Postictal state

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The postictal state is the altered state of consciousness after an epileptic seizure. It usually lasts between 5 and 30 minutes, but sometimes longer in the case of larger or more severe seizures, and is characterized by drowsiness, confusion, nausea, hypertension, headache or migraine, and other disorienting symptoms.

Contents

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:

Signs and symptoms

Jerome Engel defines the postictal state as "manifestations of seizure-induced reversible alterations in neuronal function but not structure." [2] Commonly after a seizure, a person feels mentally and physically exhausted for up to one or two days. The most common complaint is an inability to think clearly, specifically "poor attention and concentration, poor 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 epilepsy, and can have a variety of etiologies. One possible cause of these 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. Todd's paresis is a temporary regional loss of function in whatever region just experienced the seizure, and its manifestation depends on where the seizure was located. Loss of motor function is most common and can range from weakness to full paralysis. About 6% of patients who had 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 hallucinations, 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 electroshock, seizures are followed by unconsciousness and slow waves on an electroencephalogram (EEG), signs of postictal catalepsy. Administering the opiate antagonist naloxone immediately reverses this state, providing evidence that increased responsiveness or concentration of the 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, acidosis of the blood could aid in ending the seizure and also depress neuron firing following its conclusion. As muscles contract during tonic-clonic seizures they outpace oxygen supplies and go into anaerobic metabolism. With continued contractions under anaerobic conditions, the cells undergo lactic acidosis, or the production of lactic acid as a metabolic byproduct. This acidifies the blood (higher H+ concentration, lower pH), which has many impacts on the brain. For one, “hydrogen ions compete with other ions at the ion channel associated with N-methyl-d-aspartate (NMDA). This competition may partially attenuate NMDA receptor and channel mediated hyperexcitability after seizures.” [3]

Cerebral bloodflow

Cerebral autoregulation typically ensures that the correct amount of blood reaches the various regions of the brain to match the activity of the cells in that region. In other words, perfusion typically matches metabolism in all organs; especially in the brain, which gets the highest priority. However, following a seizure it has been shown that sometimes cerebral blood flow is not proportionate to metabolism. While cerebral blood flow didn’t change in the mouse hippocampus (the foci of seizures in this model) during or after seizures, increases in relative glucose uptake were observed in the region during the ictal and early postictal periods. [8] Animal models are difficult for this type of study because each type of seizure model produces a unique pattern of perfusion and metabolism. Thus, in different models of epilepsy, researchers have had differing results as to whether or not metabolism and perfusion become uncoupled. Hosokawa’s model used EL mice, in which seizures begin in the hippocampus and present similarly to the behaviors observed in human epileptic patients. If humans show similar uncoupling of perfusion and metabolism, this would result in hypoperfusion in the affected area, a possible explanation for the confusion and ‘fog’ patients experience following a seizure.

See also

Related Research Articles

<span class="mw-page-title-main">Seizure</span> Period of symptoms due to excessive or synchronous neuronal brain activity

A seizure is a period of symptoms due to abnormally excessive or synchronous neuronal activity in the brain. Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness, to shaking movements involving only part of the body with variable levels of consciousness, to a subtle momentary loss of awareness. These episodes usually last less than two minutes and it takes some time to return to normal. Loss of bladder control may occur.

<span class="mw-page-title-main">Myoclonus</span> Involuntary, irregular muscle twitch

Myoclonus is a brief, involuntary, irregular twitching of a muscle, a joint, or a group of muscles, different from clonus, which is rhythmic or regular. Myoclonus describes a medical sign and, generally, is not a diagnosis of a disease. It belongs to the hyperkinetic movement disorders, among tremor and chorea for example. These myoclonic twitches, jerks, or seizures are usually caused by sudden muscle contractions or brief lapses of contraction. The most common circumstance under which they occur is while falling asleep. Myoclonic jerks occur in healthy people and are experienced occasionally by everyone. However, when they appear with more persistence and become more widespread they can be a sign of various neurological disorders. Hiccups are a kind of myoclonic jerk specifically affecting the diaphragm. When a spasm is caused by another person it is known as a provoked spasm. Shuddering attacks in babies fall in this category.

