Nicholas-Tiberio Economou

Sleep in frontotemporal dementia is equally or possibly more disrupted, and at an earlier stage, when compared to sleep in Alzheimer's disease.

BACKGROUND Conversely to other neurodegenerative diseases (i.e., Alzheimers disease, AD), sleep in frontotemporal dementia (FTD) has not been studied adequately. Although some evidence exists that sleep-wake disturbances occur in FTD, very little is known regarding sleep macrostructure and/or primary sleep disorders. OBJECTIVE To investigate these issues in this population and compare them to similar issues in AD and in healthy elderly (HE). METHODS Twelve drug-naïve behavioral-variant FTD (bvFTD) patients (7 men/5 women) of mean age 62.5 ± 8.6 years were compared to seventeen drug-naïve AD patients (8 men/9 women) of mean age 69.0 ± 9.9 years and twenty drug-naïve HE (12 men/8 women) of mean age 70.2 ± 12.5 years. All participants were fully assessed clinically, through a sleep questionnaire, an interview, and video-polysomnography recordings. RESULTS The two patient groups were comparably cognitively impaired. However, compared to FTD patients, the AD patients had a statistically significant longer disease duration. Overall, the sleep profile was better preserved in HE. Sleep complaints did not differ considerably between the two patient groups. Sleep parameters and sleep macrostructure were better preserved in AD compared to FTD patients, regardless of primary sleep disorders, which occurred equally in the two groups. CONCLUSIONS With respect to AD, FTD patients had several sleep parameters similarly or even more affected by neurodegeneration, but in a much shorter time span. The findings probably indicate a centrally originating sleep deregulation. Since in FTD patients sleep disturbances may be obvious from an early stage of their disease, and possibly earlier than in AD patients, physicians and caregivers should be alert for the early detection and treatment of these symptoms.

Development of Parkinson and Alzheimer diseases in two cases of narcolepsy-cataplexy.

Case 1 A 69-year-old Caucasian male, suffering from NC since the age of 17, presented to us at the age of 64 years (in 2006). His history included EDS with sleep attacks, hallucinations, frequent cataplexy and occasional sleep paralysis. Patient’s psychomotor development was normal and clinical history unremarkable; in particular, he denied infectious or inflammatory cerebral diseases, head trauma and exposure to toxic agents. During his NC history, the patient underwent several drug treatments (methylphenidate, modafinil, dexedrine, imipramine) with partial benefit on EDS and cataplexy. At that time, he presented the typical HLA haplotype (HLA DQB1 * 0602), undeDear Sir, Narcolepsy (NC) is a sporadic hypersomnia (prevalence 1: 2,000), characterized by excessive daytime sleepiness (EDS) and sleep attacks, typically associated with cataplexy and other REM-sleep related phenomena such as sleep paralysis and hallucinations [1] . In human NC with cataplexy, an association with specific HLA haplotype (DR DQB1 0602) and a deficiency in hypocretin (orexin) peptide in cerebrospinal fluid (CSF) are almost constant findings. The pathogenesis of human NC is still unknown. Autoimmune and neurodegenerative processes of hypothalamic structures have been discussed with more solid evidence for the first theory [2–4] . Most of narcoleptic symptoms develop early after the onset of the disease and usually do not worsen with the progression of the neurodegeneration [2] . Moreover, the absence of ubiquitinated inclusions (cardinal neuropathological finding of most neurodegenerative diseases) in narcoleptic patients argues against the neurodegenerative hypothesis in NC [3] . An autoimmune process involving the hypocretin neurons of lateral hypothalamus has been postulated [4] . There are few reports in the literature showing the occurrence of NC-like symptoms in patients already affected by Parkinson’s disease (PD) and other neurodegenerative diseases [2, 5–7] . Hypocretin neuronal loss has been documented in Received: July 18, 2011 Accepted: October 30, 2011 Published online: December 10, 2011

