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Neurology > Harrison's Ch 445 Seizures and Epilepsy > Flashcards

Harrison's Ch 445 Seizures and Epilepsy Flashcards

1
Q

Define what seizure means in Latin. What is the clinical definition?

A

“To take possession of.” A paroxysmal event due to abnormal excessive or synchronous neuronal activity in the brain.

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2
Q

Define epilepsy

A

A condition where a person has recurrent seizures due to a chronic, underlying process.

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3
Q

How do you generally group the major types of seizures?

A

Focal or generalized

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4
Q

Define focal seizures. What are these seizures associated with?

A

originate within networks limited to one hemisphere. (partial is no longer used). structural abnormalities of the brain

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5
Q

Define generalized seizures. What are these seizures associated with?

A

arise within and rapidly engage networks distributed across both hemispheres. cellular, biochemical, or structural abnormalities that have a more widespread distribution.

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6
Q

How do you further categorize focal seizures based on cognitive impairment?

A

With or without dyscognitive features

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7
Q

What is seen on the typical EEG in between seizures of a patient with focal seizures/?

A

brief discharges called epileptiform spikes or sharp waves

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8
Q

Name the 4 divisions of types of focal seizures: MSAP

A

Motor, sensory, autonomic, or psychic symptoms without impairment

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9
Q

Name the phenomenon of focal motor seizures whereby abnormal motor movements may begin in a very restricted region (such as fingers) and gradually progresses to include a larger portion of the extremity. Who was this described by?

A

Described by Hughlings Jackson and called the “Jacksonian March”. Caused by spread of seizure activity over a larger portion of motor cortex.

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10
Q

Describe the clinical condition whereby the patient experiences localized paralysis for minutes to hours of the involved region of a focal motor seizure?

A

Todd’s paralysis

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11
Q

Name the condition when a focal motor seizure continues for hours to days? it is often refractory to medical therapy

A

epilepsia partialis continua

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12
Q

Besides motor manifestations, describe the other categories and ways that focal seizure without dyscognitive features may present?

A 
Somatic sensation: paresthesias, vision (flashing lights or hallucinations), equilibrium ( sensation of falling or vertigo)
Autonomic function (flushing, sweating, piloerection)
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13
Q

Describe the way focal seizures arising from the temporal or frontal cortex may present?

A

Alterations in hearing, olfaction, higher cortical function (psychic symptoms). Unusual, intense odors (burning rubber) or epigastric sensations

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14
Q

Subjective, internal events that are not directly observable by others seen with focal seizures are called what?

A

Auras

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15
Q

Define focal seizures with dyscognitive features

A

Focal seizures that are accompanied by a transient impairment of the patient’s ability to maintain normal contact with the environment

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16
Q

List the stages of a typical focal seizure with dyscognitive features

A

Aura -> Ictal phase (behavioral arrest) accompanied by automatisms -> post-ictal confusion -> Full recovery of consciousness (seconds up to an hour)

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17
Q

What can be seen on examination immediately following a focal seizure with dyscognitive features?

A

Anterograde amnesia or a postictal aphasia (if involved the dominant hemisphere)

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18
Q

Why is a focal seizure that progresses into a generalized seizure difficult to distinguish from a primary generalized seizure? How do you distinguish this? Why is this important?

A

Bystanders tend to only emphasize and pay attention to the more dramatic, tonic-clonic type motions. This is distinguished based on history, if the patient was feeling the onset of a seizure with auras. This is important bc there are subtle differences in treatment.

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19
Q

Name the 5 types of generalized seizures:

A 
Typical absence seizure
Atypical absence seizure
Generalized, tonic-clonic seizure
Atonic seizure
Myoclonic seizure
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20
Q

Describe a typical absence seizure

A

characterized by sudden, brief lapses of consciousness, without loss of postural control. Lasts seconds. Consciousness returns as suddenly as it was lost. No postictal confusion. Usually subtle, bilateral motor signs such as rapid blinking or chewing movements. Main type of seizure in children with epilepsy.

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21
Q

How do atypical absence seizures differ from typical absence?

A

the lapse of consciousness is usually of longer duration and less abrupt in onset and cessation. More obvious motor signs that are typically lateralizing.

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22
Q

What physical neurologic findings are associated with atypical absence seizures?

A

Diffuse or multifocal structural abnormalities of the brain

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23
Q

Genralized tonic-clonic seizures are seen in ~___% of all patients with epilepsy

A

10

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24
Q

Describe the findings in a generalized tonic-clonic seizure

A

Begins abruptly, without warning although patient may have a prodrome. Initial phase is tonic contracture leading to: load moan or “ictal cry”, respirations impaired, secretions pooled, cyanosis, biting of the tongue, increase HR, pupil size and BP. After 10-20 sec, develops into the clonic phase.

25
Q

What is the clonic phase of generzlized tonic-clonic seizures?

A

Production of suprimposed muscle relaxation on tonic muscle contraction that progressively increase until the end of the ictal phase which lasts no more than a minute.

26
Q

Describe the postictal findings in generalized tonic-clonic seizures:

A

unresponsiveness, muscle flaccidity, excessive salivation, stridorous breathing and partial airway obstruction. Bladder or bowel incontinence. Regain consciousness over minutes to hours, confusion can last many hours depending on extent of seizure and underlying CNS disease

27
Q

There are variants of generalized tonic clonic seizures such as pure tonic and pure clonic. Brief tonic seizures are significant because they are associated with typical epilepsy syndromes such as which syndrome?

