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MD4001 > Sleep, wakefulness, epilepsy and EEG > Flashcards

Sleep, wakefulness, epilepsy and EEG Flashcards

1
Q

Define sleep.

A

a) easily reversible state of inactivity with a

b) lack of interaction with the environment.

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2
Q

Define unconsciousness.

A

Unconsciousness is an inconsistent term, can be:
-coma (depressed state of neural activity, absence of
wakefulness)
-sleep ( variation in neural activity)

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3
Q

Define consciousness.

A

Having awareness; with perceptions, thoughts and feelings. – philosophical and biological aspects

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4
Q

Do all vertebrates sleep ? Mammals ?

A

Most vertebrates, and all mammals sleep, but not all sleep in the same way as humans

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5
Q

What is the function of sleep ?

A

The true function of sleep is unknown:
suggested functions include the processing and storage of memories, recuperation of the bodies immune system and to conserve energy.

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6
Q

During sleep, are neurons active ?

A

During sleep the neurons of the brain are active, but display a different type of activity from wakefulness

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7
Q

Is there a difference in amount of oxygen consumed by the brain in wakefulness cf in sleep ?

A

The sleeping brain consumes as much oxygen as the wakeful brain , and sometimes more

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8
Q

What are the main forms of external discernible sleep ?

A

There are two main forms of externally discernable sleep, they are either:
1) when the eyes move rapidly from side to side (REM sleep)
2) when they do not (non REM, slow wave or deep sleep) however there
are other determinants also (mostly starts with non REM sleep)

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9
Q

How can neuronal activity during the different stages of wakefulness (including sleep) be measured ?

A

Neuronal activity during different stages of wakefulness (including sleep) can be measured using an Electroencephalogram (EEG)

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10
Q

Explain how an EEG works.

A

-EEG electrodes are arranged in 19 pairs (or more) at internationally agreed points on the surface of the head
-Post synaptic activity of individual neurons not picked up
-Post synaptic activity of
synchronised dendritic activity (network of neurons which fire synchronously) can be picked up
(synchronisation is either by neuronal interconnections or by pacemaker)
-The more neurons that are synchronised, the bigger the peaks on the EEG.

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11
Q

What frequencies are normal adult brain waves, in the following:

  • Awake with mental activity
  • Awake and resting
  • Sleeping
  • Deep sleep
A
  • Awake with mental activity: beta (14-30 Hz)
  • Awake and resting: alpha (8-13 Hz)
  • Sleeping: theta (4-7 Hz)
  • Deep sleep: delta (<3.5 Hz)
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12
Q

Identify the main components of normal sleep, including physiological changes and EEG changes.

A

AWAKE

  • Eyes closed, alpha high frequency (8-13 Hz) and low amplitude (50 μV)
  • Eyes open beta waves (14-60 Hz) waves of activity

STAGE 1 (duration 1-5 minutes, easily roused)

  • Phys: Slow rolling eye movements
  • EEG: Some theta waves (slower frequency 4-7 Hz and higher amplitude waves)

STAGE 2 (duration 10-15 minutes)

  • Phys: No eye movement, but body movement remains possible
  • EEG: K complexes and sleep spindles (8-14 Hz bursts)

STAGE 3 (duration few minutes)

  • Phys: Harder to rouse
  • EEG: Slower frequency, delta waves (including amplitude) appear, few spindles

STAGE 4 (duration 15-30 minutes)

  • Phys: Deepest sleep, hardest to rouse, heart rate and BP lower, movement
  • EEG: >50% EEG waves at 2Hz (slow waves of synchronised firing of large groups of neurons) and high amplitude (> 200μV) called delta waves

REM

  • Phys: Subject easier to rouse than in stage 4, dreaming, recalled, low muscle tone (body effectively paralysed), rapid eye movement, increased HR, neural activity, respiration, and oxygen consumption, penile erection, body temperature drops as metabolism is inhibited
  • EEG: Fast beta waves and REM
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13
Q

Graph the different stages of sleep, especially their frequency, as a function of time.

