60.3 Epilepsy: Chronic Antiseizure Medications & Post-Stroke Care

Epilepsy Definition, Seizure Classification & Diagnostic Evaluation

Epilepsy is one of the most prevalent chronic neurological conditions managed in primary care. Under the 2014 International League Against Epilepsy (ILAE) consensus definition, epilepsy is diagnosed when a patient fulfills ANY ONE of the following three criteria:

1. At least two unprovoked (or reflex) seizures occurring >24 hours apart.
2. One unprovoked (or reflex) seizure with a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years (e.g., a patient with a single seizure occurring months after an ischemic stroke, or a patient with a single seizure whose brain MRI reveals a structural lesion and whose EEG reveals focal epileptiform discharges).
3. Diagnosis of a specific, defined epilepsy syndrome (e.g., Juvenile Myoclonic Epilepsy, Lennox-Gastaut syndrome).

                  ILAE 2017 OPERATIONAL SEIZURE CLASSIFICATION

   Classification Category     Subtypes & Clinical Manifestations                          Electroclinical Features
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Focal Onset Seizures        • Focal Aware (formerly Simple Partial): consciousness      • Originates within neuronal networks
                                 remains fully intact; sensory aura, motor twitching,        limited to one cerebral hemisphere.
                                 autonomic symptoms, or psychic phenomena.                 • Interictal EEG: focal spikes, sharp
                               • Focal Impaired Awareness (formerly Complex Partial):        waves, or focal slowing.
                                 consciousness altered/impaired; automatisms (lip-smacking,• May propagate to bilateral tonic-clonic
                                 fumbling, swallowing), post-ictal confusion.                seizures (secondary generalization).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Generalized Onset           • Absence: sudden 5-10 second behavioral arrest with        • Originates at some point within, and
   Seizures                      unresponsiveness; rapid recovery; typical 3 Hz              rapidly engages, bilaterally distributed
                                 generalized spike-and-wave discharges on EEG.               cerebral networks simultaneously.
                               • Generalized Tonic-Clonic (GTC): sudden loss of            • Interictal EEG: generalized bilateral
                                 consciousness, tonic extension followed by clonic jerking.  synchronous spike-and-wave discharges.
                               • Myoclonic: shock-like, brief muscle jerks without loss    • Broad-spectrum ASMs required; narrow-spectrum
                                 of consciousness; characteristic of Juvenile Myoclonic      sodium blockers may aggravate myoclonus/absence!
                                 Epilepsy (JME; morning jerks dropping coffee cup).
                               • Atonic: sudden loss of postural muscle tone ("drop attack").
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════

Diagnostic Workup of a First Unprovoked Seizure

• History & Collateral Account: Differentiate true seizure from syncope, psychogenic non-epileptic seizures (PNES), and transient ischemic attack (TIA).
  • High-Yield Differentiator: Lateral border tongue laceration is highly specific (99%) for generalized tonic-clonic seizures (unlike the tip of the tongue in syncope). Prolonged post-ictal confusion (>=15-30 minutes) strongly supports seizure over cardiogenic syncope.
• 12-Lead Electrocardiogram (ECG): MANDATORY for every patient presenting with a first-time seizure or transient loss of consciousness to rule out cardiogenic syncope, high-grade AV block, prolonged QTc syndrome, and Brugada syndrome mimicking convulsive syncope.
• Laboratory Evaluation: Serum glucose (hypoglycemia), basic metabolic panel (hyponatremia, hypocalcemia), magnesium, liver function tests, complete blood count, and urine toxicology screen.
• Structural Neuroimaging: Brain MRI with dedicated epilepsy protocol (including high-resolution coronal T2 and FLAIR thin-slice cuts perpendicular to the long axis of the hippocampus) is the gold standard. It detects subtle structural epileptogenic pathologies: mesial temporal sclerosis (hippocampal sclerosis), focal cortical dysplasias, cavernous malformations, low-grade tumors (gangliogliomas, DNETs), and ischemic strokes. Emergent non-contrast head CT is reserved for the acute emergency setting to exclude acute intracranial hemorrhage or large mass effect.
• Electroencephalography (EEG): Routine 30-minute awake and sleep-deprived interictal EEG should be obtained within 24 to 48 hours. A normal interictal EEG does NOT rule out epilepsy (up to 50% of initial routine EEGs in patients with proven epilepsy are normal); prolonged ambulatory or inpatient continuous video-EEG monitoring increases diagnostic yield.

