Some of the earliest work in treating sleep paralysis was done using a culturally sensitive cognitive-behavior therapy called CA-CBT. The work focuses on psycho-education and modifying catastrophic cognitions about the sleep paralysis attack. This approach has previously been used to treat sleep paralysis in Egypt, although clinical trials are lacking.

The first published psychosocial treatment for recurrent isolated sleep paralysis was cognitive-behavior therapy for isolated sleep paralysis (CBT-ISP). CBT-ISP is manualized, has an adherence manual for research purposes, and is intended to both prevent and disrupt ISP episodes. It begins with self-monitoring of symptoms, cognitive restructuring of maladaptive thoughts relevant to ISP (e.g., "the paralysis will be permanent"), and psychoeducation about the nature of sleep paralysis. Prevention techniques include ISP-specific sleep hygiene and the preparatory use of various relaxation techniques (e.g. diaphragmatic breathing, mindfulness, progressive muscle relaxation, meditation). Episode disruption techniques are first practiced in session and then applied during actual attacks. No controlled trial of CBT-ISP has yet been conducted to prove its effectiveness.

Though no large trials have taken place which focus on the treatment of sleep paralysis, several drugs have promise in case studies. Two trials of GHB for people with narcolepsy demonstrated reductions in sleep paralysis episodes.

Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.

Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal. In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the edematous cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion.

Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome. Lower extremity function is more spared than that of the faciobrachial region. The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely. Middle cerebral artery lesions mostly affect the dominant hemisphere i.e. the left cerebral hemisphere.

Note: *faciobrachial deficits greater than that of the lower limb