Focal Seizures (Partial Seizures)

1. Clinical Overview

Summary

Focal seizures originate from a localized area within one cerebral hemisphere, representing approximately 60% of all epilepsy cases. The International League Against Epilepsy (ILAE) 2017 classification replaced the older "simple partial" and "complex partial" terminology with focal onset aware and focal onset impaired awareness seizures, with further descriptors based on motor/non-motor features and potential evolution to bilateral tonic-clonic seizures.[1,2]

The clinical manifestations depend critically on the cortical region of seizure onset. Temporal lobe epilepsy (TLE) is the most common focal epilepsy syndrome, characterized by experiential phenomena (déjà vu, jamais vu, fear, epigastric aura) and oroalimentary or gestural automatisms. Frontal lobe seizures typically manifest with hypermotor activity, asymmetric tonic posturing, and brief duration with rapid recovery. Parietal and occipital lobe seizures present with somatosensory and visual phenomena respectively.[3,4]

Accurate diagnosis requires detailed seizure semiology, electroencephalography (EEG) demonstrating focal epileptiform discharges, and neuroimaging (MRI brain) to identify structural abnormalities such as hippocampal sclerosis, cortical dysplasia, tumors, or vascular malformations.[5] First-line antiseizure medications (ASMs) for focal epilepsy include carbamazepine, lamotrigine, and levetiracetam. Approximately 30% of patients develop drug-resistant epilepsy, defined as failure of adequate trials of two appropriate ASMs; these patients should be evaluated for potential epilepsy surgery, which can achieve seizure freedom in up to 60-80% of carefully selected candidates with mesial temporal sclerosis.[6,7]

Key Facts

• Epidemiology: Focal epilepsy represents ~60% of all epilepsy; incidence 20-30 per 100,000 person-years
• ILAE 2017 Classification:
  • Focal onset aware (consciousness preserved; old "simple partial")
  • Focal onset impaired awareness (consciousness impaired; old "complex partial")
  • Focal to bilateral tonic-clonic (old "secondarily generalized")
• Temporal Lobe Epilepsy: Most common focal epilepsy syndrome
  • "Mesial temporal: Aura (epigastric rising, déjà vu, fear) + automatisms"
  • "Lateral temporal: Auditory hallucinations, language disturbance"
• Frontal Lobe: Hypermotor, brief, nocturnal, preserved awareness common
• Pathology: Hippocampal sclerosis, cortical dysplasia, tumors (DNET, oligodendroglioma), vascular malformations, stroke
• Investigations: MRI brain (3T with epilepsy protocol), EEG (interictal/ictal), video-EEG telemetry
• First-line ASMs: Carbamazepine, lamotrigine, levetiracetam
• Drug-resistant: ~30% of patients; consider epilepsy surgery evaluation
• Surgery outcomes: 60-80% seizure-free for mesial temporal sclerosis

Clinical Pearls

"The Aura IS the Focal Aware Seizure": The aura (e.g., epigastric rising, déjà vu, fear) represents the initial focal seizure activity with preserved awareness. It is not a "warning" but the seizure itself, and its character provides crucial localizing information.

"Temporal Lobe = Automatisms + Memory/Emotional Phenomena": Oroalimentary automatisms (lip smacking, chewing, swallowing) and gestural automatisms (picking, fumbling) combined with experiential phenomena (déjà vu, jamais vu, fear) are pathognomonic for temporal lobe onset.

"Frontal Lobe = Hypermotor + Bizarre + Brief + Nocturnal": Frontal lobe seizures characteristically involve hypermotor activity (bicycling, thrashing), bizarre semiology (sexual automatisms, vocalization), brief duration (less than 30 seconds), clustering during sleep, and rapid post-ictal recovery—often mistaken for psychogenic non-epileptic seizures.

"Todd's Paresis = Focal Seizure Localization": Post-ictal focal neurological deficit (Todd's paresis) lasting minutes to hours indicates seizure origin in the contralateral motor cortex. If lasting > 24 hours, exclude stroke.

"Hippocampal Sclerosis = Surgery Candidate": Mesial temporal sclerosis on MRI with concordant EEG and typical semiology predicts excellent surgical outcomes (70-80% seizure freedom).