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Antiseizure Medication (ASM) Selection & Pharmacokinetic Principles

The therapeutic objective of chronic antiseizure medication (ASM) therapy is complete seizure freedom with minimal adverse effects. Monotherapy is the initial goal: approximately 50% of patients achieve seizure freedom on their first ASM monotherapy, and another 15% achieve control with a second single agent. Drug-resistant (refractory) epilepsy is defined as the failure of adequate trials of two tolerated and appropriately chosen ASM schedules (whether monotherapy or combination).

                  SPECTRUM OF ACTIVITY: BROAD-SPECTRUM VS. NARROW-SPECTRUM ASMs

   Therapeutic Category        Specific Agents                              Clinical Indications & Critical Prescribing Rules
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Broad-Spectrum ASMs         • Levetiracetam                              • First-line for ALL seizure types: focal onset,
                               • Lamotrigine                                  generalized onset (tonic-clonic, absence, myoclonic),
                               • Valproic Acid / Divalproex                   and unclassified seizures.
                               • Topiramate                                 • Mandatory choice when seizure onset type is ambiguous.
                               • Zonisamide
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Narrow-Spectrum ASMs        • Carbamazepine                              • Indicated ONLY for FOCAL onset seizures.
                               • Phenytoin                                  • DANGER: Narrow-spectrum sodium channel blockers can
                               • Oxcarbazepine                                PARADOXICALLY WORSEN generalized seizure types
                               • Lacosamide*                                  (particularly absence and myoclonic seizures in JME)!
                               • Gabapentin / Pregabalin
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════
   *Note: Lacosamide is primarily approved for focal onset seizures, though recently approved as adjunctive for generalized tonic-clonic.

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Second-Generation & Third-Generation ASMs in Clinical Practice

Second- and third-generation ASMs have largely supplanted first-generation agents as initial therapy in primary care due to predictable linear pharmacokinetics, oral and intravenous bioequivalence, absence of hepatic cytochrome P450 enzyme induction, and superior tolerability profiles.

                  SECOND- AND THIRD-GENERATION ANTISEIZURE MEDICATIONS

   Medication & Class       Target Maintenance Dosing       Metabolism & Elimination        Major Adverse Effects & High-Yield Pearls
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Levetiracetam (Keppra)   500 to 1500 mg PO BID           66% excreted unchanged in       • Rapid titration; 1:1 IV-to-PO bioequivalence.
   Synaptic Vesicle 2A      (Titrate by 500 mg/day q2w)     urine; enzymatic hydrolysis;    • No CYP metabolism or protein binding.
   (SV2A) Ligand                                            NO hepatic CYP involvement.     • NEUROPSYCHIATRIC: Agitation, aggression,
                                                                                              depression, suicidality ("Keppra rage" in 10-15%).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Lamotrigine (Lamictal)   100 to 200 mg PO BID            Hepatic glucuronidation via     • Broad-spectrum; excellent mood stabilization.
   Voltage-Gated Sodium     (Slow titration over 6-8 weeks; UGT1A4; NO CYP involvement.     • SLOW TITRATION required to prevent SJS/TEN.
   Channel Blocker          start 25 mg daily x 2 weeks)                                    • CRITICAL: ESTROGEN OCPs DOUBLE CLEARANCE,
                                                                                              slashing levels by 50% (breakthrough seizures)!
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Lacosamide (Vimpat)      100 to 200 mg PO BID            Renal excretion (40%) and       • Linear pharmacokinetics, minimal drug interactions.
   Slow Sodium Inactivation (Titrate by 50 mg BID weekly)   CYP2C19 demethylation.          • Obtain baseline ECG: dose-dependent PR interval
   Enhancer                                                                                   prolongation (caution with nodal blockers).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Topiramate (Topamax)     100 to 200 mg PO BID            70% excreted unchanged in       • Broad-spectrum; also used for migraine prophylaxis.
   Multi-Target: Na+, GABA, (Start 25 mg BID, titrate       urine; weak CYP2C19 inhibitor   • ADVERSE: Cognitive slowing ("Dopamax"),
   AMPA, Carbonic Anhydrase  by 50 mg/day weekly)           and mild CYP3A4 inducer.          weight loss, nephrolithiasis, metabolic acidosis,
                                                                                              acute myopia / angle-closure glaucoma.
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════

