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Flashcards in Epilepsy Deck (82)
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1
Q

TRUE or FALSE? Neurology is based on fancy tests and more tech = better neurology

A

False
Neurology is clinical
History and examination = 90% +
Without clear hypothesis, tests will mislead

2
Q

TRUE or FALSE? Neurologists make clever diagnoses about conditions they can’t do anything about

A

FALSE
All neurology is treatable
Much can be fully controlled

3
Q

What is the definition of epilepsy?

A

2 unprovoked seizures more than 24hrs apart

4
Q

Is a child having a seizure during a fever epilepsy?

A

No, its just a febrile seizure

5
Q

What is the definition of a seizure?

A

A manifestation of abnormal brain electrical activity

6
Q

What are the 2 main types of seizures?

A

focal and generalised

7
Q

What are the types of focal seizures?

A

simple partial seizures - retain awareness but have motor, sensory or psychological problem

Complex partial seizures - automatisms and lose awareness

Secondarily generalised seizures: initially have consciousness and then loses it and has convulsions

8
Q

What types of generalised seizures are there?

A
Absence
Myoclonus - irregular jerks of muscle or muscle group
Tonic clonic - Stiffening and jerking
Tonic -stiffening
Clonic-Rhythmic Jerking
Atonic- muscles go floppy
9
Q

What is the difference between a focal and a generlized seizure?

A

Focal: one part of brain affects the part that that part controls

Generalised: involves whole brain and thus whole body

10
Q

When making an epilepsy diagnosis what is the most important part and what are the other parts?

A

Most important: History and good communication

Less important: Examinations and investigations

11
Q

What percentage of the time is an epilepsy diagnosis correct?

A

70%

12
Q

What are the possible differential diagnoses for loss of consciousness - and which are most common?

A

Syncope (50%)
Epileptic seizure (25%)
Non-epileptic attack disorder (10%)
Other: 15%

13
Q

What sort of symptoms would you ask an eye-witness about?

A
Was there warning?
Head or eye deviation
Eyes open/pupils dilated and unresponsive
Tongue biting (lateral tongue)
Cyanosis
Tonic and/or. clonic
Rhythmic shaking
Was there incontinence?
Duration
Post-event confusion
14
Q

Why may there be head or eye deviation during a seizure?

A

Suggests a frontal lobe problem because that is where the motor cortex is

15
Q

Why might someone bite the lateral side of their tongue?

A

During tonic phase there is jaw clenching

16
Q

Why may there be cyanosis?

A

Due to person not breathing at all

17
Q

How long do seizures last and how long does post-event confusion last?

A

Seizure: <4.5 min, usually <2 min

Confusion:>10 min

18
Q

What is the problem with eye witness reports of seizure durations?

A

They tend to be overestimated

19
Q

How many people who say they have had their first seizure have actually had one before without noticing it?

A

2/3

20
Q

What are the types of seizures that are often missed?

A

Nighttime ones and aura

21
Q

What are clues that someone has had a nighttime seizure?

A

Nocturnal tongue biting
Enuresis
Morning hangover (w/o alcohol)

22
Q

What are clues that someone has had an aura seizure?

A

myoclonus
Jamais vu, deja vu
Rising epigastric sensation
Brief olfactory/gustatory aura

23
Q

What is jamais vu?

A

e.g. going to a familiar place and feeling its strange - especially if it has bad feeling

24
Q

Which is more common jamais vu or deja vu?

A

jamais vu

25
Q

What part of the brain is jamais vu associated with?

A

frontal lobe

26
Q

What is the prodrome of syncope?

A
Sweating
dizziness
chest pain
dyspnoea
palpitations
tinnitus
27
Q

What are the characteristics of syncope?

A
Prodrome
Happens from standing or sitting
<1 min
Floppy +/- myoclonus
\+/- incontinence
Pale, sweaty, clammy
Rapid recovery
28
Q

Some cases of syncope are related to problem with heart rate. How do these differ from other syncopes?

A

They can happen when the patient stands up

There is no syncope prodrome/warning

29
Q

Should we be worried about syncope?

