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-focal aware
-focal impaired awareness
what are the two types of focal seizures?
Motor: twitching, jerking in one limb/face
Sensory: tingling, visual flashes, auditory phenomena
Autonomic: flushing, nausea, epigastric rising sensation
Psychic: déjà vu, fear, jamais vu
presentation of focal aware seizure
Altered awareness/responsiveness
Automatisms: lip smacking, picking at clothes, chewing
Aura may precede (odd smell, taste, rising epigastric sensation)
Post-ictal confusion common
presentation of focal impaired awareness seizure
-absence
-tonic clonic
-tonic
-clonic
-myotonic
-atonic
name the types of generalized seizures
Sudden loss of consciousness
Tonic phase: rigidity, cry, apnea, cyanosis
Clonic phase: rhythmic jerking of limbs
Post-ictal confusion, fatigue, headache
presentation of tonic-clonic seizure
Sudden stiffening, sustained posturing
Often during sleep
presentation of tonic seizure
Repetitive, rhythmic jerking movements
presentation of clonic seizure
Sudden, brief, shock-like muscle jerks
Often bilateral and symmetric (e.g., juvenile myoclonic epilepsy)
presentation of myoclonic seizure
Sudden loss of tone → collapse, injury risk
Usually brief, may need helmet for protection
presentation of atonic seizure
foca lonset
hx of aura before seizure suggests this type of seizure
CT head non contrast
-rule out acute bleed, stroke, mass lesion (esp. if focal deficit, new-onset seizure, or trauma).
emergent imaging for seizures
MRI brain (preferred long-term) → more sensitive for structural lesions (tumor, cortical dysplasia, mesial temporal sclerosis)
preferred long term imaging in work up of seizure
ideally within 24 hours of event
how soon should you get EEG post seizure event?
Status epilepticus.
Abnormal neuro exam or persistent altered mental status.
First seizure with structural lesion on imaging.
Metabolic derangement requiring correction.
indications to hospitalize seizure pt
carbamazepine, lamotrigine, levetiracetam.
first line therapy for focal seizure if recurrence risk is high
valproate, levetiracetam., lamotrigine
first line therapy for generalized tonic-clonic seizure if recurrence risk is high
Usually continued for 2-5 years seizure-free before tapering
after first seizure, if recurrence rate is high, continue anti-seizure meds for how long?
Abnormal EEG (epileptiform discharges).
Abnormal neuroimaging (structural lesion: tumor, stroke, cortical malformation).
Prior CNS insult (TBI, stroke, meningitis).
Seizure occurred during sleep (nocturnal seizure).
first time seizure pts who have a high risk of recurrence:
About 30-40% of adults will never recur after a first seizure.
Long-term remission rates are similar whether treatment starts after the first or second seizure.
Side effects of ASMs: cognitive impairment, sedation, mood changes, teratogenicity, drug interactions.
arguments against treating after first seizure
valproate, levetiracetam.
first line treatment for myoclonic seizures
seizure >5 min, or ≥2 seizures without return to baseline
define status epilepticus
1. stabililze ABCs (0-5 min)
2. IV benzo (lorazepam preferred) (5-10 min)
3. IV antiseizure drug (10-30 min)
4. continuous IV anesthetic infusion (30-60 min)
management of status epilepticus
vasovagal syncope
what type of neurally mediated syncope?
Triggers: emotional stress, pain, prolonged standing, sight of blood.
Prodrome: nausea, warmth, diaphoresis, lightheadedness, vision changes.
carotid sinus hypersensitivity
Condition in which pressure over the carotid sinus leads to a decreased heart rate, decreased BP, and cerebral ischemia with syncope. May occur in older adults with hypertension or occlusion of the carotid artery
failure of autonomic reflelxes---> inadequate BP response to standing
causes: hypovolemia, autonomic dysfunction, medication
what causes orthostatic syncope
orthostatic syncope
what type of syncope?
Occurs within seconds to minutes of standing, improves with lying down.
Bradyarrhythmias (sinus node dysfunction, AV block).