A headache is often present in patients with epilepsy. If the headache occurs in the vicinity of a seizure, it is defined as peri-ictal headache, which can occur either before (pre-ictal) or after (post-ictal) the seizure, to which the term ictal refers. An ictal headache itself may or may not be an epileptic manifestation. In the first case it is defined as ictal epileptic headache or simply epileptic headache. It is a real painful seizure, that can remain isolated or be followed by other manifestations of the seizure. On the other hand, the ictal non-epileptic headache is a headache that occurs during a seizure but it is not due to an epileptic mechanism. When the headache does not occur in the vicinity of a seizure it is defined as inter-ictal headache. In this case it is a disorder autonomous from epilepsy, that is a comorbidity.

<span class="mw-page-title-main">Aura (symptom)</span> Symptom of epilepsy and migraine

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is a seizure.

<span class="mw-page-title-main">Neuroimaging</span> Set of techniques to measure and visualize aspects of the nervous system

Neuroimaging is the use of quantitative (computational) techniques to study the structure and function of the central nervous system, developed as an objective way of scientifically studying the healthy human brain in a non-invasive manner. Increasingly it is also being used for quantitative research studies of brain disease and psychiatric illness. Neuroimaging is highly multidisciplinary involving neuroscience, computer science, psychology and statistics, and is not a medical specialty. Neuroimaging is sometimes confused with neuroradiology.

<span class="mw-page-title-main">Electrocorticography</span> Type of electrophysiological monitoring

Electrocorticography (ECoG), a type of intracranial electroencephalography (iEEG), is a type of electrophysiological monitoring that uses electrodes placed directly on the exposed surface of the brain to record electrical activity from the cerebral cortex. In contrast, conventional electroencephalography (EEG) electrodes monitor this activity from outside the skull. ECoG may be performed either in the operating room during surgery or outside of surgery. Because a craniotomy is required to implant the electrode grid, ECoG is an invasive procedure.

ISAS is an objective tool for analyzing ictal vs. interictal SPECT scans. The goal of ictal SPECT is to localize the region of seizure onset for epilepsy surgery planning. ISAS was introduced and validated in two recent studies. This site is a technical supplement to, which should enable ISAS to be implemented at any center for further study and analysis.

Todd's paresis is focal weakness in a part or all of the body after a seizure. This weakness typically affects the limbs and is localized to either the left or right side of the body. It usually subsides completely within 48 hours. Todd's paresis may also affect speech, eye position (gaze), or vision.

<span class="mw-page-title-main">Generalized tonic–clonic seizure</span> Type of generalized seizure that affects the entire brain

A generalized tonic–clonic seizure, commonly known as a grand mal seizure or GTCS, is a type of generalized seizure that produces bilateral, convulsive tonic and clonic muscle contractions. Tonic–clonic seizures are the seizure type most commonly associated with epilepsy and seizures in general and the most common seizure associated with metabolic imbalances. It is a misconception that they are the sole type of seizure, as they are the main seizure type in approximately 10% of those with epilepsy.

<span class="mw-page-title-main">Euphoria</span> Intense feelings of well-being

Euphoria is the experience of pleasure or excitement and intense feelings of well-being and happiness. Certain natural rewards and social activities, such as aerobic exercise, laughter, listening to or making music and dancing, can induce a state of euphoria. Euphoria is also a symptom of certain neurological or neuropsychiatric disorders, such as mania. Romantic love and components of the human sexual response cycle are also associated with the induction of euphoria. Certain drugs, many of which are addictive, can cause euphoria, which at least partially motivates their recreational use.

<span class="mw-page-title-main">Spike-and-wave</span>

Spike-and-wave is a pattern of the electroencephalogram (EEG) typically observed during epileptic seizures. A spike-and-wave discharge is a regular, symmetrical, generalized EEG pattern seen particularly during absence epilepsy, also known as ‘petit mal’ epilepsy. The basic mechanisms underlying these patterns are complex and involve part of the cerebral cortex, the thalamocortical network, and intrinsic neuronal mechanisms.

Epileptogenesis is the gradual process by which a typical brain develops epilepsy. Epilepsy is a chronic condition in which seizures occur. These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure.

