Epilepsy Flashcards

1
Q

What is the most common neurological disorder?

A

Epilepsy

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2
Q

How common is epilepsy and what is it characterised by? How common are seizures?

A

1:20 will have a seizure at some point in their lifetime whereas 1:103 will have epilepsy. Epilepsy is characterised by recurrent seizures.

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3
Q

What are the two main categories of epilepsy? How is epilepsy diagnosed?

A

Focal and generalised. Epilepsy is diagnosed mainly by symptoms recounted by the individual/ witnesses and by EEG/MRI/CT scan.

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4
Q

Who characterises Epileptic type seizures? How are the categories broken down?

A

International league against epilepsy (ILAE).

Categories are broken down into either focal, focal to generalised (focal to bilateral tonic clonic), generalised, unknown (often seizures during the night), or unclassified.

Focal is further broken down into either aware or impaired awareness. Then broken down by symptoms - either motor or non-motor.

Generalised broken down into motor vs non motor.

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5
Q

Describe the characteristics/ auras of a temporal seizure

A
  • Temporal lobe houses limbic system (memory and emotion), including hippocampus and amygdala. Also responsible for integration of taste sensation, smell, understanding speech (Wernicke’s) and hearing.
  • Auras: changes in taste/ smell, deja vu, jamais vu (never seen before)
  • Seizures -> Oral automatisms (unconcious behaviours), including fidgeting and dystonia (sustained muscle contractions resulting in abnormal positioning/ tremor).
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6
Q

Describe the characteristics of a frontal lobe seizure

A
  • Frontal lobe –> primary motor cortex, supplementary motor area and pre motor cortex.
  • Motor seizures –> brief, frequent, can cluster
  • Tend to be bilateral, present with kicking/ cycling movements, violent and bizarre
  • head torsion can occur
  • often occur after waking from sleep
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7
Q

Describe the characteristics/ auras of parietal seizures

A
  • Parietal lobe –> primary somatosensory cortex, therefore sensory seizures
  • Sensory seizures present with –> tingling sensation/ warmth
  • Auras: nausea, choking, sinking sensation, illusion of body distortion
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8
Q

Describe the characteristics/ auras involved in occipital seizures

A
  • Occipital lobe —> primary visual cortex and visual association areas
  • Auras –> visual hallucinations (simple - flashing lights) or complex (scenes).
  • Vision may black out
  • visuo- spatial distortions
  • head turning, headache and nausea.
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9
Q

What are the two types of focal seizure?

Describe the characteristics of both types

A
  • Focal aware (used to be called partial simple).
    • Characterised by no loss of awareness
    • no post ictal confusion
    • symptoms depend on the lobe affected
    • tends to affect the temporal lobe (region of high plasticity which is prone to over excitation).
  • Focal w impaired awareness (used to be called partial complex).
    • Characterised by altered conciousness (but may seem fully aware)
    • may have post ictal confusion
    • Prior to concioussness change may have auras
    • Common symptom –> automatism (Chewing, swallowing, repeated displacement)
    • again commonly in temporal region
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10
Q

What is a jacksonian seizure?

What group of seizures does it fall into?

What types of jacksonian seizure are there?

A
  • A jacksonian seizure is a type of focal aware seizure that describes a seizure in which symptoms migrate from one region of the body to another, normally from distal to proximal following HAL (hand/arm/leg) pattern. Up through arms down through body.
  • Focal Aware motor –> Jacksonian motor seizure –> affecting motor cortex
    • Short lasting, ripple of muscle activity
    • may be localised to one group of muscles or progress
    • progression distal to proximal through limbs and trunk, following from hanfs up arms to trunk down legs
  • Focal Aware sensory –> Jacksonian sensory seizure –> affects primary somatosensory cortex
    • short lasting sensory changes
    • may be localised to one area or progress
    • usually distal to proximal
    • through limbs and trunk (Following HAL).
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11
Q

What are the characteristics of a focal to bilateral tonic clonic seizure?

A
  • Characteristics: focal that progresses to a generalised (tonic/ clonic or grand mal seizure).
  • Due to activation of connecting pathways or the thalamus
  • As it starts focal the patient can experience auras prior to onset
  • can have unilateral motor effects but most often are bilateral (activation of commisural fibres).
  • (note in EEG trace on bottom shows seizure starting off in the R before progressing to the L).
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12
Q

What is a generalised tonic clonic seizure?

