Daytime sleepiness and EEG abnormalities in patients treated with second generation antipsychotic agents.

BACKGROUND: The aim of this study was to verify whether or not an increased prevalence of excessive daytime sleepiness (EDS) or EEG abnormalities is observed in patients with schizophrenia spectrum disorders (SSD), and to compare the effects of second generation antipsychotics (SGA) on patients' daytime sleepiness level and EEG recordings. METHODS: EEG recordings and self-reports of EDS, assessed with Epworth (ESS) and Stanford (SSS) Sleepiness Scales, were compared between 244 patients with SSD and 82 patients with anxiety, personality or behavioral disorders (non-psychotic disorders, NPD). To examine the effects of various SGA, patients treated in monotherapy with aripiprazole, olanzapine, clozapine, risperidone and sertindole were compared. RESULTS: A higher prevalence of abnormal EEG recordings was observed in SSD patients. No significant differences in average daytime sleepiness were found between patients with SSD and NPD; however, patients with SSD had longer sleep duration. Aripiprazole treatment was associated with significantly smaller and less frequent EEG abnormalities than treatment with any other SGA, while treatment with clozapine and olanzapine was related to an increased prevalence of severe EEG abnormalities. Patients with SSD treated with SGA in monotherapy were less sleepy than unmedicated patients with NPD. CONCLUSIONS: Although antipsychotics may have profound effects on EEG patients with schizophrenia do not have higher daytime sleepiness than patients with anxiety/personality disorders. Patients with schizophrenia may compensate sedative effects of antipsychotic treatment with sleep duration prolongation and report even less sleepiness than non-psychotic patients.

[The use of event related potentials in psychiatric research]. / Zastosowanie badan potencjalów wywolanych zwiazanych z wydarzeniami poznawczymi w psychiatrii.

BACKGROUND: Event related potentials (ERPs) originate predominantly from cortical structures in response to information processing. In contrast to evoked potentials of short latency (<100 ms), long latency cognitive ERPs are not directly related to the physical characteristics of the stimulus, but rather to the information and meaning that the stimulus has for the investigated person. AIM: The aim of this review article was to present selected research questions in psychiatry that can be addressed with ERP studies. As examples we used studies performed in patients with schizophrenia and posttraumatic stress disorder (PTSD). METHODS: ERPs can be recorded during well established cognitive tests in psychiatry: go-no go, n-back, continuous performance test (CPT), Wisconsin card sorting test, Stroop test, verbal learning test and many others. Several ERP components are used as endophenotypes in genetic psychiatric research. CONCLUSIONS: ERPs can be also useful in clinic related questions: identification of subject at high-risk of psychosis, assessment of attention deficits or selective attention problems in anxiety disorders, evaluation of early response to psychopharmacological treatment and efficacy of psychotherapeutic interventions.

[Sleep quality and daytime sleepiness in schizophrenia spectrum disorders during antipsychotic treatment]. / Jakosc snu i sennosc w ciagu dnia w zaburzeniach psychotycznych z kregu schizofrenii w trakcie leczenia lekami przeciwpsychotycznymi.

AIM: Patients with schizophrenia frequently report disturbed sleep and excessive daytime sleepiness. In this study the sleep quality and daytime sleepiness of patients hospitalized due to psychotic disorders was assessed shortly before the discharge from the hospital. METHOD: 62 patients treated with antipsychotics (20 F/ 42 M, mean age 25.7 +/- 3.5) were examined. The patients performed a vigilance task (Mackworth clock test), clinical scales were used for the assessment of: sleep quality (Athens insomnia scale - AIS), daytime sleepiness (Epworth sleepiness scale - ESS), clinical global impression (CGI scale), drug side effects (UKU scale), psychopathology and depressive symptoms (PANSS and CDSS scales). RESULTS: Excessive daytime sleepiness (EDS) was reported in the UKU scale in 58% of the patients. This subjective sensation of EDS was not reflected in the results of the standardized methods for the assessment of EDS. In the ESS scale EDS was found in 20% of the patients. A disturbed vigilance was found in the vigilance task in 32% of the patients. CONCLUSION: Subjective feeling of EDS is common in patients treated with antipsychotics. The ESS scale allows to verify the patients' claims. EDS resulting from disturbed or shortened sleep, should be differentiated from sedation resulting from pharmacological treatment and fatigue that may be related to somatic or mental disorders.

REM sleep behaviour disorder in narcolepsy.

