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Term 5: Neuro > 6/1- Epilepsy > Flashcards

6/1- Epilepsy Flashcards

1
Q

Seizure/Epilepsy outline/flowchart

A
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2
Q

Seizure (def)?

A

Latin: sacire “to take posession of”

  • Paroxysmal, abnormal, excessive, hypersynchronous discharge of cortical neurons, resulting in a change in behavior or in an EEG discharge
  • Can be “provoked” or “unprovoked”
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3
Q

Epilepsy (def)?

A
  • Recurrent unprovoked seizures
  • …or one unprovoked seizure and high likelihood of more based on history/exam/studies
  • … or provoked by something that shouldn’t provoke seizures (“reflex epilepsy”)
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4
Q

Potential differential diagnoses for seizures?

A
  • Gastroesophageal reflux
  • Breath-holding spells
  • Sleep myoclonus
  • Night terrors
  • Movement disorders
  • Migraines
  • Syncope
  • Transient ischemic attacks
  • Vertebrobasilar insufficiency
  • Hypoglycemia
  • Hypoxia
  • Psychogenic seizures
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5
Q

What percentage of the population will experience seizures/epilepsy?

A
  • Single seizure lifetime prevalence = 9-10%
  • Epilepsy lifetime prevalence = 0.5-1% (3% by age 75)

(no racial/gender/geographic preference for epilepsy)

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6
Q

ILAE Classification History (pic)

A
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7
Q

Two division of seizure based on onset

A

Focal Onset seizure

  • “initial activation of a system of neurons limited to one cerebral hemisphere.”
  • Previously called “partial” or “localization-related”

Generalized Onset seizure

  • “first clinical changes indicate involvement of both hemispheres.”
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8
Q

Focal seizures further divided based on what? Details?

A

Level of consciousness:

  • No alteration of consciousness (“auras” or focal motor seizures); previously “simple partial seizures”
  • Impaired or altered, but no loss of consciousness = “dyscognitive”; previously “complex partial seizures”
  • Both types may evolve into generalized seizures (“secondarily generalized”)
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9
Q

Generalized seizures include?

A
  • Absence seizures
  • Atypical substance seizure
  • Clonic seizure
  • Tonic seizure
  • Tonic-clonic seizure
  • Myoclonic seizure
  • Atonic seizure
  • Infantile spasms
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10
Q

Aura- definition and characteristics?

A

Brief stereotypic prodrome that precedes the more obvious clinical event by seconds to minutes

  • Does not impair cognition
  • Ex) taste, smell, fear, dissociation, deja vu
  • Is actually a FOCAL SEIZURE
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11
Q

Ictus- defintion

A

(Latin- “to strike”)

The “seizure” itself

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12
Q

Automatisms (def) and examples?

A

Semipurposeful or non-purposeful “automatic” behaviors during the seizure

  • Ex) picking at clothes, lipsmacking, swallowing
  • Can occur in both partial and generalized epilepsies
  • In partial epilepsies tend to be unilateral
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13
Q

Postictal state (def) and examples?

A
  • Confusion, somnolence & fatigue (complex partial and some generalized seizures)
  • Aphasia (partial seizures affecting language areas)
  • Focal weakness- “Todd’s paralysis” (partial seizures)
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14
Q

Behavioral change reflecting the anatomic location of abnormal discharge for frontal lobe?

A
  • Clonic mvts, tonic posturing, or atonia
  • Contralateral tonic posturing or bizarre bilateral hyperkinetic mvts
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15
Q

Behavioral change reflecting the anatomic location of abnormal discharge for temporal lobe?

A
  • Aura of smell, taste, emotion
  • Followed by confusion and staring
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16
Q

Behavioral change reflecting the anatomic location of abnormal discharge for parietal lobe?

A
  • Somatosensory changes
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17
Q

Behavioral change reflecting the anatomic location of abnormal discharge for occipital lobe?

A
  • Flashing lights
  • Visual distortions
  • Eye movements
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18
Q

Take Home:

  • Not everything that shakes is a seizure
  • Not every seizure is epileptic
  • Note very epileptic seizure involves shaking
A

(:

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19
Q

In a broad sense, normal CNS function is determined by what?