"2 Failed ASMs = Drug-Resistant = Surgery Referral": Failure of adequate trials of two appropriately chosen and tolerated ASMs defines drug-resistant epilepsy and mandates referral to a comprehensive epilepsy center for surgical evaluation.

Why This Matters Clinically

Focal seizures indicate a localized brain abnormality—identifying the etiology is critical for prognosis and management. Structural lesions such as tumors, vascular malformations, and cortical dysplasia require specific interventions. Approximately 30% of focal epilepsy patients become drug-resistant, but epilepsy surgery offers potential cure in carefully selected candidates. Early referral for surgical evaluation is essential, as prolonged uncontrolled seizures are associated with cognitive decline, psychiatric comorbidity, increased SUDEP risk, and reduced quality of life.[8,9]

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2. Epidemiology

Incidence & Prevalence

Age Distribution

Risk Factors

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3. Aetiology & Pathophysiology

Molecular Mechanisms of Focal Seizure Generation

Exam Detail: Focal seizures arise from a localized network of hyperexcitable neurons capable of generating synchronous, excessive electrical discharges. The fundamental mechanism involves an imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission.

Key Pathophysiological Mechanisms:

1. Ion Channel Dysfunction

   • Mutations in sodium channels (SCN1A, SCN2A) → altered neuronal excitability
   • Potassium channel mutations → prolonged depolarization
   • Calcium channel abnormalities → enhanced neurotransmitter release

2. Neuronal Loss and Reorganization

   • Hippocampal sclerosis: selective loss of CA1, CA3 pyramidal neurons and dentate hilar interneurons
   • Mossy fiber sprouting → recurrent excitatory circuits
   • Loss of inhibitory interneurons → reduced GABAergic tone

3. Glial Dysfunction

   • Astrocytic dysfunction → impaired glutamate and potassium buffering
   • Disrupted blood-brain barrier → albumin extravasation → TGF-β receptor activation → reduced Kir4.1 channels

4. Network Reorganization

   • Formation of "epileptogenic zone" with intrinsic seizure-generating capacity
   • "Irritative zone" producing interictal spikes on EEG
   • "Seizure onset zone" where ictal activity begins
   • Potential propagation pathways to bilateral tonic-clonic seizure

Structural Pathology

Genetic Causes

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4. Clinical Presentation

ILAE 2017 Classification of Focal Seizures

The International League Against Epilepsy (ILAE) revised classification in 2017 provides a comprehensive framework:[1,2]

FOCAL SEIZURE CLASSIFICATION (ILAE 2017)

FOCAL ONSET
    │
    ├─ AWARE (consciousness fully preserved)
    │   └─ Motor or Non-motor onset
    │
    ├─ IMPAIRED AWARENESS (consciousness impaired)
    │   └─ Motor or Non-motor onset
    │
    └─ AWARENESS UNKNOWN
        └─ Motor or Non-motor onset

MOTOR ONSET:
  • Automatisms (oroalimentary, gestural)
  • Atonic
  • Clonic
  • Epileptic spasms
  • Hyperkinetic
  • Myoclonic
  • Tonic

NON-MOTOR ONSET:
  • Autonomic (epigastric rising, pallor, flushing, piloerection)
  • Behavior arrest
  • Cognitive (déjà vu, jamais vu, forced thinking)
  • Emotional (fear, pleasure)
  • Sensory (visual, auditory, olfactory, gustatory, somatosensory, vestibular)

FOCAL TO BILATERAL TONIC-CLONIC
  (Evolution from focal onset to bilateral convulsive seizure)

Temporal Lobe Seizures

Mesial Temporal Lobe Epilepsy (Hippocampal Onset)

Lateral Temporal Lobe Epilepsy

Clinical Pearl: Ictal Vomiting: Rare but highly localizing feature for non-dominant temporal lobe or insular onset. If a patient reports nausea/vomiting during seizure, strongly consider mesial temporal or insular focus.

Dystonic Limb Posturing: Unilateral dystonic posturing of upper limb during seizure suggests contralateral temporal lobe onset (particularly in basal ganglia involvement via temporal lobe spread).

