The functional role of dreaming in emotional processes

Dream experience (DE) represents a fascinating condition linked to emotional processes and the human inner world. Although the overlap between REM sleep and dreaming has been overcome, several studies point out that emotional and perceptually vivid contents are more frequent when reported upon awakenings from this sleep stage. Actually, it is well-known that REM sleep plays a pivotal role in the processing of salient and emotional waking-life experiences, strongly contributing to the emotional memory consolidation. In this vein, we highlighted that, to some extent, neuroimaging studies showed that the processes that regulate dreaming and emotional salience in sleep mentation share similar neural substrates of those controlling emotions during wakefulness. Furthermore, the research on EEG correlates of the presence/absence of DE and the results on EEG pattern related to the incorporated memories converged to assign a crucial role of REM theta oscillations in emotional re-processing. In particular, the theta activity is involved in memory processes during REM sleep as well as during the waking state, in line with the continuity hypothesis. Also, the gamma activity seems to be related to emotional processes and dream recall as well as to lucid dreams. Interestingly, similar EEG correlates of DE have been found in clinical samples when nightmares or dreams occur. Research on clinical samples revealed that promoting the rehearsal of frightening contents aimed to change them is a promising method to treat nightmares, and that lucid dreams are associated with an attenuation of nightmares. In this view, DE can defuse emotional traumatic memories when the emotional regulation and the fear extinction mechanisms are compromised by traumatic and frightening events. Finally, dreams could represent a sort of simulation of reality, providing the possibility to create a new scenario with emotional mastery elements to cope with dysphoric items included in nightmares. In addition, it could be hypothesized that the insertion of bizarre items besides traumatic memories might be functional to “impoverish” the negative charge of the experiences

Conceitos atuais no tratamento das ataxias hereditárias

Hereditary ataxias (HA) represents an extensive group of clinically and genetically heterogeneous neurodegenerative diseases, characterized by progressive ataxia combined with extra-cerebellar and multi-systemic involvements, including peripheral neuropathy, pyramidal signs, movement disorders, seizures, and cognitive dysfunction. There is no effective treatment for HA, and management remains supportive and symptomatic. In this review, we will focus on the symptomatic treatment of the main autosomal recessive ataxias, autosomal dominant ataxias, X-linked cerebellar ataxias and mitochondrial ataxias. We describe management for different clinical symptoms, mechanism-based approaches, rehabilitation therapy, disease modifying therapy, future clinical trials and perspectives, genetic counseling and preimplantation genetic diagnosis.As ataxias hereditárias representam um grupo complexo de doenças neurodegenerativas, e se caracterizam por ataxia cerebelar progressiva, associada a sinais e sintomas extra-cerebelares e sistêmicos, os quais incluem: neuropatia periférica, sinais piramidais, distúrbios do movimento, convulsões e disfunção cognitiva. Não existe um tratamento efetivo para a cura das ataxias hereditárias. Até o momento os tratamentos disponíveis são apenas sintomáticos. Nesta revisão vamos abordar tratamento sintomático das principais ataxias autossômicas recessivas, ataxias autossômicas dominantes, ataxias ligadas ao X e ataxias mitocondriais. Descrevemos os diferentes sintomas, abordagens terapêuticas baseadas no mecanismo fisiopatológico, terapia de reabilitação, terapia modificadora da doença, futuros ensaios clínicos, perspectivas, níveis de evidência, aconselhamento genético e diagnóstico genético pré-implantacional.74324425

Conceitos Atuais No Tratamento Das Ataxias Hereditárias

Hereditary ataxias (HA) represents an extensive group of clinically and genetically heterogeneous neurodegenerative diseases, characterized by progressive ataxia combined with extra-cerebellar and multi-systemic involvements, including peripheral neuropathy, pyramidal signs, movement disorders, seizures, and cognitive dysfunction. There is no effective treatment for HA, and management remains supportive and symptomatic. In this review, we will focus on the symptomatic treatment of the main autosomal recessive ataxias, autosomal dominant ataxias, X-linked cerebellar ataxias and mitochondrial ataxias. We describe management for different clinical symptoms, mechanismbased approaches, rehabilitation therapy, disease modifying therapy, future clinical trials and perspectives, genetic counseling and preimplantation genetic diagnosis. © 2016, Associacao Arquivos de Neuro-Psiquiatria. All rights reserved.74324425

