Epilepsy is diagnosed by any one of three criteria:

1. At least two unprovoked seizures occurring more than 24 hours apart;
2. One unprovoked (or reflex) seizure with at least a 60% risk of recurrence over the next 10 years;
3. Diagnosis of an epilepsy syndrome (a characteristic seizure plus abnormal EEG and MRI findings in a recognisable pattern).

Seizure activity arises three ways: stimulation of excitatory pathways, inhibition of the inhibitory pathways, or withdrawal of a long-term CNS depressant. Any disorder that alters the neuronal environment can provoke one — metabolic and electrolyte disturbances, trauma, infection, tumour, vascular disease, drugs or alcohol, and toxins — and the cause is often never found.

Structural/metabolic causes shift with age (Table 18.9):

The evaluation:

• History — subjective sensations, altered consciousness, motor signs, behaviour change, and the setting; a witness account is often decisive.
• Blood and urine labs — blood glucose, serum calcium, BUN, urine sodium, creatinine clearance — to catch systemic disease that presents as seizures.
• EEG — assesses the seizure type and helps localise its focus; combined EEG + functional MRI maps the networks involved.
• Brain imaging and CSF exam — to identify an underlying neurologic disease.

Seizures are classified (ILAE 2017) on three axes: where it starts (focal vs generalized onset), awareness (retained vs impaired), and movement (motor vs nonmotor). Separating focal from generalized epilepsy is vital to treatment and prognosis.

The phases of a seizure, in order:

The aura is tied to cortical spreading depression — a self-propagating wave of neuronal and glial depolarisation that starts in the occipital cortex and spreads forward. It releases excitatory neurotransmitters that activate the trigeminovascular system (afferents of cranial nerve V), producing vasodilation of dural vessels, neurogenic inflammation, and sensitisation of pain receptors. Neuropeptides — CGRP, substance P, PACAP — drive the meningeal inflammation and pain and are the target of newer drugs.

Three classes:

• Migraine with aura;
• Migraine without aura — the most common form;
• Chronic migraine — ≥15 days/month for >3 months, often from analgesic overuse (rebound headache).

Four phases of an attack:

Who gets migraines (demographics):

• Women 18%, men 6%, children 10% in the US — roughly 3:1 female;
• Most common at 18–44 years; onset typically in childhood, adolescence, or young adulthood;
• A family history is common — migraine comes from combined genetic and environmental factors;
• Hormonal — most frequent before and during menstruation, tied to cyclic estrogen withdrawal.

Triggers that lower the threshold for an attack:

• Fatigue, oversleeping, missed meals, overexertion;
• Weather change; stress, or the letdown after stress;
• Hormonal changes (menstrual periods);
• Excess afferent stimulation — bright lights, strong smells;
• Chemicals — alcohol, nitrates.

The picture:

• Unilateral — orbit, temple, cheek; severe, stabbing, throbbing, steady;
• Begins without warning and may switch sides between episodes;
• Men, 20–50 years; no family history;
• Ipsilateral autonomic signs — lacrimation (tearing), ptosis, nasal congestion/rhinorrhea (Horner syndrome).

The clustering pattern — its signature:

• Up to 8 attacks a day, each lasting minutes to hours;
• Recur over days, then a long spontaneous remission;
• The chronic form (no sustained remission) is 10–20% of cases;
• Circadian, rhythmic timing points to hypothalamic involvement. Triggers: caffeine, alcohol, smoking.

The boundary with acute ischemic stroke is dual-gated: a deficit that lasts more than 24 hours, or shows infarction on imaging regardless of how briefly it lasted, is a stroke — so the distinction is tissue-based, not just time-based. A short event with an infarct is still a stroke, not a TIA.

Symptoms — sudden, focal, temporary:

• Hemiparesis or numbness;
• Sudden confusion; loss of balance;
• Loss of vision; speech disturbance;
• A sudden, severe headache.

Modifiable — most of the list:

• Hypertension (poorly or uncontrolled);
• Smoking — raises stroke risk 2–4×;
• Insulin resistance and diabetes; atrial fibrillation;
• Polycythemia and thrombocythemia; high total or low HDL cholesterol, high lipoprotein(a);
• Carotid artery disease; heart, valvular, and peripheral vascular disease; hyperhomocysteinemia;
• Postmenopausal hormone therapy; high sodium >2300 mg / low potassium <4700 mg; obesity;
• Obstructive sleep apnea; depression; physical inactivity; Chlamydia pneumoniae infection.

Non-modifiable:

• Family history of ischemic stroke;
• Black American;
• Female;
• Sickle cell disease.

The two inflows:

• Internal carotid arteries (the larger share) enter the skull base and divide into the anterior and middle cerebral arteries;
• Vertebral arteries ascend through the cervical transverse foramina, enter at the foramen magnum, and join at the pons–medulla to form the basilar artery, which divides into the posterior cerebral arteries (and supplies the cerebellum via PICA, AICA, and superior cerebellar arteries).

The Circle of Willis — anterior cerebral, anterior communicating, internal carotid, posterior communicating, and posterior cerebral arteries — is a ring that provides collateral flow when one contributing artery is obstructed. (The middle cerebral artery leaves the circle; it is not part of the ring.) The brain takes ~20% of cardiac output (~800–1000 mL/min), and CO₂ is its main vasodilator.

Which artery, which deficit (Table 15.5):