A

No, this is usually benign and not frequent or too troublesome

30
Q

What is the history of non-epileptic attack syndrome?

A
Remembers event
Detached description
Variable seizure types
Other illnesses
Dependency/support structure
Previous abuse
31
Q

What should the examination during a NEAD attack show?

A
Normal colour
eyes closed, resist opening
Distractable
Waxing and waning
Triggers (e.g. clinic visits)
reactive pupils
flexor plantars (reflex)
Episodes are often long
32
Q

Are NEAD diagnoses fast?

A

No, it takes forever and in the meantime the patient has to take useless antiepileptics

33
Q

What do you look at in an examination of epilepsy patients?

A

General: BP, pulse, heart
Raised intracranial pressure - papilloedema
Neurological/structural abnormalities: tumour/stroke
Focal signs
Genetic causes
Asymmetry of limbs

34
Q

What are some signs that suggest genetic causes of epilepsy?

A

Skin lesions suggest tuberous sclerosis

35
Q

Why do we look for limb asymmetry in epilepsy examinations?

A

Suggests a long standing lesion on opposite hemisphere - one side of the body is smaller if the seizure happened before the end of puberty due to weakness on one side

36
Q

What are the components of good communication after epilepsy diagnosis?

A

Explaining the limitations of the tests

Explaining what they can or cannot do - e.g. don’t drive but don’t have unnecessary restrictions

Explain benefits of treatment and risk w/o

Empower: they can do almost anything they want

Work to reduce stigma

Educate colleagues

37
Q

Why should we explain limitations of tests to the patients?

A

So they know that tech doesn’t trump the clinical aspect and they know to tell us as many details as they can

38
Q

Why do we need to explain the benefits of treatment and the risk w/o it?

A

Some ppl have no symptoms for about a year and stop taking meds (only 40-60% regularly take meds)

But this can lead to death

39
Q

What sort of investigations do you do for epilepsy?

A

Blood
ECG
Imaging
EEG

40
Q

What is the most important test in clinical epilepsy investigations and why?

A

ECG bc it is important to check whether they are having a cardiac event which leads to the symptom

41
Q

Why are routine EEGs less useful to do for clinical investigations of epilepsy?

A

Its not as effective as ECG because the waves are attenuated : waves are smaller than in heart , physical barrier of scalp and skull, some structures deep in the brain cannot be seen well especially in frontal seizures

42
Q

What is the yield (ability to diagnose) with EEG?

A

50% of ppl with epilepsy have a normal EEG

43
Q

What are the different ways of improving EEG yield?

A

Provocation tests:
Sleep deprivation
Photic stimulation

Video-telemetry

Stereo EEG

Functional Mapping

MEG - alternative to EEG

44
Q

How much does sleep deprivation improve EEG yield?

A

50%–>80%

45
Q

What % of people with epilepsy are photosensitive?

A

5%

46
Q

What kinds of epilepsy is video-telemetry used to diagnose?

A

Refractory - doesn’t respond to meds

Non-epileptic (NEAD)

47
Q

What is stereo EEG?

A

Implanting very thin electrodes through small holes in skull to measure deeper structures

48
Q

Why do we only do stereo EEG if epilepsy is severe?

A

It can cause haemorrhage

49
Q

What is functional mapping?

A

It looks at the metabolic activity of the brain to find abnormal seizure activity

50
Q

What is MRS?

A

It is like an MRI but instead of looking at anatomy/structure, it measures the chemical metabolism of a suspected tumour (profiles of e.g. AA/lipids might differ in tumour compared to normal)

51
Q

Why is MEG useful?

A

It’s very good at localising problem area more precisely

52
Q

When (at what ages) do the onset/indences of epilepsy peak?

A

Young people/children and very old people ~80

53
Q

How common is epilepsy?

A

Incidence: 50-180/100,000/Year

Prevalence of active epilepsy: 10/1000

Lifetime prevalence: 2-5%

54
Q

What is the outcome of a febrile seizure?

A

Usually one off and good recovery

If more seizures occur there might be temporal lobe sclerosis leading to temporal epilepsy

55
Q

What are the top causes of epilepsy in order of contribution?

