Pathophysiology Of Cataplexy

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The muscle atonia seen in cataplexy is the result of postsynaptic hyperpolar-ization of the spinal cord motor neurons, with active inhibition of muscle tone (Glen et al., 1978). The spinal cord makes no essential contribution to the muscle atonia of cataplexy or normal REM sleep. Lesions of the ventral quadrant of the spinal cord, especially the ventrolateral funiculus corresponding to the ventrolateral reticulo spinal tract, inhibit muscle atonia. Because there is a strong analogy in man and dog between cataplexy and the muscle atonia seen during normal REM sleep, it may be that similar final pathways are involved. Siegel (1985) has shown in the cat, using transection experiments and cellular unit activity recordings, that pontine and medullary mechanisms are needed to produce muscle atonia. If transection is made at the pontomedullary junction, no muscle atonia is seen, while in midbrain decerebrate cats, complete bilateral inhibition of the antigravity muscles is seen. Therefore, pontine mechanisms contribute to medullary induction of atonia.

It has been shown that chemical destruction of the locus ceruleus a (LCa) and the perilocus ceruleus a (peri-LCa) neurons with local injections of kainic or ibotenic acid result in permanent abolition of muscle atonia and REM sleep (Sakai, 1985). Thus, the dorsolateral pontine tegmentum seems to be involved in the muscle atonia of REM sleep. LCa and peri-LCa appear to contain cholinergic neurons and receive noradrenergic afferents from the LC complex.

In summary, while we understand that the central neurological defects responsible for cataplexy ultimately impact the spinal cord motor neurons, causing hyperpolarization and active inhibition of muscle tone, investigations of receptors in the brains of narcoleptic humans and dogs have yet to fully explain the etiology of the disease.

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