A

Refer to slide 8

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14
Q

Which stages of sleep are spindles present in ?

A

Stages 2 and 3

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15
Q

How many cycles occur in a typical night’s sleep ?

A

Consists of several cycles through the five stages of sleep. Note that Stage 4 is only reached in the initial cycles, thereafter the deepest sleep attained is Stage 3. Also, increasing time spent in REM sleep (and shorter intervals between REMs, towards morning tend to be dreaming more)

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16
Q

What is the relationship between muscle activity and depth of sleep ?

A

Muscle activity (head) decreases with depth of sleep.

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17
Q

Why can the characteristic penile erection associated with REM sleep be useful ?

A

Penile erection is associated with REM sleep and this characteristic can be used in discrimination between different types of erectile dysfunction.

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18
Q

Describe the changes in movement and breathing as subject goes deeper into non REM sleep.

A

As the subject goes deeper into non REM sleep, movement and breathing is depressed however movement is still possible

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19
Q

What is the function of slow waves ?

A

Slow waves are thought to be involved with inhibiting sections of the relevant cortex

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20
Q

Why is there no body movement but there is eye movement during REM sleep ?

A

One source of activity in REM is concerned with inhibiting motor output (excepting breathing and eye movement)

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21
Q

What are the main structures forming the reticular formation ? What is its function ?

A

diffuse collection of at least 100 networks of neuromodulatory neurones spanning all three divisions of the brainstem

  • NOT homogeneous (main NTs are NAdr, 5HT, Ach)
  • DIVERSE functions (posture, respiration, heart rate and sleep/arousal)
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22
Q

Where does the reticular formation project ?

A

It has projections to: the thalamus, the hypothalamus, some brainstem nuclei, the cerebellum, the spinal cord and, the cerebral cortex

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23
Q

Where does the reticular formation receive inputs from ?

A

It receives input from: the cerebra (collaterals from the corticospinal pathways), the visual and auditory systems, sensory spinal systems, the cerebellum, certain brainstem nuclei

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24
Q

Which parts of the brain are involved in sleep ?

A

Sleep mechanisms rely on communication between the Reticular Formation and the Thalamus (being the main relay station to and from the cortex.

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25
Q

What is the effect of inhibiting, and exciting the thalamus ?

A

Inhibiting the thalamus decreases the sensory throughput and exciting the thalamus increases the sensory throughput.

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26
Q

How can specific site and general excitability of the thalamus be controlled ?

A

Specific site, and general excitability of the thalamus can be controlled by the reticular formation via a number of pathways

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27
Q

What is the main function of the thalamus ?

A

The thalamus acts as a major relay between the sensory systems (including sight) and the cerebral cortex.

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28
Q

Describe neural control of non REM sleep.

A

NonREM characterised by synchronised cortical slow waves caused by a hyperpolarised
thalamus and decreased activity in the arousal centers of the reticulum

  • Sleep spindles and K complexes (refer to slide 13 for graph) are caused in part by the inherent rhythmicity of thalamic neurons as they hyperpolarise due to reduced ascending reticular formation input. Seen in in Non REM stage 2 sleep.
  • As thalamic cells hyperpolarise further, they develop slow wave rhythmicity (due to thalamic interconnections) which serves to block ascending sensory input. This rhymicity is transmitted to the cortex and due to a strong reciprocity between these two areas, the waves becomes synchronised across the cortex.
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29
Q

What is the main NT of sleep ? Where in the brain is this found ?

A

Orexin

Orexinergic neurons are situated in the lateral hypothalamus.

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30
Q

When are orexinergic neurons active ?

A

Orexinergic neurons are normally active during wakefulness

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31
Q

Where do Orexinergic neurons project ? Relate this to the functioning of Orexin?

A

These neurons project to the cerebra, the arousal nuclei and the Ventro- lateral pre-optic nucleus in the anterior hypothalamus (VLPO) however the VLPO has no orexin receptors.

Therefore these neurons enhance the arousal nuclei and by doing so cause indirect inhibition of the VLPO via reciprocal inhibition pathways between the arousal centres and the VLPO.

