in 13 of the 15 antisocial patients. Nine of the antisocial patients scored 2 or 3 (mild to moderate akathisia) on the BARS. Thus, the motor hyperactivity of antisocial ADHD patients has common features with mild akathisia. This may be due to a common hypodopaminergic etiology of ADHD and akathisia.

Decreased production of reactive oxygen species by blood monocytes caused by clozapine correlates with EEG slowing in schizophrenic patients.

We have earlier reported an increased theta-power value in clozapine (CLO)-treated patients with schizophrenia, nonresponsive to conventional antipsychotics. We also found that the decrease in the production of reactive oxygen species (ROS), induced by CLO, by peripheral blood monocytes (MO) of these patients correlates with clinical improvement. MO share the capability of ROS production with their more mature descendants, microglia of the brain. We hypothesized that the CLO-related changes in peripheral blood MO might be related to a parallel process in microglia and thus be reflected in brain activity. In those 8 patients for whom both QEEG and MO data were available, we explored possible relationships between these parameters. A clear-cut correlation between ROS production (R(2) = 0.929, p < 0.05) for nonstimulated MO, and (R(2) = 0.907, p < 0.001) for stimulated MO and theta-power values in the central frontal electrode (F(z)) was found. It is intriguing to speculate that the EEG slowing is a result of the modulatory action of the activated microglial cells in the central nervous system via production of ROS or cytokines or both. However, this proposition has to be confirmed by future research.

Growth hormone-insulin-like growth factor-1 axis, leptin and sleep in anorexia nervosa patients.

The present study characterizes the relationships between severe malnutrition, sleep, growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis, and leptin levels in anorexia nervosa (AN) patients before and after weight gain. Eleven restricting-type anorectic females (mean age = 19.7 years) with severe starvation state [mean body mass index (BMI) = 13.3] were studied using polysomnography and spectral power analysis. The hormone levels were measured in the morning after sleep recording. Eleven normal-weight, age- and gender-matched healthy volunteers without a history of any eating disorder served as controls. After nutritional treatment for about 2 months (65.7 +/- 6.4 days), sleep examinations and blood tests were repeated. At this stage, the study group consisted of 5 patients (mean BMI = 15.6). Higher IGF-1 and leptin levels were associated with longer and deeper sleep among anorectics. The sleep parameters including the percentages of stage 1 sleep and SWS as well as IGF-1 tended to normalize after only limited weight gain. Sleep disturbances in anorectics may be mediated through changes in the levels of the GH-IGF-1 axis hormones, as well as the levels of leptin.

REM sleep and prolactin in patients with non-affective psychoses.

Reduced REM latency is a common polysomnographic finding in patients with schizophrenia. This has been attributed to cholinergic hyperactivity secondary to increased dopaminergic tone. We studied polysomnographic sleep recordings, and morning serum prolactin levels as a measure of dopaminergic tone in 17 drug-free patients suffering from non-affective psychoses, hypothesizing that REM-latency and prolactin would correlate. A clear-cut positive correlation between prolactin and REM latency was found, as well as a negative correlation between prolactin and REM sleep. The findings may be explained by dopaminergic and secondary hypercholinergic and/or serotonergic mechanisms responsible for the regulation of REM sleep and the secretion of prolactin.

Neopterin and macrophage inflammatory protein-1alpha in the cerebrospinal fluid of schizophrenic patients: no evidence of intrathecal inflammation.

BACKGROUND: Numerous reports support the idea that inflammatory and/or immunological processes contribute to the etiopathogenesis of schizophrenia. Most of the data are, however, based on findings from body compartments outside the central nervous system (CNS). We measured the concentrations of the inflammatory marker neopterin and the chemokine macrophage inflammatory protein-alpha (MIP-1alpha) in the cerebrospinal fluid (CSF) of acutely psychotic schizophrenic patients and of healthy controls. METHODS: The concentration of neopterin was measured in the CSF of 11 schizophrenic patients by radioimmunoassay, and of MIP-1alpha in the CSF from 8 patients using ELISA. Control CSF was collected from 10 and 8 healthy individuals. RESULTS: No statistically significant differences in CSF neopterin or MIP-1alpha were detected between patients and controls or between the patient samples obtained on hospital admission and after the treatment period associated with clinical improvement. CONCLUSIONS: These findings argue against the hypothesis that active inflammatory processes are part of the pathophysiology of acute psychotic episodes in schizophrenia. The possible mechanisms explaining the previously reported aberrations of mononuclear cells and cytokines in schizophrenia are discussed.