Epilepsy Part 2 Flashcards
Investigations into a seizure
EEG: support diagnosis of epilepsy, also used to monitor treatment effect. Usually can find abnormalities in under 24 hours.
- Look for the double Banana signal.
Video EEG monitoring:
- Indicated to characterize spells (seizure vs syncope vs PNES vs other)
- Localize seizures for presurgical workup
- Determine seizure type to select ASD, quantify seizures, monitor treatment effect.
CT, MRI, Presurgical (SPECT, PET)
- Cerebral Calcifications: Sturge Weber Syndrome. Seen on CT
- Hippocampal Sclerosis can be seen on MRI: Other common temporal lobe auras include olfactory and gustatory hallucinations, jamais vu, and sudden intense panic. Hippocampal sclerosis is the most common cause of new onset epilepsy in adulthood.
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Management of Seizures: after first unprovoked seizure
CBCd, lytes, BUN, glucose, Ca2+, Mg2+, PO4-, ECG, CT head, routine EEG
- restrict class 5 license and other risky activities for 3 months
management of seizures: after second unprovoked seizure
MRI brain, sleep-deprived EEG if the routine EEG is non-diagnostic
management: restrict class 5 license and other risky activities for at least 6 months and start antiseizure drug. Daily folic acid supplementation for young feamles (>1mg)
Lamotrigine and levetiracetam are emerging as first-line treatments for epilepsy, which people may be more likely to keep taking than carbamazepine. Reducing the risk of adverse events and treatment withdrawal is important when selecting an anti-epilepsy drug as it usually will need to be taken long-term.
2 hallmarks of neuron characteristics in epilepsy
Due to imbalance of excitation (___+ and ___2+ channels and __ receptors) and inhibition (__+ channel receptors and ___ receptors)
Hyperexcitability of neurons
Hypersynchrony of circuits
Generally there is an imbalance between excitation and inhibition.
Need a large network of firing neurons to cause a seizure→ a single neuron is not sufficient to cause a seizure.
Due to imbalance of excitation (Na+ and Ca2+ channels and glutamate receptors) and inhibition (K+ channel receptors and GABA receptors)
Triggers of epilepsy
Triggers: sleep deprivation, alcohol, flashing lights, stress, ovulation/menstruation, infection, fever, non-adherence to treatment, rec drugs, stress.
Risk Factors/Etiology: genetics, febrile convulsions, developmental disorders, metabolic disorders (hypoglycemia, chronic liver/kidney failure), infections, head injury, neurodegenerative disorder.
Interictal to Ictal transition on EEG
Pathophysiology of Focal Seizures
- Focal seizures arise from a localized brain area
- Can spread through synaptic and nonsynaptic mechanisms to subcortical structures and through commissures, to eventually involve the whole cortex.
NOrmally, the activity is low voltage and desynchronized. Interictal: there are large spikes are seen focally= synchronized firing of large population of hyperexcitable neurons. Ictal: long runs of spikes.
Ictal = during the seizure
Pathophysiology of focal and generalized epilepsy
Pathophysiology of Focal Seizures
Focal seizures arise from a localized brain area
Can spread through synaptic and nonsynaptic mechanisms to subcortical structures and through commissures, to eventually involve the whole cortex.
Pathophysiology of generalized Epilepsy
Bilateral tonic-clonic seizures in generalized epilepsy begin with abnormal electrical discharges in both hemispheres and involve thalamocortical connections.
T-Type Ca2+ channels are involved in ABSENCE generalized (petit mal) epilepsy:
- Normally, they are found in thalamic relay and reticular neurons
- Ethosuximide and valproic acid suppresses the T current.
- Deactivated by prolonged hyperpolarization.
T-Type Ca2+ channels are involved in ___ generalized (__ ___ epilepsy:
T-Type Ca2+ channels are involved in ABSENCE generalized (petit mal) epilepsy:
- Normally, they are found in thalamic relay and reticular neurons
- Ethosuximide and valproic acid suppresses the T current.
- Deactivated by prolonged hyperpolarization.
General Mechanisms of Actions for anticonvulsants
Na+ channel blocker: inhibits axonal transmission (ex/ carbamazepine, oxcarbazepine, phenytoin, lamotrigine)
Inhibition of glutamate release (gabapentin)
Inhibition of glutamate receptors (topiramate)
overall, they reduce excitation of neurons
focal ASMs
levetiracetam, carbamazepine, phenytoin, clobazam, lamotrigine
generalized ASMs
valproic acid, lamotrigine, ethosuximide.
definition of drug resistant epilesy
failure of 2 tolerated and appropriately chosen and used AED
Epilepsy Surgical candidates must have;
- drug resistant epilepsy that is disabling
- epileptic symptos for 1-2 years
- good support system
- well localized area
- relatively low risk of severe neurological deficit post-resection
But undergo MRI, EEG, SPECT, PET, intracranial video-EEG monitoring, psychology/psych consultation prior to surgery
Types of surgical procedures: anterior temporal lobectomy, selective amygdalohippocampectomy.
Other options: deep brain stim, responsive neurostim, vagal nerve stimulation, ketogenic/atkins diet.
Status Epilepticus
prolonged epileptic seizure, or two or more sequential seizures without full recovery in between.
Duration (for treatment purposes):
Convulsive: 5 min
Non-convulsive: 10 min
Absence: 10-15 min.
Overall Mortality: 7-20%, 80% if >12 hrs in duration.
Etiology: • Remote symptomatic • Stroke • Low antiseizure drug levels • Metabolic • Hypoxia • Alcohol • Idiopathic
Management of Status Epilepticus
Management:
Immediate stabilization of ABCs
Stopping seizures, both electrographic and clinical (protect neurons)
Treat cause and precipitant of status epilepticus
Prevention of medical complications (aspiration, myoglobinuria, renal failure)
Phenytoin in ER, propofol or midazolam in iCU
