Refers to the consciousness after an epileptic seizure.
The postictal state manifests as seizure-induced reversible alterations in neuronal function but not structure.
The postictal state usually lasts between 5 and 30 minutes.
It can sometimes last longer in the case of more severe seizures.
It presence is characterized by drowsiness, confusion, nausea, hypertension, headache or migraine, and other disorienting symptoms.
The emergence from this state is often accompanied by amnesia or other memory defects.
It is the period of brain recovery from the trauma of the seizure.
The ictal period refers to the seizure itself.
The interictal period reflects the time between seizures, when brain activity is more normal.
The preictal period is the time leading up to a seizure.
The interictal state corresponds to more than 99% of life.
EEGs often show small interictal spiking and other abnormalities to be subclinical seizures.
Following a seizure mental and physical exhaustion may be experienced for one-two days.
Postictally the most common complaint is the inability to think clearly, to have a poor attention span, and decreased concentration, with poor short term memory, decreased verbal and interactive skills, and other cognitive defects specific to individuals.
Postictal migraine headaches are a major complaint among persons with epilepsy, and may be due to high intracranial pressure resulting from postictal cerebral edema.
Depression is common after a seizure, as is anxiety.
Todd’s paresis is a temporary regional loss of function postictally in the region just experienced the seizure.
Todd’s paresis loss of motor function can range from weakness to full paralysis.
Among patients who experience tonic-clonic seizures 6% have Todd’s paresis afterward: with loss of motor function sometimes accompanied with temporary numbness, blindness, or deafness.
Postictally anterograde amnesia can occur if the seizure includes the bilateral hippocampi.
Postictally aphasia can occur if the seizures began in the language-dominant hemisphere.
Symptoms typically last about 15 hours, but can continue for 36 hours.
Postictal psychosis is a neuropsychiatric sequel to seizures of chronic epilepsy, that occur with bilateral seizure types and is characterized by auditory and visual hallucinations, delusions, paranoia, affective change, and aggression.
After postictal confusion and lethargy, the patient gradually recovers to a normal lucid state.
Postictal psychosis, can continue at least 6 hours or up to a week followed by the psychosis lasting 12 hours to more than 3 months.
Postictal psychosis is typically treated using atypical antipsychotics and benzodiazepines.
Epilepsy surgery can also resolve the psychotic episodes.
Postictal euphoria has been also reported following seizures.
Absence seizures do not produce a postictal state.
The lack of typical postictal symptoms, such as confusion and lethargy following a seizures suggests alternative diagnoses.
The postictal state can also help determining the focus of the seizure.
Seizures in the dominant hemisphere, are associated with decreased verbal memory.
Seizures in the non-dominant hemisphere manifest with decreased visual memory.
Inability to read after a seizure suggests seizure foci in the language areas of the left hemisphere.
Following a seizure semivoluntary movements tend to be done with the hand ipsilateral to the seizure site.
The ability of the neuron to carry an action potential following a seizure is not decreased.
There are four hypotheses regarding what cellular and molecular mechanisms cause the observed postictal systems:
neurotransmitter depletion
changes in receptor concentration
active inhibition
cerebral bloodflow changes.
No evidence for neurotransmitter depletion following seizures has been identified.
Opioid receptors are upregulated in the regions near the focus of the seizure during the ictal phase, gradually returning to baseline availability during the postictal phase.
After seizures regional bloodflow can increase by as much as 70-80%, but normalizes after 30 minutes.
The presence of leftover inhibitory signals may explain a period in which the threshold for provoking a second seizure is high, and lowered excitability may account for some of the postictal symptoms.
Inhibitory signals could be through GABA receptors, calcium-activated potassium receptors, or other changes in ion channels or signal receptors.
These changes would likely have a residual effect for a short time after successfully ending the high activity of neurons: lasting seconds to minutes, but cannot account for the fog that lasts for hours after a seizure.
Acidosis of the blood could aid in ending the seizure and also depress neuron firing following its conclusion.
Acidosis occurs as a result of sustained tonic-clonic seizures they outpace oxygen supplies and go into anaerobic metabolism, with the cells undergoing lactic acidosis.
Hydrogen ions compete with other ions at the ion channel associated with N-methyl-d-aspartate (NMDA), and
may partially attenuate NMDA receptor and channel mediated hyperexcitability after seizures.
Cerebral autoregulation typically ensures that perfusion matches metabolism in all organs; especially in the brain.
Sometimes following a seizure cerebral blood flow is not proportionate to the necessary metabolic needs.