BACKGROUND AND PURPOSE: Narcolepsy is characterized by excessive daytime sleepiness, cataplexy, sleep paralysis and hypnagogic hallucinations. The aim of the study was to evaluate the incidence of REM sleep behaviour disorder (RBD) in consecutive patients with narcolepsy referred to our sleep disorders centre. MATERIAL AND METHODS: Among patients examined because of hypersomnia, a diagnosis of narcolepsy was established in 30 patients (mean age 34.1 +/-13.6; 13 females, 17 males) on the basis of clinical features, polysomnography (PSG) and Multiple Sleep Latency Test. Polysomnographic analysis included assessment of muscle activity during REM sleep, recorded from chin and anterior tibialis muscles. Video recordings were reviewed for intense motor activity during REM periods, manifested as excessive, violent body movements (especially legs) and vocalization, reflecting dream-enacting behaviour. Questions about RBD symptoms were asked as a standard in all newly diagnosed patients and those reporting for follow-up visits. RESULTS: Symptomatic, polysomnographically documented RBD was found in three patients. In one of them RBD symptoms appeared during anticataplectic treatment with antidepressive medications. Disturbances of muscle tone regulation during REM sleep without clinical symptoms were found in polysomnography in a further four patients. Among patients reporting for follow-up visits, three subjects confirmed clinical symptoms corresponding to RBD of various severity. CONCLUSIONS: RBD occurs in narcolepsy more frequently than it was previously considered. Questions about symptoms of this disorder that may be injurious for the patient or patient's bed partner should be routinely asked during the clinical interview.

[Cardiac, respiratory and sleep disorders in patients with myotonic dystrophy]. / Zagrozenia kardiologiczne i oddechowe oraz zaburzenia snu u pacjentów z dystrofia miotoniczna.

Myotonic dystrophy (MD) is a genetically determined disease with autosomal dominant mode of inheritance. Relatively recently, MD has been divided into two sub-types (MD1 and MD2). Clinical symptoms of MD1 result from the expansion of a (CTG)n trinucleotide of the gene coding for serine/threonine protein kinase and clinical symptoms in MD2 are associated with the expansion of (CCTG)n in I intron of the zinc-finger protein 9 (ZNF9). Myotonic dystrophies MD1 and MD2 are multisystem diseases with numerous symptoms and high interfamily variability, resulting from the fact that different organs are affected. Until now the mechanisms that lead to the damage of the central and peripheral nervous systems, heart muscle and endocrine system have not been fully understood. Symptoms that are characteristic of MD1 and MD2 are myotonic symptom, muscular weakness and muscular atrophy. In MD2, muscular weakness and muscular atrophy are expressed more significantly in proximal segments, which is a differentiating factor for patients with MD1 who have muscular weakness and muscular atrophy in distal segments. Apart from myotonia and symptoms of skeletal muscle damage, the disease affects smooth muscles, heart muscle and the central nervous system, causing cataract, endocrine disorders, cognitive dysfunctions, intellectual and personality disturbances as well as sleep disordered breathing with nocturnal hypoventilation, obstructive, central and mixed apneas and hypopneas. The symptoms of sleep disordered breathing is fatigue, reduced cognitive performance and excessive daytime sleepiness. The pathophysiology of the breathing disorders includes weakness of the respiratory muscles and disorder of the respiratory drive. Of some interest are the works in which authors evaluated the incidence and character of abnormalities in the peripheral and central nervous systems. It has been shown that the number of CTG-repeats in the same person with MD1 is not stable over time and may increase, which leads to disease progression and new clinical symptoms. Cardiologic disorders associated with myotonic dystrophy are common and are part of the clinical picture of the disease. The dominant pathology are conduction disturbances and cardiac arrhythmias. It is estimated that 40 to 80% of patients with MD1 have abnormalities in ECG, and rapid supra-ventricular and ventricular cardiac arrhythmias are the second common cause of death in patients with MD1. Unfortunately, most of these pathologies are asymptomatic until life-threatening conduction blocks and/or supra-ventricular tachyarrhythmias occur. Sometimes, prodromal symptoms such as collapsing, fainting or feeling of palpitation occur and they should always draw attention of the treating doctor of a patient with muscular dystrophy. This paper is aimed at characterizing some common cardiologic and sleep related respiratory disorders of patients with myotonic dystrophy which if not recognized in good time may lead to sudden death.

Electroencephalogram slowing, sleepiness and treatment response in patients with schizophrenia during olanzapine treatment.