A

Balance between excitation (glutamate) and inhibition (GABA)

  • Modulated by: ACh, serotonin, DA, somatostatin, CCK, dynorphin, nitric oxide, arachidonic acid, endocanabinoids…
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20
Q

Examples of provoked seizures (NOT epilepsy!)

Exceptions?

A
  • Alcohol withdrawal seizures
  • Hyponatremia
  • Hypoglycemia
  • Cocaine

Exceptions- “reflex epilepsy” (typically genetic)

  • Photosensitive epilepsy
  • Rarely: bath (hot water), eating, music-induced epilepsy
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21
Q

What is the process of developing epilepsy (epileptogenesis)?

A

Eliptogenesis:

  • Sequence of events leading to abnormal activity sufficient to convert a normal neuronal network into an abnormally hyperexcitable and hypersynchronous one

Latent period:

  • A “clinically silent period” between an initial injury or insult and the development of epilepsy
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22
Q

Pathophysiology of epilepsy: what goes wrong (broad)?

A
  • Loss of inhibition
  • Intrinsic excitability
  • Abnormal excitation (and excessive synchronization)
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23
Q

Pathophysiology of loss of inhibition? Examples?

A

Loss of inhibition

  • Some interneurons are particularly vulnerable to cell death
  • Disinhibition of primary neurons -> hyperexcitability and excessive neuronal activity
  • Axons may sprout and synapse on other principal cells

Examples: Generalized epilepsy with febrile seizures plus (GEFS+)

24
Q

Characteristics of Generalized Epilepsy with Febrile Seizures plus (GEFS+)?

A

(Abnormal inhibition)

Onset usually in 1st decade Clinically heterogeneous

  • Febrile seizures that persist beyond 5 yrs of age
  • Afebrile generalized seizures (tonic-clonic, absence, myoclonic, atonic, others)

Severity ranges from mild to severe

EEG: generalized spike and wave

Some of the mutations described are in the GABA-A recepetor

25
Q

Pathophysiology of intrinsic excitability? Example?

A
  • Decreased hyperpolarizing current
  • Increased depolarizing current

Ex) decreased K conductance with Benign Familial Neonatal Convulsions

26
Q

Characteristics of decreased K conductance with Benign Familial Neonatal Convulsions?

A
  • Associated with 2 K channel genes (KCNQ2 and KCNQ3)
  • Both subunits form a heterodimeric complex underlying a slow potassium conductance which regulates excitability (the M current)
  • Though to be loss of function mutations
  • Example of a “channelopathy”
27
Q

Childhood Absence Epilepsy Circuit caused by what underlying biochemistry?

A
  • Bursting mediated by T-type Ca channels
  • Blocked by Ethosuximide
28
Q

Categorizing Causes of Epilepsy?

A

Structural/Metabolic

  • Evident (usually structural) cause
  • For example: cortical dysplasia
  • Previously “Symptomatic” Genetic
  • Known or presumed genetic cause
  • For example: Childhood absence epilepsy or one of the “channelopathies”
  • Previously “Idiopathic” Unknown
  • Previously “Cryptogenic”
  • “Hidden cause” (practically: “I don’t know”)
29
Q

Classification schemes can be combined as far as etiology of epilepsy and onset of seizure

Ex)

  • Structural epilepsy with focal onset seizures due to cortical dysplasia
  • Genetic generalized epilepsy
A

(:

30
Q

Approach to diagnosis?

A
  • Medical and Family Hx
  • Complete description of typical events
  • Complete neurological exam
  • Depending on the above: Lab studies (first seizure with chemistries and tox screne, recurrents seizures with possible genetic testing), Neuroimaging (usually MRI), electroencephalography
31
Q

What is this?

A

Electroencephalogram (EEG) “recording squiggles” of interictal discharges

32
Q

What is this?

A

Electroencephalogram (EEG) “recording squiggles” of generalized seizure

33
Q

What is this?

A

Electroencephalogram (EEG) “recording squiggles” of focal seizure

34
Q

What are the recurrence rates following a 1st unprovoked seizure?