Frontal Lobe Seizures

Frontal Lobe Seizure Subtypes by Region:

Clinical Pearl: Frontal Lobe vs Non-Epileptic Attack Disorder (NEAD): Frontal lobe seizures are frequently misdiagnosed as psychogenic non-epileptic seizures due to bizarre, hypermotor semiology with preserved awareness. Key differentiators:

• Frontal seizures: Stereotyped, brief (less than 1 min), nocturnal clustering, rapid recovery, scalp EEG often normal
• NEAD: Prolonged (> 2 min), variable semiology, eyes closed forcefully, triggered by stress, normal prolactin

Parietal Lobe Seizures

Occipital Lobe Seizures

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5. Clinical Examination

Inter-ictal Neurological Examination

Post-ictal Examination (Todd's Paresis)

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6. Differential Diagnosis

Focal vs Generalized Epilepsy

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7. Investigations

First-Line Investigations

MRI Brain (Essential for All Focal Seizures)

Key MRI Findings:

Electroencephalography (EEG)

Interictal EEG Findings:

Ictal EEG Findings:

Exam Detail: Why is Scalp EEG Often Normal in Frontal Lobe Seizures?

Frontal lobe seizures, particularly from orbitofrontal or mesial frontal regions, frequently show no abnormality on scalp EEG due to:

1. Deep sources: Electrical activity from deep frontal structures (e.g., anterior cingulate, orbitofrontal cortex) may not reach scalp electrodes
2. Rapid spread: Seizure propagates quickly before localized ictal pattern develops
3. Muscle artifact: Hypermotor activity generates extensive muscle artifact that obscures underlying EEG

This is why video-EEG telemetry capturing typical seizure semiology is critical for diagnosis, even with normal scalp EEG.

Advanced Investigations (Pre-Surgical Evaluation)

