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Epilepsy Flashcards

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

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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

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3
Q

What is the definition of epilepsy?

A

2 unprovoked seizures more than 24hrs apart

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4
Q

Is a child having a seizure during a fever epilepsy?

A

No, its just a febrile seizure

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5
Q

What is the definition of a seizure?

A

A manifestation of abnormal brain electrical activity

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6
Q

What are the 2 main types of seizures?

A

focal and generalised

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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

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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
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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

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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

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11
Q

What percentage of the time is an epilepsy diagnosis correct?

A

70%

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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%

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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
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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

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15
Q

Why might someone bite the lateral side of their tongue?

A

During tonic phase there is jaw clenching

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16
Q

Why may there be cyanosis?

A

Due to person not breathing at all

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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

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18
Q

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

A

They tend to be overestimated

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19
Q

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

A

2/3

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20
Q

What are the types of seizures that are often missed?

A

Nighttime ones and aura

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21
Q

What are clues that someone has had a nighttime seizure?

A

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

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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

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23
Q

What is jamais vu?

A

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

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24
Q

Which is more common jamais vu or deja vu?

A

jamais vu

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25
What part of the brain is jamais vu associated with?
frontal lobe
26
What is the prodrome of syncope?
``` Sweating dizziness chest pain dyspnoea palpitations tinnitus ```
27
What are the characteristics of syncope?
``` Prodrome Happens from standing or sitting <1 min Floppy +/- myoclonus +/- incontinence Pale, sweaty, clammy Rapid recovery ```
28
Some cases of syncope are related to problem with heart rate. How do these differ from other syncopes?
They can happen when the patient stands up There is no syncope prodrome/warning
29
Should we be worried about syncope?
No, this is usually benign and not frequent or too troublesome
30
What is the history of non-epileptic attack syndrome?
``` Remembers event Detached description Variable seizure types Other illnesses Dependency/support structure Previous abuse ```
31
What should the examination during a NEAD attack show?
``` 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
Are NEAD diagnoses fast?
No, it takes forever and in the meantime the patient has to take useless antiepileptics
33
What do you look at in an examination of epilepsy patients?
General: BP, pulse, heart Raised intracranial pressure - papilloedema Neurological/structural abnormalities: tumour/stroke Focal signs Genetic causes Asymmetry of limbs
34
What are some signs that suggest genetic causes of epilepsy?
Skin lesions suggest tuberous sclerosis
35
Why do we look for limb asymmetry in epilepsy examinations?
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
What are the components of good communication after epilepsy diagnosis?
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
Why should we explain limitations of tests to the patients?
So they know that tech doesn't trump the clinical aspect and they know to tell us as many details as they can
38
Why do we need to explain the benefits of treatment and the risk w/o it?
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
What sort of investigations do you do for epilepsy?
Blood ECG Imaging EEG
40
What is the most important test in clinical epilepsy investigations and why?
ECG bc it is important to check whether they are having a cardiac event which leads to the symptom
41
Why are routine EEGs less useful to do for clinical investigations of epilepsy?
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
What is the yield (ability to diagnose) with EEG?
50% of ppl with epilepsy have a normal EEG
43
What are the different ways of improving EEG yield?
Provocation tests: Sleep deprivation Photic stimulation Video-telemetry Stereo EEG Functional Mapping MEG - alternative to EEG
44
How much does sleep deprivation improve EEG yield?
50%-->80%
45
What % of people with epilepsy are photosensitive?
5%
46
What kinds of epilepsy is video-telemetry used to diagnose?
Refractory - doesn't respond to meds | Non-epileptic (NEAD)
47
What is stereo EEG?
Implanting very thin electrodes through small holes in skull to measure deeper structures
48
Why do we only do stereo EEG if epilepsy is severe?
It can cause haemorrhage
49
What is functional mapping?
It looks at the metabolic activity of the brain to find abnormal seizure activity
50
What is MRS?
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
Why is MEG useful?
It's very good at localising problem area more precisely
52
When (at what ages) do the onset/indences of epilepsy peak?
Young people/children and very old people ~80
53
How common is epilepsy?
Incidence: 50-180/100,000/Year Prevalence of active epilepsy: 10/1000 Lifetime prevalence: 2-5%
54
What is the outcome of a febrile seizure?
Usually one off and good recovery If more seizures occur there might be temporal lobe sclerosis leading to temporal epilepsy
55
What are the top causes of epilepsy in order of contribution?
1. Genetic 2. Infections 3. Structural/Vascular 4. Other
56
TRUE or FALSE? The cause of your epilepsy depends on your age/ country / socioeconomic status
TRUE
57
Map out the road to remission for epilepsy patients
Diagnosis --> drugs --> remission or more drugs --> remission or surgery --> if no remission, possible stimulation
58
What percentage of people remit after their first drug treatment?
70%
59
What is one reason why treatment may not be working?
Incorrect diagnosis
60
What were the first 2 entiepiletics?
Bromide (1850) | Phenobarbital (1910)
61
TRUE or FALSE? There are currently only a few antiepileptics available
False (there are many)
62
What are the problems with barbituates?
if you suddenly stop, ppl can have very severe seizures
63
Has remission rate on treatment improved in recent years?
No, it has stayed at 70%
64
What kinds of drugs are used for primary/generalised epilepsy?
Broad spectrum
65
What happens if you give narrow spectrum drugs to someone with generalised epilepsy?
They get worse (e.g. making absence seizures longer)
66
What are side effects of epilepsy meds?
GI problems sedation mood changes Allergic reactions
67
How has imaging e.g. MRI improved epilepsy treatment?
It helps us explain some of the unexplained pathologies in epilepsy and treat some of them via surgery
68
What proportion of people gave a genetic cause of epilepsy?
25-50%
69
Are genetic epilepsies caused by one gene?
No, they tend to be caused by multiple genes and thier interaction with the environment
70
What are some potential improvements in epilepsy treatment?
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
Explain how pharmacogenomics helps with epilepsy treatment
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
What are the most common type of epilepsy related channelopathy?
Na
73
Name and describe a brain inflammation that can lead to epilepsy
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
What kind of antibodies are associated with limbic encephalitis?
Anti-NMDAR, AMPA, GABA-B, VG K channel
75
What is missing from current epilepsy treatment?
Basic symptomatic treatment (LEDCs) Treatment for underlying epilepsy cause Treatment for the 30% who have refractory epilepsy
76
What percentage of people in Africa and the developing world don't get treatment?
90% - Africa LEDCs - 75%
77
TRUE or FALSE? People in Africa can't get AEMs bc they are too expensive
No, they are quite cheap (especially the older ones)
78
What are the things we can and cannot treat in epilepsy?
Can: seizures, structural lesions, injuries ``` Cannot: Epileptogenesis Progressive memory deficits subclinical seizures stigma ```
79
What are progressive memory deficits?
Some have treatment and don’t have seizures but still have memory problems.
80
What are subclinical seizures?
They are ones that aren't very bad so people might not go to the doctor
81
What is the problem with subclinical seizures?
They may not cause much discomfort but they may be causing damage to e.g. the temporal lobe
82
Finally, what do we need to do to improve epilepsy treatment?
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

Neuro (23 decks)

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