A

Lennox-Gastaut syndrome

28
Q

Describe atonic seizures

A

sudden loss of postural muscle tone lasting 1-2 sec. Consciousness is briefly impaired but no post-ictal confusion. Usually associated with known epilepsy syndromes.

29
Q

Describe myoclonic seizures

A

Sudden and brief muscle contraction, can involve one part of the body or the entire body. (ex: falling asleep).

30
Q

Pathological myoclonus is associated with what 3 conditions?

A

Metabolic disorders, degenerative CNS disease, anoxic brain injury

31
Q

What are the 3 main epilepsy syndromes?

A

Juvenile myoclonic epilepsy
Lennox-Gastaut syndrome
Mesial temporal lobe epilepsy

32
Q

Characterize Juvenile myoclonic epilepsy

A

Generalized seizure disorder of unknown cause that starts in early adolescence, bilateral myoclonic jerks single or repetitive. Most frequent in the morning after awakening, provoked by sleep deprivation. Consciousness is preserved. Also experience generalized tonic-clonic seizures and absence seizures

33
Q

Characterize Lennox-Gastaut syndrome

A

Occurs in children. Defined by a triad: 1) multiple seizure types 2) EEG with slow spike and wave discharges and other abnormalities 3) impaired cognitive function. Nonspecific response of the brain to diffuse neuronal injury.

34
Q

Characterize mesial temporal lobe epilepsy

A

MTLE is the most common syndrome associated with focal seizures with dyscognitive features. MRI shows hippocampal sclerosis that is essential in the pathophysiology. Refractory to AED treatment, but responds to surgery.

35
Q

What endogenous factors are involved that cause seizures or epilepsy?

A

genetic factors and maturational stages of the brain

36
Q

severe, penetrating head trauma is associated with up to ___% risk of subsequent epilepsy

A

45

37
Q

What other processes are associated with epileptogenesis?

A

stroke, infections, abnormalities in CNS development

38
Q

What are known triggers for seizures?

A

Psychological or physical stress, sleep deprivation, hormonal changes, toxic substances and certain meds

39
Q

What are the most common causes of seizures in neonates?

A

hypoxic-ischemic encephalopathy, trauma, CNS infection, congenital CNS abnormalities, and metabolic disorders

40
Q

the most common seizures arising in late infancy or early childhood

A

febrile seizures

41
Q

What are the most common causes of seizures in adolescents and early adults?

A

head trauma, CNS infections, brain tumors, congenital CNS abnormalities, illicit drug use, or EtOH withdrawal

42
Q

A patient with a penetrating head wound, depressed skull fracture, ICH, or prolonged post traumatic coma or amnesia has a ___ risk of developing epilepsy?

A

30-50%

43
Q

Patient with a closed head injury and cerebral contusion has a ___ risk

A

5-25%

44
Q

Causes of seizures in older adults:

A

Cerebrovascular disease, trauma (SDH), CNS tumors and degenerative diseases

45
Q

Describe the sequence of events on a cellular level during a seizure:

A

bursting neuronal activity caused by long-lasting depolarizing of the neuronal membrane caused by influx of extracellular calcium -> opening of voltage dependent Na+ channels -> influx of Na+ -> repetitive action potentials

46
Q

What causes slowing and halting of seizure wavefront on a cellular level?

A

hyperpolarizing afterpotential (“surround” inhibition) by GABA receptors or K+ channels

47
Q

How are seizures propagated through neural tissue?

A

1) increase in extracellular K+ which blunts hyperpolarization and depolarizes neighboring neurons 2) accumulation of Ca2+ in presynaptic terminals leading to enhanced neurotransmitter release 3) depolarization induced activation of NMDA subtype of the excitatory amino acid receptor which causes additional Ca+ influx and neuronal activation 4) ephaptic interactions related to changes in tissue osmolarity and cell swelling

48
Q

AEDs that inhibit Na+ dependent action potentials in a frequency dependent manner

A 
phenytoin (Dilantin) 
carbamazepine (Tegretol)
lamotrigine (Lamictal)
topiramate (Topamax)
zonisamide (Zonegran)
lacosamide (Vimpat)
rufinamide (Banzel)
49
Q

AEDs that voltage gated Ca+ channels

A

phenytoin
gabapentin
pregabalin

50
Q

AED that facilitates the opening of K+ channels

A

ezogabine

51
Q

AEDs that attenuate glutamate activity

A

lamotrigine
topiramate
felbamate

52
Q

AEDs that potentiate GABA receptor function

A

benzodiazepines

barbituates

53
Q

AEDs that increase the availability of GABA

A

valproic acid
gabapentin
tiagabine

54
Q

AED that modulates release of synaptic vesicles

A

levetiracetam (Keppra)

55
Q

AEDs that inhibit T type Ca+ channels in thalamic neurons

A

ethosuximide

valproic acid

56
Q

Clues to a predisposition to seizures obtained in history include:

A

history of febrile seizures
earlier auras or seizures not identified as such
FH of seizures

57
Q

Epileptogenic factors identified in history:

A

prior head trauma, stroke, tumor or CNS infection

58
Q

Precipitating factors for seizures obtained in history:

A

sleep deprivation, systemic disease, electrolyte or metabolic derangements, acute infection, drugs that lower seizure threshold or EtOH or illicit drugs

Neurology (3 decks)

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