Epilepsy/Seizures Flashcards
the clinical manifestation of an abnormal and excessive excitation and synchronization of a population of cortical neurons
seizure
a tendency toward recurrent seizures UNPROVOKED by any systemic or acute neurologic insults
epilepsy
sequence of events that converts a normal neuronal network into a hyperexcitable network
epileptogenesis
Principal or pyramidal neurons form what type of synapse?
excitatory synapse on post-synaptic neurons
Interneurons or basket cells form what type of synapse?
inhibitory synapse on principal cells or other inhibitory neurons
When does recurrent inhibition occur?
when a principal neuron forms synapses on an inhibitory neuron, which in turn forms synapses back on the principal cells to achieve a negative feedback loop
excitatory NTs?
GLUTAMATE and aspartate
inhibitory NTs?
GABA and glycine
Describe the ionotropic glutamate receptor.
fast synaptic transmission; NMDA, AMPA, and kainate; Gated Ca2+ and gated Na+ channels
Describe the metabotropic glutamate receptor?
slow synaptic transmission; quisqualate; regulation of second messengers (cAMP and inositol); modulation of synaptic activity
Modulation of glutamate receptors
glycine, polyamine sites, zinc, redox site
Describe GABA-A receptor.
post-synaptic, specific recognition sites, linked to Cl- channel, mediate
Describe GABA-B receptor.
presynaptic autoreceptors, mediated by K+ currents, prolong activation of K+ channels
What is burst firing?
firing very rapidly in “bursts,” results from repetitive activation of action potentials
Where does burst firing frequently occur?
HIPPOCAMPUS (very important in seizure pathology bc lots of seizures generated here)
Where do recurrent excitatory pathways occur?
in the hippocampus and neocortex via pyramidal collateralls
What do recurrent excitatory pathways do?
promote spread of the seizure discharge
Describe hippocampal sclerosis
common in temporal lobe epilepsy; good reason for surgery; results from having many seizures over time
What is facilitation?
increased glutamate release
What is potentiation?
enhanced synaptic activity
High frequency repetitive firing results in…?
results in increased accumulation of Ca2+ near the presynaptic terminal and results in facilitation and potentiation; it also depresses inhibitory synaptic activity
in areas with densely packed neurons (i.e.. hippocampus), how do neurons directly interact?
gap junctions; emphatic transmission due to close apposition of membranes allowing direct propagation of the seizure discharge
List the 8 cellular mechanisms of epilepsy. (*important)
1 modification or alteration of ion channels; 2 synaptic reorganization and modification; 3 modulation of gene expression; 4 burst firing; 5 recurrent excitatory connections; 6 synaptic enhancement resulting in facilitation and potentiation produced by rapid firing; 7 depression of inhibitory synapses by high frequency firing; 8 non synaptic spread of electrical activity
When can an acute seizure turn into epilepsy?
if an acute seizure is the result of trauma, and later that develops scaring, you can develop epilepsy bc of the pathway created
What are spike and sharp waves?
spikes (
are spike and sharp waves generalized, focal or both?
there are generalized and focal spike waves; and just focal sharp waves
myoclonic seizure?
very fast jerk seizure
atonic seizure?
they just fall. (walk around normal and then just fall and bust lip or something)
convulsive seizure?
the kind you see on TV. different terms to describe how they move (tonic, clonic, tonic-clonic, clonic-tonic-clonic)
absence seizure?
starring gaze (a lot of school teachers refer kids for this)
focal seizure?
means originating in a particular part of the brain and staying in networks in that one hemisphere; if a focal seizure goes long enough it can generalize
Generalized seizures?
conceptualized as originating at some point within and rapidly engaging bilaterally distributed networks
Describe focal seizures at different levels of impairment.
1) w/o impairment of consciousness or awareness, with observable motor or autonomic components (old term: simple partial); 2) with impairment of consciousness or awareness (old term: complex partial); 3) evolving to bilateral, convulsive seizures [involving tonic, clonic, or tonic and clonic components] (old term: secondarily generalized)
West syndrome (infantile spasms)*
these come in clusters after the baby is startled. kids w/ brain injuries are more likely to have these (shaken baby syndrome; cerebellar palsy; etc) but they don’t have to. flexion or extension spasms, cryptogenic vs. symptomatic, onset = birth - 2 years, 80% develop mental retardation, 60-70% have lifelong epilepsy, hypsarrhythmia pattern on EEG
Atonic seizure description
no warning, abrupt onset; injuries common; very difficult to treat; may respond well to VNS (vagal nerve stimulator); corpus callosotomy may prevent falls
Lennox-Gastaut syndrome
onset in early childhood; many underlying etiologies, often cryptogenic; MULTIPLE SEIZURE TYPES including atypical absence, generalized convulsive, atonic, myoclonic, partial; negative neurodevelopment impact – mental retardation; slow spike and wave (2 hertz)
Focal seizure (parietal) – example
ex: keeps saying “okay okay…” to try to calm himself down bc has some feeling of being not right. he was having recurrent episodes of sudden fear or panic that increased in frequency. during these he maintained consciousness
Focal seizure (frontal)
harder to diagnose; stereotypically it is exactly the same every time; does not look like a normal seizure; most commonly diagnosed pseudoseizure they see
Focal seizure without impairment of consciousness (simple partial)
focal onset; aura is common; clinical manifestation is typically based on cerebral location of origin (i.e. frontal lobe – motor, parietal lobe – sensory, occipital lobe – vision); may secondarily generalize
Focal seizure (temporal)
vocalization stuff is very common
focal seizure with impairment of consciousness (complex partial)
aura is common, represents the ictal onset, stereotypical but may be difficult to describe; alteration of consciousness; automatisms (ex: fumbling w/ the sheets); postictal confusion; may secondarily generalize. if this lasts several minutes they are usually very confused
Benign epilepsies of childhood*
centrotemporal or occipital spikes (benign epilepsy with centrotemporal spikes BECTS; panayiotopoulos syndrome or benign epilepsy w/ occipital spikes); nocturnal seizures are common; seizures are usually infrequent; remits by 15-16 years of age or earlier
Absence description
brief stare with unresponsiveness; may have associated eye flutter (eyelid myoclonia); sudden onset with arrest of activity; no aura or postictal confusion; generalized 3 per second spike and wave; childhood absence – typical onset 5-9 years of age; juvenile absence – onset during early adolescence. usually noticed by the family, pt may have no idea.
generalized tonic-clonic (and other generalized convulsive types)
no warning, abrupt onset; tonic, clonic, tonic-clonic or clonic-tonic-clonic activity; bowel and bladder incontinence common; postictal unresponsiveness or confusion; generalized spike and wave.
Myoclonic seizure*
SUDDEN SINGLE JERKS of the arms and head; single or in clusters; no alterations in consciousness; may progress to clonic-tonic-clonic seizure; generalized multispike wave
juvenile myoclonic epilepsy (JME)
MYOCLONIC SEIZURES with onset in late childhood or adolescence; may develop generalized convulsive (80%) or absence seizures (30%); autosomal dominant inheritance pattern, but many may represent new mutations with no family history
What are some of the epilepsy surgeries performed?
temporal lobectomy, extratemporal lesional resection, extratemporal non-lesional resection, functional hemispherectomy; corpus callosotomy (especially for atonic and brief tonic seizures)