Blood Tests

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8. Management

Management Algorithm

FOCAL SEIZURE MANAGEMENT PATHWAY
                    ↓
┌──────────────────────────────────────────────────────────────┐
│                   FIRST SEIZURE                               │
├──────────────────────────────────────────────────────────────┤
│  IMMEDIATE:                                                   │
│  ➤ Assess safety, recovery, post-ictal state                │
│  ➤ Check capillary glucose                                  │
│  ➤ Consider benzodiazepine if ongoing seizure > 5 min        │
│                                                               │
│  INVESTIGATIONS:                                              │
│  ➤ MRI brain (URGENT if focal deficit, age > 25, concern     │
│     for structural lesion)                                   │
│  ➤ EEG (routine, sleep-deprived)                            │
│  ➤ Bloods: FBC, U&E, LFTs, glucose, calcium, magnesium      │
│                                                               │
│  REFERRAL:                                                    │
│  ➤ First seizure clinic / Neurology (within 2 weeks)        │
│                                                               │
│  COUNSELING:                                                  │
│  ➤ Driving: MUST NOT drive; notify DVLA                     │
│     - Car/motorcycle: 6 months seizure-free (UK)            │
│     - HGV/PSV: 10 years off ASM, seizure-free (UK)         │
│  ➤ Safety advice (bathing, heights, machinery)              │
│  ➤ SUDEP discussion (if recurrent seizures)                 │
│  ➤ Epilepsy specialist nurse contact                        │
└──────────────────────────────────────────────────────────────┘
                    ↓
┌──────────────────────────────────────────────────────────────┐
│         DECISION TO START ANTISEIZURE MEDICATION (ASM)       │
├──────────────────────────────────────────────────────────────┤
│  CONSIDER ASM IF:                                             │
│  ➤ ≥2 unprovoked seizures                                    │
│  ➤ High risk of recurrence (abnormal EEG, structural lesion) │
│  ➤ Patient preference (occupation, driving)                  │
│                                                               │
│  SHARED DECISION-MAKING:                                      │
│  • Recurrence risk after first seizure: 40-50% (2 years)    │
│  • ASM reduces risk to ~20-25%                               │
│  • Weigh benefits vs side effects, teratogenicity (women)   │
└──────────────────────────────────────────────────────────────┘
                    ↓
┌──────────────────────────────────────────────────────────────┐
│              FIRST-LINE ANTISEIZURE MEDICATIONS              │
├──────────────────────────────────────────────────────────────┤
│  FIRST-LINE OPTIONS (Focal Seizures):                        │
│                                                               │
│  1️⃣ LAMOTRIGINE (LTG)                                        │
│     • Mechanism: Sodium channel blocker                      │
│     • Starting dose: 25 mg OD (12.5 mg if on valproate)     │
│     • Titration: Increase by 25-50 mg every 2 weeks         │
│     • Maintenance: 100-400 mg/day (divided BD)              │
│     • Pros: Well tolerated, no weight gain, mood stabilizer │
│     • Cons: SLOW titration (rash risk), drug interactions   │
│     • Monitoring: Rash (Stevens-Johnson syndrome risk)      │
│                                                               │
│  2️⃣ LEVETIRACETAM (LEV)                                      │
│     • Mechanism: SV2A modulator                              │
│     • Starting dose: 250-500 mg BD                           │
│     • Titration: Rapid (can increase weekly)                │
│     • Maintenance: 1000-3000 mg/day (divided BD)            │
│     • Pros: RAPID titration, minimal interactions, renal    │
│     • Cons: Mood/behavioral (irritability, depression 10%)  │
│     • Monitoring: Mood, psychiatric symptoms                │
│                                                               │
│  3️⃣ CARBAMAZEPINE (CBZ)                                      │
│     • Mechanism: Sodium channel blocker                      │
│     • Starting dose: 100-200 mg BD (slow-release preferred) │
│     • Titration: Increase by 100-200 mg weekly              │
│     • Maintenance: 600-1600 mg/day (divided BD)             │
│     • Pros: Highly effective focal seizures, cheap          │
│     • Cons: Enzyme inducer (many interactions), side effects│
│     • Monitoring: FBC, LFTs, Na (SIADH), HLA-B*1502 (Asian) │
│     • ⚠️ AVOID in women of childbearing potential (interactions)│
│                                                               │
│  SECOND-LINE OPTIONS:                                         │
│  ➤ Oxcarbazepine (fewer interactions than CBZ)              │
