Post-Ictal State

Definition and Timing

• Rosen's Emergency Medicine, p. 173: "A postictal state of variable duration, which correlates with the duration of the preceding seizure."
• Bradley and Daroff's Neurology, p. 487: "The postictal state seems to correlate with severity and duration."

Which Seizure Types Cause a Postictal State?

Clinical Features

General features

• Lethargy and somnolence (often deep sleep follows a generalized tonic-clonic seizure)
• Confusion and disorientation
• Impaired recollection of the seizure event (amnesia)
• Headache (often pronounced after generalized tonic-clonic seizures)
• Generalized muscle soreness
• Stertorous (snoring) respirations immediately after a convulsive seizure

Focal Neurological Deficits - Todd's Paralysis

• Can be motor, sensory, visual, cognitive, emotional, or related to consciousness
• Results from a prolonged depression of one brain region after seizure termination
• Usually transient but can last hours - clinically important as a stroke mimic
• Plum and Posner's, p. 407: "...the postictal state, which may include confusion or a postictal deficit (Todd's paralysis) of the cortical area in which the seizure was most intense"
• Kandel's Principles of Neural Science, p. 1508: "A neurological exam in the postictal period can lead to insights about the locus of the seizure focus when there is prolonged depression of one brain region or function."

Postictal Aphasia

• Particularly follows left temporal lobe seizures
• Can be mistaken for TIA or stroke if seizure was unwitnessed (as illustrated by the vignette in Plum & Posner)

Mechanism (Neurophysiology)

1. Post-seizure neuronal exhaustion - neurons undergo cycles of depolarization/repolarization during the clonic phase, and the postictal silence reflects a rebound hyperpolarization and suppression of neuronal firing
2. Neurotransmitter depletion - exhaustion of excitatory neurotransmitters and accumulation of inhibitory mediators (adenosine, GABA)
3. Metabolic changes - local hypoxia, lactic acidosis, and ionic shifts (e.g., K+ accumulation extracellularly) in the seizure focus all contribute to neuronal suppression

Psychiatric Manifestations of the Postictal Period

Postictal Psychosis

• Onset: within one week of a seizure or seizure cluster
• Duration: >1 day and <3 months
• Features: disorientation, delusions, delirium, or hallucinations in clear or clouded consciousness
• Exclusions: must rule out anticonvulsant toxicity, non-convulsive status epilepticus (NCSE), prior interictal psychosis, head trauma, or drug/alcohol intoxication
• More common with: age >30, male sex, focal (especially temporal) seizures, rapid secondary generalization, prior history of psychosis
• Kaplan & Sadock's Comprehensive Textbook of Psychiatry, p. 2077

Clinically Important Points

1. Prolonged postictal confusion - especially following right temporal focal seizures - should raise suspicion for unwitnessed seizure or NCSE. An EEG may be required.
2. Todd's paralysis as a stroke mimic - unwitnessed seizure followed by hemiplegia can be indistinguishable from acute stroke; history, tongue biting, incontinence, and upgoing plantar reflexes provide clues.
3. Persistent vital sign abnormalities beyond the immediate postictal period (e.g., sustained fever, hypertension, tachycardia) suggest an underlying cause (infection, toxic ingestion, CNS lesion) rather than simply the post-ictal period itself.
4. Absence seizures are the key exception - they do not produce a postictal state; abrupt return to full awareness is characteristic.
5. For pharmacotherapy of postictal psychosis, avoid clozapine, chlorpromazine, and loxapine due to their seizure threshold-lowering effects. Be aware of drug-drug interactions (e.g., enzyme-inducing antiseizure drugs reduce levels of ziprasidone).