A considerable number of theories exist as to the pathophysiology: *Epileptiform discharges in the diencephalon, or the interbrain, are a potential theory for PSH. These discharges can be identified using electroencephalography. *Increased intracranial pressure is another theory. Currently, this theory seems to be less likely than the others. Intracranial pressure has been seen to have no correlation to PSH episodes. *Disconnection via lesions of the inhibitory efferent pathways from cortical and subcortical areas of the brain is a potential theory. This theory deals with inhibitory pathways being ablated or malfunctioning post-injury. This leads to sympathetic pathways from the cortical and subcortical areas being less controlled, resulting in a 'sympathetic storm'. *Excitatory-inhibitory models suggest that lesions in the mesencephalic area lessen inhibition pathways from the brain. This is thought to lead to pathways that are usually non-nociceptive becoming nociceptive, which results in the peripheral sympathetic nervous system being over activated. *Another theory deals with malfunction of the brainstem, specifically excitatory centers in the brainstem. In this case, rather than inhibitory pathways malfunctioning and allowing sympathetic pathways to propagate unhindered, excitatory centers are up-regulated, increasing sympathetic activity. There are many theories dealing with the pathophysiology of<unk> . It is possible that none or multiple of these theories are correct. Research that is being conducted on PSH is focused on figuring out these pathways.
Paroxysmal sympathetic hyperactivity
Cholinergic crisis
Parasympathetic rebound
Postural orthostatic tachycardia syndrome
False awakening
Postanesthetic shivering
Heat syncope
Thalamocortical dysrhythmia