Conceitos atuais no tratamento das ataxias hereditárias

Hereditary ataxias (HA) represents an extensive group of clinically and genetically heterogeneous neurodegenerative diseases, characterized by progressive ataxia combined with extra-cerebellar and multi-systemic involvements, including peripheral neuropathy, pyramidal signs, movement disorders, seizures, and cognitive dysfunction. There is no effective treatment for HA, and management remains supportive and symptomatic. In this review, we will focus on the symptomatic treatment of the main autosomal recessive ataxias, autosomal dominant ataxias, X-linked cerebellar ataxias and mitochondrial ataxias. We describe management for different clinical symptoms, mechanism-based approaches, rehabilitation therapy, disease modifying therapy, future clinical trials and perspectives, genetic counseling and preimplantation genetic diagnosis.Hereditary ataxias (HA) represents an extensive group of clinically and genetically heterogeneous neurodegenerative diseases, characterized by progressive ataxia combined with extra-cerebellar and multi-systemic involvements, including peripheral neuropat743244252sem informaçãosem informaçãoAs ataxias hereditárias representam um grupo complexo de doenças neurodegenerativas, e se caracterizam por ataxia cerebelar progressiva, associada a sinais e sintomas extra-cerebelares e sistêmicos, os quais incluem: neuropatia periférica, sinais pirami

Exploring Addictive Online Behaviors in Patients with Narcolepsy Type 1

Background: Narcolepsy type 1 (NT1) is a rare neurological sleep disorder caused by the loss of neurons that produce hypocretin—a peptide that plays a crucial role in addictive behaviors. We aimed to compare, for the first time, levels of problematic online gaming, problematic social media use, and compulsive Internet use between NT1 patients and healthy controls (HC), and to evaluate the association between anxiety, depression, and emotion dysregulation with addictive online behaviors in NT1 patients. Methods: A total of 43 patients with NT1 and 86 sex- and age-matched HC participated in an online cross-sectional survey. Results: NT1 patients did not differ from HC in terms of problematic social media use and compulsive Internet use but displayed higher levels of problematic online gaming compared to HC. Higher levels of emotion dysregulation were significantly associated with higher levels of problematic social media use and compulsive Internet use, while none of the tested factors were associated with problematic online gaming. Conclusion: NT1 patients and HC had similar levels of problematic social media use and compulsive Internet use, but NT1 patients showed higher levels of problematic online gaming. Emotion dysregulation might be an intervention target for reducing compulsive Internet use and problematic social media use

Narcolepsy beyond sleepiness : endocrine, metabolic and other aspects

The thesis contains a large study in which eight male hypocretin deficient narcolepsy with cataplexy patients and eight matched controls were enrolled. Blood was sampled before and on the 5th day of SXB administration. SXB was taken 2 times 3g per night for 5 consecutive nights. Both groups underwent 24-h blood sampling and many hormones (prolactin, Growth hormone, melatonin, ghrelin, leptin) were measured and compared before and during SXB treatment. A study using the golden standard on insuline sensitivity is decribed to compare insuline sensitivity between patients and controls, and between patients, before and during satisfactory SXB treatment. ANother study describes body and skintemperature differences between narcolepsy patients and controls. Another chapter describes a rarely described, common feature in narcolepsy, in which patients mistake the memory of a dream for a real experience. In another chapter describes that date of birth is not a risk factor for narcolepsy.SEIN, UCB Pharma, Koninklijke Auping, Wave Medical, Nederlandse vereniging voor Narcolepsie, Nederlandse vereniging voor slaap- en waak onderzoek, Heinen en Löwenstein, ChipsoftUBL - phd migration 201

