Pathophysiol of seizures Flashcards
OVERVIEW OF SEIZURES
i) what is a seizure?
ii) what do clinical manifestations of epileptic seizures depend on?
iii) how long do seizures normally last? what are they followed by?
i) abnormal synchronous (lots of neurons firing at the same time - not physiological) neural electrical discharge of the cerebral cortex >
- results in sudden transient disturbance of function
ii) depend on area of the cortex involved (usually cortical)
iii) usually self limiting and last 1-2 mins
- followerd by period of post ictal cerebral depression
PATHOPHYSIOLOGY OF SEIZURES
i) what happens to the neurons? what happens to balance of neuronal processes? what is favoured?
ii) name two mechanisms that can terminate a seizure? what may they also contribute to?
iii) which two brain area loops are involved in generalised epilepsies? name a type of seizure these can cause
i) hyper synchronisation > balance of excite and inhibitory neuronal process (excitatory is favoured)
ii) adenosine, endogenous opiate peptide NTs
- can also contrib to the negative phenomenom seen after seizures eg post ictal and paresis
iii) generalised epilepsies linked to circuits between the thalamus and the cortex
- petit mal seizure
EPILEPTIC SEIZURES
i) name four causes of provoked seizures? name three drugs that may cause a seizure
ii) name four medical things that can cause a provoked seizure?
iii) what % of people will have at least 1 seizure in a lifetime? what proportion of these go on to develop epilepsy?
iv) what does epilepsy increase the risk of?
i) acute response to brain insult > brain trauma, stroke, encephalitis, meninigits
- drugs > cocaine, OD of antideps, alcohol withdraw, benzo or barbit withdraw
ii) fever, acute renal fail, hypoglycaemia, acute porphoria, elec deraangement > go back to normal once problems are corrected
iii) 10% of people have at least 1 seizure > 1/3 will go on to develop epilepsy
iv) increased risk of unprovoked seizures
SEIZURE SPREAD
i) what are the majority of seizures seen in elderly people in relation to spread?
ii) what happens if the seizure spreads across a commisure? how does the patient appear?
iii) what does a complex seizure mean?
iv) which brain structure does a seizure starting in the temporal lobe often spread to? what does this result in? what type of seizure results?
i) localisation related - start somewhere in the brain then spread
ii) involves both sides of brain > alteration in conciousness
- patient appears confused, poor memory afterwards
iii) conciousness has been affected in some way (not lost but impaired)
iv) spread to the thalamus > lots of connections to the cortex therefore seizure spread to cortex and complete LOC
- tonic clonic seizure (decorticate posture, tongue biting, cyanosis)
PRIMARY GENERALISED EPILEPSY
i) what are they due to?
ii) what type of seizure falls into this category?
iii) what is a myoclonic seizure?
iv) what is an absence seizure/petit mal? how long is loss of awareness/how long is recovery? which thalamic nuclei is involved
i) instability in the thalamo cortical feedback circuitry > re entrant loop
ii) tonic clonic
iii) series of jerks affecting one side of the body (like clonic phase)
iv) loss of awareness <30s, can be just a split second
- immediate recovery
- reticular nucleus of the thalamus > inhibits the cortex > dont manifest as tonic clonic
JUVENILE MYOCLONIC EPILEPSY
i) what type of epilepsy is it?
ii) what is usual age of onset?
iii) what type of seizures occur? (3)
iv) what two drugs are there excellent response to?
i) most common type of primary generalised epilepsy (instab betweeen thalamus and cortex)
ii) age of onset 8-30yrs
iii) myoclonic, absence, generalised tonic clonic
iv) good response to valproate +- clonazepam
LOCALISED EPILEPSY
i) which area of the brain do they most commonly arise from? why may this be? which things are linked with this area
ii) why may you get smells or taste at the onset of a seizure?
iii) which area is implicated in feelings of flushing or epigastric rising (butterflies)
iv) which automatism movements may be seen? (3)
v) what time of day to frontal lobe seizures often occur? how do they manifest?
vi) what do primary somatosensory seizures present with? do they travel
i) medial temporal lobe (hippocampus) > area is very susceptible to injury/hypoxia
- memory/de ja vu
ii) olfactory cortex is close to frontal/medial temporal lobe
iii) hypothalamus (control of the ANS)
iv) chewing, lip smacking, swallowing
v) often occur at night with motor manifestations (jacksonian seizure, assymetrical posturing)
vi) tingling > travel down body
AUTOMATISMS
i) what are they? give an example
ii) which brain area do they often involve?
