Epilepsy Part 2 Flashcards

1
Q

Investigations into a seizure

A

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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2
Q

Management of Seizures: after first unprovoked seizure

A

CBCd, lytes, BUN, glucose, Ca2+, Mg2+, PO4-, ECG, CT head, routine EEG

  • restrict class 5 license and other risky activities for 3 months
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3
Q

management of seizures: after second unprovoked seizure

A

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.

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4
Q

2 hallmarks of neuron characteristics in epilepsy

Due to imbalance of excitation (___+ and ___2+ channels and __ receptors) and inhibition (__+ channel receptors and ___ receptors)

A

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)

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5
Q

Triggers of epilepsy

A

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.

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6
Q

Interictal to Ictal transition on EEG

A

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

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7
Q

Pathophysiology of focal and generalized epilepsy

A

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.
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8
Q

T-Type Ca2+ channels are involved in ___ generalized (__ ___ epilepsy:

A

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.
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9
Q

General Mechanisms of Actions for anticonvulsants

A

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

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10
Q

focal ASMs

A

levetiracetam, carbamazepine, phenytoin, clobazam, lamotrigine

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11
Q

generalized ASMs

A

valproic acid, lamotrigine, ethosuximide.

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12
Q
A
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13
Q

definition of drug resistant epilesy

A

failure of 2 tolerated and appropriately chosen and used AED

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14
Q

Epilepsy Surgical candidates must have;

A
  • 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.

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15
Q

Status Epilepticus

A

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

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16
Q

Management of Status Epilepticus

A

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

17
Q
A