1. Levetiracetam (Keppra)

• Mechanism: Binds stereoselectively to synaptic vesicle protein 2A (SV2A) in presynaptic terminals, inhibiting presynaptic vesicle exocytosis and reducing action-potential-dependent neurotransmitter release.
• Pharmacokinetics: Completely absorbed, linear kinetics, minimal protein binding (<10%), not metabolized by hepatic cytochrome P450 enzymes (cleared primarily by renal elimination; dose-reduce in renal impairment).
• Neuropsychiatric Adverse Effects: In 10% to 15% of patients, levetiracetam triggers behavioral irritability, hostility, emotional lability, anxiety, depression, and paranoia (colloquially termed "Keppra rage"). It is relatively contraindicated in patients with active severe psychiatric illness (bipolar disorder, major depression with suicidal ideation). Pyridoxine (vitamin B6, 100 mg daily) can occasionally mitigate mild irritability.

2. Lamotrigine (Lamictal)

• Mechanism: Voltage-gated sodium channel blocker and glutamate release inhibitor; broad-spectrum activity with favorable cognitive and mood-stabilizing effects.
• Titration & Stevens-Johnson Syndrome (SJS) Risk: Rapid dose escalation substantially increases the risk of severe dermatologic reactions, including Stevens-Johnson syndrome and Toxic Epidermal Necrolysis (TEN). Lamotrigine must be titrated slowly over 6 to 8 weeks (e.g., 25 mg daily for weeks 1-2, 50 mg daily for weeks 3-4, 100 mg daily for week 5, then 200 mg daily).
• The Estrogen Oral Contraceptive Interaction (BOARD FAVORITE): Lamotrigine is cleared predominantly via hepatic glucuronidation mediated by UGT1A4. Ethinyl estradiol (found in combined oral contraceptive pills, transdermal contraceptive patches, and vaginal rings) induces UGT1A4 glucuronidation, increasing lamotrigine clearance by >100% and cutting serum lamotrigine concentrations by 50% within days. This precipitous drop triggers catastrophic breakthrough seizures and status epilepticus. Conversely, during the placebo "pill-free" week, lamotrigine levels double back up, inducing acute dizziness, ataxia, and diplopia. Management: When starting an estrogen-containing contraceptive, the maintenance lamotrigine dose typically must be doubled; alternatively, recommend a progestin-only intrauterine device (e.g., levonorgestrel IUD), which does not affect glucuronidation.
• Valproic Acid Interaction: Valproate strongly inhibits lamotrigine glucuronidation, doubling its elimination half-life and dramatically amplifying the risk of fatal SJS/TEN. If lamotrigine is added to valproate, the starting dose must be halved (25 mg every other day) using a dedicated low-dose titration kit.

First-Generation ASMs: Mechanisms, Toxicities & Drug Interactions

First-generation ASMs have narrow therapeutic indices, exhibit extensive hepatic metabolism, and induce or inhibit cytochrome P450 enzymes, leading to multiple drug interactions and long-term end-organ toxicities.

