Seizure without Status Epilepticus

Background

Risk factors: birth trauma, perinatal ischemia, prematurity, TBI with loss of awareness > 1 hour or penetrating wound, strokes, brain masses (tumors, abscesses), prior CNS infections, and recent brain surgery
Key for seizures: rhythmic, stereotyped event with sudden onset/offset o If bilateral seizure-like activity (eg tonic-clonic), then there will also be loss of awareness
- If focal, can have loss of awareness or retained awareness

A clear description or recording of seizure semiology is helpful, including preceding aura, event description, duration, loss of awareness, post-ictal confusion with duration, tongue biting (and location), urination/defecation, frequency of events, and triggers
Provoked seizures can develop with new medications (lower threshold), ASM/benzodiazepine/EtOH withdrawal, physical/mental/emotional stressors, hypo/hyperglycemia, significant electrolyte abnormalities (e.g. hyponatremia), CNS infections
In pts with new seizures, important to work-up potential underlying etiology
If patient has a known seizure disorder with a reversible underlying trigger or typical frequency of seizures and has returned to their baseline neurologic exam, EEG may not be necessary
In patients with new first-time seizures who have returned to baseline, would be reasonable to perform EEG in the outpatient setting if there is not a clear reason that the patient would be at risk for a repeat seizure (eg alcohol withdrawal).
MRI brain with and without contrast (can be done with epilepsy protocol) once stable

You do not need to acutely treat a seizure with medication unless there is concern for status epilepticus. I woud leave the 5 minutes here because IM resident’s may not known the definition: ...unless there is generalized tonic clonic activity lasting 5 minutes or greater”

ASMAED	Adverse Effects
Levetiracetam (Keppra) (PO/IV)	Sedation and agitation, worsening of underlying mood disorders. Can trial B6 supplementation to help with mood effects
Valproic acid (Depakote) (PO/IV)	Sedation, hirsutism, PCOS, P450 inhibitor, nausea, liver injury, hyperammonemia, teratogenicity
Phenytoin (Dilantin) (PO)/ Fosphenytoin (IV)	Sedation, gingival hyperplasia, arrhythmias
Lacosamide (Vimpat) (PO/IV)	Heart block, dizziness, ataxia
Topiramate (Topamax) (PO)	Kidney stones, metabolic acidosis, paresthesias, weight loss, cognitive slowing
Carbamazepine (Tegretol) (PO)	Hyponatremia, SJS (in Han Chinese check HLA), bone marrow suppression (rare)
Oxcarbazepine (Trileptal) (PO)	Similar to Carbamazepine
Lamotrigine (Lamictal) (PO)	SJS/TEN, nausea, least sedating
Zonisamide (Zonegran) (PO)	Sedation, ataxia, nausea, confusion

Can be very difficult to distinguish from epileptic seizures
Not all NES are psychogenic, such as myoclonus, tremors, and syncope
Features more common in PNES
- Retained awareness with bilateral extremity “seizing”
- Opisthotonus (arching the back)
- Talking during a spell
- Excessively long spells (e.g. lasts hour or days)
- Forced eye closure
- Truncal thrusting
- Suppressibility to touch
- Coachability during a spell or reacting to external stimuli
- Heavy breathing during a spell with lots of rigorous movement
- Immediately returning to baseline after a spell
Features more common in epileptic seizures:
- Seizures arising out of sleep
- Highly stereotyped
- Incontinence
- Severe injuries (e.g. burns)
Management
- Try to avoid excessive BZD use that could compromise airway protection
- This requires good clinical judgement as you wouldn't want to withhold Ativan and discover that the pt was having true atypical seizures. The compromise would be do not repeatedly administer BZDs when there is suspicion for PNES as well as no evidence of response to prior BZD administration.