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32
Q

What is the result of a VLPO lesion on sleep ?

A

VLPO lesions cause insomnia

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33
Q

What is the role of the VLPO of the thalamus ? Which structures is this linked to ?

A

The ventrolateral pre-optic nucleus (VLPO) has been identified as the centre of non REM sleep promotion.

1) Has inhibitory projections to all the major direct arousal centres (which in return reciprocally inhibit it by projections (NA, GABA, and 5HT)), and is active during sleep
2) Also innervates neurons in the lateral hypothalamus (including the orexin neurons)
3) Also innervates inter-neurons in the MRF cell groups (PPT and LDT)

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34
Q

What is the extended VLPO ? What is its function ?

A

The extended VLPO (eVLPO) (area round the VLPO)

promotes REM sleep

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35
Q

Describe how we alternate between arousal and sleep.

A

1) When Orexin is released it stimulates the arousal centres and so causes inhibition of the VPLO (would otherwise send you to sleep). As long as Orexin is released the balance is shifted towards wakefulness.

2) When the VPLO begins to fire, it inhibits both the orexinergic neurons and the arousal centres. This:
- Removes the inhibition of VLPO by the arousal centre
- Cuts off the excitation from the orexinergic neurons thus pushing the balance quickly towards sleep.

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36
Q

Describe how circadian rhythms influence the flip-flop switch.

A

• The suprachiasmatic nucleus (SCN) is located in the hypothalamus and controls:
1. circadian cycles and
2. influences many physiological and behavioural rhythms occurring over a
24-hour period, including the sleep/wake cycle.

• In humans “free running” of the SCN clock gene gives a periodicity of about 24.5 hours
This cycle is therefore re-set each day by a variety of zeitgebers (time givers in German), the most dominant of which is the light dark cycle

• Receptors in the retina (not rods or cones) containing melanopsin react to light and synapse directly onto the SCN resetting the clock gene.

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37
Q

Identify the main causes of Narcolepsy.

A
  • Onset due to specific loss of the Orexin containing neurons in the Lateral Hypothalamus
  • Thought to be an inherited auto immune condition linked to chromosome 6.
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38
Q

Identify the main symptoms of narcolepsy.

A

Presents as a tetrad of symptoms:

  1. Repeatedly falling asleep during the day, regardless of current activity (go straight into REM sleep) (with very short sleep latency)
  2. Limb weakness during emotional episodes (mild to extreme cataplexy)
  3. Night time or morning wakening accompanied by muscular paralysis (sleep paralysis).
  4. Vivid dream recollection just prior to wakening (hypnagogic hallucinations)
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39
Q

Describe treatment of Narcolepsy.

A
  • Modafanil
  • Amphetamines
  • Methylphenidate
  • Sodium oxybate (GHB)
  • SSRIs and tricyclic antidepressants suppress REM sleep
  • Venlafaxine may help cataplexy
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40
Q

Identify examples of sleep disorders.

A
  • Narcolepsy
  • Insomnia (lack of ability to sleep)
  • Sleep apnoea (XS daytime sleepiness because lack of quality of sleep during night)
  • REM sleep disorder (associated with PD)
  • Somnambulism
  • Epilepsies
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41
Q

What proportion of the population is affected by epilepsy. What is the overall lifetime risk of seizure ?

A

Epilepsy affects about 0.5% of the population

Overall lifetime risk of seizure is 1 in 50

42
Q

Define epilepsy. Define seizure.

A

Epilepsy is a continuing tendency to have seizures

Seizures are sudden discharges of abnormal electrical activity

43
Q

Define SUDEP.

A

Sudden unexpected death in epilepsy (very rare risk, 1 in 1000)

44
Q

Describe the effect of epilepsy on driving.

A

If seizure, in UK, not allowed to drive for 6 months (then able to drive if 6 months free)

If continuing ones, one year free before able to drive

45
Q

How is a diagnosis of epilepsy performed ?

