IM20.1-2 | Seizure Disorder Foundations and Diagnosis — Summary & Reflection

KEY TAKEAWAYS

Seizure = transient excessive synchronous neuronal discharge (motor or non-motor, convulsive or non-convulsive, provoked or unprovoked). Convulsion = motor subtype of a seizure. Epilepsy (ILAE 2014) = ≥2 unprovoked seizures >24 h apart, OR one unprovoked seizure with ≥60% recurrence probability, OR diagnosis of an epilepsy syndrome.

ILAE 2017 seizure classification: Focal onset (retained awareness / impaired awareness / focal to bilateral); Generalised onset (tonic-clonic, tonic, clonic, myoclonic, atonic, absence); Unknown onset.

Six aetiological categories: Structural (NCC, post-stroke, TBI, hippocampal sclerosis — NCC is the leading identifiable cause in Indian adults), Genetic (SCN1A/Dravet, JME, CAE), Infectious (TB meningitis, viral encephalitis, cerebral malaria), Metabolic (hypoglycaemia, hyponatraemia, hypocalcaemia, uraemia), Immune (anti-NMDAR, anti-LGI1, CNS lupus), Unknown.

Pathophysiology: PDS from excess excitation (glutamate/AMPA/NMDA) or reduced inhibition (GABA-A dysfunction). Absence seizures = thalamo-cortical 3 Hz T-Ca²⁺ channel oscillation → ethosuximide target. GABA-A internalisation in prolonged seizures → benzodiazepine resistance in status epilepticus.

Differential diagnosis: Syncope (rapid recovery, pallor, no tongue bite, brief jerks only), PNES (waxing-waning, pelvic thrust, eye closure, no post-ictal confusion), TIA (negative symptoms), hypoglycaemia (corrects with glucose), migraine with aura (slow spread over minutes).

Key investigations: Blood glucose (first), electrolytes (Na⁺, Ca²⁺, Mg²⁺), prolactin (post-ictal within 20 min), EEG (3 Hz spike-wave = CAE; polyspike on awakening = JME; focal temporal spikes = TLE), MRI epilepsy protocol (hippocampal sclerosis, NCC, dysplasia), CT (acute emergency), LP (meningitis/encephalitis).

Never use carbamazepine or phenytoin in absence or myoclonic epilepsy — they worsen these seizure types.

REFLECT

Return to the opening hook: the 'funny turn' three months before the tonic-clonic episode — a blank stare with chewing movements and no recollection of what was said — is the description of a focal impaired awareness seizure arising from the temporal lobe. The tonic-clonic event was likely a secondarily generalised focal seizure. Together, these two episodes fulfil the ILAE definition of epilepsy (two unprovoked seizures >24 hours apart) — a diagnosis that was missed when the first episode was dismissed as vasovagal. Reflect on this: how would you take a structured seizure history to avoid this diagnostic miss in your own future practice? And when a family asks 'doctor, will this happen again?' — what are the clinical, EEG, and aetiological factors that would inform your answer about recurrence risk? Connecting the framework to a real conversation with a frightened patient is the goal of your preparation.