Tachyarrhythmias (VT, SVT, WPW, long QT, Brugada).
arrhythmias that can cause syncope
Aortic stenosis (exertional syncope).
Hypertrophic obstructive cardiomyopathy (HOCM).
Pulmonary embolism.
Acute MI or ischemia.
Cardiac tamponade.
structural causes of cardiac syncope
sudden, no prodrome, exertional or while supine, family history of SCD.
historical features pointing to cardiac syncope
Prodrome (nausea, diaphoresis), triggers like pain/stress
prodrome associated with vasovagal syncope
vertigo
true spinning sensation
BPPV (most common cause), vestibular neuritis, Ménière's disease, labyrinthitis.
common causes of peripheral vertigo
stroke (posterior circulation), multiple sclerosis, cerebellar tumor.
causes of central vertigo
Benign Paroxysmal Positional Vertigo (BPPV)
most common cause of vertigo in adults (esp. >50 yrs).
Reassurance (benign in most).
Avoid triggers (prolonged standing, dehydration).
Physical counterpressure maneuvers (leg crossing, handgrip).
Severe recurrent cases: medications (fludrocortisone, midodrine).
treatment of neurally mediated syncope
Hydration, salt/fluid intake.
Compression stockings.
Review/adjust medications.
Pharmacologic: midodrine, fludrocortisone.
tx of orthostatic hypotension causing syncope
epley maneuver
Series of head movements to relieve symptoms of benign positional vertigo

low-salt diet, diuretics
tx of Menieres disease
benign paroxysmal positional vertigo
Brief, recurrent episodes of vertigo (seconds-minutes).
Triggered by head position changes (rolling over in bed, looking up).
No hearing loss or tinnitus.
Dix-Hallpike maneuver
Rapidly moving the pt from a sitting position to the supine position with the head turned 45 degrees to the Right. After waiting apx. 20-30 sec, the pt is returned to the sitting position. If no Nystagmus is observed, the procedure is then repeated on the Left side.
-+ nystagmus indicates BPPV

Otoliths displaced into semicircular canals → transient vertigo.
what causes BPPV
vestibular neuronitis
Acute onset of severe, continuous vertigo lasting days.
Often follows viral upper respiratory infection.
No hearing loss or tinnitus.
Unidirectional, horizontal nystagmus (away from affected side).
Positive head impulse test (catch-up saccade when turning head toward lesion).
physical exam findings associated with vestibular neuronitis
Isolated inflammation of vestibular nerve.
cause of vestibular neuritis
labyrinthitis
Similar to vestibular neuronitis (acute, prolonged vertigo).
Associated with hearing loss and tinnitus (distinguishes from neuronitis).
Often post-viral or bacterial infection.
Nystagmus (unidirectional, horizontal).
Sensorineural Hearing deficit on exam (audiometry confirms).
physical exam findings associatedd with labyrinthitis
Inflammation involves both vestibular and cochlear portions of labyrinth → vertigo + hearing loss.
pathophys of labyrinthitis
RINNE:
SNHL: still AC > BC (test remains "positive"), but hearing is diminished overall.
Helps differentiate from conductive hearing loss, where BC > AC (negative Rinne).
WEBER:
SNHL: sound lateralizes to the normal (unaffected) ear.
Conductive loss: sound lateralizes to the affected ear.
how do you distinguish between sensorineural and conductive hearing losss
vestibular rehabilitation therapy
Core treatment for persistent dizziness and imbalance due to vestibular dysfunction.
Supervised physical therapy program focusing on:
Habituation exercises: repeated exposure to movements that provoke dizziness (reduces sensitivity).
Gaze stabilization: improves visual focus during head movements.
Balance training: improves posture and reduces fall risk.
physical therapy components off vestibulalr rehabililtation therapy
chronic vestibular neuritis, labyrinthitis recovery, bilateral vestibular loss, central compensation after vestibular damage.
indications for vestibular rehab
Avoid alcohol, caffeine, nicotine (can worsen vestibular symptoms).
avoid these substancess in pts with chronic dizziness
meclizine, benzodiazepines, antihistamines
vestibular suppressants useful in short term tx of vertigo