12/10/2023 0 Comments Narcolepsy without cataplexy 347.00![]() We review recent anatomical and physiological evidence for the role of histamine and hypocretin in normal sleep–wake behaviours, as well as recent findings concerning their involvement in a variety of pathologies, including narcolepsy, Alzheimer disease (AD), Parkinson disease (PD), Huntington disease (HD) and Tourette syndrome (TS). 7– 12 This Review focuses on the contribution of histamine and hypocretin to the control of the sleep–wake cycle. 5, 6īoth histamine and hypocretin have been implicated in the modulation of brain functions, such as sleep–wake regulation, energy and endocrine homeostasis, reward-motivated behaviours and motor functions. 4 Recently, two groups reported a massive increase in the number of histamine neurons in narcolepsy type 1. By contrast, patients with narcolepsy type 2 (initially called narcolepsy without cataplexy) also demonstrate mean sleep latencies of ≤8 min and at least two sleep-onset REM periods, but do not experience cataplexy, have normal CSF levels of hypocretin peptide 1 (if tested), and their hypersomnolence and/or sleep latency findings cannot be better described by another cause. In narcolepsy type 1 (also called hypocretin deficiency syndrome or narcolepsy with cataplexy), patients demonstrate one or both of the following: cataplexy plus mean sleep latencies of ≤8 min and at least two sleep-onset rapid eye movement (REM) periods on a multiple sleep latency test, and/or low levels of hypocretin peptide 1 (≤110 pg/ml) in the cerebrospinal fluid (CSF). Narcolepsy is diagnosed in patients who have a daily irrepressible need for sleep. The discovery of this hypocretin deficiency led to a change in the International Classification of Sleep Disorders, with the ‘narcolepsy’ category being divided into ‘narcolepsy type 1’ and ‘narcolepsy type 2’. ![]() More than a decade ago, two groups 2, 3 identified loss of hypocretin neurons as the cause of human narcolepsy with cataplexy. In normal individuals, hypocretin neurons are present throughout the hypothalamus. 1 The posterior hypothalamus is a heterogeneous structure that includes neurons containing histamine, glutamate, γ-aminobutyric acid (GABA), hypocretin (also known as orexin) and melanin-concentrating hormone (MCH). The involvement of the posterior hypothalamus in the maintenance of wakefulness was first recognized during an encephalitis lethargica epidemic (1918–1926) by the neurologist von Economo, who described extreme sleepiness associated with damage to this area. The hypothalamus is a brain area with a critical role in the control of autonomic function and sleep. ![]() Finally, we discuss novel therapeutic approaches for manipulation of the histamine system. We also review the changes in the hypocretin and histamine systems, and the associated sleep disruptions, in Parkinson disease, Alzheimer disease, Huntington disease and Tourette syndrome. Furthermore, we summarize the neuropathological changes to these two systems in narcolepsy and discuss the possibility that narcolepsy-associated histamine abnormalities could mediate or result from the same processes that cause the hypocretin cell loss. Here, we review the role of the histamine and hypocretin systems in sleep–wake modulation. In narcolepsy, 90% of hypocretin neurons are lost in addition, two groups reported in 2014 that the number of histamine neurons is increased by 64% or more in human patients with narcolepsy, suggesting involvement of histamine in the aetiology of this disorder. Narcolepsy type 1, also known as narcolepsy with cataplexy, is a neurological disorder characterized by excessive daytime sleepiness, impaired night-time sleep, cataplexy, sleep paralysis and short latency to rapid eye movement (REM) sleep after sleep onset. Histamine and hypocretin neurons are localized to the hypothalamus, a brain area critical to autonomic function and sleep.
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