Patients often do fall asleep rapidly but are unable to stay asleep for more than a few hours at a time. Hypnagogic hallucinations – vivid, sometimes disturbing dreamlike experiences that occur while dozing, falling asleep and/or upon awakening.Īutomatic behavior – a person continues to function or talk while being half asleep, and awakens with no memory of doing these activities.ĭifficulties maintaining sleep – Nighttime sleep is disturbed. Sleep paralysis - the temporary inability to talk or move when waking it may last a few seconds to minutes. Cataplexy is a cardinal symptom as it almost always indicates that the cause of the narcolepsy is a lack of hypocretin in the brain. While cataplexy can manifest as something as minor as a slight slackening of the facial muscles, in extreme cases, a person may experience total collapse or even muscle paralysis. Subcoereulus vlPAG, ventrolateral periaqueductal grey.Beside excessive daytime sleepiness, patients may display the following symptoms:Ĭataplexy – a sudden weakening of the muscles, often triggered by a strong emotion. Medial medulla mPFC, medial prefrontal cortex REM, rapid eye movement SubC, Locus coeruleus LH, lateral hypothalamus LPT, lateral pontine tegmentum MM, Neuronal activity cancels out the inhibitory effect of amygdalar neurons.Ībbreviations: CeA, central amygdala GABA, γ-aminobutyric acid LC, In healthy individuals, orexin-expressing Muscle paralysis inĬataplexy is also enabled by loss of noradrenergic input from LC neurons, whichĪre inhibited during cataplexy. Neuron circuit, triggering muscle paralysis and cataplexy. LC–vlPAG–LPT circuit, which in turn disinhibits the SubC to motor GABAergic CeA neurons inhibit neurons in the The LC–vlPAG–LPTĬircuit normally prevents muscle paralysis during wakefulness by suppressing theĪctivity of SubC neurons. When a positive emotion is experienced, GABAergic neurons in the CeA switch onĪnd inhibit cells in the LC, vlPAG and LPT. Neurons in the SubC trigger REM paralysis by activating GABAergic or glycinergicĬells in the MM, which in turn project to and inhibit skeletal motor neurons. Two-part brainstem circuit-the SubC and MM connection. Paralysis is thought to underlie cataplexy, and is probably triggered by a Activation during wakefulness of neural circuits involved in REM sleep Hypothetical circuits and pathways controlling cataplexy in the rodentīrain. This Review describes the clinical and pathophysiological aspects of cataplexy, and outlines optimal therapeutic management strategies. Despite major advances in understanding disease mechanisms in cataplexy, therapeutic management is largely symptomatic, with antidepressants and γ-hydroxybutyrate being the most effective treatments. The amygdala and medial prefrontal cortex contain neural pathways through which positive emotions probably trigger cataplectic attacks. Muscle weakness during cataplexy is caused by decreased excitation of noradrenergic neurons and increased inhibition of skeletal motor neurons by γ-aminobutyric acid-releasing or glycinergic neurons. One pathogenetic mechanism that has been hypothesized for cataplexy is the activation, during wakefulness, of brainstem circuitry that normally induces muscle tone suppression in rapid eye movement sleep. This disorder occurs almost exclusively in patients with depletion of hypothalamic orexin neurons. Occurring spontaneously, cataplexy is typically triggered by strong positive emotions such as laughter and is often underdiagnosed owing to a variable disease course in terms of age of onset, presenting symptoms, triggers, frequency and intensity of attacks. Cataplexy is incapacitating because it leaves the individual awake but temporarily either fully or partially paralyzed. Cataplexy is the pathognomonic symptom of narcolepsy, and is the sudden uncontrollable onset of skeletal muscle paralysis or weakness during wakefulness.
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