A
  • 30% for pt with normal EEG, MRI, and exam - > 90% when all three are abnormal
  • Multiple seizures in the same 24 hr period have same risk as a single seizure
35
Q

Treatment for seizures?

A

New guidelines for first seizures: treat first unproviked seizure with an anti-epileptic drug. Treatment depends on:

  • Syndrome classification (e.g. Childhood Absence Epilepsy, use ethosuximide)
  • Type of seizures (focal-onset use narrow-spectrum agents; generalized onset use broad spectrum agents)
  • Other medical problems
36
Q

What is the general principle underlying AEDs (antiepileptic drugs)? Examples?

A

Act by restoring balance:

Reduce excitation:

  • Phenytoin
  • Carbamazepine
  • Oxcarbazepine

Increase inhibition:

  • Phenobarbital
  • Benzodiazepines

Both:

  • Valproic acid
  • Topiramate
37
Q

AEDs (list)

A
38
Q

Mechanisms of action of AEDs with examples?

A
  • Block Na channels: Carbamazepine
  • Block Ca channels: Ethosuximide
  • Block AMPA/NMDA Rs: Perampanel
  • Enhance GABA receptors: Clobazam
  • Enhance K channel conductance: Ezogabine
  • Block NT release: Levetiracetam
39
Q

Adverse effects of AEDs?

A
  • All AEDs can cause drowsiness, dizziness, and rash
  • Drugs which act on GABA system tend to be more sedating
  • Not antiepileptic has been shown to be entirely safe in pregnancy (older drugs have clear teratogenic effects [2-4x increase] while newer are more likely safe, but less experience)
40
Q

Serious and specific adverse effects for Valproic acid?

A

Acute hemorrhagic pancreatitis, hepatic failure

(1/50,000 but 1/500 for kids under 2)

41
Q

Serious and specific adverse effects for Felbamate?

A

Aplastic anemia

(up to 1/5000 adults; not seen in kids)

42
Q

Serious and specific adverse effects for Carabamazepine?

A

Aplastic anemia

(1/500,000)

43
Q

Serious and specific adverse effects for Phenytoin?

A

Hepatotoxicity, aplastic anemia

(1/500,000)

44
Q

Which drug used to treat epilepsy with focal-onset seizures?

A

- First line: oxcarbazepine, levetiracetam, carbamazepine, phenytoin

- Second line: lacosamide, lamotrigine, topiramate, zonisamide

45
Q

Which drug used to treat epilepsy with generalized-onset seizures?

A

- Absence: ethosuximide, lamotrigin, valproate

- Others: lamotrigine, levetiracetam, valproate, topiramate, zonisamide, pregabalin

46
Q

Success with AED Regimens?

A
  • 47% seizure free with 1st drug
  • 13% seizure free with 2nd drug
  • 4% seizure free with 3rd/multiple drugs
  • 36% not seizure free
47
Q

Treatments for medically refractory patients?

A
  • Ketogenic diet (an extremes Atkins: high fat low carb diet induces ketosis which has anticonvulsant effects for unclear reasons)
  • Epilepsy surgery
  • Vagus nerve stimulator
  • Responsive focal cortical stimulation
48
Q

Types of epilepsy surgery?

A
  • Lesionectomy: take out the lesion
  • Lobectomy: take out the offending lobe
  • Hemispherectomy: take out the whole hemisphere
  • Corpus callosotomy: cut the corpus collosum
49
Q

Outcomes of epilepsy surgery depend on what?

A
  • Type of epilepsy
  • Type of surgery
  • Age
50
Q

For whom is epilepsy surgery considered?

A

Patients with intractable epilepsy

(done on about 250,000)

51
Q

Mechanism of action of Carbamazepine?

A

Block Na channels

52
Q

Mechanism of action of Ethosuximide?

A

Block Ca channels

53
Q

Mechanism of action of Perampanel?

A

Block AMPA/NMDA

54
Q

Mechanism of action of Clobazam?

A

Enhance GABA receptors

55
Q

Mechanism of action of Ezogabine?

A

Enhance K channel conductance

56
Q

Mechanism of action of Levetiracetam?

A

Block NT release

Term 5: Neuro (24 decks)

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