We recently discovered, using Fos immunostaining, that the tuberal and mammillary hypothalamus contain a massive population of neurons specifically activated during paradoxical sleep (PS) hypersomnia. We further showed that some of the activated neurons of the tuberal hypothalamus express the melanin concentrating hormone (MCH) neuropeptide and that icv injection of MCH induces a strong increas...

We report on patients with post-traumatic fatigue and hypersomnia who showed injury of the lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation (RF) and the intralaminar thalamic nucleus (ILN) following mild traumatic brain injury (TBI), using diffusion tensor tractography (DTT).Two patients with mild TBI resulting from a car accident were en...

Abstract Introduction Idiopathic hypersomnia (IH) is a rare neurologic disorder that can cause debilitating symptoms, including excessive daytime sleepiness, severe sleep inertia, prolonged nighttime sleep, long and unrefreshing naps, cognitive dysfunction. Limited research has investigated the clinical burden associated with IH. This study compared profile of patients diagnosed IH versus match...

STUDY OBJECTIVES To evaluate the prevalence and natural history of sleepiness following traumatic brain injury. METHODS This prospective cohort study used the Sickness Impact Profile to evaluate sleepiness in 514 consecutive subjects with traumatic brain injury (TBI), 132 non-cranial trauma controls, and 102 trauma-free controls 1 month and 1 year after injury. RESULTS Fifty-five percent of...

Sleep disorders are very prevalent in the general population and are associated with significant medical, psychological, and social disturbances. Insomnia is the most common. When chronic, it usually reflects psychological/behavioral disturbances. Most insomniacs can be evaluated in an office setting, and a multidimensional approach is recommended, including sleep hygiene measures, psychotherap...

Primary hypersomnia, a rare clinical syndrome, was diagnosed in a 14-year-old boy. The syndrome showed partial response to high dose fluoxetine therapy (120 mg/day) which recruited insomnia, an adverse effect of the drug, for therapeutic purposes. Response was enhanced with intermittent methylphenidate in association with a lower dose of fluoxetine. A possible pharmacokinetic interaction develo...