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Neuro > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Define Epilepsy*

A

the hyper-synchronisation of electrical activity in the brain, this includes the alpha, beta, theta and delta signalling (evident on EEG)

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2
Q

what are the types of seizures?

A
  1. Ictal (during the seizure)

2. interictal (between the seizures, consecutive ones)

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3
Q

What are the two types of symptoms in ictal seizure?

A

positive symptoms like twitching of thumb and hallucinations

negative symptom - loss of speech and amnesia

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4
Q

how is the interictal clinical presentation characterised?

A
  1. neurological - similar EEG is seen for hippocampal sclerosis and brain tumour under epileptic conditions however, the neurobiological response will be different for tumour
  2. cognitive
  3. psychological/psychiatric- depression, anxiety, psychosis
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5
Q

what are the classification of seizure?*

A
  1. focal onset
  2. generalised onset
  3. unknown onset
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6
Q

what is the lifetime risk of seizure?*

A

8-10%

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7
Q

what is the lifetime risk of epilepsy?*

A

2-5%

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8
Q

how is epilepsy characterised in a population*?

A

U shaped curve with

  1. children - usually due to genetic mutations
  2. older adulthood - cerebrovascular disease causing stroke and dementia
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9
Q

what is the prevalence of active epilepsy?*

A

4-7/1000

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10
Q

In which cases do you find “seizure with loss of awareness”?

A
  1. epilepsy
  2. syncope or loss of consciousness/ fainting
  3. non-epileptic attack disorder e.g. blacking out when stressed or depressed
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11
Q

In which cases do you find focal seizure?

A
  1. focal epilepsy
  2. migraine
  3. transient ischemic attack (TIA)
  4. pre-syncopal
  5. ‘functional’ (psychological conditions)
  6. metabolic e.g. hypoglycaemia
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12
Q

what are the key investigations in a patient with suspected epilepsy and their shortcomings?

A
  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
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13
Q

why would you look at the AchR in chronic epilepsy?

A

Frequent nocturnal seizures and they have a family history is when you will be interested in Ach receptor

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14
Q

what are the causes of epilepsy?*

A
  1. inherited - mutattions in ion channels, NTs, NTRs (determinante of excitability in the brain)
  2. acquired - VINTAMEDIP and developmental
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15
Q

what is vintamedip?

A 
V - vascular (stroke)
I - inflammatory 
N - neuroplastic brain injury 
T - trauma head injury 
A - allergy 
M - metabolic 
E- endocrine 
DI - drug induced 
P - psychiatric 
and developmental abnormalities in brain
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16
Q

what is the pathophysiology of epilepsy?

A
  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
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17
Q

what are the multiple zones in focal epilepsy?

A

IIEESF

  1. ictal onset zone
  2. epileptic zone
  3. irritative zone
  4. symptomatogenic zone
  5. epileptogenic lesion
  6. functional deficit core
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18
Q

what are the management techniques for epilepsy?

A
  1. information
  2. lifestyle factors like
  3. medication
  4. contraception and pregnancy
  5. surgery
  6. comorbidities, specially mood/cognition related like depression
  7. Multidisciplinary team (MDT) esp. specialist nurse, psychologist, psychiatrist, surgeon
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19
Q

what are the life style factors for the management of epilepsy?

A
  1. alcohol - an anti-convulsant so leaves the brain in a jittery state once it comes pff the next day
  2. sleep deprivation
  3. driving
  4. safety
  5. career
20
Q

on what factors does the prognosis of epilepsy vary?

A
  1. context
  2. seizure type
  3. epilepsy syndrome
21
Q

what is the general prognosis of epilepsy?

A
  1. 2/3 referred/remit for drug treatment
  2. 1/3 - treatment resistant
  3. Sudden Unexpected Death in Epilepsy (SUDEP)
22
Q

what is transient epileptic amnesia (TEA)?

A

the loss of memory for a short period of time in epilepsy, could be total or partial loss

23
Q

what are the diagnostic criteria for TEA?

