Postictal state

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(Redirected from
Postictal
)
Not to be confused with
icteric
.

The postictal state is the

drowsiness, confusion, nausea, hypertension, headache or migraine
, and other disorienting symptoms.

The

ictal
period is the seizure itself; the interictal period is the time between seizures, when brain activity is more normal; and the preictal period is the time leading up to a seizure:

  • Ictal period refers to a physiologic state or event such as a seizure, stroke, or headache. The word originates from the Latin word ictus, meaning a blow or a stroke. In electroencephalography (EEG), the recording during a seizure is said to be "ictal". The following definitions refer to the temporal relation with seizures.[1]
  • Pre-ictal refers to the state immediately before the actual seizure, stroke, or headache.
  • Post-ictal refers to the state shortly after the event.
  • Interictal refers to the period between seizures, or
    subclinical seizures
    . Interictal EEG discharges are those abnormal waveforms not associated with seizure symptoms.

Signs and symptoms

short term memory, decreased verbal and interactive skills, and a variety of cognitive defects specific to individuals."[3]

Postictal migraine headaches are a major complaint among persons with

migraines is high intracranial pressure resulting from postictal cerebral edema. At times, a person may be unaware of having had a seizure, and the characteristic migraine is their only clue.[3]

Other symptoms associated with the postictal state are less common.

tonic-clonic seizures experienced Todd's paresis afterward, with loss of motor function sometimes accompanied with temporary numbness, blindness, or deafness.[3] Todd's paresis can also cause anterograde amnesia if the seizure included the bilateral hippocampi, and aphasia if the seizures began in the language-dominant hemisphere.[2] Symptoms typically last about 15 hours, but can continue for 36 hours.[3]

Postictal psychosis is a neuropsychiatric sequel to seizures of chronic epilepsy in adults. Tending to occur with bilateral seizure types it is characterized by auditory and visual

delusions, paranoia, affective change, and aggression. Following the typical postictal confusion and lethargy, the person gradually recovers to a normal lucid state. In persons who experience postictal psychosis, this "lucid phase" usually continues at least 6 hours (and up to a week) followed by the psychosis lasting as little as one hour to more than 3 months (the mean is 9–10 days). The psychosis is typically treated medically using atypical antipsychotics and benzodiazepines, and successful epilepsy surgery can resolve the psychotic episodes.[4]

Postictal bliss or euphoria is also reported following seizures. This has been described as a highly blissful feeling associated with the emergence from amnesia. Feelings of depression before a seizure may lead to postictal euphoria.[5]

Some of postictal symptoms are almost always present for a period of a few hours up to a day or two.

Absence seizures do not produce a postictal state[6] and some seizure types may have very brief postictal states. Otherwise, the lack of typical postictal symptoms, such as confusion and lethargy following convulsive seizures, may be a sign of non-epileptic seizures. Usually such seizures are instead related to syncope or have a psychogenic origin ("pseudoseizures").[3]

The postictal state can also be useful for determining the focus of the seizure. Decreased verbal memory (short term) tends to result from a seizure in the dominant hemisphere, whereas seizures in the non-dominant hemisphere tend to manifest with decreased visual memory. Inability to read suggests seizure foci in the language areas of the left hemisphere, and "after a seizure semivoluntary events as mundane as nose wiping tend to be done with the hand ipsilateral to [that is, on the same side as,] the seizure focus."[3]

Mechanism

While it might seem that the neurons become “exhausted” after the near-constant firing involved in a seizure, the ability of the neuron to carry an action potential following a seizure is not decreased. Neurons of the brain fire normally when stimulated, even after long periods of status epilepticus.[3]

Neurotransmitters

Neurotransmitters must be present in the axon terminal and then exocytosed into the synaptic cleft in order to propagate the signal to the next neuron. While neurotransmitters are not typically a limiting factor in neuronal signaling rates, it is possible that with extensive firing during seizures neurotransmitters could be used up faster than new ones could be synthesized in the cell and transported down the axon. There is currently no direct evidence for neurotransmitter depletion following seizures.[3]

