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. Numerous other accommodation solutions may exist.Cataplexy is the pathognomonic symptom of narcolepsy, and is the sudden uncontrollable onset of skeletal muscle paralysis or weakness during wakefulness. The following is only a sample of the possibilities available. Be aware that not all people with cataplexy will need accommodations to perform their jobs and many others may only need a few accommodations. Also, the degree of limitation will vary among individuals. People with cataplexy may develop some of the limitations discussed below, but seldom develop all of them. For more information about how to determine whether a person has a disability under the ADA, see How to Determine Whether a Person Has a Disability under the Americans with Disabilities Act Amendments Act (ADAAA). Instead, the ADA defines a person with a disability as someone who (1) has a physical or mental impairment that substantially limits one or more "major life activities," (2) has a record of such an impairment, or (3) is regarded as having such an impairment. The ADA does not contain a definitive list of medical conditions that constitute disabilities. Cataplexy and the Americans with Disabilities Act Some of the most common limitations stemming from a cataplectic attack are weakened speech, vision issues, trouble balancing, upper extremity weakness, and/or collapsing. While a cataplectic attack is usually very short in duration and leaves no residual effects, there may be symptoms that would require workplace accommodations. Other symptoms may include balance issues, upper extremity weakness, and/or collapsing. Some people with narcolepsy can have cataplectic attacks almost daily, while there are some people with narcolepsy that have never experienced cataplexy.ĭuring a cataplectic attack the person will remain conscious however, the person may experience jaw dropping, which can cause speech limitations, or eyelids drooping, which can interfere with vision. These episodes tend to have few, if any, residual effects. Most episodes are short in duration, lasting a few seconds up to five minutes. Cataplexy by itself is considered a rare disease. Cataplexy is the sudden loss of voluntary muscle tone or temporary paralysis that is often triggered by extreme emotion, such as laughter or fear.
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