                  FIRST-GENERATION ANTISEIZURE MEDICATIONS: COMPARISON

   Agent & Class            Therapeutic Window & Kinetics   Enzyme Effects & Interactions   Toxicities & Clinical Monitoring
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Carbamazepine (Tegretol) 4 to 12 mcg/mL                  POTENT CYP3A4 INDUCER           • AUTOINDUCTION: Induces its own metabolism;
   Sodium Channel Blocker   Linear clearance;               Induces metabolism of OCPs,       half-life drops from 36h to 15h after 3-4w.
                            98% hepatic metabolism.         warfarin, statins, and DOACs.   • SIADH with hyponatremia (check Na+).
                                                                                            • Aplastic anemia, agranulocytosis (monitor CBC).
                                                                                            • HLA-B*1502 screening in Asian patients (SJS).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Phenytoin (Dilantin)     Total: 10 to 20 mcg/mL          POTENT INDUCER of CYP3A4,       • ZERO-ORDER (SATURATION) PHARMACOKINETICS;
   Sodium Channel Blocker   Free: 1.0 to 2.0 mcg/mL         CYP2C9, CYP2C19, and UGT.         small dose increments produce massive toxic jumps.
                            Nonlinear Michaelis-Menten.     Decreases DOACs, warfarin.      • Acute toxicity: Nystagmus, ataxia, lethargy.
                                                                                            • Chronic: Gingival hyperplasia, hirsutism,
                                                                                              peripheral neuropathy, cerebellar vermian atrophy.
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
   Valproic Acid /          50 to 100 mcg/mL                ENZYME INHIBITOR                • Broad-spectrum of choice for generalized/JME.
   Divalproex (Depakote)    Linear protein binding;         Inhibits CYP2C9 and UGT;        • Hyperammonemic encephalopathy (normal LFTs!).
   GABA Transaminase        hepatic glucuronidation         doubles lamotrigine levels.     • Weight gain, alopecia, pancreatitis, tremor.
   Inhibitor & Na+ Blocker  and beta-oxidation.                                             • SEVERE TERATOGENICITY: Neural tube defects,
                                                                                              lower IQ; CONTRAINDICATED IN PREGNANCY.
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════════

1. Carbamazepine & Genetic Screening

• Autoinduction: Carbamazepine induces its own hepatic CYP3A4 metabolism. When initiated, its half-life is approximately 30 to 40 hours, but after 3 to 5 weeks of continuous therapy, autoinduction reduces the elimination half-life to 12 to 18 hours, frequently requiring dosage re-titration.
• Hyponatremia: Carbamazepine enhances collecting duct sensitivity to ADH (SIADH-like effect); monitor serum sodium routinely.
• HLA-B*1502 Screening: The FDA mandates HLA-B*1502 allele screening prior to initiating carbamazepine in patients of Asian ancestry (Han Chinese, Filipino, Thai, Malaysian, Indian). Carriage of this allele confers an astronomical (>100-fold) relative risk of fatal Stevens-Johnson syndrome and Toxic Epidermal Necrolysis.

2. Phenytoin & Nonlinear Pharmacokinetics

• Michaelis-Menten (Zero-Order) Elimination: At low plasma levels, phenytoin clearance is first-order (rate of elimination is proportional to drug concentration). However, within the therapeutic range (10 to 20 mcg/mL), hepatic metabolizing enzymes (CYP2C9 and CYP2C19) become fully saturated. Once saturated, elimination switches to zero-order kinetics (a constant amount of drug is cleared per unit time). Beyond this saturation point, small, seemingly trivial dosage increases (e.g., increasing from 300 mg to 330 mg daily) produce disproportionately massive spikes in serum drug levels, precipitating acute cerebellar toxicity (horizontal nystagmus, gait ataxia, diplopia, dysarthria, and stupor).
• Protein Binding Adjustments: Phenytoin is 90% bound to serum albumin. In hypoalbuminemia (cirrhosis, nephrotic syndrome, malnutrition, elderly), total measured phenytoin levels are falsely depressed while active unbound free phenytoin remains elevated. The Sheiner-Tozer equation must be used to calculate corrected phenytoin: $\text{Corrected Phenytoin} = \frac{\text{Measured Total Phenytoin}}{0.2 \times \text{Serum Albumin (g/dL)} + 0.1}$

3. Valproic Acid / Divalproex Sodium

• Broad-Spectrum Efficacy: Valproate remains the most effective ASM for primary generalized tonic-clonic seizures, idiopathic generalized epilepsies, and Juvenile Myoclonic Epilepsy (JME).
• Non-Hepatic Encephalopathy: Valproate inhibits the urea cycle enzyme carbamoyl phosphate synthetase I, which can trigger valproate-induced hyperammonemic encephalopathy (VHE) characterized by acute lethargy, confusion, asterixis, and increased seizure frequency in the setting of completely normal transaminases and bilirubin; check serum ammonia immediately in any patient on valproate who develops delirium.