A

1) History is most important, both from patient and witness. Specifically ask about:

  • Possible precipitant lowering seizure treshold (lack of sleep, alcohol, drugs, infection ?)
  • ? Aura/warning
  • Abnormal movements (e.g. wet themselves)
  • Colour
  • Position (in which it occurred)
  • When? (what doing at the time, what time of day)
  • After effects? (most epileptic attacks, confused and disorientated after)

2) Examination is usually normal in most seizures
3) Investigations include ECG (to check for possible arrythmias), EEG (but can have abnormal EEG patterns in people who have never had seizures before), MRI

46
Q

How may one distinguish between a seizure and syncope ?

A

Seizures of epileptics can often occur when standing up, but also in bed when lying down at night. Very unusual to faint when lying flat so if unsure reason of blackout between syncope and seizure, and it only occurs when standing up, may suggest more of a syncopal problem rather than epilepsy.

47
Q

Explain how/why auras/warnings may occur in an epileptic seizure.

A

Lots of seizures start in temporal lobe, which can scar easily, possibly resulting in hypoC sclerosis. The latter can be congenital or develop early in life, and may lead to abnormal focus of electrical activity. Because hypoC deals with memory, can get auras related to sense of deja vu, or a certain taste or smell, or feeling of anxiety (latter because amygdala and emotional circuits also situated in temporal lobe)

As a result, must ask patient if felt strange taste/smell associated with the seizure.

48
Q

Identify possible classifications of seizures.

A
  • Partial, i.e. comes from one part of the brain (can be simple or complex, both of which can evolve to secondarily generalised)
  • Generalised, i.e. abnormal electrical activity from all over the brain, including both hemispheres from the outset (can be primary or secondary) (e.g. absence, myoclinc, clonic, tonic, tonic-clonic, atonic)
49
Q

Define absence seizures.

A
  • Staring ahead being blank

- Common in children

50
Q

Distinguish between simple and complex partial seizure.

A

SIMPLE PARTIAL
• Focal with minimal spread of abnormal discharge (e.g. starts in hand, moves up the arm but able to keep talking)
• normal consciousness and awareness are maintained

COMPLEX PARTIAL 
• Local onset, then spreads (often involve abnormal mouth movements, possibly hand gestures) 
• Impaired consciousness
• Clinical manifestations vary with site of origin and degree of spread
– Presence and nature of aura
– Automatisms
– Other motor activity
• Temporal lobe epilepsy
most common
51
Q

Define secondarily generalised seizure, including clinical features, and duration.

A
  • Begins focally (e.g. in temporal lobe), with or without focal neurological symptoms
  • Variable symmetry, intensity, and duration of tonic (stiffening) and clonic (jerking) phases. Also associated with Postictal confusion and somnolence
  • Typical duration up to 1-2 minutes
52
Q

Give an example of secondary generalised seizure.

A

Tonic Clonic Seizure, go stiff, then start jerking, unable to talk, go blue (due to lack of breathing), may bite their tongue, may be incontinent

53
Q

What determines the manifestations of generalised seizures ?

A

Manifestations of the seizure are determined by the

cortical site at which the seizure arises.

54
Q

What proportion of all epileptic syndromes are generalised seizures present in ?

A

40%

55
Q

Describe possible manifestations of generalised seizure starting in the frontal lobe.

A

May force eyes across to the other side, because

frontal eye fields on the R area force the eyes to the L

56
Q

Identify examples of primary generalised seizures.

A

Absence seizures (petit mal)
Myoclonic seizures
Atonic seizures
Tonic-clonic seizures (grand mal)

57
Q

Define absence seizures, including onset, duration, clinical features, and EEG pattern.

A

Absence seizures (Petit mal):

  • Sudden onset and abrupt cessation
  • Brief duration
  • Consciousness is altered; attack may be associated with mild clonic jerking of the eyelids or extremities, postural tone changes, autonomic phenomena and automatisms (difficult diagnosis from partial)
  • Characteristic 2.5-3.5 Hz spike-and wave pattern
58
Q

Define myoclonic seizures, and give one such example.

