Flashcards in Epilepsy Deck (45):
the hyper-synchronisation of electrical activity in the brain, this includes the alpha, beta, theta and delta signalling (evident on EEG)
what are the types of seizures?
1. Ictal (during the seizure)
2. interictal (between the seizures, consecutive ones)
What are the two types of symptoms in ictal seizure?
positive symptoms like twitching of thumb and hallucinations
negative symptom - loss of speech and amnesia
how is the interictal clinical presentation characterised?
1.neurological - similar EEG is seen for hippocampal sclerosis and brain tumour under epileptic conditions however, the neurobiological response will be different for tumour
3.psychological/psychiatric- depression, anxiety, psychosis
what are the classification of seizure?*
1. focal onset
2. generalised onset
3. unknown onset
what is the lifetime risk of seizure?*
what is the lifetime risk of epilepsy?*
how is epilepsy characterised in a population*?
U shaped curve with
1. children - usually due to genetic mutations
2. older adulthood - cerebrovascular disease causing stroke and dementia
what is the prevalence of active epilepsy?*
In which cases do you find “seizure with loss of awareness”?
2. syncope or loss of consciousness/ fainting
3. non-epileptic attack disorder e.g. blacking out when stressed or depressed
In which cases do you find focal seizure?
1. focal epilepsy
3. transient ischemic attack (TIA)
5. 'functional' (psychological conditions)
6. metabolic e.g. hypoglycaemia
what are the key investigations in a patient with suspected epilepsy and their shortcomings?
1. Scan - CT, MRI, metabolic, functional
2. EEG - (needs to be monitored) routinely, sleep deprived, ambulatory (while walking around), video telemetry
3. Bood tests - acute vs chronic
Acute - Ca2+, Mg2+, glucose
chronic - special tests e.g. AchR genetics, Kuf's disease
why would you look at the AchR in chronic epilepsy?
Frequent nocturnal seizures and they have a family history is when you will be interested in Ach receptor
what are the causes of epilepsy?*
1. inherited - mutattions in ion channels, NTs, NTRs (determinante of excitability in the brain)
2. acquired - VINTAMEDIP and developmental
what is vintamedip?
V - vascular (stroke)
I - inflammatory
N - neuroplastic brain injury
T - trauma head injury
A - allergy
M - metabolic
DI - drug induced
P - psychiatric
and developmental abnormalities in brain
what is the pathophysiology of epilepsy?
1. fundamental disorder of brain network and oscillations
2. ion channels and neurotransmitters - determinants of excitability, key to primary generalised epilepsy
3. multiple zones of focal epilepsy
what are the multiple zones in focal epilepsy?
1. ictal onset zone
2. epileptic zone
3. irritative zone
4. symptomatogenic zone
5. epileptogenic lesion
6. functional deficit core
what are the management techniques for epilepsy?
2. lifestyle factors like
4. contraception and pregnancy
6. comorbidities, specially mood/cognition related like depression
7. Multidisciplinary team (MDT) esp. specialist nurse, psychologist, psychiatrist, surgeon
what are the life style factors for the management of epilepsy?
1. alcohol - an anti-convulsant so leaves the brain in a jittery state once it comes pff the next day
2. sleep deprivation
on what factors does the prognosis of epilepsy vary?
2. seizure type
3. epilepsy syndrome
what is the general prognosis of epilepsy?
1. 2/3 referred/remit for drug treatment
2. 1/3 - treatment resistant
3. Sudden Unexpected Death in Epilepsy (SUDEP)
what is transient epileptic amnesia (TEA)?
the loss of memory for a short period of time in epilepsy, could be total or partial loss
what are the diagnostic criteria for TEA?
1. recurrent, witnessed episode of transient amnesia
2. other cognitive functions intact
3. evidence of epilepsy
a. other clinical features of epilepsy
b. response to anti-convulsant medications
c. epileptiform abnormalities on EEG
what are the diagnostic methods involved in TIME?
1. history and examination
4. structural MRI
what are the clinical features of TEA?
