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Pathophysiology - Neurology > Seizures and Epilepsy > Flashcards

Seizures and Epilepsy Flashcards

1
Q

How is epilepsy defined? Three definitions.

A
  1. At least two unprovoked seizures occurring more than 24 hours apart (could be 60 years).
  2. One unprovoked seizure and a probability of further seizures (i.e. tumor was due to a tumor, trauma, or stroke and will likely recur)
  3. Diagnosis of an epilepsy syndrome
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2
Q

How is resolution of epilepsy defined?

A

Remaining seizure-free for the last 10 years, with no seizure medication used for the last 5.

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3
Q

How is drug resistant / medically intractable seizures defined?

A

Failure of seizure control after trying two anti-epileptic drugs which were tolerated well.

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4
Q

What is the usual cause of epilepsy and what age groups get it most?

A

Bimodal distribution: highest prevalence in young children and older adults

Etiology: 65% idiopathic, but may be congenital, traumatic, degenerative, vascular, CNS infections, etc

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5
Q

What are a few proposed mechanisms of seizure generation?

A

Enhanced glutamate / excitatory transmission, with impaired inhibition (GABA) -> higher basal activities to bring patients near seizure threshold in epilepsy

Lesions like scar tissues interrupting the macroenvironment -> i.e. mesial temporal sclerosis, or TBI scar

Abnormal glial function alters extracellular balance

Abnormal neural connections

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6
Q

What is one cause of increased NMDA or AMPA receptor activation?

A

Non-ketotic hyperglycemia

-> upregulates glycine and modulates NMDA

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7
Q

What vitamin should children be given in epileptic seizures?

A

Pyridoxine -> B6 is needed to convert glutamate to GABA

-> decreased GABA is thought to underlie problems of juvenile myoclonic epilepsy and angelman syndrome

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8
Q

What are the new names for simple partial and complex partial seizures?

A

Simple partial = focal onset seizures without loss of awareness

Complex partial = focal onset seizures WITH loss of awarness

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9
Q

What is a myoclonic vs tonic-clonic seizure?

A

Myoclonic - quick, repetitive jerks

Tonic-clonic - grand mal seizure if generalized -> alternating stiffening and jerking

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10
Q

What is tonic vs atonic seizures? What can the latter be mistaken for?

A

Tonic - stiffening / sustained contraction of a muscle group

Atonic - “drop” seizures - complete loss of muscle tone. Can be mistaken for syncope since you fall to the floor.

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11
Q

What is a versive seizure? What part of the brain is affected?

A

Forced head deviation to one side or the other

Frontal eye field (area 8) is affected -> seizure is contralateral to side you are turning your head towards.

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12
Q

What is meant by the semiology of a seizure?

A

Clinical description of the progression of a seizure

  • > seizures are repetitive and stereotypic, always progressing the same way
  • > patient may able to describe an aura or warning sign before the seizure starts
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13
Q

Why is it important to identify seizure type?

A

Primary generalized epilepsy syndromes (i.e. Absence) can worsen in response to Na+ channel blockers (i.e. carbamazepine) which are first line AEDs for other disorders.

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14
Q

What is a Jacksonian march?

A

When a focal motor seizure marches up the homunculus starting from your fingers up your arm until you lose consciousness

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15
Q

What side to automatisms happen in relation to where the seizure focus begins?

A

Will happen on ipsilateral side
-> i.e. seizure of right hemisphere will cause right-sided automatisms, since left side will be dystonic due to the seizure and the right side will “automatically” do things

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16
Q

If one arm is extended and one arm is flexed during the tonic phase of a tonic-clonic seizure, which side did the seizure start on?

A

Generally seizure started on the contralateral side as the extended arm.

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17
Q

What is the cause of a complex visual imagery hallucination aura vs flashes of light / color / scotoma aura?

A

Complex visual imagery - visual association cortex -> seizure likely starting in occipital-temporo-parietal junction

Flashes of light / color / scotoma -> occipital lobe (primary visual cortex)

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18
Q

What anatomical defect is gelastic seizure most associated with?

A

Hypothalamic hamartoma

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19
Q

What areas of the brain cause autonomic dysfunction auras? (palpations / feeling hot/cold)

A

Insula
Amygdala
Anterior cingulate gyrus

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20
Q

Where does a hypermotor seizure arise from?

A

Frontal lobe -> precentral gyrus

21
Q

What causes alteration of consciousness during a seizure?

A
  1. Bilateral medial temporal lobe seizure activity (when seizure spreads to bilateral hemispheres)

or

  1. Seizure is focal in medial temporal lobe, but opposite medial temporal lobe is damaged
22
Q

What should you be thinking if a person says they can remember their bilateral tonic-clonic seizure? How is this diagnosed?

A

Think of a psychogenic non-epileptic spell
-> it is impossible to remember things during a tonic-clonic seizure

Diagnosed via video capture and EEG showing no abnormal electrical activity during the spell

23
Q

What normally terminates a seizure and what are some common symptoms of a post-ictal state?

A

huge GABA surges from brain, or pharmacologic help

Confusion, disorientation, exhaustion, anterograde / retrograde amnesia

Rarer - post-ictal psychosis days after, Todd’s paralysis

24
Q

When does Todd’s paralysis occur and what is it?

A

When there is a seizure of the premotor cortex

  • > post-ictal paresis contralateral to seizure side
  • > occurs due to depletion of glutamate during seizure
25
Q

Where do primary generalized seizures generally start from?

A

Generally start from the thalamus, and spread nearly instantly through the commissures and corpus callosum leading to bilateral synchronous activity

26
Q

Where does focal epilepsy generally start from and how does it spread?

