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Neuropysch > Seizures > Flashcards

Seizures Flashcards

1
Q

“Occasional, sudden, excessive, rapid and local discharges of gray matter”

“Alteration of behavior that results from abnormal and excessive activity of a group of cerebral neurons

A

seizure

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2
Q

What is going on in seizure pathophysiology

A

Cells here trigger seizure; synchronized high freuqnecy firing

cells bursting and transitions to seizures

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3
Q

Trigger for seizure pathophysiology

A
  • Genetic predisposition
  • Trauma, ischemia, stroke, malformation of cortical development

•Febrile illness, Sleep deprivation

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4
Q

excitatory/inhibitory factors in seizure pathophysiology

A
  • GABA, K&Cl, Basal ganglia
  • NMDA, AMPA; alteration of voltage-gated channels

•Bursting neurons

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5
Q

Synchronization process seein in Seizure pathophysiology

A
  • Recurrent excitatory connections, coupling of gap junctions
  • Networks – electrical field effects and ephaptic effects
  • Clinical Seizure
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6
Q

What are Partial seizures

A

simple and complex

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7
Q

What are generalized seizures

A

Absence

Complex

Tonic

Atonic

GTC

Myoclonic

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8
Q

What do you need to diagose pt with epilepsy

A

EEG, MRI or labs

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9
Q

What’s the difference between epilepsy or seizures

A

 Epilepsy: Tendency to have recurrent, unprovoked seizures

 Seizure: abnormal electrical activity of a group of neurons with stereotypic behavioral change

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10
Q

Neuronal network, you see these conditions: cerebral dysgenesis, post-traumatic, mesial temporal sclerosis (MTS)

A

Altered neuronal circuits, formaiton of aberrant excitatory connections

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11
Q

Level of brain: see down syndrome which leads to seizures how

A

abnormal structure of dendrites and dendritic spines; altered flow in neurons

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12
Q

Neurotransmitter synthesis; see prodioxine deficiency which leads to

A

Decreased GABA synthesis; B-vit cofactor for GAD

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13
Q

NTS inhibition seen in Angelman syndromea and juvenile myoclonic epilepsy; we see

A

abnormal GAGA receptor subunites

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14
Q

NT exication issue: see non-ketotic hyperglycemia with the pathophysiologic consequence of

A

excess glycine that activates NMDA

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15
Q

Synaptic development can lead to neonatal seizures based on pathopys consequences

A

depolarizing action of GABA in premature

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16
Q

Ion channelopathies are seen in benign familial convulsions

A

Potassium channel mutation with impaired repolarizaiton

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17
Q

 Consciousness is not impaired: Signs and symptoms depends on localization

• Clonic movements of face, arm, leg , Somatosensory, Autonomic, Psychic Symptoms

‐ De’ja vu

‐ Hallucinations

‐ Illusions

A

Simple Partial Seizures

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18
Q

 Brief

 No post-ictal symptoms
 Todd paralysis can occur
 Formerly Jacksonian seizures

A

Simple Partial Seizure

19
Q

 Consciousness is impaired
 “Temporal Lobe” or “Psychomotor” seizures

 Manifestations: Staring or Automatisms

A

Complex Partial Seizures

20
Q

 Automatisms
• Facial grimacing, gestures, chewing, lip smacking, finger snapping, and repetitive speech

Continuation of activity and Fragmented but coordinated motor task

A

Complex Partial Seizures

21
Q

 Patient without recall

Lasts 30 seconds to minute

 Post-ictal impairment:

Lethargy and Confusion and Lasts minutes to hours

A

Complex Partial Seizure

22
Q

Complex partial seizure preceded by aura is located in what origin

A

Temporal lobe origin

23
Q

What syptoms are associated with aura

A

Aura in complex partial is Temporal

Fear

Stomach pain

Light headedness

Rising sensation in head or chest

Distortion of memory or time

De’ja vu or De’ja entendu

* Often with Autonomic Symptoms

24
Q

 Temporal Lobe Origin has something called a : Post-Ictal Phase

describe this

A

May still have automatism,

Fatigue or deep sleep‐ Not well for hours afterwards

  • Headache
  • Emesis
25
Q

In this seizure you see arrest of activity (motor manifestations/blank stare/brief attacks), head and neck movments and these are on and off, very brief

A

Complex partial with Frontal Lobe Origin

26
Q

List of generalized seizures

A

 Tonic - Clonic

 Absence
 Clonic
 Tonic

 Atonic
 Myoclonic

27
Q

Loss of consciousness with stiffening of limb(s) ===• (tonic phase)
 Evolution to generalized jerking of muscles == (clonic phase)
 Deep sleep post-ictal

A

Tonic-Clonic

type of generalized seizures

28
Q

 Majority of GTC in childhood
 Focal onset

A

 Partial with secondary generalization

29
Q

Abrupt cessation of actvity + change facial expression to blank stare

Lasts less 30 secs, no aura, behaviour change = motor/behavioral/autonomic

A

Absence seizures

30
Q

What clonic movements, Head movments and autonomic phenomena are associated with absence seizures

A

Clonic eye mvm: nystagmus + blinking.. Head nod/dropping of object.

Perserverance of actions, speech

Autonomic symptoms = pupils dialate, pallow, flushing, salivation

31
Q

Focal/multifocal; rarely ever generalized. See EEG changes. Migrating = metabolic or anoxic damage

A

Clonic Seizures

32
Q

Brief, 60 secs, sudden onset of increased extensor tone + impaired consiousness

A

Tonic seizures

33
Q

‘Drop attack’, sudden loss tone + bried loss consciousness; rare (Lennox-Gastaut syndrome)

A

Atonic seizure

34
Q

Sudden, brief, <350 mS, Shock-like, on face or trunk. Can be prior to absence, tonic or T/C may be sign of diffuse brain injury

A

Myoclonic

35
Q

Define Status Epilepticus

A

30 mns sustained seizure OR 2 or more seizure w/ou full recovery consciousness btwn them

36
Q

Extent of the work-up • For example:

‐ Focal seizure =____

‐ Primary generalized epilepsy - ____

‐ Developmental regression -_____

A

MRI

EEG only

extensive evaluation

37
Q

what do we use to eval seizures

A

Lab EEG MRI

Labs

38
Q

What is involved in initial studies when working up seizures

A

Glucose, electrolytes, BUN

ABG

Antiepileptic drug level(s)

CBC

Urinalysis

39
Q

Second phase studies for seizure eval

A

Lumbar puncture

Liver function tests

Toxicology screen

Metabolic testing

EEG

Brain imaging (CT vs MRI)

40
Q

Risk of therapy for seizures

A

Idiosyncratic reaction

Systemic toxicity

Stigma
Expense

41
Q

Risk of seizures

A

Status epilepticus

Cognitive impairment

Restriction of activities Injury

Sudden death

42
Q

Negative side effects of anti-seizures

A

 Direct Toxicity

 Dermatologic
• carbamazepine, lamotrigine

 Bone Marrow effects
• phenobarbital, ethosuximide, carbamazepine, phenytoin,

 Hepatic Effects
• phenytoin, carbamazepine, valproic acid

43
Q

key for treatment of seizures when dosing

A

 Start low/go slow

 Partial, secondarily generalized ACD’s  carbamazepine

 (gabapentin)
 Oxcarbazepine  phenytoin

44
Q

 _______ respond to first or second ACD : Controlled and ACD withdrawn after 2 years seizure free

_____ have medically intractable epilepsy which Interferes with
• health and development

  • QOL
  • financial hardship
A

70-80%

20-30%

Neuropysch (18 decks)

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