│  ➤ Lacosamide (sodium channel, well-tolerated)              │
│  ➤ Zonisamide (multiple mechanisms)                         │
│  ➤ Perampanel (AMPA receptor antagonist)                    │
│                                                               │
│  AVOID AS FIRST-LINE:                                         │
│  ⚠️ Valproate (less effective for focal; teratogenic)        │
│  ⚠️ Phenytoin (narrow therapeutic index, cosmetic effects)   │
└──────────────────────────────────────────────────────────────┘
                    ↓
┌──────────────────────────────────────────────────────────────┐
│              DRUG-RESISTANT EPILEPSY (DRE)                   │
├──────────────────────────────────────────────────────────────┤
│  DEFINITION:                                                  │
│  ➤ Failure of adequate trials of 2 tolerated, appropriately │
│     chosen ASMs (monotherapy or combination)                 │
│  ➤ Occurs in ~30% of focal epilepsy patients                │
│                                                               │
│  ACTIONS:                                                     │
│  1️⃣ RE-EVALUATE DIAGNOSIS                                    │
│     • Is it truly epilepsy? (consider video-EEG, PNES)      │
│     • Is classification correct? (focal vs generalized)     │
│     • Are seizures provoked? (sleep deprivation, alcohol)   │
│                                                               │
│  2️⃣ OPTIMIZE CURRENT ASM                                     │
│     • Ensure adequate dose, compliance, drug levels         │
│     • Address side effects (may limit dosing)               │
│                                                               │
│  3️⃣ ADJUNCTIVE ASM THERAPY                                   │
│     • Add second/third ASM with different mechanism         │
│     • Options: Clobazam, brivaracetam, cenobamate           │
│                                                               │
│  4️⃣ REFER TO COMPREHENSIVE EPILEPSY CENTER                   │
│     ⚠️ CRITICAL: Early referral (don't delay years!)         │
│     • Video-EEG telemetry                                    │
│     • High-resolution MRI (3T epilepsy protocol)            │
│     • Neuropsychological assessment                         │
│     • Multidisciplinary team evaluation                     │
│     • Consider:                                              │
│       - Epilepsy surgery                                     │
│       - Vagus nerve stimulation (VNS)                       │
│       - Responsive neurostimulation (RNS)                   │
│       - Deep brain stimulation (DBS)                        │
│       - Dietary therapy (ketogenic diet)                    │
└──────────────────────────────────────────────────────────────┘
                    ↓
┌──────────────────────────────────────────────────────────────┐
│                 EPILEPSY SURGERY EVALUATION                  │
├──────────────────────────────────────────────────────────────┤
│  INDICATIONS:                                                 │
│  ✅ Drug-resistant focal epilepsy                            │
│  ✅ Identifiable epileptogenic zone                          │
│  ✅ Seizure-free outcome would significantly improve QoL     │
│  ✅ Acceptable risk of neurological/cognitive deficit        │
│                                                               │
│  IDEAL CANDIDATE (Mesial Temporal Sclerosis):                │
│  ➤ Typical semiology (aura + impaired awareness + automatisms)│
│  ➤ MRI: Unilateral hippocampal sclerosis                    │
│  ➤ EEG: Concordant temporal lobe epileptiform discharges    │
│  ➤ Neuropsych: Memory deficits ipsilateral to MRI lesion    │
│  ➤ No bilateral hippocampal abnormality                     │
│                                                               │
│  SURGICAL PROCEDURES:                                         │
│  • Anterior temporal lobectomy (ATL)                         │
│  • Selective amygdalohippocampectomy (SAH)                  │
│  • Lesionectomy (tumor, FCD, cavernoma)                     │
│  • Multiple subpial transection (eloquent cortex)           │
│                                                               │
│  OUTCOMES (Mesial Temporal Sclerosis):                        │
│  ➤ 60-80% seizure-free at 2 years (Engel Class I)           │
│  ➤ 50-70% seizure-free at 5-10 years                        │
│  ➤ Verbal memory decline risk (dominant hemisphere 30-40%)  │
│  ➤ Visual field defect (superior quadrantanopia) common     │
│                                                               │
│  NON-RESECTIVE OPTIONS:                                       │
│  • Vagus nerve stimulation (VNS): 50% responder rate        │
│  • Responsive neurostimulation (RNS): Closed-loop device    │
│  • Deep brain stimulation (anterior thalamus)               │
└──────────────────────────────────────────────────────────────┘