What are the characteristic features of a tonic clonic seizure? (describe onset, duration, recovery)

What would their EEG trace show?

A
  • Generalised tonic clonic seizure (used to be known as grand mal seizure) is a seizure that affects the whole brain (starts in both sides), isn’t preceeded by a warning (although patients can know their triggers) and is generally the easiest to diagnose.
  • when it starts in one side of the brain and spreads this is focal to bilateral tonic clonic seizure
  • usually lasts 1-3 minutes, more than 5 minutes is a medical emergency
  • Characterised by a tonic phase followed by a clonic phase.
  • Tonic phase –>
    • increase in tone of muscles, sudden stiffening, loss of conciousness, fall to the ground
    • Air can rush past vocal cords –> scream as they fall
    • may bite on their tongue
  • Clonic phase –>
    • sudden rythymic contractions of muscles in arms and legs
    • altered breathing and cyanosis
  • During recovery phase patient will slowly regain conciousness and muscles will start to relax.
  • Could also be: loss of bladder/ bowel control as their body relaxes, confusion, no recollection of episode, drowsy, headaches, aching limbs
  • EEG tract will show large amplitude deflections, affecting both hemispheres and synchrony. Rythmic activity shown –> thought gap junctions could be involved.
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13
Q

What is generalised absence?

A
  • Generalised abscence is a seizure in which the person is said to become blanked out/ switched off/ stare into space but cannot be alerted or woken up.
  • Most commonly affects children (6-12 yrs) and rarely affects adults
  • affects girls more than boys
  • Responds very well to anti epileptic drugs
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14
Q

What is status epilepticus?

A
  • Status epilepticus is a medical emergency, where there is generalised tonic clonic activity affecting the whole brain for a prolonged period of time (greater than 5 mins) or repeatedly without recovery (longer than 30 mins)
  • Either ictal period > 5 mins
  • or repeated seizure without recovery
  • or repeated seizures for 30 mins
  • Always treated as a medical emergency as prolonged seizuring can cause permanent brain damage
  • Other forms of status epilepticus are long lasting, absence or focal type seizures.
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15
Q

Outline 4 other forms of seizures (not including focal aware/ w impaired awareness/ Jacksonian/ absence/ generalised tonic clonic/ status epilepticus).

A
  • Generalised myoclonic –> sudden shock like jerks of groups of muscles, (like falling asleep), possibly familial
  • Generalised clonic –> repeated muscle twitches and jerks w/ no stiffness
  • Generalised tonic –> all muscles contract, whole body stiffens
  • Generalised atonic –> “drop attacks”, muscle tone lost, head/ body become limp.
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16
Q

What is NEAD?

What is its other name?

How is it diagnosed?

What are the differences between NEAD and generalised tonic clonic?

How does this affect treatment?

A
  • NEAD = non epileptic attack disorder
  • Also known as psychogenic seizures
  • Seizures that mimick generalised tonic clonic seizures exactly but there seems no be no physical reason or any changes in brain activity
  • Diagnosis requires EEG
  • May be slight differences to generalised tonic clonic in:
    • duration (may last seconds to 2-3 mins)
    • eye opening - eyes firmly shut in NEAD vs open in generalised
    • tongue biting - tip of tongue in NEAD vs lateral tongue generalised
    • Recollection - NEAD can recollect
  • Treatment not with antiepileptics but with antidepressants, antianxiety and psychological
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17
Q

What are the benefits and uses of EEG?

A
  • Useful for determining the type of epilepsy, epileptiform changes depending on the type
  • can pinpoint the focus of a seizure, often correlates to auras or auditory hallucinations
  • monitor the progression of the seizure throughout the brain and correlate this to changes in the patients physiological state. (not always poss as patient no control over seizure occurence and EEG recording).
  • non invasive, cost effective, can be used over long periods
  • used for diagnosis of sleep disorder, epilepsy and brain death/coma
18
Q

How is the EEG recorded?

A
  • 24- 158 plate electrodes
  • records voltage deflections relative to a ground electrode (usually the ear).
  • Polysomnography/sleep study records brain waves and simulataneously compares this to the physiological status of the patient:
    • records breathing and HR
    • BP
    • oxygen saturation
    • eye and leg movements (oculogram and electromyogram)
19
Q

What does the EEG actually measure?

