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Block 3 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is epilepsy?

A

The most common neurological disorder characterised by recurrent seizures - main categories are focal and generalised (ICD-10;G40)

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2
Q

How is epilepsy diagnosed?

A

MRI
CAT
EEG (not commonly as takes long time to analyse brainwaves)

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3
Q

How is epilepsy classified?

A

International League Against Epilepsy (ILAE):

  1. Focal onset (aware/impaired awareness): motor/non-motor onset or focal to bilateral tonic-clonic
  2. Generalized onset: motor or non-motor (absence) onset
  3. Unknown onset: motor/non-motor onset or unclassified
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4
Q

What typically might you see if you get temporal lobe seizures?

A

Auras: smell/taste, ‘deja vu’, ‘jamais vu’ + emotional changes

Oral automatisms: gestures e.g. dystonic or fidgeting

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5
Q

What typically might you see if you get frontal lobe seizures?

A

Motor seizures: brief, frequency + cluster

Often bilateral e.g. kicking, cycling, violent, bizarre head version and commonly occur on waking from sleep

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6
Q

What typically might you see if you get parietal lobe seizures?

A

Auras: nausea, choking, sinking sensations + illusions of body distortion

Sensory seizures: somatosensory (tingling/warmth)

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7
Q

What typically might you see if you get occipital lobe seizures?

A

Visual hallucinations (simple or complex i.e. shapes-scenes), vision may black out, visuo-spatial distortions, head turning, headache and nausea

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8
Q

What do temporal lobe seizures affect?

A

Auditory and limbic system along with the amygdala near the hippocampus

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9
Q

What are focal aware (simple partial) seizures?

A

Characterised by NO loss of consciousness or post-ictal confusion

Symptoms depend on focal site but commonly temporal lobe in origin (area of learning and memory so brain is has high plasticity making it more likely to become over-excited)

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10
Q

What are focal seizures with impaired awareness?

A

Characterised by altered consciousness but may seem fully aware and may have some post-ictal confusion commonly temporal lobe in origin

Common symptoms: auras, automatisms (chewing, swallowing, repeating displacement behaviour)

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11
Q

What are focal aware motor Jacksonian seizures?

A

Short-lasting ripple of muscle activity that may be localised to one group of muscles or progress usually distal to proximal through the limbs and trunk (following HAL)

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12
Q

What are focal aware sensory Jacksonian seizures?

A

Short-lasting sensory changes that may be localised to one area or progress usually distal to proximal through the limbs and trunk (following HAL)

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13
Q

What are focal to bilateral tonic clonic (partial to 2ndary generalised/secondarily generalised) seizures?

A

Focal seizure progressing to generalised tonic-clonic seizure

May experience auras prior to onset and have unilateral motor effects (if interconnecting areas e.g. commissure not hit)

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14
Q

Why might a focal seizure become generalised?

A

Once the activity hits the thalamus, the key relay area of the brain, activity will spread very rapidly to all over the brain

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15
Q

What are generalised tonic-clonic seizures?

A

Characterised by tonic and then clonic phase followed by unconsciousness, muscle relaxation, slow regain of consciousness, confusion, sleepy, headaches, aching limbs and no episode recall

Easiest to diagnose but there is no warning i.e. aura even though whole brain is involved but can identify triggers

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16
Q

What are the 2 phases of a generalised tonic clonic seizure?

A
  1. Tonic: whole body stiffness, breathing may stop (cyanosis) and loss of bladder control
  2. Clonic: muscle jerks
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17
Q

What must you consider regarding patients coming around from a generalised tonic clonic seizure?

A

They are very suggestible so anything you say to them, they will take on board and may act on

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18
Q

What is a generalised absence seizure?

A

Whole brain is involved but with low level activity where patient seems to ‘switch-off’ and cannot be alerted or woken up

Rare in adults, generally starts between 6-12yrs (girls > boys) and responds well to AEDs

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19
Q

What is status epilepticus?

A

Prolonged seizure state (ICD10;G41) that can be generalised tonic clonic where whole brain is involved with ictal period of >5mins but repeated seizures with no recovery between for >30mins OR long-lasting, absence of focal-type seizures

MEDICAL EMERGENCY as can cause long-term damage

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20
Q

What are some other forms of seizures?