Performance evaluation of an Artificial Neural Network automatic spindle detection system

Sleep spindles are transient waveforms found in the electroencephalogram (EEG) of non-rapid eye movement (NREM) sleep. Sleep spindles are used for the classification of sleep stages and have been studied in the context of various psychiatric and neurological disorders, such as Alzheimers disease (AD) and the so-called Mild Cognitive Impairment (MCI), which is considered to be a transitional stage between normal aging and dementia. The visual processing of wholenight sleep EEG recordings is tedious. Therefore, various techniques have been proposed for automatically detecting sleep spindles. In the present work an automatic sleep spindle detection system, that has been previously proposed, using a Multi-Layer Perceptron (MLP) Artificial Neural Network (ANN), is evaluated in detecting spindles of both healthy controls, as well as MCI and AD patients. An investigation is carried also concerning the visual detection process, taking into consideration the feedback information provided by the automatic detection system. Results indicate that the sensitivity of the detector was 81.4%, 62.2%, and 83.3% and the false positive rate was 34%, 11.5%, and 33.3%, for the control, MCI, and AD groups, respectively. The visual detection process had a sensitivity rate ranging from 46.5% to 60% and a false positive rate ranging from 4.8% to 19.2%.

EEG-based investigation of brain connectivity changes in psychotic patients undergoing the primitive expression form of dance therapy: a methodological pilot study

Primitive expression (PE) is a form of dance therapy (DT) that involves an interaction of ethologically and socially based forms which are supplied for re-enactment. There exist very few studies of DT applications including in their protocol the measurement of neurophysiological parameters. The present pilot study investigates the use of the correlation coefficient (ρ) and mutual information (MI), and of novel measures extracted from ρ and MI, on electroencephalographic (EEG) data recorded in patients with schizophrenia while they undergo PE DT, in order to expand the set of neurophysiology-based approaches for quantifying possible DT effects, using parameters that might provide insights about any potential brain connectivity changes in these patients during the PE DT process. Indication is provided for an acute potentiation effect, apparent at late-stage PE DT, on the inter-hemispheric connectivity in frontal areas, as well as for attenuation of the inter-hemispheric connectivity of left frontal and right central areas and for potentiation of the intra-hemispheric connectivity of frontal and central areas, bilaterally, in the transition from early to late-stage PE DT. This pilot study indicates that by using EEG connectivity measures based on ρ and MI, the set of useful neurophysiology-based approaches for quantifying possible DT effects is expanded. In the framework of the present study, the causes of the observed connectivity changes cannot be attributed with certainty to PE DT, but indications are provided that these measures may contribute to a detailed assessment of neurophysiological mechanisms possibly being affected by this therapeutic process.

CPAP and quality of life: A still unresolved issue

In their recent study on ‘‘Health related quality of life (QoL) in Greek patients with sleep apnea–hypopnea syndrome treated with continuous positive airway pressure,” Tsara and colleagues [1] found an impaired QoL at baseline and a significant improvement following 3 months of CPAP therapy in sleep apnea–hypopnea syndrome (SAHS) patients. This is a well acknowledged observation, but replication on a Greek population is welcome and therefore of merit. Several issues, however, may limit the significance of their findings. First, the authors report data from a prospective study of unselected, consecutive SAHS patients who were screened only for respiratory diseases but not for other diseases, co-morbidities (e.g., chronic medical or neuropsychiatric conditions), concomitant medications or even for other sleep disorders [2,3], which may seriously affect QoL [3] and therefore influence their results. Second, it would have been more interesting to study outcome in SAHS following a longer treatment period than 3 months. In a recent meta-analysis [4] on the impact of CPAP treatment on general QoL it is suggested that long-term trials are able to provide more solid evidence on this issue and that such studies are important because of their ability to capture important information regarding persistence of benefits from CPAP. Thus, studies with longer follow-ups [2,5] are crucial given the debatable advantage of CPAP over conservative treatment [4,6]. Third, data on the outcome of the GHQ-30 in the 3-month follow-up of the patients who underwent conservative therapy are not explicitly presented, which does not allow for clear comparisons between the two types of treatment. Finally, due to the large difference in sample size between the two treatment subgroups on the 3-month follow-up (140 patients on CPAP vs. 15 patients on conservative therapy), a power calculation of the statistical comparisons should be provided.

