Postictal Seizure State

Etiology

The underlying process responsible for the postictal state is thought to be related to neuronal exhaustion and hyper-inhibition.

Epidemiology

There is no clear data on the incidence of the postictal state in patients with epilepsy. A study showed that most patients with epilepsy (72%) reported postictal behavioral impairment.[2]

Pathophysiology

A seizure is terminated by a variety of potential mechanisms, including depletion of energy substrate, desensitization of receptors to the excitatory neurotransmitter, depolarization block, desynchronization of the neuronal networks, the effect of inhibitory neuromodulators such as endogenous opiate receptor agonists, and various other possible mechanisms. These mechanisms can be classified as[3]:

• Mechanisms acting at the cellular level: Energy failure, potassium current, ion gradients
• Mechanisms acting on local networks: Glutamate depletion, glial buffering of glutamate, the role of gap junctions on synchrony, increased GABA-ergic inhibition, effects of neuromodulators (endocannabinoids, adenosine, and neuropeptide Y)
• Mechanisms acting remotely to limit excitation and seizure spread: Effect of other cortical regions and subcortical nuclei on modifying ictal activity

History and Physical

Different neurological functions are affected by the inhibitory processes in the postictal period. These involve speech, motor, and memory. Patients with left temporal lobe epilepsy develop a more prominent verbal memory deficit in the postictal period while those with right temporal lobe epilepsy suffer from visual memory deficit.[4] The duration of such impairment depends on the preictal cognitive deficit (higher with the higher pre-ictal deficit). The memory is affected in such a way that 30% of the patients do not remember any seizure, and only a quarter remember all of their seizures.[5] Postictal motor weakness (Todd paresis) has a lateralizing value. It points to seizure onset in the contralateral hemisphere. Automatism is a phenomenon that can be seen both during ictal and postictal states. Other postictal symptoms include postictal coughing, spitting, hypersalivation, nose-wiping, psychosis, and mania.

The duration of the postictal state depends on how different mechanisms associated with seizure termination interact with each other. Whether the resolution of the postictal state requires the resolution of all the inhibitory processes is a question yet to be answered. Postictal deficits recover at different rates. Postictal deficits in a patient with focal seizure with impaired awareness may resolve in 1 to 2 hours. Todd paresis may take up to 1 to 2 days for resolution. Some patients would have cognitive, mood, and change in energy levels that may last days.

Evaluation

The decision to intervene during the postictal state depends on the postictal symptoms and the individual patient's epilepsy history. Knowledge of the previous ictal and postictal events is of great importance to determine if all the symptoms can be attributed to the postictal state. A patient with a history of a postictal headache does not require urgent brain imaging. A patient presenting with a new focal sign (e.g., unilateral weakness) after an unwitnessed but suspected seizure requires brain imaging to rule out alternative etiology like a stroke.

Similarly, a patient presenting with new-onset seizure with prolonged postictal alteration of mental status requires an elaborate workup, including cerebrospinal fluid analysis, to look for an etiological diagnosis. Nonconvulsive status epilepticus should be in the differential of a patient with prolonged postictal confusion. As already mentioned above, determining the end of a seizure and the beginning of the postictal state is often difficult. Electroencephalogram (EEG) helps distinguish between the two states. Neuroimaging may detect changes in the postictal brain, but its clinical utility is yet to be established and is more a research tool at this time.  

EEG

The transition from ictal to postictal EEG can be classified either by rate or location; some seizures end abruptly, while others have gradual termination. In terms of location, some seizures terminate in all involved regions of the brain at the same time, while others terminate at various regions at various times. Postictal EEG typically shows attenuation or slowing (usually in delta frequency range) or a combination of both.[6] As further recovery ensues, delta slowing transitions to theta frequencies before background rhythms return. Some patients enter sleep in the course of recovery. Brain regions involved in postictal attenuation/slowing may be of localizing value. The EEG changes tend to be more pronounced with prolonged seizures but have less lateralizing value in such cases[7]. A retrospective study showed that the average time for EEG to return to baseline was 120 minutes, with a maximum of 420 minutes in adults.[8] The postictal slowing was found to match with the site of surgery in 96% of the times in temporal lobe epilepsy.[9]

Neuroimaging

Positron emission tomography (PET) scan of the brain can be used to study the changes in neurotransmitters and receptors in the postictal state. In one study,[8], it was found that opioid receptors were upregulated in the postictal period in a patient with temporal lobe epilepsy in the epileptogenic side. PET scan also showed that benzodiazepine receptor levels vary with the duration of the postictal period. The shorter the duration, the lower is the levels of benzodiazepine receptors.[10] Perfusion magnetic resonance imaging (MRI) is used to detect variation in cerebral blood flow (CBF) in the postictal state. One study showed that CBF, ipsilateral to the focus, doubles within 5 minutes of a seizure and drops below average after 1 hour.[11] Diffusion-weighted imaging also shows diffusion restriction postictally.

Treatment / Management

Postictal deficits, once alternative causes are ruled out, only require supportive care and monitoring. Postictal delirium typically lasts for hours but may continue up to 1 to 2 days. It is usually of the hypoactive type, but some may evolve to hyperactive type. Supportive care is usually enough unless the patient gets agitated; medications should be avoided unless the patient is extremely agitated.

Differential Diagnosis

• Central nervous system (CNS) secondary causes, e.g., stroke
• Ongoing seizure
• Systemic causes:
  • Drug/toxin
  • Infection
  • Metabolic