A

Generalised:

  • Myoclonic: sudden jerks (possibly familial)
  • Clonic: repeated twitches + jerks with no stiffness
  • Tonic: all muscles contract + whole body stiffness
  • Atonic: ‘drop attacks’ where all muscle tone lost
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21
Q

What is non-epileptic attack disorder (NEAD)/psychogenic seizures?

A

No physical reason or changes in brain activity but has similar symptoms to epilepsy - when diagnosed through video EEG, there may be differences in duration, eye opening (tightly shut), location of tongue biting (tip) and recollection

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22
Q

Why is electroencephalogram (EEG) useful to diagnose epilepsy?

A

Good for determining TYPE of epilepsy as epileptiform activity shows distinct patterns according to type and focus of activity easy to pinpoint correlating to presence of auras and auditory hallucinations for e.g. - also shows progression of seizure throughout brain but patient MUST seize when doing EEG

23
Q

What are the advantages of the electroencephalogram (EEG)?

A

Non-invasive/painless
Used over long periods
Cost-effective

24
Q

What is the electroencephalogram (EEG) used for?

A

Investigating gross cortical activity in sleep disorders, epilepsy and coma/brain-death

25
Q

How do you record a electroencephalogram (EEG)?

A

24-158 (256 for research) electrodes that record voltage deflections relative to ‘ground’ electrode usually the ear to record

26
Q

What measures does polysomnography add to the typical electroencephalogram (EEG)?

A 
EOG (oculo)
EMG (myo)
Abdominal/chest wall (respiratory) movement
CV measurements (BP, HR)
Skin responses
O2 measurements
27
Q

What do you record on an electroencephalogram (EEG)?

A
  1. Activity patterns of populations of neurons by recording changes in gross current flow
  2. Levels of synchrony between neurons causing changes in patterns (if fire together give larger amplitude oscillations)
  3. Patterns of synchrony causing rhythms
28
Q

What types of rhythms are seen in an electroencephalography (EEG)?

A
  1. Alpha (8-13Hz): mainly occipital, quiet, eyes shut, meditation
  2. Beta (>14Hz): parietal + frontal, activity + tension, sleep spindles
  3. Gamma (40Hz): ‘binding’, L&M
  4. Theta (4-7Hz): parietal + temporal, alertness, L&M, reinforcement of L&M in sleep
  5. Delta (<3.5Hz): cortical, deep sleep, coma
  6. Flat line: death
29
Q

What changes in neuronal excitability occur in seizures?

A
  1. Reduction in GABA
  2. Increase in ACh transmission enhancing glutamate
  3. Increase in Na+ channel activity
  4. Decrease in K+ channel activity
30
Q

What are channelopathies?

A

Mutations in channel structure (K+, Na+, ACh + GABA receptors) that are often linked to congenital forms of seizures, seizure syndromes and juvenile seizures

31
Q

What types of treatment are available for epilepsy?

A
  1. Pharmacological: AEDs
  2. Surgical: removal of aberrant areas found by MRI/CAT/electrical stimulation
  3. Implants: VNS and DBS (like pacemakers training brain to work at certain frequencies)
32
Q

What drugs would you give to non-epileptic forms of seizure?

A

CBT +/- ADs/antipsychotics

33
Q

Why are implants more popular than surgical removal of a brain area?

A

Removing an area causing a seizure may mean scar areas arise making this area more likely to trigger seizures too

34
Q

What is the treatment for focal and focal-generalised seizures?

A
  1. Carbamazepine > Lamotrigine > Sodium Valproate (Na+ channel blockers)
  2. Adjuncts e.g. Clobazam
35
Q

What is the treatment of generalised tonic clonic seizures?

A
  1. Sodium Valproate > Lamotrigine > Carbamazepine (Na+ channel blockers)
  2. Adjuncts e.g. Clobazam
36
Q

What group of patients should you not use Sodium Valproate in?

A

Premenopausal women or women of child bearing age due to teratogenicity

37
Q

What is the treatment of generalised absence typical seizures?

