Editing Morvan's syndrome (section)

===Insomnia===
In all of the reported cases, the need for [[sleep]] was severely reduced and in some cases not necessary.  The duration of sleep in one case decreased to about 2–4 hours per 24-hour period.<ref name=indian/>  Clinical features pertaining to insomnia include daytime drowsiness associated with a loss of ability to sleep, intermingled with confusional oneiric status, and the emergence of atypical [[Rapid eye movement sleep|REM]] sleep from wakefulness.  The [[polysomnogram]] (PSG) picture of this disease is characterized by an inability to generate physiological sleep (key features are the suppression of the hallmarks of stage 2 non-REM sleep: spindles and K complexes) and by the emergence of REM sleep without [[atonia]].  The involvement of the [[thalamus]] and connected limbic structures in the pathology indicate the prominent role that the limbic thalamus plays in the pathophysiology of sleep.<ref name=oneiricisms/>  In a case documented in 1974, PSG findings documented the sustained absence of all sleep rhythms for up to a period of 4 months.<ref name=agrypnia/>

[[Electroencephalography]] (EEG) in one case was dominated by "[[wakefulness]]" and “subwakefulness” states alternating or intermingled with short (< 1 min) atypical REM sleep phases, characterized by a loss of muscle atonia.  The “subwakefulness” state was characterized by 4–6&nbsp;Hz theta activity intermingled with fast activity and desynchronized lower voltage theta activity, behaviourally associated with sleep-like somatic and autonomic behavior.  The subject was said to have “agrypnia excitata”, which consists of severe total insomnia of long duration associated with decreased vigilance, mental confusion, hallucinations, motor agitation, and complex motor behavior mimicking dreams, and autonomic activation.  CNS and autonomic symptoms were caused by impaired corticolimbic control of the subcortical structures regulating the sleep-wake and autonomic functions.<ref name=cardiac/>