A

Starts usually in medial temporal lobe, may spread outward through corpus callosum, commissures, and subthalamic structures

27
Q

What else is on the differential diagnosis of seizures?

A
  1. Movement disorders
  2. REM sleep behavior disorder (may be mistaken for frontal lobe epilepsy)
  3. Migraines with auras (vs simple partial seizures)
  4. Limb-shaking transient ischemic attacks
  5. Syncope
  6. Hyperventilation syndrome
  7. Psychogenic non-epileptic spells
28
Q

What type of syncope mimics seizures? How is it told apart?

A

Convulsive syncope where patient can have myoclonus, hallucinations, automatisms, etc

Syncope is precipitated by postural changes, has a long prodrome, is precipitated by emotion, pain, heat, is not associated with post-ictal confusion, and is commonly associated with cardiovascular signs

29
Q

What is the most common epilepsy syndrome and what is the most common neuropathologic finding in patients when it is medically refractive?

A

Temporal lobe epilepsy

-> commonly caused by hippocampal sclerosis / mesial temporal sclerosis

30
Q

What pathology is typically involved in mesial temporal sclerosis?

A

Neuronal cell loss and gliosis in the CA1/C3 region of the hippocampus (Ammon’s horn)

Also involved can be:
Subiculum, dentate gyrus, amygdala, and entorhinal cortex (parahippocampal gyrus)

31
Q

What predisposes to mesial temporal sclerosis and what is the treatment?

A

Finding is more likely if you had complicated febrile seizures before age 5

Treatment: temporal lobectomy or amygdallohippocampectomies of affected side

32
Q

What is Benign Epilepsy with CentroTemporal Spikes (BECTS) and what is the prognosis?

A

Focal epilepsy syndrome characterized by epileptiform spikes on EEG

Occurs in children age 3-13 years, can have hemifacial motor seizures and facial twitching which usually occurs at night -> may progress to bilateral tonic clonic

No treatment is generally required because there will be remission by mid-teens

33
Q

What type of seizure is “petit mal” and how is it diagnosed? What are the symptoms? Is there post-ictal confusion?

A

Primary generalized epilepsy

  • > absence seizure
  • > diagnosed via 3 Hz spike and wave on EEG

Symptoms: Mild tonic, clonic oral automatisms and eye fluttering. Last 10-20 seconds and there is no post-ictal confusion

34
Q

What are the two general types of absence seizures and what is the treatment?

A

Childhood absence - usually between 4-8 years and spontaneously remits

Juvenile absence - starting closer to puberty, may progress to a worse seizure disorder

Treatment is ethosuximide

35
Q

What seizures characterize juvenile myoclonic epilepsy (JME)? What precipitates them?

A
  1. Myoclonic jerks of arms (usually early morning)
  2. Generalized tonic-clonic
  3. Behavioral arrest / staring spells

Precipitated by sleep deprivation, alcohol use, and stress

36
Q

What is the age of onset for JME, how is it diagnosed, and what is the prognosis?

A

Puberty to early 20s

Diagnosed via 4-6 Hz spike and waves

Wellcontrolled with medication, but will have seizures for life

37
Q

What is the diagnostic triad of Lennox Gastaut syndrome? Prognosis?

A
  1. Multiple seizure types (atonic, absence, tonic, generalized tonic-clonic)
  2. Developmental delay
  3. Slow 1-2.5 spike and wave on EEG as a baseline (not just during seizures)

-> patient will have static encephalopathy with poor prognosis

38
Q

What is an atypical absence seizure?

A

EEG spike and wave activity is more heterogenous than 3 Hz, and has more pronounced signs and automatisms than usual

39
Q

What is EEG actually recording? And what is the gold standard for seizure diagnosis?

A

Summation of excitatory or inhibitory post synaptic potentials -> NOT action potentials

Gold standard: Epilepsy monitoring unit -> video recording of seizure with EEG

40
Q

What are the non-pharmacologic treatment options for focal seizures?

A
  1. Resective surgery
  2. Vagus nerve stimulator
  3. Responsive neurostimulator device (i.e. deep brain stimulation) -> implanted near brain foci to terminate seizure
41
Q

What are the non-pharmacologic treatment options for generalized seizures?

A
  1. Vagal nerve stimulation

2. Corpus callosum resection

42
Q

What is the efficacy of pharmacotherapy in treating seizure disorders?

A

60-65% of patients can be controlled with one or two AEDs

43
Q

What is the definition of status epilepticus? Can it occur with focal seizures?

A

Continuous seizures (5-30 minutes) without return to baseline (without regaining consciousness), or recurring seizures resulting in brain injury

Yes, it can occur with focal seizures, not just generalized tonic-clonic

44
Q

What do you want to do as a baseline before treating status epilepticus?

A

Assess patient’s true status, assessing bloodwork (AED levels, CBC, chemistry), blood glucose, toxicology screen, vitals, respiratory state, etc

45
Q

What is the first-line treatment for status epilepticus? SEcond line?

A

1st line: Benzodiazepines i.e. lorazepam or midazolam

2nd line: Fosphenytoin, phenytoin

46
Q

What are the side effects of concern when adding phenytoin or fosphenytoin?

A

Hypotension and CNS depression

May cause purple glove syndrome rarely: a thrombophlebitis which could require amputation (more common with phenytoin)

47
Q

What are the thirdline treatments for status epilepticus?

A

Propofol, phenobarbital, possibly putting patient in a phenobarbital coma if patient is severely decompensating with lactic acidosis and hypoxia / hyperthermia

48
Q

What two drugs should never be given together in status epilepticus?

A

Diazepam followed by phenobarbital -> may cause hypotension / severe respiratory depression

Pathophysiology - Neurology (21 decks)

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