A
  1. Ethosuximide (Ca2+ channel blocker T-type) > Sodium Valproate
  2. Lamotrigine
38
Q

How do you treat generalised tonic clonic status epilepticus?

A
  1. IV Lorazepam (repeat after 10 mins) OR buccal Midazolam/IV or rectal Diazepam (GABA PAM/co-agonist at γ-subunit)
  2. After 25 mins give Phenytoin Sodium or Phenobarbital Sodium
  3. After 45 mins anaesthetize with Thiopental, Midazolam or Propofol
39
Q

How do you treat other types of status epilepticus?

A

Depends on severity but oral AEDs if aware/orientated or as for convulsive but anaesthetic rarely required

40
Q

How do you treat Non-Epileptiform Attack Disorders (NEAD)?

A

Remove any AEDs in use and give ADs/antipsychotics along with psychotherapy/CBT

41
Q

How do you treat other types of seizure?

A

1st line: Sodium Valproate

For everything but generalised myoclonic give 2nd line (adjunct) Lamotrigine as they generally respond poorly to typical AEDs

42
Q

What are epilepsy syndromes?

A

Specific types of epilepsy, often congenital, characterised according to a no. of features including seizure type, age of onset and EEG characteristics

43
Q

How do you treat epilepsy syndromes?

A

Some drugs licensed for use in particular epilepsy syndromes e.g. Lennox-Gastaut syndrome - treat with Lamotrigine

44
Q

What is antiepileptic hypersensitivity syndrome?

A

Major side-effect of AEDs starting 1-8 weeks from treatment initiations causing fever, rash and swollen lymph nodes initially but can become more severe causing blood, liver, kidney and respiratory abnormalities, vasculitis and organ failure

45
Q

How do you treat antiepileptic hypersensitivity syndrome?

A
  1. Withdraw drug immediately
  2. Topical steroids and antihistamines for rash
  3. Systemic corticosteroids perhaps
  4. BEWARE of rebound seizure activity - put on another AED as no crossreactivity between 2 drugs
46
Q

How do the barbiturates work? What are they commonly used for?

A

GABA PAM/co-agonist at β subunit used as:

  • Anaesthetics
  • Anxiolytics

E.G. Pentobarbital (euthanasia) and Phenobarbital (1st line neonatal seizures)

47
Q

How do Na+ channel blockers work?

A

Drug blocks channel in inactivated state preventing neurotransmitter going through

48
Q

What are the side effects of Na+ channel blockers?

A 
CNS effects
Cognitive impairment
Visual impairment
Peripheral neuropathy
Skin problems
Gum hyperplasia
Anaemia/other blood disorders
Osteomalacia
Teratogenicity
49
Q

How is GABA targeted in these drugs?

A

Enhance activation of GABA-A mediated channels via:

  • Action at co-agonist sites
  • Inhibition of GABA breakdown
  • Inhibition of GABA uptake
  • GABAmimetics (PAMs)
50
Q

What are the side effects of benzodiazepines (BDZs) and Barbiturates?

A

Only use for short-term (<12wks) in emergencies as tolerance and dependency can develop with withdrawal on termination

Also:

  • Impaired motor coordination (decreased muscle tone)
  • Impaired cognitive performance
  • Sedation
  • Disturbed sleep patterns (decreased SWS)
  • Retrograde amnesia
51
Q

What drugs affect GABA uptake and breakdown? What are they used for?

A

Tiagabine: inhibit GABA transporter
Vigabatrin: inhibit GABA transaminase

By tertiary specialists as adjuncts - not for generalized seizures as it can worsen absence, tonic + myoclonic seizure forms

52
Q

What drugs are low-threshold Ca2+ channel blockers?

A

Ethosuximide (T-type)
Gabapentin
Perhaps Lamotrigine too

53
Q

What are future epilepsy targets?

A
  1. Glutamate antagonists (AMPA/metabotropic)
  2. Gap junction inhibitors
  3. Enzymes
  4. Cannabinoids
  5. Steroids
  6. CO2
54
Q

What diet has been shown to useful in epilepsy?

A

Ketone diets as it changes the gut microbiota

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