Seizures, Absence (Petit Mal)

Incidence of absence seizures in USA is 1.9–8 cases per 100,000 population.

Seizures are most common in children aged 4–14 y but rare in adults.

Risk of transition of absence seizures into tonic-clonic seizures or SE is low but still possible.

Seizure induced sequelae, including physical injuries, tachycardia, hypertension, hypoxia, metabolic acidosis, pulm aspiration, elevated ICP, and cerebral edema.

Seizure induction with periop drugs and hyperventilation can occur, especially with sevoflurane induction.

Altered pharmacokinetics and dynamics with anticonvulsants: Resistance to neuromuscular blockers and opioids with chronic therapy

Maintain serum anticonvulsant levels.

Absence seizures are a common seizure disorder of childhood; up to two-thirds of pts are girls.

Age of onset has bimodal distribution, with the first peak at 6–7 y (childhood) and the second around 12 y (juvenile).

International League against Epilepsy classification of absence seizures:

• Absence seizures: Typical or atypical.

• Absence with special features: Includes myoclonic absence and eyelid myoclonia.

Typical absence seizures are brief absence (5–20 sec), with impairment of consciousness and an abrupt onset/offset, often accompanied by one or more mild motor manifestations: staring, behavioral arrest, eyelid fluttering, or hand/face automatisms.

Atypical seizures have a less rapid onset/offset with more motor features and prolonged seizures.

Hyperventilation and bright flickering lights are common triggers for absence seizures, except for atypical absence seizures, which often occur during drowsiness.

Attacks may be few or occur >100 times per d.

Accidental injuries are rare.

Minimal postictal sequelae occurs: EEG and consciousness return immediately.

SE may occur: Convulsive and nonconvulsive SE are possible

Remission rate for childhood absence epilepsy is 80%; juvenile myoclonic epilepsy carries a high risk of generalized tonic-clonic seizures.

Strong genetic predisposition in otherwise normal children.

A mutation in the GABA (A) receptor gene was found in some pts with childhood absence epilepsy.

Structural lesions in adults.