Special Populations

Women of Childbearing Potential

Elderly

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9. Complications

SUDEP Risk Factors and Mitigation

Exam Detail: Sudden Unexpected Death in Epilepsy (SUDEP) is the leading cause of epilepsy-related mortality. Incidence: 1-2 per 1,000 patient-years in epilepsy population; higher in drug-resistant epilepsy (6-9 per 1,000).

Mechanism: Likely multifactorial involving:

• Seizure-induced respiratory dysfunction (central apnea, laryngospasm)
• Cardiac arrhythmia (ictal bradycardia, asystole)
• Autonomic dysregulation

Risk Factors:

• Uncontrolled generalized tonic-clonic seizures (most important)
• Young age (20-40 years)
• Nocturnal seizures
• Polytherapy (marker of drug resistance)
• Prone sleeping position post-ictally

Risk Reduction:

• Optimize seizure control (most important intervention)
• Medication adherence education
• Nocturnal supervision/monitoring devices
• Avoid prone sleeping
• Treat comorbid sleep apnea

Counseling: NICE recommends discussing SUDEP with all patients with epilepsy; balance awareness without causing undue anxiety.

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10. Prognosis & Outcomes

Prognostic Factors

Epilepsy Surgery Outcomes

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11. Evidence & Guidelines

Key Guidelines

Landmark Studies

Exam Detail: 1. MESS Trial (Multicentre Study of Early Epilepsy and Single Seizures): Immediate vs deferred ASM treatment after first or early seizures. ASM reduced 2-year seizure recurrence (32% vs 51%) but no difference in long-term remission.[10]

2. SANAD Trial (Standard and New Antiepileptic Drugs): Largest RCT comparing ASMs for focal epilepsy. Lamotrigine vs carbamazepine: similar efficacy, lamotrigine better tolerated.[11]

3. Wiebe et al. (NEJM 2001): RCT of temporal lobe surgery vs medical therapy for drug-resistant TLE. Surgery group: 58% seizure-free at 1 year vs 8% in medical group. Landmark trial establishing efficacy of epilepsy surgery.[7]

4. Kwan & Brodie (NEJM 2000): Prospective cohort showing 47% seizure freedom with first ASM, 13% with second, only 4% with third or more—defining concept of drug-resistant epilepsy and futility of multiple ASM trials without surgical evaluation.[12]

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12. Examination Focus

High-Yield Exam Topics

Sample MRCP PACES Viva Scenario

Scenario: A 28-year-old woman presents with recurrent episodes over the past 2 years. She describes a sudden rising sensation from her stomach lasting 5-10 seconds, followed by staring and unresponsiveness lasting about 60 seconds. Her partner reports she makes chewing movements and picks at her clothes during these episodes. Afterwards, she is confused for several minutes and cannot recall what happened. She has had 6 such episodes despite treatment with levetiracetam 1500 mg BD.

Questions and Model Answers:

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Q1: What is your diagnosis and how would you classify this epilepsy using the ILAE 2017 classification?

Model Answer:

This is focal epilepsy with seizures originating from the mesial temporal lobe, most likely the hippocampus.

ILAE 2017 Classification:

• Focal onset impaired awareness seizure (formerly "complex partial")
• Non-motor onset (autonomic and cognitive features in aura)
• Progressing to motor features (oroalimentary automatisms)

Supporting Features:

1. Aura: Epigastric rising sensation is classic for mesial temporal onset (autonomic non-motor onset)
2. Impaired awareness: Staring, unresponsiveness during seizure
3. Automatisms: Chewing (oroalimentary) and picking at clothes (gestural automatisms) are pathognomonic for temporal lobe seizures
4. Post-ictal confusion: Typical of temporal lobe epilepsy; prolonged confusion suggests temporal origin

Localization: Mesial temporal lobe (hippocampus/amygdala) based on aura and automatisms.

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Q2: What investigations would you perform and what findings would you expect?

Model Answer:

Essential Investigations:

1. MRI Brain (3 Tesla with epilepsy protocol):

   • Coronal oblique sequences perpendicular to hippocampus
   • T2/FLAIR: Look for increased signal in hippocampus
   • Volumetric T1: Assess hippocampal volume
   • Expected finding: Hippocampal sclerosis (mesial temporal sclerosis)—unilateral hippocampal atrophy, T2 hyperintensity, loss of internal architecture
   • Rule out: Tumor (DNET, ganglioglioma), vascular malformation, cortical dysplasia

2. Video-EEG Telemetry:

   • Capture habitual seizures with simultaneous video and EEG
   • Interictal: Anterior temporal spikes or sharp waves
   • Ictal: Rhythmic temporal theta activity, evolving to rhythmic alpha/beta; localize to one temporal lobe
   • Confirm seizures are epileptic (exclude PNES)

3. Neuropsychological Assessment:

   • Verbal memory deficits (if dominant hemisphere affected)
   • Visual memory deficits (if non-dominant hemisphere)
   • Helps lateralize and predict post-surgical outcomes

4. Functional Imaging (if considering surgery):

   • FDG-PET: Interictal hypometabolism in affected temporal lobe
   • Ictal SPECT: Hyperperfusion in seizure onset zone

Blood Tests (if not already done):

• FBC, U&E, LFTs (baseline for ASMs)
• Drug levels (levetiracetam level to assess compliance, though therapeutic monitoring not routine)

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Q3: She has failed levetiracetam. What is your next management step?

Model Answer:

This patient has drug-resistant epilepsy, defined as failure of adequate trials of two appropriately chosen ASMs. She requires urgent referral to a comprehensive epilepsy center for evaluation for epilepsy surgery.

