Seizures Flashcards
“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
seizure
What is going on in seizure pathophysiology
Cells here trigger seizure; synchronized high freuqnecy firing
cells bursting and transitions to seizures
Trigger for seizure pathophysiology
- Genetic predisposition
- Trauma, ischemia, stroke, malformation of cortical development
•Febrile illness, Sleep deprivation
excitatory/inhibitory factors in seizure pathophysiology
- GABA, K&Cl, Basal ganglia
- NMDA, AMPA; alteration of voltage-gated channels
•Bursting neurons
Synchronization process seein in Seizure pathophysiology
- Recurrent excitatory connections, coupling of gap junctions
- Networks – electrical field effects and ephaptic effects
- Clinical Seizure
What are Partial seizures
simple and complex
What are generalized seizures
Absence
Complex
Tonic
Atonic
GTC
Myoclonic
What do you need to diagose pt with epilepsy
EEG, MRI or labs
What’s the difference between epilepsy or seizures
Epilepsy: Tendency to have recurrent, unprovoked seizures
Seizure: abnormal electrical activity of a group of neurons with stereotypic behavioral change
Neuronal network, you see these conditions: cerebral dysgenesis, post-traumatic, mesial temporal sclerosis (MTS)
Altered neuronal circuits, formaiton of aberrant excitatory connections
Level of brain: see down syndrome which leads to seizures how
abnormal structure of dendrites and dendritic spines; altered flow in neurons
Neurotransmitter synthesis; see prodioxine deficiency which leads to
Decreased GABA synthesis; B-vit cofactor for GAD
NTS inhibition seen in Angelman syndromea and juvenile myoclonic epilepsy; we see
abnormal GAGA receptor subunites
NT exication issue: see non-ketotic hyperglycemia with the pathophysiologic consequence of
excess glycine that activates NMDA
Synaptic development can lead to neonatal seizures based on pathopys consequences
depolarizing action of GABA in premature
Ion channelopathies are seen in benign familial convulsions
Potassium channel mutation with impaired repolarizaiton
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
Simple Partial Seizures
Brief
No post-ictal symptoms
Todd paralysis can occur
Formerly Jacksonian seizures
Simple Partial Seizure
Consciousness is impaired
“Temporal Lobe” or “Psychomotor” seizures
Manifestations: Staring or Automatisms
Complex Partial Seizures
Automatisms
• Facial grimacing, gestures, chewing, lip smacking, finger snapping, and repetitive speech
Continuation of activity and Fragmented but coordinated motor task
Complex Partial Seizures
Patient without recall
Lasts 30 seconds to minute
Post-ictal impairment:
Lethargy and Confusion and Lasts minutes to hours
Complex Partial Seizure
Complex partial seizure preceded by aura is located in what origin
Temporal lobe origin
What syptoms are associated with aura
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
Temporal Lobe Origin has something called a : Post-Ictal Phase
describe this
May still have automatism,
Fatigue or deep sleep‐ Not well for hours afterwards
- Headache
- Emesis
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
Complex partial with Frontal Lobe Origin
List of generalized seizures
Tonic - Clonic
Absence
Clonic
Tonic
Atonic
Myoclonic
Loss of consciousness with stiffening of limb(s) ===• (tonic phase)
Evolution to generalized jerking of muscles == (clonic phase)
Deep sleep post-ictal
Tonic-Clonic
type of generalized seizures
Majority of GTC in childhood
Focal onset
Partial with secondary generalization
Abrupt cessation of actvity + change facial expression to blank stare
Lasts less 30 secs, no aura, behaviour change = motor/behavioral/autonomic
Absence seizures
What clonic movements, Head movments and autonomic phenomena are associated with absence seizures
Clonic eye mvm: nystagmus + blinking.. Head nod/dropping of object.
Perserverance of actions, speech
Autonomic symptoms = pupils dialate, pallow, flushing, salivation
Focal/multifocal; rarely ever generalized. See EEG changes. Migrating = metabolic or anoxic damage
Clonic Seizures
Brief, 60 secs, sudden onset of increased extensor tone + impaired consiousness
Tonic seizures
‘Drop attack’, sudden loss tone + bried loss consciousness; rare (Lennox-Gastaut syndrome)
Atonic seizure
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
Myoclonic
Define Status Epilepticus
30 mns sustained seizure OR 2 or more seizure w/ou full recovery consciousness btwn them
Extent of the work-up • For example:
‐ Focal seizure =____
‐ Primary generalized epilepsy - ____
‐ Developmental regression -_____
MRI
EEG only
extensive evaluation
what do we use to eval seizures
Lab EEG MRI
Labs
What is involved in initial studies when working up seizures
Glucose, electrolytes, BUN
ABG
Antiepileptic drug level(s)
CBC
Urinalysis
Second phase studies for seizure eval
Lumbar puncture
Liver function tests
Toxicology screen
Metabolic testing
EEG
Brain imaging (CT vs MRI)
Risk of therapy for seizures
Idiosyncratic reaction
Systemic toxicity
Stigma
Expense
Risk of seizures
Status epilepticus
Cognitive impairment
Restriction of activities Injury
Sudden death
Negative side effects of anti-seizures
Direct Toxicity
Dermatologic
• carbamazepine, lamotrigine
Bone Marrow effects
• phenobarbital, ethosuximide, carbamazepine, phenytoin,
Hepatic Effects
• phenytoin, carbamazepine, valproic acid
key for treatment of seizures when dosing
Start low/go slow
Partial, secondarily generalized ACD’s carbamazepine
(gabapentin)
Oxcarbazepine phenytoin
_______ 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
70-80%
20-30%
