T1S1 seizures and epilepsy Flashcards
epilepsy definition
recurring, unprovoked seizures
acute symptomatic seizures can be triggered by -
stoke, alcohol withdrawal, metabolic disturbance
seizure types
generalised onset- electrical discharges appear to start over the whole brain at the same time
focal onset- electrical discharge appears to start in one cortical region and then may remain localized or spread over the whole brain (secondary generalized)
seizure classifications
- tonic clonic seizures
- absences
- tonic seizures
- atonic seizures
- myoclonic seizures
idiopathic generalised seizures
- onset in childhood and adolescence
- usually no focal symptoms or signs
- polygenic cause
- generalised discharges on eeg
- may be photosensitive
juvenile myoclonic epilepsy
- commonest form of generalised epilepsy
- lifelong usually
- early morning myoclonic jerks
- photosensitive/ sleep deprived triggers
- generalised tonic clonic seizures, without warning
tonic clonic seizures
no warning (injury risk)
- tonic phase
- continuous muscle spasm, fall, cyanosis, tongue biting, inconcinence - clonic phase
- rhythmic jerks which slow down and get larger in amplitude as attack ends - post seizure phase
- coma, drowsiness, confusion, headache
- muscle ache
abences
- abrupt
- 5-20 secs
- multiple times a day, can lead to learning difficulties
- unresponsive, amnesia
- rapid recovery
- eyelid flickering
3hz spike and wave on eeg
focal onset seizures
simple partial seizure (SPS)- patient aware- aura (warning)
complex partial seizure (CPS)
- aura with level of reduced awareness (warning)
- can be secondary generalised ie patient may experience CPS or SPS before tonic clonic seizure
aura is knowing its about to happen- may be altered smell, fear, deja vu, epigastric rising sensation
secondary tonic clonic seizures
- aura
- cant abort attack
- 1-3 mins before falling
- then tonic clonic seizure
most seizures are in the - lobe
temporal (70%) symptoms: - hallucination of taste, speech, smell, visuals - epigastric rising sensation - pallor/flushing/hr changes - lip smacking/chewing motions - dystonic posturing (limbs rise)
If words are formed during attack, it is in non dominant hemisphere
frontal lobe seizures
10-30 secs
- rapid recovery
- frequent but usually nocturnal
- eyes and head forced to contralateral side
- thrashing motor activity
- eeg often normal
- automatisms, distonic posturing
parietal lobe seizures
- positive sensory symptoms
- tingling, pain
- distortion of body shape/image
- jacksonian march of +ve sensory symptoms
occipital lobe seizures
- visual hallucinations (balls of coloured or flashing lights)
- 25% blackout or whiteout
epileptogenesis
- the process by which parts of a normal brain are converted to a hyperexcitable brain
epileptic seizure def
- an explosion of synchronous activity by lots of neurons at once that has a tendancy to spread throughout the cerebral cortex causing an electrical brainstorm
- this causes a brief change in behaviour
why is the brain prone to seizure activity
- action potentials rely on positive feedback so are inherently unstable
- a single neuron can fire a train of action potentials simultaneously without external stimulation (intrinsic excitability)
thus a network of connected excitatory neurons is potentially explosive; stimulation of any one can lead to a chain reaction due to the progressive spread of activity over a large area
to avoid this we have inhibitory synpases
EPILEPSY REPRESENTS A FAILURE OF INHIBITORY REGULATION, EITHER FOCALLY OR GENERALLY
channelopathies
- Na+ inactivation is too slow
- eg generalised epilepsy with febrile seizures
- action potential repolarisation impaired - reduction in the number of functional k+ channels
- eg benign familial neonatal convulsions
- action potential repolarisation impaired
eeg
- electroencephalogram
- highest synchronous activity when the brain is at rest
- when stimulated the brain becomes dyssynchronous
- hyperexcitation of seizure leads to synchronous eeg activity
origin and spread of focal to generalized seizures
- focal (1000 neurons)
- caused by paroxysmal depolarising shift
spread to other brain regions along normal neuronal pathways
secondary generalization: when activity spreads to thalamus (tonic clonic)
primary generalized seizures reach the cerebral cortex via normal neuronal pathways from the thalamus
see pic s8 x
antiepileptic drugs (AEB) general
- do not prevent development of epilepsy
- prevent spread of the excitation across the lobes
- control the symptom (seizure) rather than the cause
how do AEDs prevent generalisation
causes of increase excitation:
- increased membrane permeability
- increased efficiency of excitatory synaptic transmission (glutamate)
- decrease efficiency of inhibitory synaptic transmission (GABA)
treatments may be aimed at opposing these actions, eg na channel blockers and gaba enhancers
na channel blockers
- block repetitive neuron firing
- normal neuronal functioning is not impaired
phenytoin, lamotrigine, zonisamide, lacosomide
carbamazine, oxcarbazepine and eslicarbazepine
- competitively inhibit voltage gates Na channel by binding to receptor in its inactive state, prolonging the period between successive firings
