dear Abdulhafeez (sorry I changed your name!): suposedly is caused by either activation of sympathic autonomic system or/and excessive motor  activity. On occasions potictal hyprthermia is part of febrile seizures and might be considered as a phenotype feature of some Na channelopathies, such as mutations on SCNA1 gene

Dear Abdulhafeez,

I would postulate that post-seizure fever may be due to tissue (e.g. muscle) damage due to excessive and powerful involuntary contractions of the muscle due to synaptic hyperactivity.  Although part of this heat energy may arise directly from the excessive muscle contractions, the prolonged fever is likely due to activation of immune system in response to tissue damage.

best wishes,

Refik

In addition to the suggestions above one can speculate that the  hypothalamic temperature setpoint is increased  by unknown  circulating "substances" and or neural input. we have limited knowledge   about the control of the temperature setpoint - just think about  cyclic hotflushes during menopause. 

Although fever may induce seizures especially among children but its occurance following epileptic episodes is rare but then again since the response of the human body is different in every stress. Excessive muscle contractility would activate hypothalmus and release of C-reative protiens in unknown amount or other substance may alter the set point. Quite possible, there can be some idiopathic increase in pyrogenic substances via other some latent underlying pathology. Autonomic system disorders should always be considered among generalised symptoms.

post ictal hyperthermia is due to combination of factors, out of which excessive muscle activity and autonomic surge are the important one. contribution of hypothalamus is also proposed in different studies

Thank you all for sharing your thoughts.

In my opinion a manyfold response needed: violent muscle contraction leads to hyperthermia, as seen in exercise, hard physical work, etc.. But given there is also leucocytosis, elements of the stereotyped stress reaction add. There may be even other more telencephalic mechanisms implied. Interestingly, similar phenomena can be observed in migraine attacks.

Quite possible as well. Thank you.

Dear Dr. A.Hafeez M Khair 

Your question is very informative and interesting. The postictal changes in general are explained by the cellular and molecular mechanisms whereby changes occur in concentration of receptors and transmitters, active inhibition and cerebral blood flow. This indicates that neurons still generate action potentials even after status epilepticus. 

Although fever in children may cause seizures, the occurrence of fever after epileptic seizures or by transient GABA A activity impairment in susceptible people, and due to of repetitive muscular contractions or homeostatic deregulations in status epilepticus or other types of generalized seizures showing convulsions,   shows a  rare symptom exclusively peri-ictally, except  generalized convulsive status epilepticus. 

Fever that is a physiological response eliciting upregulation of central homeostatic control, differs from hyperthermia that occurs without resetting the temperature centre. Changes in temperature following non-convulsive seizures may occur by gene upregulation in hypothalamus, nucleus tractus solitaries and other brain areas. Hence, considering pathophysiology of fever and seizure spread, less consistency of direct propagation of discharges appears with the timing of symptogenesis.

Seizures occurring in view of febrile involvement might indicate an infectious etiology and postictal symptom in view of repetitive occurrence. The most common causes in this respect are: fever, inflammation or malignancy.

Post-ictal cause  either as activation of sympathetic autonomic system or/and excessive motor  activity/ phenotype feature of some Na channelopathies, such as mutations on SCNA1 gene suggested by Dr Antonio Gil-Nagel; response of excessive motor activity and activation of immune system as explained by Dr Refik Kanjhan; suggestion by Dr Marianne Thoresen as hypothalamic temperature setpoint increase  by unknown  circulating "substances" and or neural input; role of excessive muscle contractility activating hypothalamus, and CRP / other substances altering setpoint, idiopathic increase in pyogenic substances via latent pathology/ autonomic system disorders as suggested by Dr. Nehan Syed; contribution of excessive muscle activity/ autonomic involvement and prominent role of hypothalamus suggested by Dr Arshad Yahya; violent muscle contarction, leukocytosis and telencephalon mechanisms suggested by Dr Dirk Ulbricht; and appreciating suggestion of Dr Ghulam Md Ashraf, all these and other creative thoughts for post-ictal convulsive or non-convulsive seizures are quite interesting factors explaining the pathophysiological mechanisms for the development of occasional pyrexia in post epileptic seizures.

Regards…

It is as a results of tissue damages which may elicit immunological changes leading to release of cytokines which will show up as fever in the patients.