Panayiotopoulos syndrome is a common idiopathic childhood-related seizure disorder that occurs exclusively in otherwise normal children and manifests mainly with autonomic epileptic seizures and autonomic status epilepticus. An expert consensus has defined Panayiotopoulos syndrome as "a benign age-related focal seizure disorder occurring in early and mid-childhood. It is characterized by seizures, often prolonged, with predominantly autonomic symptoms, and by an EEG [electroencephalogram] that shows shifting and/or multiple foci, often with occipital predominance."

Migralepsy is a rare condition in which a migraine is followed, within an hour period, by an epileptic seizure. Because of the similarities in signs, symptoms, and treatments of both conditions, such as the neurological basis, the psychological issues, and the autonomic distress that is created from them, they individually increase the likelihood of causing the other. However, also because of the sameness, they are often misdiagnosed for each other, as migralepsy rarely occurs.

Forced Normalization (FN) is a psychiatric phenomenon in which a long term episodic epilepsy or migraine disorder is treated, and, although the electroencephalogram (EEG) appears to have stabilized, acute behavioral, mood, and psychological disturbances begin to manifest. If, or when, treatment for the disorder is halted, the disturbances go away, but the episodic spikes on the EEG reappear. H. Landolt coined the term 'Forced Normalization' in 1953 in response to a change he witnessed in epileptic EEGs, which monitor electrical activity in the brain. These changes were followed by abrupt behavioral changes in the patient. Landolt concluded that forced normalization is "the phenomenon characterized by the fact that, with the occurrence of psychotic states, the electroencephalography becomes more normal or entirely normal, as compared with previous and subsequent EEG findings." Forced normalization, as described by Landolt, was therefore an electrophysiological phenomenon with the electroencephalograph at its helm.

Idiopathic childhood occipital epilepsy of Gastaut (ICOE-G) is a pure but rare form of idiopathic occipital epilepsy that affects otherwise normal children and adolescents. It is classified amongst benign idiopathic childhood focal epilepsies such as rolandic epilepsy and Panayiotopoulos syndrome.

<span class="mw-page-title-main">Ulegyria</span> Type of cortical scarring deep in the sulci

Ulegyria is a diagnosis used to describe a specific type of cortical scarring in the deep regions of the sulcus that leads to distortion of the gyri. Ulegyria is identified by its characteristic "mushroom-shaped" gyri, in which scarring causes shrinkage and atrophy in the deep sulcal regions while the surface gyri are spared. This condition is most often caused by hypoxic-ischemic brain injury in the perinatal period. The effects of ulegyria can range in severity, although it is most commonly associated with cerebral palsy, mental retardation and epilepsy. N.C. Bresler was the first to view ulegyria in 1899 and described this abnormal morphology in the brain as “mushroom-gyri." Although ulegyria was first identified in 1899, there is still limited information known or reported about the condition.

A neonatal seizure is a seizure in a baby younger than age 4-weeks that is identifiable by an electrical recording of the brain. It is an occurrence of abnormal, paroxysmal, and persistent ictal rhythm with an amplitude of 2 microvolts in the electroencephalogram,. These may be manifested in form of stiffening or jerking of limbs or trunk. Sometimes random eye movements, cycling movements of legs, tonic eyeball movements, and lip-smacking movements may be observed. Alteration in heart rate, blood pressure, respiration, salivation, pupillary dilation, and other associated paroxysmal changes in the autonomic nervous system of infants may be caused due to these seizures. Often these changes are observed along with the observance of other clinical symptoms. A neonatal seizure may or may not be epileptic. Some of them may be provoked. Most neonatal seizures are due to secondary causes. With hypoxic ischemic encephalopathy being the most common cause in full term infants and intraventricular hemorrhage as the most common cause in preterm infants.

<span class="mw-page-title-main">Occipital epilepsy</span> Medical condition

Occipital epilepsy is a neurological disorder that arises from excessive neural activity in the occipital lobe of the brain that may or may not be symptomatic. Occipital lobe epilepsy is fairly rare, and may sometimes be misdiagnosed as migraine when symptomatic. Epileptic seizures are the result of synchronized neural activity that is excessive, and may stem from a failure of inhibitory neurons to regulate properly.

