What are the different types of seizures - just name them!
FOCAL SEIZURES: Simple Partial, Complex Partial
GENERALIZED: Absence, Convulsive/Generalized Tonic-Clonic (GTC)/Gran Mal, Myoclonic, Atonic
Can be Primary or Secondary Generalized
What is a simple partial seizure and how does it present? What is the most common area involved?
Simple Partial Seizure- can be an aura, any seizure without loss of consciousness
Temporal lobe is very common
Can present with Aura (start of event leading to deja vu, fear, confusion etc but itself also actually a seizure)
Consciousness intact as have either motor-like symptoms (ex. twitch), sensory (ex. numbness), Autonomic (ex. fear or increased HR)
What is a Complex Partial seziure? How doe sthat present?
Complex Partial Seizure: Impaired consciousness/loss of consciousness - alteration and so not normally interacting with environment (can be as subtle as zoning out) --> confusion
Can have Automatisms (non-conscious movements like lip-smacking etc)
Focal seizures with dyscognitive features, confusion and can't communicate
On EEG from Inter-Ictal PDS to bloom over time and space to involve more brain
Overall, what are generalized seizures?
Not all generalized seizures are Tonic Clonic!!!
Generalized Seizures just means that lots of area of brains are involved
- If Primary - starts in deeper areas of brain like Basal/Thalamus
-- Can be convulsive or non-convulsive but either way whole brain involved at once
How does a focal seizure turn into gran mal/generalized? Difference between Primary Generalized and Secondarily Generalized?
Simple Focal/Partial seizure can become secondarily generalized when it starts in the cortex and spreads discharge so far that it ihits most areas and becomes generalized - LOTS of brain area involved
Primarary Generalized start in the basal areas/Thalamus and spread out to whole brian from there; typically have more genetic propensity to lower threshold for seizures - ex. JME or absenteeism
What are the ways to differentiate seizure types?
EEG Features - Inter-Ictal or Ictal (gold standard but only get if lucky usually)
RF for epilepsy --> damage to brain or family history
What is the main problem/ result from seizures that's an emergency? What's difficult about them?
Seizures that persist for > 5minutes, repetitive seizures that recur without recovery of consciousness and need seizure rescue or if can't return to baseline mental status
Can be Convulsive or Non-convulsive (hard to recognize!!)
Non-convulsive can seem like comatose or prolonged confusion, change in personality, autism/language loss, or comatose with subtle twicthing
What are some of the different familial epilepsy forms?
Juvenile Myoclonic Epilepsy
Ion channel mutations
What is Juvenile Myoclonic Epilepsy? How does it present?
see smart, college age kids starting to get jerks and then eventually get a gran mal for first time
do NOT outgrow
Genetic condition with lower threshold for Primary Generalized seizures
What is chilhood absence? How do you treat it?
Childhood absence is good bc is benign and often don't have to treat it bc kids can outgrow it
Familial generalized seizure disorder where get lots of absent seizures
What are some Ion Channel mutation syndromes?
Generalized epilepsy with febrile seizures
AD nocturnal frontal lobe epilepsy
Benign familial neonatal convulsions
Episodic ataxia Type 1 with partial seizures
What is a Paroxysmal Depolarization Shift (PDS)? What is the mechanism for it?
Essentially, is just the fancy way of saying enhanced excitability
Like an Inter-Ictal spark that goes off that can sometimes ignite and become a seizure when bursts of firing lasts for long enough periods that can see something happening
*Altered receptor protein conductance channels --> decreased GABA mediated inhibition and increased excitation by Glu/Asp
- increased calcium conductance at post-syn membrane and reduced outward K currents = Net INWARD current
- Triggereing depolarization resulting in PDS = BURST of spikes seen on EEG
Functional vs Structural Alterations in excitability from environment that can lead to epileptic foci?
Functional Alterations include changes in cation/anion concentrations, metabolic alterations, changes in NT levels
Structural Alterations in network include neurons/glia reactions
How are catecholamines involved in seizures?
Decreases in Da lower the threshold for seizures --> suggests Noradrenergic hyper-innervation of forebrain for absence seizures
How can glia help in seizures?
Glia buffer K+ concentrations and can correct increased extracellular K during seizures
Gliosis means that there is less buggering capacity and more likely to have more seizures
What are the structural changes involved in temporal lobe epilepsy that increase excitability? (specifically Mesial Temporal Sclerosis) How do these structural changes occur?
Mossy Fiber Sprouting!!! involved in Mesial Temporal Sclerosis
Neuronal alteration that increases excitability for Focal Temporal lobe epilepsy with Hippocampal Sclerosis
- MFS turns dentate granules cells (normally inhibitory) into epileptogenic population of neurons with recurrent excitatory synapsing
- Can resent bad brain and be seizure free
Bilateral BAD can be seen after meningitis/encephalitis
Clinically, how can you tell the difference sometimes between primary generalized tonic-clonic seizure and secondary generalized tonic clonic seizure (from partial onset)?
Sceondary might start with stiffening tone and clonic activity occuring more on one side
on EEG is blooms over time and space as opposed to all of a sudden everything everywhere
Clinical and EEG findings in Absence Seizure?
Typically, fast and can have hundreds / day
EEG - shows generalized spike and wave distribution in 3 cycles/sec in Typical Absence but can be slower in Atypical absence
Typical Absence very amenable to medications!
When do you treat seizures?
When you know it's epilepsy -> unprovoked and more than 1
Treat at second seizure