A
  • EEG measures the patterns of activity of population of neurons by recording changes in gross current flow.
  • Measures the level of syncrhony between neurons –> higher synchrony, changes in patterns
  • When neurons fire together there is an increase in amplitude of the oscillations and patterns of synchrony cause rhythms.
20
Q

What are the waveforms seen in the EEG?

Reference their frequency and what this relates to functionally

A
  • Dont Take Anyone Before Granted (Delta, Theta, Alpha, Beta, Gamma –> from lowest frequency to highest).
  • Delta < 3.5 Hz:
    • lowest frequency, deep sleep, coma
    • Cortical
  • Theta 4-7 Hz:
    • recorded in both sleep and awake states, deep meditation or REM sleep.
    • Involved in learning and memory, theta waves reactivate during sleep in learning states.
    • Temporal and parietal lobes
  • Alpha 8-13 Hz:
    • quiet, relaxed, eyes shut, concious but resting, meditation
    • occipital lobe
  • Beta > 14 Hz (14- 38 Hz):
    • Split into Lo-Beta, Beta and High Beta
    • Lo- Beta –> active during light sleep –> sleep spindles –> bursts of oscillatory activity during sleep
    • Beta –> normal concious contemplation (Activity)
    • High beta –> highly complex thought processing –> high anxiety/ excitement states
    • Parietal and frontal lobes
  • Gamma 40 Hz:
    • Highest frequency brain wave
    • Learning and memory –> frequency fast enough to allow synapse to make plastic changes
21
Q

Describe the aetiology of seziures in epilepsy

A
  • Epileptic seizure aetiology all relates to increase in neuronal excitability:
    • Decrease in inhibitory GABA transmission
    • Increase in Ach –> affects excitatory glutamatergic activity
    • Decrease in K+ channel activity
    • Increase in Na+ channel activity
  • Channelopathies = inherited mutations in channel structure. Affects : Na+/K+/GABA/Ach channels in CNS, often seen in juvenile seizures, can only treat symptoms.
22
Q

Describe briefly the treatment options for epilepsy

A
23
Q

What is the pharmacological treatment for focal and focal –> generalised seizures?

A
  • 1st line :
    • Carbs, marzipan, lamb and terrine, pro salt eating can lead to focal seizures that become generalised.
    • Carbmazepine
    • Lamotrigine
    • Sodium valproate
  • 2nd line/ adjuncts:
    • Clobazam
    • Topiramate
    • gabapentin
24
Q

What is the pharmacological treatment for generalised tonic clonic seizures?

What issues may arise from treatment?

Is this treatment used to treat any other forms of seizure?

A
  • 1st line:
    • Sodium valproate
    • lamotrigine
    • Carbamazepine
  • 2nd line/ adjuncts:
    • Clobazam
    • topiramate
    • levetiracetam
  • Issues: Sodium valproate:
    • Do not use in premenopausal women –> teratogenic effects (disturbs fetal development).
  • Generally sodium valproate is 1st choice for other seizures too: generalised myoclonic, atonic and tonic seizures.
25
Q

What is the pharmacological treatment of abscence seizures?

A
  • 1st line –> ethosuximide (ethan sucks when he hides (abscence) or sodium valproate
  • Adjuncts: lamotrigine
26
Q

Describe the treatment for status epilepticus

A
  • Basic life support- open and secure airway, 100% oxygen
  • IV access- take bloods look for U&E, FBC, Glucose, Ca2+, toxicology screen if indicated, anticonvulsant levels
  • IV lorazepam (or iv diazepam) - repeat if no response within 10 minutes- must have resucitation facilities available as risk of respiratory arrest
  • Or if in community/ no resusc facilities available –> buccal midazolam or rectal diazepam
  • No response within 25 mins –> IV infusion barbiturates –> phenytoin or phenobarbital
  • No response within 45 mins —> Anaesthetise –> used barbiturates -Thiopental, non barbiturate –> propofol or benzodiazepine –> midazolam
27
Q

Describe the treatment for NEAD

A
  • remove off any antiepileptics drugs
  • Antipsychotic / antidepressants
  • Psychotherapy and cbt
28
Q

What is the treatment for generalised myoclonic seizures?

