Seizures

Question 1

“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

Answer 1

seizure

Question 2

What is going on in seizure pathophysiology

Answer 2

Cells here trigger seizure; synchronized high freuqnecy firing

cells bursting and transitions to seizures

Question 3

Trigger for seizure pathophysiology

Answer 3

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

•Febrile illness, Sleep deprivation

Question 4

excitatory/inhibitory factors in seizure pathophysiology

Answer 4

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

•Bursting neurons

Question 5

Synchronization process seein in Seizure pathophysiology

Answer 5

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

Question 6

What are Partial seizures

Answer 6

simple and complex

Question 7

What are generalized seizures

Answer 7

Absence

Complex

Tonic

Atonic

GTC

Myoclonic

Question 8

What do you need to diagose pt with epilepsy

Answer 8

EEG, MRI or labs

Question 9

What’s the difference between epilepsy or seizures

Answer 9

 Epilepsy: Tendency to have recurrent, unprovoked seizures

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

Question 10

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

Answer 10

Altered neuronal circuits, formaiton of aberrant excitatory connections

Question 11

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

Answer 11

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

Question 12

Neurotransmitter synthesis; see prodioxine deficiency which leads to

Answer 12

Decreased GABA synthesis; B-vit cofactor for GAD

Question 13

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

Answer 13

abnormal GAGA receptor subunites

Question 14

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

Answer 14

excess glycine that activates NMDA

Question 15

Synaptic development can lead to neonatal seizures based on pathopys consequences

Answer 15

depolarizing action of GABA in premature

Question 16

Ion channelopathies are seen in benign familial convulsions

Answer 16

Potassium channel mutation with impaired repolarizaiton

Question 17

 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

Answer 17

Simple Partial Seizures

Question 18

 Brief

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

Answer 18

Simple Partial Seizure

Question 19

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

 Manifestations: Staring or Automatisms

Answer 19

Complex Partial Seizures

Question 20

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

Continuation of activity and Fragmented but coordinated motor task

Answer 20

Complex Partial Seizures

Question 21

 Patient without recall

Lasts 30 seconds to minute

 Post-ictal impairment:

Lethargy and Confusion and Lasts minutes to hours

Answer 21

Complex Partial Seizure

Question 22

Complex partial seizure preceded by aura is located in what origin

Answer 22

Temporal lobe origin

Question 23

What syptoms are associated with aura

Answer 23

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

Question 24

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

describe this

Answer 24

May still have automatism,

Fatigue or deep sleep‐ Not well for hours afterwards

• Headache
• Emesis

Question 25

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

Answer 25

Complex partial with Frontal Lobe Origin

Question 26

List of generalized seizures

Answer 26

 Tonic - Clonic  Absence  Clonic  Tonic  Atonic  Myoclonic

Question 27

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

Answer 27

Tonic-Clonic type of generalized seizures

Question 28

 Majority of GTC in childhood  Focal onset

Answer 28

 Partial with secondary generalization

Question 29

Abrupt cessation of actvity + change facial expression to blank stare Lasts less 30 secs, no aura, behaviour change = motor/behavioral/autonomic

Answer 29

Absence seizures

Question 30

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

Answer 30

Clonic eye mvm: nystagmus + blinking.. Head nod/dropping of object. Perserverance of actions, speech Autonomic symptoms = pupils dialate, pallow, flushing, salivation

Question 31

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

Answer 31

Clonic Seizures

Question 32

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

Answer 32

Tonic seizures

Question 33

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

Answer 33

Atonic seizure

Question 34

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

Answer 34

Myoclonic

Question 35

Define Status Epilepticus

Answer 35

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

Question 36

Extent of the work-up • For example: ‐ Focal seizure =\_\_\_\_ ‐ Primary generalized epilepsy - \_\_\_\_ ‐ Developmental regression -\_\_\_\_\_

Answer 36

MRI EEG only extensive evaluation

Question 37

what do we use to eval seizures

Answer 37

Lab EEG MRI Labs

Question 38

What is involved in initial studies when working up seizures

Answer 38

Glucose, electrolytes, BUN ABG Antiepileptic drug level(s) CBC Urinalysis

Question 39

Second phase studies for seizure eval

Answer 39

Lumbar puncture Liver function tests Toxicology screen Metabolic testing EEG Brain imaging (CT vs MRI)

Question 40

Risk of therapy for seizures

Answer 40

Idiosyncratic reaction Systemic toxicity Stigma Expense

Question 41

Risk of seizures

Answer 41

Status epilepticus Cognitive impairment Restriction of activities Injury Sudden death

Question 42

Negative side effects of anti-seizures

Answer 42

** Direct Toxicit**y ** Dermatologi**c • carbamazepine, lamotrigine ** Bone Marrow effects** • phenobarbital, ethosuximide, carbamazepine, phenytoin, ** Hepatic Effects** • phenytoin, carbamazepine, valproic acid

Question 43

key for treatment of seizures when dosing

Answer 43

** Start low/go slow**  Partial, secondarily generalized ACD’s  carbamazepine  (gabapentin)  Oxcarbazepine  phenytoin

Question 44

 _______ 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

Answer 44

70-80% 20-30%