1. late onset
2. male predominance
3. attacks every 30-60 mins (like TGA)
4. attacks once/month
5. attacks on waking up are common
6. amnesia could be the sole feature
7. olfactory hallucinations, automatism, brief unresponsiveness
8. partial recall is common
9. diagnosis usually delayed (due to stress, TGA, TIA, sleep inertia)
10. excellent treatment response
11. interictal memory complaints are common
what are the common interictal memory complaints in TEA?
1. 2/3 autobiographical amnesia
2. 1/2 accelerated forgetting
3. 1/3 topographical amnesia
1. TIME - time in memory impairment
2. TGA - transient global amnesia
3. TEA - transient epileptic amnesia
4. TIA - transient ischemic attack
5. ALF - accelerated long term forgetting
6. REM - remote memory impairment
what are. the neuroimaging options available for epilepsy?
1. MRI (structural, DTI, fMRI)
what are the structural changes in TEA?
reduced hippocampal (head + body and not tail) volume
what are the affected domain is accelerated long-term forgetting (ALF)?
- memory specially, long term anterograde memory
- poor word and design recalls
which are the affected memory domain in TEA?
1. event recall
2. contiguous event recall
3. thoughts recall
what are the features for the following in ALF?
- adequate acquisition
- rapid loss at extended delays
- encoding/ early consolidation
- later phases of consolidation
- episodic vs semantic
- physiological (epileptic discharges) and structural (loss of HC volume) changes
what are the features of autobiographical amnesia?
- cannot remember where, when and who
- temporal lobectomy
- presentation of TLE (subtle seizures, prodromal)
- adult onset drug sensitive
- chronic refractory (migraine??)
what are the characters for the following for autobiographical amnesia?
1. clinical - extensive autobiographical memory loss despite of serviceable day to day memory
2. cognitive - impairment of encoding/consolidation, storage and retrieval of memory
3. neurobiological - physiological and structural changes
what is the memory formation process?
perception -> encoding -> consolidation (fast/slow) -> storage -> retrieval
which components of the memory does TEA, accelerated long term forgetting (ALF) and remote memory impairment (REM) affect?
1. TEA - encoding + retrieval
2. ALF - consolidation
3. REM - mainly storage + consolidation and retrieval
why is epilepsy more than seizures? what are its major comorbidities?*
anxiety, depression, cerebrovascular disease causing epilepsy
what are the mechanisms of actions used to treat epilepsy?*
- drugs specialised to target specific channels and receptors
- promotes K+ channels, Cl- channels, GABAaR activity
- inhibits Na+, Ca2+, NMDARs, AMPARs
- the goal is to reduce abnormal brain activity without affecting the normal brain activity
what conditions can epilepsy be confused with?*
1. syncope (fainting) and pre-syncopal
2. non-epileptic attack disorder
5. functional - psychological conditions like depression and anxiety
6. metabolic - hypotension
list four reasons for which cognitive impairment might occur in epilepsy?*
1. Temporal lobe lesions
3. Active epilepsy
4. Treatments - interfering with critical parts of brain development
5. Hippocampal volume reduction
when can surgery be helpful is epilepsy?*
1. focal epilepsy
2. when epileptic zone is known
by the lesion of region responsible for triggering seizure (multiple zones)
why does epilepsy affect memory so often?*
1. temporal lobe lesions
2. subtle hippocampal volume loss (mTL in TEA)
3. fundamental disorder of brain network oscillations (gamma and theta oscillations involved in memory formation)
what are the types of focal onset?
2. impaired awareness
3. motor onset - automatisms, atonic, clonic, tonic, epileptic spasms, myoclonic
4. non-motor onset - atomic, behaviour arrest, cognitive, emotional, sensory
what are the types of generalised onset?
1. motor - tonic-clonic, clonic, tonic, myoclin, myclonic-tonic-clonic, myoclonic-atonic, epileptic spams
2. non-motor (absence) - typical, atypical, myoclonic, eyelid myoclonia