On returning to normality there is no memory of what has occurred during the trance. In psychic terms, this is a deliberately desired trance-like state when a medium is in a state of deep hypnosis and taken over by some other intelligence, which uses the medium's body to speak and act. As opposed to suspended animation or coma, respiration and heart rate are virtually normal. Intentional cataleptic states may be induced by pressure on certain arteries, by occult techniques or by drugs. Catalepsy may arise in a number of nervous disorders, being characteristic of hysteria it also occurs in some forms of schizophrenia or it may result from emotional shock. The person is unconscious (as opposed to the cataplexic state) and may remain in the state for several days. Even if the limbs may be moved, they remain exactly where they are placed. Subcoereulus vlPAG, ventrolateral periaqueductal grey.Description: The characteristics of this deep trance are rigidity of the limbs and insensitivity to pain. 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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