Immediate Management:

1. Optimize Current ASM or Trial Second-Line ASM:

   • Ensure compliance with levetiracetam (check drug levels if available)
   • Consider adding or switching to:
     • Lamotrigine (sodium channel blocker; slow titration; well-tolerated)
     • Carbamazepine (highly effective for focal; enzyme inducer—discuss contraception)
     • Lacosamide (sodium channel; good tolerability)
   • Adjunctive therapy: Clobazam (benzodiazepine; particularly useful for temporal lobe epilepsy)

2. Referral to Tertiary Epilepsy Center (CRITICAL—do not delay):

   • Multidisciplinary team evaluation
   • Comprehensive epilepsy surgery workup (as above)

Surgical Evaluation:

If investigations confirm:

• Unilateral hippocampal sclerosis on MRI
• Concordant EEG (unilateral temporal lobe onset)
• Typical semiology (aura + automatisms + post-ictal confusion)
• Neuropsychology consistent with unilateral temporal dysfunction

→ She is an excellent candidate for anterior temporal lobectomy or selective amygdalohippocampectomy

Expected Surgical Outcome:

• 60-80% seizure-free at 2 years (Engel Class I)
• Risks: Verbal memory decline (~30-40% if dominant hemisphere), superior quadrantanopia (common but usually asymptomatic)

Shared Decision-Making:

• Discuss risks vs benefits of surgery
• Neuropsychological counseling re: memory outcomes
• Consider SAH (selective amygdalohippocampectomy) vs ATL (anterior temporal lobectomy)—SAH may preserve more memory but outcomes similar

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Q4: What safety counseling would you provide?

Model Answer:

Driving:

• Must NOT drive until seizures controlled
• Notify DVLA (legal requirement in UK)
• Car/motorcycle: Must be seizure-free for 12 months (or 6 months if first seizure only)
• Failure to notify DVLA: invalidates insurance, illegal

Bathing/Showering:

• Avoid baths (drowning risk); showers preferred with door unlocked
• Supervision if seizures frequent

Swimming:

• No unsupervised swimming
• Inform lifeguard, swim with companion

Heights/Machinery:

• Avoid working at heights, operating heavy machinery, open fires

Alcohol:

• Avoid excessive alcohol (lowers seizure threshold, impairs compliance)

Sleep Deprivation:

• Maintain regular sleep schedule (sleep deprivation is major trigger)

Contraception (if switching to carbamazepine):

• Enzyme inducer reduces efficacy of combined oral contraceptive
• Use alternative contraception (IUD, barrier) or higher-dose pill (50 mcg)

Pregnancy Planning:

• High-dose folic acid 5 mg daily (not 400 mcg) pre-conception and through pregnancy
• Preconception counseling to optimize ASM (monotherapy, lowest effective dose)
• Avoid valproate

SUDEP Discussion:

• Sudden unexpected death in epilepsy is rare but real risk
• Best prevention: Seizure control, medication adherence
• Nocturnal supervision/monitoring devices if nocturnal GTC seizures

Epilepsy Specialist Nurse:

• Provide contact details for ongoing support, education, counseling

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Q5: If she undergoes anterior temporal lobectomy, what post-operative complications should you counsel her about?

Model Answer:

Common/Important Complications:

1. Memory Decline (most important functional outcome):

   • Verbal memory decline: 30-40% risk if dominant (usually left) hemisphere surgery
   • Visual memory decline: 10-20% if non-dominant (usually right) hemisphere
   • Mechanism: Removal of hippocampus disrupts memory consolidation
   • Mitigation: Pre-operative neuropsychology assessment; consider SAH (selective amygdalohippocampectomy) vs ATL

2. Visual Field Defect:

   • Superior quadrantanopia (loss of upper quadrant of vision contralateral to surgery)
   • Mechanism: Damage to Meyer's loop (optic radiation fibers passing through temporal lobe)
   • Frequency: Very common (60-80%); usually asymptomatic; patient often unaware
   • Impact: May affect driving eligibility (must meet visual field standards)

3. Dysphasia (if dominant hemisphere):

   • Transient dysphasia common post-operatively
   • Permanent dysphasia rare (less than 5%) with careful surgical technique

4. Infection:

   • Meningitis, wound infection (~1-2%)

