Epileptiform Fits (Seizures & Epilepsy)

Definition

A single seizure or brief burst during a medical illness (e.g., fever, electrolyte disturbance) does not necessarily constitute epilepsy. — Harrison's Principles of Internal Medicine 22E

Classification (ILAE 2017)

Types of Seizures

1. Focal Onset Seizures

• With intact awareness: The patient remains conscious. Motor forms include tonic, clonic, or myoclonic movements contralateral to the focus (e.g., involuntary left hand movements from a right motor cortex focus). Sensory forms include numbness/tingling (parietal lobe), olfactory hallucinations ("uncinate fits" — unpleasant smells from medial temporal lobe), visual flashes (occipital lobe), or auditory phenomena (superior temporal gyrus).
• With impaired awareness (formerly complex partial): Typically temporal lobe origin. The patient stares blankly and performs automatisms (lip smacking, picking movements). There may be a prior aura (e.g., rising epigastric sensation, déjà vu, fear).
• Focal to bilateral tonic-clonic: A focal seizure that evolves into full generalized convulsion — previously called "secondary generalisation."

2. Generalized Onset Seizures

• Tonic phase (10–20 s): Sudden loss of consciousness, fall, brief flexion then sustained extension of the body, forced air expulsion ("epileptic cry"), cyanosis, pupils dilated and fixed
• Clonic phase (~30 s): Rhythmic jerking at ~8/s, coarsening to 4/s, then subsiding; autonomic features prominent (tachycardia, hypertension, salivation, incontinence)
• Postictal phase: Deep stupor then gradual confusion, headache, myalgia, amnesia for the event

Pathophysiology

• Ictal discharge initiation: Involves changes in ion channel conductance, receptor sensitivity, and extracellular ion concentrations. A paroxysmal depolarisation shift (PDS) in individual neurons, with synchronous firing in a population of neurons.
• Absence seizures: Linked to oscillatory thalamocortical circuits involving GABA_A receptors, T-type Ca²⁺ channels, and K⁺ channels. Genetic mutations in these components are well established.
• Epileptogenesis: The process by which a normal neural network becomes chronically hyperexcitable, often after an initial CNS injury (trauma, stroke, infection) with a delay of months to years before the first seizure. Structural changes include hippocampal neuronal loss and mossy fibre sprouting.
• Genetic channelopathies: Many idiopathic epilepsies are now known to involve mutations in ion channel genes — notably SCN1A (Dravet syndrome), KCNQ2, CHRNA4, and GABA receptor subunits.

Diagnosis

EEG

• Normal interictal EEG does not exclude epilepsy
• Epileptiform spikes/sharp waves predict higher recurrence risk
• 3-Hz spike-wave: Absence epilepsy
• Video-EEG monitoring is the gold standard for seizure characterisation
• High-density EEG (up to 257 electrodes) and MEG allow source localisation for surgical planning

Neuroimaging

• MRI is preferred — detects hippocampal sclerosis, cortical dysplasia, tumours, vascular malformations
• PET/SPECT for presurgical evaluation of refractory epilepsy

Blood tests

Aetiology

Special Situations

Status Epilepticus

1. 0–5 min: ABC, IV access, glucose check, thiamine if nutritionally at risk
2. 5–20 min: IV/IM benzodiazepine (lorazepam 0.1 mg/kg IV; or midazolam 10 mg IM)
3. 20–40 min: IV levetiracetam, valproate, or fosphenytoin
4. >40 min (refractory): Anaesthetic agents (propofol, midazolam, thiopental) with ICU intubation

Febrile Seizures

• Simple: Single generalised tonic-clonic, <15 min, in child 6 months–5 years with fever; benign prognosis
• Complex: Focal, prolonged (>15 min), or recurrent within 24 h; higher risk of future epilepsy
• Temperature usually >38°C; herpesvirus 6 is a common precipitant

Treatment: Antiseizure Drug (ASD) Selection

• Start with monotherapy; if inadequate at maximum tolerated dose, switch to another monotherapy before adding a second agent
• Initiate treatment after a second unprovoked seizure, or after a first seizure with high recurrence risk (structural lesion, abnormal EEG, nocturnal onset)
• Common dose-related side effects: sedation, ataxia, dizziness, diplopia
• Idiosyncratic risks: rash (carbamazepine, lamotrigine), hepatotoxicity (valproate), bone marrow suppression
• Valproate: teratogenic — avoid in women of childbearing age unless no alternative
• Drug-resistant epilepsy (failure of ≥2 appropriate ASDs): refer for surgical evaluation; other options include responsive neurostimulation (RNS), vagus nerve stimulation (VNS), ketogenic diet

When to Stop Driving / Lifestyle Advice

• Driving restrictions (typically seizure-free for 6–12 months depending on jurisdiction)
• Avoiding unsupervised swimming, bathing, heights, and operating heavy machinery
• Sleep deprivation and alcohol as seizure triggers
• Contraception/pregnancy planning (enzyme-inducing ASDs affect oral contraceptives; folate supplementation mandatory)

• Harrison's Principles of Internal Medicine 22E, Chapter 436 — Seizures and Epilepsy
• Adams and Victor's Principles of Neurology 12E — Epilepsy and Other Seizure Disorders
• Recent systematic review on status epilepticus management guidelines (Vignatelli et al., Epilepsia 2024, PMID: 38606469)