Electroencephalogram (EEG) slowing is associated with clozapine side effects, e.g., sedation, and may predict treatment response during clozapine treatment. As olanzapine and clozapine share many pharmacological properties, we investigated whether EEG slowing during olanzapine treatment was related to therapy outcome and sleepiness in patients with schizophrenia. Participants were age- and gender-matched schizophrenic patients treated with olanzapine (n 54), receiving no pharmacological treatment (n 54), or cotreated with olanzapine and some other psychotropic drug (n 38). Their EEG recordings were assessed visually by the same rater blind to clinical data. The EEG scores were categorized using standardized forms. Patients with a poor treatment response did not differ significantly from those with a good response to treatment either in EEG patterns or in frequency of sleepiness. Olanzapine treatment was associated with increased rates of slow (70.4% vs. 22.3%) and sharp waves (22.2% vs. 7.4%), as well as of paroxysmal slow wave discharges (14.8% vs. 1.9%), but did not induce spike- or sharp-slow-wave complexes. Cotreatment with another antipsychotic further increased EEG abnormalities, whereas benzodiazepine administration diminished the olanzapine-induced EEG changes. The results show that olanzapine inducing both slow and sharp waves, as well as paroxysmal discharges, has a strong impact on EEG. However, as no spike- or sharp-slow-wave complexes were observed, the risk of epileptic seizure during olanzapine treatment can be regarded as low, as long as olanzapine is not combined with some other antipsychotic.

[Spinocerebellar ataxias type 1 and 2: comparison of clinical, electrophysiological and magnetic resonance evaluation]. / Ataksja rdzeniowo-mózdzkowa typu 1 i 2 - porównanie oceny klinicznej, elektrofizjologicznej i rezonansu magnetycznego.

BACKGROUND AND PURPOSE: Spinocerebellar ataxias type 1 (SCA1) and type 2 (SCA2) belong to neurodegenerative disorders of autosomal dominant inheritance, genetically and clinically heterogeneous, caused by the expansion of CAG trinucleotides. Trunk and limb ataxia, dysarthria, dysphagia, gaze palsy, sensory and motor axonal neuropathy are the dominant features in both entities. The aim of the study was to evaluate the differences between genotype and phenotype based on clinical and electrophysiological assessment of the visual, auditory pathways, and EEG alterations in comparison with the cerebellar and brain atrophy in MRI. MATERIAL AND METHODS: 44 patients with SCA1 and 24 cases with SCA2 confirmed molecularly were examined neurologically and using the International Cooperative Ataxia Rating Scale (ICARS). A correlation of clinical symptoms and signs, and CAG repeat numbers with EEG, visual (VEP) and brainstem auditory (BAEP) evoked potentials, and MRI alterations were evaluated. RESULTS: A statistically significant negative correlation between the age of disease onset and number of CAG repeats in both types of SCA was found. Examined patients with SCA2 were younger, with longer disease duration and more pronounced cerebellar and brain atrophy in MRI. We found a significant correlation between ICARS and CAG repeats in this group. The dysphagia, pyramidal tract involvement and depressive reaction were significantly frequent in SCA1 patients. However in SCA2 patients, the peripheral nerve damage and extrapyramidal signs were more prominent. The amplitude of P100 visual evoked potentials was significantly lower in SCA1 patients and negatively correlated with CAG repeats. CONCLUSIONS: These results provide further evidence for the phenotypic differences of genetically defined SCA1 and SCA2 patients, expressed by more frequent involvement of the pyramidal tract and depression reaction in SCA1, in contrast to peripheral nerve involvement and extrapyramidal signs in the clinical feature of SCA2 phenotype. Furthermore, atrophy of the brain and cerebellum revealed in MRI was more pronounced than electrophysiological functional alterations, especially in SCA2. The decreased amplitude of P100 VEP in SCA1 patients was the only electrophysiological parameter differentiating between both groups of patients.

[Clinical and genetic study of juvenile form of Huntington's disease]. / Badania kliniczne i genetyczne w mlodzienczej postaci choroby Huntingtona.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by high instability and extension of CAG sequences within the coding region of IT15 gene. It affects both sexes and age at onset of the disease may be different but usually occurs in midlife. The term Juvenile Huntington's disease is generally applied to 10% of the cases with onset before 20. We present clinical features and results of DNA analysis in 16 patients from 14 families aged 9 to 36. The age of onset was between 5 to 20 years; duration of the disease was from 2 to 16 years. In 10 cases the mutated gene was transmitted by the affected father; only in two cases by the mother. In all cases anticipation manifested by earlier onset of the disease in subsequent generations and expansion of CAG repeats was documented. The number of CAG repeats was between 50 and 92 (mean 67.3). Progressive mental deterioration, declining school performance, hyperactivity and emotional disturbances were the first symptoms of juvenile HD. Neuropsychological assessment showed mean IQ in Wechsler test 59.6 and Mini-Mental State Examination scores 22.8. Rigidity and bradykinesia were predominant features in the cases with juvenile onset, the remaining ones developed choreatic movements. Three persons had epileptic seizures; two (both females) revealed behaviour and psychiatric disturbances. Amplitudes of somatosensory evoked potentials, visual evoked potentials and brainstem auditory evoked potentials were markedly reduced. MRI of the brain showed atrophy of heads of the caudate nuclei, putamen and globus pallidus.