A
  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
24
Q

what are the diagnostic methods involved in TIME?

A
  1. history and examination
  2. neuropsychology
  3. EEG
  4. structural MRI
25
Q

what are the clinical features of TEA?

A
  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
26
Q

what are the common interictal memory complaints in TEA?

A
  1. 2/3 autobiographical amnesia
  2. 1/2 accelerated forgetting
  3. 1/3 topographical amnesia
27
Q

what is

  1. TIME
  2. TGA
  3. TEA
  4. TIA
  5. ALF
  6. REM
A
  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
28
Q

what are. the neuroimaging options available for epilepsy?

A
  1. MRI (structural, DTI, fMRI)

2. PET

29
Q

what are the structural changes in TEA?

A

reduced hippocampal (head + body and not tail) volume

30
Q

what are the affected domain is accelerated long-term forgetting (ALF)?

A
  • memory specially, long term anterograde memory

- poor word and design recalls

31
Q

which are the affected memory domain in TEA?

A
  1. event recall
  2. contiguous event recall
  3. thoughts recall
32
Q

what are the features for the following in ALF?

  1. clinical
  2. cognitive
  3. neurobiological
A
  1. clinical
    - adequate acquisition
    - rapid loss at extended delays
  2. cognitive
    - encoding/ early consolidation
    - later phases of consolidation
    - episodic vs semantic
  3. neurobiological
    - physiological (epileptic discharges) and structural (loss of HC volume) changes
33
Q

what are the features of autobiographical amnesia?

A
  • cannot remember where, when and who
  • temporal lobectomy
  • presentation of TLE (subtle seizures, prodromal)
  • adult onset drug sensitive
  • chronic refractory (migraine??)
34
Q

what are the characters for the following for autobiographical amnesia?

  1. clinical
  2. cognitive
  3. neurobiological
A
  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
35
Q

what is the memory formation process?

A

perception -> encoding -> consolidation (fast/slow) -> storage -> retrieval

36
Q

which components of the memory does TEA, accelerated long term forgetting (ALF) and remote memory impairment (REM) affect?

A
  1. TEA - encoding + retrieval
  2. ALF - consolidation
  3. REM - mainly storage + consolidation and retrieval
37
Q

why is epilepsy more than seizures? what are its major comorbidities?*

A

anxiety, depression, cerebrovascular disease causing epilepsy

38
Q

what are the mechanisms of actions used to treat epilepsy?*

A
  • 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
39
Q

what conditions can epilepsy be confused with?*

A
  1. syncope (fainting) and pre-syncopal
  2. non-epileptic attack disorder
  3. migraine
  4. TIA
  5. functional - psychological conditions like depression and anxiety
  6. metabolic - hypotension
40
Q

list four reasons for which cognitive impairment might occur in epilepsy?*

A
  1. Temporal lobe lesions
  2. Seizures
  3. Active epilepsy
  4. Treatments - interfering with critical parts of brain development
  5. Hippocampal volume reduction
41
Q

when can surgery be helpful is epilepsy?*

A
  1. focal epilepsy
  2. when epileptic zone is known
    by the lesion of region responsible for triggering seizure (multiple zones)
42
Q

why does epilepsy affect memory so often?*

A
  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)
43
Q

what are the types of focal onset?

A
  1. aware
  2. impaired awareness
  3. motor onset - automatisms, atonic, clonic, tonic, epileptic spasms, myoclonic
  4. non-motor onset - atomic, behaviour arrest, cognitive, emotional, sensory
44
Q

what are the types of generalised onset?

A
  1. motor - tonic-clonic, clonic, tonic, myoclin, myclonic-tonic-clonic, myoclonic-atonic, epileptic spams
  2. non-motor (absence) - typical, atypical, myoclonic, eyelid myoclonia
45
Q

what are the types of unknown onset?

A
  1. motor - tonic-clonic, epileptic spams
  2. non-motor - behaviour arrest
  3. unclassified

Neuro (8 decks)

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