A
  1. Genetic
  2. Infections
  3. Structural/Vascular
  4. Other
56
Q

TRUE or FALSE? The cause of your epilepsy depends on your age/ country / socioeconomic status

A

TRUE

57
Q

Map out the road to remission for epilepsy patients

A

Diagnosis –> drugs –> remission or more drugs –> remission or surgery –> if no remission, possible stimulation

58
Q

What percentage of people remit after their first drug treatment?

A

70%

59
Q

What is one reason why treatment may not be working?

A

Incorrect diagnosis

60
Q

What were the first 2 entiepiletics?

A

Bromide (1850)

Phenobarbital (1910)

61
Q

TRUE or FALSE? There are currently only a few antiepileptics available

A

False (there are many)

62
Q

What are the problems with barbituates?

A

if you suddenly stop, ppl can have very severe seizures

63
Q

Has remission rate on treatment improved in recent years?

A

No, it has stayed at 70%

64
Q

What kinds of drugs are used for primary/generalised epilepsy?

A

Broad spectrum

65
Q

What happens if you give narrow spectrum drugs to someone with generalised epilepsy?

A

They get worse (e.g. making absence seizures longer)

66
Q

What are side effects of epilepsy meds?

A

GI problems
sedation
mood changes
Allergic reactions

67
Q

How has imaging e.g. MRI improved epilepsy treatment?

A

It helps us explain some of the unexplained pathologies in epilepsy and treat some of them via surgery

68
Q

What proportion of people gave a genetic cause of epilepsy?

A

25-50%

69
Q

Are genetic epilepsies caused by one gene?

A

No, they tend to be caused by multiple genes and thier interaction with the environment

70
Q

What are some potential improvements in epilepsy treatment?

A

Spotting genetic abnormalities which cause epilepsy and treating these

Pharmacogenomics identifies variablity in response to meds

Identifying and treating channelopathies

Looking at inflammation in the brain as a source of epilepsy and stopping it with Mabs

Maybe trying to treat epilepsy before it happens too many times and becomes entrenched

71
Q

Explain how pharmacogenomics helps with epilepsy treatment

A

Some people are just more sensitive to medications because of genetic differences in liver enzymes, so looking at these different variants of the P450 enzymes may help choose the doses and meds of patients

72
Q

What are the most common type of epilepsy related channelopathy?

A

Na

73
Q

Name and describe a brain inflammation that can lead to epilepsy

A

limbic encephalitis - inflammation of the limbic system (usually caused by tumour)

May be caused by cross-reacting of tumour antigens and the antibodies to them

74
Q

What kind of antibodies are associated with limbic encephalitis?

A

Anti-NMDAR, AMPA, GABA-B, VG K channel

75
Q

What is missing from current epilepsy treatment?

A

Basic symptomatic treatment (LEDCs)

Treatment for underlying epilepsy cause

Treatment for the 30% who have refractory epilepsy

76
Q

What percentage of people in Africa and the developing world don’t get treatment?

A

90% - Africa

LEDCs - 75%

77
Q

TRUE or FALSE? People in Africa can’t get AEMs bc they are too expensive

A

No, they are quite cheap (especially the older ones)

78
Q

What are the things we can and cannot treat in epilepsy?

A

Can: seizures, structural lesions, injuries

Cannot: 
Epileptogenesis
Progressive memory deficits
subclinical seizures
stigma
79
Q

What are progressive memory deficits?

A

Some have treatment and don’t have seizures but still have memory problems.

80
Q

What are subclinical seizures?

A

They are ones that aren’t very bad so people might not go to the doctor

81
Q

What is the problem with subclinical seizures?

A

They may not cause much discomfort but they may be causing damage to e.g. the temporal lobe

82
Q

Finally, what do we need to do to improve epilepsy treatment?

A

2 main things: good basic care + tackling epileptogeneis by

Make new research models

Make regulatory process better so truely novel drugs can be researched

Research (and get funding for): clinical, national databases, mortality and morbidity, epilepsy and complications, why people don’t want to take treatments