Adult neurogenesis in the orexin/ataxin-3 mouse

Introduction: The adult mammalian brain retains neural stem cells (NSCs) that continually generate new neurons within two restricted regions, the subventricular zone (SVZ) of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus in the hippocampus (HC). This process is called adult neurogenesis. Controlled stimulation of endogenous neurogenesis might be an elegant way to treat neurodegenerative diseases. It is therefore important to understand the molecular signals, which govern the proliferation, migration, and differentiation of endogenous NSCs in the neurogenic niches. Regulatory mechanisms in the so-called neurogenic niches have already been shown by in vivo studies for various factors, including numerous neurotransmitters, and behavioral and environmental factors. However, our knowledge is still insufficient to exploit adult neurogenesis for controlled brain repair or for stimulation of its physiological function. The sleep disorder narcolepsy is considered to be a neurodegenerative disease because there is a massive progressive loss of neurons containing the neuropeptide orexin. Consequently narcoleptic patients have very low cerebrospinal fluid levels of orexin. Narcolepsy is defined as a sleep-wake disorder with REM and non-REM sleep associated symptoms existing longer than 6 months, such as daytime sleepiness, cataplexy, fractionated sleep at night and automatic behaviors. The postulated pathophysiology of human narcolepsy is mimicked very closely in a transgenic mouse model called orexin/ataxin-3 mouse, in which orexin-containing neurons are ablated progressively by specific overexpression of a truncated cytotoxic ataxin-3 gene product under the orexin-promoter. Aim: We aimed to study the possible role of the protein orexin in the regulation of adult neurogenesis in the orexin/ataxin-3 mouse. Study design: Adult neurogenesis in the SGZ, SVZ and rostral migratory stream (RMS), where the cells migrate from the SVZ to the olfactory bulb (OB), was studied by immunohistology. For the evaluation of the stem cell proliferation in SVZ and SGZ and migration in the RMS, orexin/ataxin-3 mice (n = 8) and wild type (WT) mice (n = 8) received a single intraperitoneal injection of 100 mg BrdU (bromodeoxyuridine)/kg body weight 2 hour prior to sacrifice. For the analysis of differentiation and survival of newly built cells, BrdU was administered intraperitoneally on 5 consecutive days once per day to orexin/ataxin-3 mice (n = 8) and WT mice (n = 8) and they were sacrificed 30 days after the last injection. Results: We found a significantly higher proliferation of stem/precursor cells in the orexin/ataxin-3 mice in both neurogenic regions, the SGZ and the SVZ. Also in the RMS, higher levels of newly built cells in the orexin/ataxin group were found, but these differences were not significant. We were able to demonstrate a significantly higher survival of newly built cells in the granular zone, but not for the periglomerular zone of the OB in the orexin/ataxin group. A tendency for higher survival rates could be shown for the HC of the orexin/ataxin-3 mice (not significant). By triple staining we could show that the proportion of newly born neurons relative to the total number of newly built cells in the HC was significantly higher with 90 % in the orexin-ataxin group compared to 83 % in the control group. In both the granular zone and the periglomerular zone of the OB, over 90 % of the total amount of new built cells differentiated into neurons in both groups. Also the rate of differentiation into a dopaminergic phenotype of the newly born neurons in the periglomerular zone of the OB was not significantly changed with 93 % in the orexin/ataxin-3 mice compared to 91 % in the WT mice. Conclusion: In the absence of orexin in the adult mouse brain, the proliferation of adult neural stem/precursor cells was increased, the survival rate was significantly increased in the granular zone of the OB and a consistent not significant trend was seen in the HC. The proportion of newborn neurons among all newly born cells was higher in the HC, however, no significant differences in the differentiation of newly built cells could be found in the OB. Together, these observations lead to the assumption that orexin suppresses the proliferation of adult NSC, affects the survival rate in the OB negatively and hinders the differentiation of newly built cells into neurons in the HC

“It’s like tumbleweeds everywhere”: An Interpretative Phenomenological Analysis of the lived experience of being diagnosed with and living with narcolepsy

There is a lack of awareness of how sleep health and sleep disorders are experienced. Previous research has found that living with narcolepsy has a debilitating impact on several areas of an individual’s life alongside significant diagnostic delays. This study uses a phenomenological, qualitative methodology to explore experiences of being diagnosed with and living with narcolepsy. Six women with type 1 narcolepsy participated in semi-structured interviews. Transcripts were analysed using Interpretative Phenomenological Analysis. Capturing the whole illness experience of narcolepsy, our analysis illuminated three superordinate themes; ‘minimising, dismissing and downplaying symptoms’, ‘navigating the winding journey to diagnosis’ and ‘a different way of living’. Through our analysis, we are able to demonstrate the affective impact lack of awareness of sleep and sleep disorders has; resulting in significant diagnostic delays and a lack of support post-diagnosis. Findings demonstrate a need for greater awareness and increased support