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Teratogenicity, Reproductive Health & Pregnancy Management in Epilepsy

Over 90% of women with epilepsy deliver healthy infants. However, uncontrolled maternal convulsive seizures carry significant risks of fetal hypoxia, intracranial hemorrhage, miscarriage, and maternal mortality. The fundamental management rule is to achieve complete seizure control with the lowest effective dose of a single ASM (monotherapy) prior to conception.

                  TERATOGENIC RISK PROFILES OF COMMONLY PRESCRIBED ASMs

   Antiseizure Medication   Major Congenital Malformation (MCM) Risk   Specific Teratogenic Phenotypes & Cognitive Impact
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Valproic Acid            HIGHEST RISK (10% to 11%)                  • Neural tube defects (spina bifida in 1-2%), cleft palate,
   (Depakote)               Dose-dependent (> 800 mg/day extreme)        craniosynostosis, cardiac septal defects.
                                                                       • NEURODEVELOPMENTAL DEFICITS: Offspring suffer an average
                                                                         7 to 10 point reduction in IQ and higher autism rates.
                                                                       • ABSOLUTE CONTRAINDICATION in reproductive-aged females.
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Topiramate               MODERATE RISK (4% to 5%)                   • 5-fold increased risk of oral clefts (cleft lip/palate);
   (Topamax)                                                           • Fetal growth restriction (small for gestational age [SGA]).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Carbamazepine &          MODERATE RISK (3% to 4%)                   • Neural tube defects, cardiac anomalies, craniofacial defects
   Phenytoin                                                             (fetal hydantoin syndrome).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Levetiracetam &          LOWEST RISK (2% to 3%)                     • Malformation rates EQUIVALENT to baseline unexposed
   Lamotrigine              SAFEST FIRST-LINE CHOICES IN PREGNANCY       general population risk (2% to 3%).
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════

Preconception Counseling & Gestational Management

1. High-Dose Folic Acid: All women of childbearing potential taking any antiseizure medication should receive oral folic acid supplementation (4.0 mg daily) starting at least 1 to 3 months prior to conception and continuing through the first trimester to minimize the risk of neural tube defects.
2. Therapeutic Drug Monitoring During Pregnancy: Plasma clearance of lamotrigine and levetiracetam accelerates dramatically during pregnancy (due to increased renal blood flow and progesterone/estrogen-mediated UGT induction), with serum levels dropping by 50% to 70% as early as the first trimester. Baseline preconception serum levels must be established, and serum ASM levels monitored monthly throughout gestation, with upward dosage titration to prevent gestational breakthrough seizures. Immediately postpartum, clearance normalizes rapidly, requiring prompt dose reduction to pre-pregnancy levels over 7 to 14 days to prevent maternal toxicity.

ASM-Induced Metabolic Bone Disease

Long-term use of hepatic cytochrome P450 enzyme-inducing ASMs (Carbamazepine, Phenytoin, Phenobarbital, Primidone) induces the hepatic microsomal enzyme CYP24A1, which accelerates the catabolism of 25-hydroxyvitamin D into inactive calcitroic acid metabolites. This produces hypocalcemia, secondary hyperparathyroidism, accelerated bone turnover, osteopenia, osteoporosis, and high fragility fracture rates.

• Management: Patients on chronic enzyme-inducing ASMs require baseline and periodic serum 25-hydroxyvitamin D monitoring, routine supplementation with vitamin D3 (1000 to 2000 IU daily) and calcium (1000 to 1200 mg daily), and a screening DEXA scan after 2 to 5 years of continuous therapy.

