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Insomnia in neurological disorders: Prevalence, mechanisms, impact and treatment approaches.

Insomnia is more prevalent in neurological disorders compared to the general population, with rates ranging from 11 to 74.2% in neurodegenerative disorders, 20 to 37% in vascular diseases, 13.3 to 50% in inflammatory diseases, 28.9 to 74.4% in epilepsy, and nearly 70% in migraines. Insomnia in neurological disorders stems from a variety of factors, encompassing physical and neuropsychiatric factors, behavioral patterns, and disruptions in the biological clock and circadian rhythm. There are bidirectional connections between neurological disorders and insomnia. Insomnia in neurological disorders worsens symptoms, resulting in heightened depressive symptoms, elevated mortality rates, reduced quality of life, and intensified acute symptoms. Managing comorbid sleep disorders, especially in the presence of psychiatric comorbidities, is crucial. Cognitive behavioral therapy for insomnia (CBT-I) is the first-line recommendation for insomnia management in neurological disorders. Other treatments are second-line strategies. Melatonin may demonstrate effectiveness in addressing insomnia, with soporific and chronobiotic effects. Furthermore, it has the potential to alleviate "sundowning" and behavioral disturbances, while generally being well-tolerated. Other treatment options that may be of interest include morning bright light therapy, sedative antidepressants, new orexin dual antagonists and levodopa specifically indicated for Parkinson's disease. Benzodiazepines and z-drugs can be used primarily during acute phases to prevent pharmacotolerance and minimize side effects. However, they should be avoided in patients with neurological disorders and not used in patients over 75 years old due to the risk of falls and confusion. In neurological disorders, insomnia has a profound impact on daytime functioning, making its management crucial. Effective treatment can result in improved outcomes, and additional research is necessary to investigate alternative therapeutic options and enhance patient care.

The effectiveness and safety of non-pharmacological intervention for pain management in Parkinson's disease: A systematic review.

Chronic pain is a non-motor symptom affecting from 60 to 80% of patients with Parkinson's disease (PD). PD patients can suffer from different types of pain, either specific or not specific of the disease, and depending on various pathophysiological mechanisms (nociceptive, nociplastic or neuropathic), which can be present at any stage of the disease. Non-pharmacological interventions (NPIs) are essential to complement routine care interventions in PD pain management. Moreover, in the literature, it has been shown that 42% of PD patients are already using complementary therapies. Hence, our aim was to investigate the effectiveness and safety of NPIs for pain management in PD. A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Eighteen published randomized control trials (RCTs) were included between 2004 and 2021 leading to a total of 976 PD patients. From them, we reported fifteen different NPIs classified in seven categories: physical exercises, balneotherapy, manual therapy, acupuncture, botanical preparation, body-psychological practice and multiprotection care. Our results have shown that NPIs for PD pain management had a low-to-moderate level of evidence showing mainly favourable results, even if some NPIs presented inconclusive results. Moreover, our review highlighted the clinical relevance of some specific NPIs in PD pain management: NPIs consisting of active physical activities, opposed to passive activities. The safety of NPIs was also confirmed since only few minor transient adverse events were reported. Nevertheless, even if some interesting results were found, the methodology of future studies needs to be more robust and to include comprehensive descriptions in order to offer reliable and sound recommendations to clinicians.

How we sleep: From brain states to processes.

All our lives, we alternate between wakefulness and sleep with direct consequences on our ability to interact with our environment, the dynamics and contents of our subjective experience, and our brain activity. Consequently, sleep has been extensively characterised in terms of behavioural, phenomenological, and physiological changes, the latter constituting the gold standard of sleep research. The common view is thus that sleep represents a collection of discrete states with distinct neurophysiological signatures. However, recent findings challenge such a monolithic view of sleep. Indeed, there can be sharp discrepancies in time and space in the activity displayed by different brain regions or networks, making it difficult to assign a global vigilance state to such a mosaic of contrasted dynamics. Viewing sleep as a multidimensional continuum rather than a succession of non-overlapping and mutually exclusive states could account for these local aspects of sleep. Moving away from the focus on sleep states, sleep can also be investigated through the brain processes that are present in sleep, if not necessarily specific to sleep. This focus on processes rather than states allows to see sleep for what it does rather than what it is, avoiding some of the limitations of the state perspective and providing a powerful heuristic to understand sleep. Indeed, what is sleep if not a process itself that makes up wake up every morning with a brain cleaner, leaner and less cluttered.

Open Access
Narcolepsies, update in 2023.

Narcolepsy type 1 (NT1) and type 2 (NT2), also known as narcolepsy with and without cataplexy, are sleep disorders that benefited from major scientific advances over the last two decades. NT1 is caused by the loss of hypothalamic neurons producing orexin/hypocretin, a neurotransmitter regulating sleep and wake, which can be measured in the cerebrospinal fluid (CSF). A low CSF level of hypocretin-1/orexin-A is a highly specific and sensitive biomarker, sufficient to diagnose NT1. Orexin-deficiency is responsible for the main NT1 symptoms: sleepiness, cataplexy, disrupted nocturnal sleep, sleep-related hallucinations, and sleep paralysis. In the absence of a lumbar puncture, the diagnosis is based on neurophysiological tests (nocturnal and diurnal) and the presence of the pathognomonic symptom cataplexy. In the revised version of the International Classification of sleep Disorders, 3rd edition (ICSD-3-TR), a sleep onset rapid eye movement sleep (REM) period (SOREMP) (i.e. rapid occurrence of REM sleep) during the previous polysomnography may replace the diurnal multiple sleep latency test, when clear-cut cataplexy is present. A nocturnal SOREMP is very specific but not sensitive enough, and the diagnosis of cataplexy is usually based on clinical interview. It is thus of crucial importance to define typical versus atypical cataplectic attacks, and a list of clinical features and related degrees of certainty is proposed in this paper (expert opinion). The time frame of at least three months of evolution of sleepiness to diagnose NT1 was removed in the ICSD-3-TR, when clear-cut cataplexy or orexin-deficiency are established. However, it was kept for NT2 diagnosis, a less well-characterized disorder with unknown clinical course and absence of biolo biomarkers; sleep deprivation, shift working and substances intake being major differential diagnoses. Treatment of narcolepsy is nowadays only symptomatic, but the upcoming arrival of non-peptide orexin receptor-2 agonists should be a revolution in the management of these rare sleep diseases.