Sleepiness, fatigue, anxiety and depression in Chronic Obstructive Pulmonary Disease and Obstructive Sleep Apnea – Overlap – Syndrome, before and after continuous positive airways pressure therapy

Patients with Chronic Obstructive Pulmonary Disease (COPD) and / or Obstructive Sleep Apnea (OSA) often complain about sleepiness, fatigue, anxiety and depression. However, common screening questionnaires, like Epworth Sleepiness Scale (ESS), Fatigue Severity Scale (FSS) and Hospital Anxiety and Depression Scale (HADS) have not been previous evaluated in patients with overlap–coexisting COPD and OSA–syndrome versus patients with OSA alone. Our study compared ESS, FSS and HADS between patients with overlap syndrome and patients with OSA, before and after treatment with Continuous Positive Airways Pressure (CPAP). We examined 38 patients with coexisting COPD and OSA versus 38 patients with OSA-only and 28 subjects without respiratory disease, serving as controls. All patients underwent pulmonary function tests (PFTs), oximetry and overnight polysomnography and completed the questionnaires, before and after 3 months of CPAP therapy. The two patient groups did not differ significantly in terms of age, Body Mass Index (BMI), neck, waist and hip circumferences, and arterial blood pressure values. They also had similar comorbidities. They differed significantly, as expected, in PFTs (Forced Vital Capacity–FVC, 2.53±0.73 vs 3.08±0.85 lt, p = 0.005, Forced Expiratory Volume in 1sec–FEV1, 1.78±0.53 vs 2.60±0.73 lt/min, p<0.001) and in daytime oximetry (94.75±2.37 vs 96.13±1.56%, p = 0.007). ESS, HADS–Anxiety and HADS–Depression scores did not differ statistically significant between these two groups, whereas overlap syndrome patients expressed significantly more fatigue (FSS) than OSA-only patients, a finding that persisted even after 3 months of CPAP therapy. We conclude that sleepiness, anxiety and depression were similar in both groups, whereas fatigue was more prominent in patients with overlap syndrome than in sleep apneic patients and did not ameliorate after treatment.

Intrusion of rapid eye movement (REM) behavior disorder episodes into NREM sleep in a case of Lewy body dementia

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Sleep-Related Drug Therapy in Special Conditions: Children

see front matter 2012 Elsevier B.V. All rights reserved. doi:10.1016/j.sleep.2012.08.018 ⇑ Corresponding author. Address: Neurology Department, Neurocenter of Southern Switzerland, Via Tesserete 46, Lugano 6900, Switzerland. Tel.: +41 (0)91 811 6825; fax: +41 (0)91 811 6915. E-mail address: nt_economou@yahoo.it (N.-T. Economou). will be enriched by the contributions of our colleagues who wish to offer stimulating opportunities for discussion and new insights into the field of sleep.

Agomelatine may improve REM sleep behavior disorder symptoms.

Sleep disorders in children may lead to neurodevelopmental and neurocognitive deficits; it is important to diagnose and treat them properly. Apart from the existing challenges in diagnosis, another drawback is that few therapies are currently approved. In this article, a comprehensive summary of the most common pediatric sleep disorders, along with the various pharmacologic and nonpharmacologic approaches for their management, is presented. Special attention has been paid to the currently available treatment options for pediatric insomnia, obstructive sleep apnea, parasomnias, narcolepsy, and restless legs syndrome, and comparisons are made with the corresponding treatment options for sleep disorders in adults.