Receptor concentration

In studies that stimulate seizures by subjecting rats to

opiate receptors may be occurring during seizures and may be partially responsible for the weariness humans experience following a seizure. When humans were given naloxone in-between seizures, researchers observed increased activity on their EEGs, suggesting that opioid receptors may also be upregulated during human seizures.[3] To provide direct evidence for this, Hammers et al. did positron emission tomography (PET) scanning of radiolabelled ligands before, during, and after spontaneous seizures in humans. They found that opioid receptors were upregulated in the regions near the focus of the seizure during the ictal phase, gradually returning to baseline availability during the postictal phase.[7] Hammers notes that cerebral bloodflow after a seizure can not account for the increase in PET activity observed. Regional bloodflow can increase by as much as 70-80% after seizures but normalizes after 30 minutes. The shortest postictal interval in their study was 90 minutes and none of the patients had seizures during the scanning. It has been predicted that a decrease in opioid activity following a seizure could cause withdrawal symptoms, contributing to postictal depression. The opioid receptor connection with mitigating seizures has been disputed, and opioids have been found to have different functions in different regions of the brain, having both proconvulsive and anticonvulsive effects.[3]

Active inhibition

It is possible that seizures cease spontaneously, but it is much more probable that some changes in the brain create inhibitory signals that serve to tamp down the overactive neurons and effectively end the seizure. Opioid peptides have been shown to be involved in the postictal state and are at times anticonvulsive, and adenosine has also been implicated as a molecule potentially involved in terminating seizures. Evidence for the theory of active inhibition lies in the postictal refractory period, a period of weeks or even months following a series of seizures in which seizures cannot be induced (using animal models and a technique called kindling, in which seizures are induced with repeated electrical stimulation).[2]

Leftover inhibitory signals are the most likely explanation for why there would be a period in which the threshold for provoking a second seizure is high, and lowered excitability may also explain some of the postictal symptoms. Inhibitory signals could be through

GABA receptors (both fast and slow IPSPs), calcium-activated potassium receptors (which give rise to afterhyperpolarization), hyperpolarizing pumps, or other changes in ion channels or signal receptors.[3]

While not an example of active inhibition,

NMDA). This competition may partially attenuate NMDA receptor and channel mediated hyperexcitability after seizures.”[3]

Cerebral bloodflow

Cerebral

hypoperfusion
in the affected area, a possible explanation for the confusion and ‘fog’ patients experience following a seizure.

See also

References

  1. PMID 21447894. Archived from the original
    on 18 June 2015. Retrieved 22 July 2021.
  2. ^
    LCCN 89007930. Retrieved 22 July 2021 – via Google Books
    .
  3. ^
    S2CID 20393636. Archived from the original
    on 2 June 2018. Retrieved 22 July 2021.
  4. PMID 18330462
    .
  5. ^ Engel 2013, p. 332, Chapter 9: Periictal PhenomenaQuote: "Patients who are aware of increased depression or tension prior to generalized tonic-clonic or limbic seizures occasionally report a feeling of euphoria or release during the postictal period[...] [P]atients with interictal or preictal depression can report relief or euphoria postictally, which is consistent with the well-known beneficial effect of electroconvulsive shock therapy (ECT). Postictal hypomania can occur, particularly after repeated limbic seizures."
  6. PMID 20821849. Archived from the original on 21 January 2011. Retrieved 22 July 2021 – via NCBI (National Center for Biotechnology Information)/NLM (United States National Library of Medicine)
    . Absence ... seizures begin and end suddenly. There is no warning before the seizure, and immediately afterward the person is alert and attentive. This lack of a postictal period is a key feature that allows one to distinguish between absence and partial complex seizures.
  7. PMID 17301080. Archived from the original
    on 2 June 2018. Retrieved 22 July 2021.
  8. PMID 9098212
    . Retrieved 22 July 2021.
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