A
  • 1st line –> sodium valproate
  • 2nd line topiramate and levetiracetam
29
Q

What is the treatment for generalised abscence atypical, generalised atonic and generalised tonic seizures?

A
  • generally respond poorly to AED’s
  • 1st line –> sodium valproate
  • 2nd line –> lamotrigine
30
Q

What is the general mechanisms of action for antiepileptic drugs?

A
  • Na+ channel blocker
  • Ca2+ channel blocker
  • GABA modulation
  • GABA mimetics
31
Q

What is the mechanism of action for Na+ channel blockers?

Give examples of Na+ blocking AED’s

A
  • Na+ channel blockers block voltage dependent Na+ channels
  • Enter the channel when open and then stabilise it in the inactive state –> unable to reopen
  • Examples:
    • Lamotrigine
    • Carbamazepine
    • Sodium valproate –> also thought to potentiate GABA by inhibiting breakdown
32
Q

What are the side effects of Na+ channel blockers?

A
  • CNS and NS —> cognitive and visual impairment, peripheral neuropathy
  • Blood and bone —> anaemia, other blood disorders, osteomalacia (soft bones)
  • Fetal —> teratogenicity
33
Q

Describe how we can modulate GABA to treat epilepsy?

What drugs are included in modulating the GABA pathway?

A
  • Enhance GABA transmission –> potentiate receptor activity by positive allosteric regulation of GABA receptor subunits
  • Inhibit GABA breakdown or uptake
  • GABA mimetics:
    • Gabapentin (thought to increase GABA synthesis)
    • pregabalin (thought to increase GABA transport)
    • Both indirectly enhance GABA r activity thought via inhibition of voltage dependent calc channel
  • Other drugs that modulate GABA pathway:
    • Benzodiazepines –> bind to gamma subunit GABAa receptor +ve allosteric modulator
    • Barbiturates –> Bind to beta subunit GABAa receptor +ve allosteric modulator
34
Q

Name the Benzodiazepines for epilepsy treatment

Mechanism of action

how this aids epilepsy treatment

A
  • Lorazepam
  • Diazepam
  • midalozam
  • All bind to alpha/ gamma subunit interface of GABAa receptor –> +ve allosteric modulators
  • Aids epilepsy treatment as enhances inhibitory GABA signalling, which reduces neuronal transmission
35
Q

Name the barbiturate drugs used in epilepsy treatment

What is their mechanism of action?

How does this aid epilepsy treatment?

A
  • Phenobarbitone
  • Pentobarbitone
  • Primidone
  • Mechanism of action –> binds at a binding site between alpha/ beta subunits of GABA receptor –> +ve allosteric modulator
  • Aids in treatment of epilepsy as it enhances inhibitory GABA signalling which reduces neuronal transmission.
36
Q

What are the side effects of benzodiazepine and barbiturate treatment?

A
  • Can only be used for short term emergency epileptic treatment (< 12 wks)
  • Otherwise:
    • Tolerance
    • Dependency
    • Withdrawal on removal
  • Cognitive impairment and impairment of motor coordination
  • Sedation
  • Sleep disturbance
  • Retrograde amnesia
37
Q

What are other GABA modulating drugs that act on uptake and transport?

A
  • Inhibiting the GABA transporter –> Tiagabine
  • Inhibiting GABA breakdown –> inhibit GABA transaminase –> vigabatrin
38
Q

Name the Ca2+ channel blockers used in epilepsy treatment

A
  • Block voltage gated Ca2+ channels or low threshold T type Ca2+ channels.
  • Main examples:
    • Ethosuximide –> block T type Ca2+ channel
    • GABApentin —> GABA mimetic that actually blocks T type Ca2+ channel
    • Lamotrigine also thought to block Ca2+ as well a Na+ channels
39
Q

What is antiepileptic hypersensitivity syndrome?

A
  • Antiepileptic hypersensitivity syndrome is a severe reaction to anticonvulsant therapy and has been reported in patients on carbamazepine, phenobarbitone, lamotrigine, phenytoin.
  • Starts within 1- 8 weeks of treatment
  • initial signs are a rash, fever and swollen lymph nodes
  • Severe signs : blood, liver, kidney and respiratory abnormalities, vasculitis and organ failure
  • Withdraw drug immediately
  • treat rash with topical steroid and antihistamines
  • Potentially systemic corticosteroids
  • Be aware of rebound seizures
40
Q
A