5. Stroke:

   • Rare (less than 1%); damage to vascular structures (anterior choroidal artery, MCA branches)

6. Hemorrhage:

   • Intracranial hemorrhage (less than 1%)

7. Seizure Recurrence:

   • 20-40% will NOT achieve complete seizure freedom
   • Some may have improved seizure control (Engel Class II-III)

8. Psychiatric:

   • Post-operative depression (~10-20%)
   • Rarely, psychosis

Expected Benefits:

• 60-80% seizure-free at 2 years
• Improved quality of life, potential to drive, reduced SUDEP risk
• May be able to reduce or withdraw ASMs (gradual, if seizure-free 2+ years)

Informed Consent:

• Detailed discussion with neurosurgeon
• Weigh functional risks (memory, visual field) vs benefit (seizure freedom)
• Neuropsychological counseling essential

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13. Patient/Layperson Explanation

What is a Focal Seizure?

A focal seizure (also called a partial seizure) starts in one specific part of your brain, rather than affecting the whole brain at once. Think of it like a small electrical storm beginning in one area, rather than spreading everywhere immediately.

What Causes Focal Seizures?

Focal seizures happen because there's an area of your brain that's irritable and produces abnormal electrical signals. This can be due to:

• Scarring in the brain (e.g., from a high fever in childhood, head injury, or stroke)
• A small growth or tumor (often benign)
• Abnormal blood vessels in the brain
• Brain development differences from birth

What Are the Symptoms?

The symptoms depend on which part of your brain is affected:

Temporal Lobe Seizures (most common):

• A strange rising feeling in your stomach
• Sudden intense fear or anxiety
• Feeling like you've experienced something before (déjà vu)
• Unusual smells or tastes
• Staring blankly and not responding
• Repetitive movements like lip smacking, chewing, or fidgeting with clothes
• Confusion afterwards and not remembering what happened

Frontal Lobe Seizures:

• Sudden jerking or stiffening of one side of your body
• Unusual movements like thrashing, kicking, or making sounds
• Often happen during sleep
• Usually very brief (less than a minute)

Visual or Sensory Symptoms:

• Flashing lights or visual hallucinations (if affecting the back of the brain)
• Tingling or numbness in part of your body (if affecting the sensory area)

How Is It Diagnosed?

1. MRI Brain Scan: Takes detailed pictures of your brain to look for scars, tumors, or other abnormalities
2. EEG (Electroencephalogram): Records electrical activity in your brain using sensors on your scalp
3. Video Monitoring: Sometimes you stay in hospital for a few days to record your brain waves during a seizure

How Is It Treated?

Medication:

• Most people take daily anti-seizure medication (like lamotrigine, levetiracetam, or carbamazepine)
• About half of people become seizure-free with the first medication
• If one medication doesn't work, your doctor may try a different one or add a second medication

Surgery:

• If two medications don't control your seizures (about 1 in 3 people), you may be a candidate for brain surgery
• Surgery removes or disconnects the small area of brain causing the seizures
• For the right candidates (e.g., scarring in one part of the brain), surgery can cure epilepsy in 60-80% of cases
• Risks include memory changes and visual field problems, but these are carefully discussed beforehand

Lifestyle and Safety:

• Avoid triggers: Sleep deprivation, excessive alcohol, flashing lights (for some people)
• Safety precautions: Shower instead of bath, no unsupervised swimming, inform employer/school
• Driving: You cannot drive until seizure-free (usually 6-12 months depending on country rules)

What Is the Outlook?

• With medication, many people become seizure-free and live normal lives
• If medications don't work, surgery offers a potential cure for carefully selected patients
• Even if seizures continue, treatments can often reduce their frequency and severity
• Regular follow-up with a neurologist is important to optimize treatment

Important Safety Information

SUDEP (Sudden Unexpected Death in Epilepsy):

• This is rare but important to know about
• The best way to reduce this risk is to control seizures and take medication regularly
• If you have frequent convulsive seizures, consider nocturnal monitoring devices

When to Seek Emergency Help:

• Seizure lasting more than 5 minutes
• Multiple seizures without recovery in between
• Difficulty breathing after a seizure
• Injury during seizure
• First-ever seizure

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