Computational models in epilepsy mainly focus on describing an electrophysiological manifestation associated with epilepsy called seizures. For this purpose, computational neurosciences use differential equations to reproduce the temporal evolution of the signals recorded experimentally. A book published in 2008, Computational Neuroscience in Epilepsy. summarizes different works done up to this time. The goals of using its models are diverse, from prediction to comprehension of underlying mechanisms.

References

  1. ↑ Mula, Marco; Monaco, Francesco (23 March 2011). Cavanna, A.E.; Trojano, Luigi (eds.). "Ictal and peri-ictal psychopathology". Behavioural Neurology . 24 (1). London, England, United Kingdom: Hindawi: 21–25. doi:10.3233/ben-2011-0314. ISSN   0953-4180. OCLC   37773567. PMC   5377957 . PMID   21447894. Archived from the original on 18 June 2015. Retrieved 22 July 2021.
  2. 1 2 3 Engel, Jerome Jr. (2013) [1989]. Seizures and Epilepsy. Conteporary neurology series (2nd ed.). Oxford, England, United Kingdom: Oxford University Press. ISBN   9780803632011. LCCN   89007930 . Retrieved 22 July 2021– via Google Books.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 Fisher, Robert S.; Schachter, Steven C. (1 February 2000). Schachter, Steven C. (ed.). "The postictal state: a neglected entity in the management of epilepsy". Epilepsy & Behavior . 1 (1). Oxford, England, United Kingdom: Elsevier Inc.: P52–P59. doi:10.1006/ebeh.2000.0023. ISSN   1525-5050. LCCN   sn99008772. OCLC   41569329. PMID   12609127. S2CID   20393636. Archived from the original on 2 June 2018. Retrieved 22 July 2021.
  4. ↑ Devinsky, Orrin (26 February 2008). Spencer, David; Jehi, Lara E.; Won, Michael; Danzer, Steve C. (eds.). "Postictal Psychosis: Common, Dangerous, and Treatable". Epilepsy Currents . 8 (2). Chicago, Illinois, United States of America: American Epilepsy Society/SAGE Journals: 31–34. doi:10.1111/j.1535-7511.2008.00227.x. ISSN   1535-7597. LCCN   2001215107. OCLC   47195748. PMC   2265810 . 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. ↑ Bromfield, Edward B.; Cavazos, José E.; Sirven, Joseph I. (2006). "Chapter 2: Clinical Epilepsy". In Bromfield, Edward B.; Cavazos, José E.; Sirven, Joseph I.; Rogawski, Michael A. (eds.). An Introduction to Epilepsy. West Hartford, Connecticut, United States of America: American Epilepsy Society. 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. ↑ Hammers, Alexander; Asselin, Marie-Claude; Hinz, Rainer; Kitchen, Ian; Brooks, David J.; Duncan, John S.; Koepp, Matthias J. (14 April 2007). Newsom-David, John; Husain, Masud; Al-Chalabi, Ammar; Mallucci, Giovanna (eds.). "Upregulation of opioid receptor binding following spontaneous epileptic seizures". Brain . 130 (4). Oxford, England, United Kingdom: Guarantors of Brain (charitable organization)/Oxford University Press (OUP): 1009–1016. doi: 10.1093/brain/awm012 . ISSN   0006-8950. LCCN   66084758. OCLC   1536984. PMID   17301080. Archived from the original on 2 June 2018. Retrieved 22 July 2021.
  8. ↑ Hosokawa, Chisa; Ochi, Hironobu; Yamagami, Sakae; Yamada, Ryusaku (1 April 1997). Goldsmith, Stanley J.; Murphy, Dawn; Sonnemaker, Robert E.; Silver, Stacey; Tapscott, Eleanore (eds.). "Regional cerebral blood flow and glucose utilization in spontaneously epileptic EL mice" (PDF). Journal of Nuclear Medicine . 38 (1). Society of Nuclear Medicine and Molecular Imaging (SNMMI): 613–616. ISSN   0161-5505. OCLC   807503641. PMID   9098212 . Retrieved 22 July 2021.
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