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Comprehensive Post-Stroke Care in Primary Care Practice

Stroke is a leading cause of long-term adult disability. Primary care physicians play a central role in managing chronic secondary prevention, coordinating multidisciplinary neurorehabilitation, and screening for underdiagnosed neuropsychiatric complications.

                  CHRONIC POST-STROKE SECONDARY PREVENTION BUNDLE

   Intervention Domain         Clinical Target / Guideline Recommendation                  First-Line Pharmacotherapy / Actions
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
   Lipid Optimization          Target LDL-C < 70 mg/dL (or >= 50% reduction from           High-intensity statin: Atorvastatin 80 mg
                               baseline) for all atherosclerotic ischemic strokes.         or Rosuvastatin 40 mg daily; add Ezetimibe
                                                                                           if LDL remains >= 70 mg/dL.
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Blood Pressure Control      Target BP < 130/80 mmHg after the acute period              ACE inhibitor / ARB, Thiazide-like diuretic
                               to prevent recurrent lacunar and territorial strokes.       (Chlorthalidone/Indapamide), or DHP CCB.
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Antithrombotic Therapy      • Non-Cardioembolic Stroke / TIA: Single antiplatelet       • Aspirin 81 mg daily OR Clopidogrel 75 mg daily.
                               • Short-term DAPT (Aspirin + Clopidogrel x 21 days)        • DAPT beyond 21-90 days increases major bleed
                                 for minor stroke (NIHSS <=3) or high-risk TIA (ABCD2 >=4).  risk without added ischemic benefit!
                               • Cardioembolic (Atrial Fibrillation): Full anticoagulation • Direct Oral Anticoagulant (DOAC: Apixaban,
                                 is superior to antiplatelet therapy.                       Rivaroxaban) preferred over warfarin.
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Neuropsychiatric Screen     Mandatory screening for POST-STROKE DEPRESSION (PSD;        Routine PHQ-9 screening at every visit;
                               affects ~30% of survivors; impairs functional recovery).    First-line: SSRIs (Sertraline, Escitalopram).
   ─────────────────────────────────────────────────────────────────────────────────────────────────────────
   Functional Rehabilitation   Multidisciplinary referrals based on deficits:              • Physical Therapy (gait, balance, spasticity).
                                                                                           • Occupational Therapy (IADLs, ADLs, home safety).
                                                                                           • Speech Therapy (dysphagia screen, aphasia).
   ═════════════════════════════════════════════════════════════════════════════════════════════════════════

Post-Stroke Depression (PSD) & Cognitive Impairment

• Post-Stroke Depression: Affects approximately one-third of all stroke survivors, with the peak incidence occurring in the first 3 to 6 months post-stroke. Left frontal cortical and basal ganglia infarctions carry particularly high vulnerability. PSD directly impedes participation in physical and occupational rehabilitation, doubles 5-year all-cause mortality, and diminishes quality of life. Clinicians must screen routinely using the Patient Health Questionnaire-9 (PHQ-9). First-line therapy consists of Selective Serotonin Reuptake Inhibitors (SSRIs) (such as Sertraline 25-100 mg daily or Escitalopram 10-20 mg daily), which promote neuroplastic recovery alongside mood improvement.
• Post-Stroke Cognitive Impairment (PSCI): Up to 50% of stroke survivors experience cognitive deficits within 6 months. Screen at 3 to 6 months using the MoCA, which is highly sensitive for post-stroke subcortical and executive dysfunction.

Driving Safety & Post-Stroke Seizures

• Driving Restrictions: Most state motor vehicle departments mandate driving cessation for a minimum of 1 to 3 months following an ischemic stroke or TIA, provided no persistent visual field cut (homonymous hemianopia) or motor deficits remain.
• Post-Stroke Seizures: Ischemic stroke is the most common etiology of new-onset epilepsy in older adults (>65 years). A single unprovoked late seizure occurring >7 days post-stroke carries an approximately 70% risk of recurrence, meeting the ILAE definition for epilepsy and mandating initiation of chronic ASM monotherapy (with Levetiracetam or Lamotrigine being preferred choices due to minimal vascular and drug interactions).