iii) name three situations they usually occur in?
iv) what is release phenomena?
v) what type of seizure do you see one arm extended on flexed (fencing stance)
i) automatic, involuntary, non purposeful, stereotyped repititive behaviours
- lip smacking, chewing
ii) temporal lobe (usually both due to travel along corpus callosum)
iii) usually occur in situations of impaired awareness eg concussion, syncope, complex partial seizures
iv) loss of inhibition of specific parts of the brain
v) SMA frontal seizure
IMPAIRMENT OF CONC IN TEMPORAL LOBE EPILEPSY
i) which main network is probably inhibited?
ii) which brain area that is important in conciousness may be implicated? (2)
iii) what is the left hemisphere important for?
iv) what happened when subcortical spread of seizures was blocked in rats by cutting the fornix? what does this show?
i) fronto parietal network
ii) thalamus and temporal lobe
iii) speaking > reporting conciousness
iv) prevented neocortical slow wave activity and behavioural arrest
- sub cortical areas eg brainstem are important for seizure spread/loss of conc
CAUSES OF EPILEPSY
i) what is the most common cause?
ii) what accounts for 15% of cause?
iii) name three other causes
iv) what can happen to the hippocampus to cause seizures? what does this cause in childhood?
v) what % of epilepsy does monogenic causes account for
i) idiopathic
ii) CVD is 15%
iii) stroke, infarction, cerebral contusion, astrocytoma
iv) hippocampal sclerosis > febrile convulsions in childhood
v) 1-2%
EPILEPTOGENESIS - GLIOSIS
i) what is gliosis? when does it happen?
ii) name one things that is upregulated in astrocytes and one things upregulated in microglia?
iii) name three factors that may be released by the glial cells to cause this
iv) how are glutamate transporters on astrocytes implicated?
v) how does astrocyte buffering of K+ change?
i) hypertrophy of cell bodies and processes of astrocytes and microglia
- happens after an insult eg stroke
ii) upreg of intermediate filament proteins in AC
upreg of ionised calcium binding adaptor molecule 1 in MG - makes them more epileptogenic
iii) rel of cytokines, chemokines anfd growth factors
iv) reduced glu transporters > excitotoxicity
v) astrocytes fail to buffer K+ by not taking it up > more suscep to excitation
OTHER EPILEPTOGENIC CHANGES
i) how does ECM change?
ii) how may vascular supply be impacted?
iii) what can happen to synapses to make them more excitatory?
i) increase in ECM molecules such as chondroitin sulphate proteoglycans
ii) impaired vascular supply
iii) abherrant synaptic reorganisation > more exciteable
PRODROMAL FEATURES
i) name three
ii) what area may a seizure be in if patient has deja vu, piloerection, smell, taste?
iii) name three context/location that indicate its more likely to be epilepsy?
iv) what may happen to the skin pre vasovagal syncope?
i) visual tunneling, light headed, vertigo, sense of LOC, sleepiness
ii) temporal lobe seizure
iii) sleep related episode, first thing in the morning, in the nightclub
iv) flushing (not pallor)
TONGUE BITING AND INCONTINENCE
i) what part of a tonic clonic seizure does tongue biting occur?
ii) if there is lateral tongue biting - what is it due to 99% of the time?
iii) does presence of urinary incontinence have diagnostic value in epileptic episodes?
iv) what % of syncope will there be myoclonic jerks?
i) tonic phase
ii) seizure (not syncope but can occasionally happen in syncope)
iii) no - low sensitivity and specificity so no value in dx of syncope or seizure
iv) 90% - often leads to misdiagnosis
SYNCOPE DIFFERENTIALS
i) what are the three main types of syncope?
ii) name four other differentials
iii) how quick is recovery usually?
iv) is it common to have tongue biting/tonic clonic phase
v) what can trigger hypervent > seizure? what can trigger vomiting > syncope?
i) reflex (vasovagal, cough, defacation), orthostatic, cardiogenic
ii) seizures, hypoxia, hypoglycaemia, intoxication
iii) very quick, few seconds
iv) no tongue biting or tonic/clonic phase
v) panic > hypervent > seizure/syncope
vertigo > vomiting > syncope