A

Myoclonic seizures: myoclonic jerking is seen in a wide variety of seizures but when this is the major seizure type it is treated differently to some extent from partial leading to generalized

E.G. JUVENILE MYOCLONIC EPILEPSY

  • Myoclonus first thing in the morning, with other features of seizures
  • Certain drugs make it worse
59
Q

Describe the clinical features of atonic seizures.

A

Atonic seizures: sudden loss of postural tone; most often in children but may be seen in adults

60
Q

Describe the clinical features of tonic-clonic seizures. Why do they occur ?

A

Tonic-clonic seizures (grand mal):

Major seizures, usually with two phases:

1) Tonic phase: muscles will suddenly tense up (rigidity, tonic), causing the person to fall to the ground if they are standing.
2) Clonic phase: muscles will start to contract and relax rapidly (jerking), causing seizures

Tonic and clonic phases slow over 60-120 sec followed by stuporous state (post-ictal depression)

Occur due to recruitment of neurons throughout the cortex

61
Q

Define convulsions.

A

Convulsions:
 motor manifestations
 may or may not be present during seizures
 excessive neuronal discharge

62
Q

Which types of seizures do convulsions occur in ? Which do these not occur in ?

A

Convulsions appear in Simple Partial and Complex Partial Seizures if the focal neuronal discharge includes motor centers; they occur in all Generalized Tonic-Clonic Seizures regardless of the site of origin.

Atonic and absence Seizures are non-convulsive

63
Q

Define status epilepticus.

A

MEDICAL EMERGENCY

  • More than 30 minutes of continuous seizure activity
  • Two or more sequential seizures spanning this period without full recovery between seizures
64
Q

What is an anti-epileptic drug ? Does it treat symptoms or cause ? What is its goal ?

A
  • A drug which decreases the frequency and/or severity of seizures in people with epilepsy
  • Treats the symptom of seizures, not the underlying epileptic condition
  • Goal—maximize quality of life by minimizing seizures and adverse drug effects
65
Q

Are there any anti-epileptogenic drugs available ?

A

No

66
Q

Draw the EEG:

  • normal
  • GSCT
  • Generalised seizure- absence
  • Parietal seizure
A

Refer to slide 34

67
Q

What proportion of all people with epilepsy can become seizure free with drug therapy ?
What proportion can drug therapy drastically reduce seizures ?
What proportion are refractory to currently available AEDs ?

A
  • Just under 60% of all people with epilepsy can become seizure free with drug therapy
  • In another 20% the seizures can be drastically reduced
  • ~ 20% epileptic patients, seizures are refractory to currently available AEDs
68
Q

Do most people start anti-epileptics after one seizure ?

A

If have one seizure, you don’t know if gonna have another attack. Most people don’t start treatment after one attack, only usually start if an epilepsy diagnosis has been made (i.e. continuous tendency to have seizures)

69
Q

Identify the main relevant factors in choose antiepileptic drug.

A
  • Seizure type
  • Epilepsy syndrome
  • Pharmacokinetic profile
  • Interactions/other medical conditions
  • Efficacy
  • Expected adverse effects
  • Cost
70
Q

Explain cellular mechanisms of seizure generation.

A

Seizure:

  • Na+ influx
  • Glutamate (main excitatory NT)

Control

  • K+ efflux
  • GABA (main inhibitory NT)
71
Q

Identify possible targets of Anti-Epileptic Drugs, wrt the cellular mechanism of seizure generation.

A
  • Increase inhibitory neurotransmitter system— GABA
  • Decrease excitatory neurotransmitter system—glutamate
  • Block voltage-gated inward positive currents— Na+ or Ca++
  • Increase outward positive current—K+

(many AEDs pleiotropic—act via multiple mechanisms)

72
Q

Identify the main glutamate receptors.

A

– Ionotropic—fast synaptic transmission
• NMDA, AMPA, kainate receptors
• Gated Ca++ and Gated Na+ channels

– Metabotropic—slow synaptic transmission
• Regulation of second messengers (cAMP and Inositol)
• Modulation of synaptic activity

73
Q

Identify substances which can modulate Glutamate receptors.

A

Glycine, polyamine sites, Zinc, redox site

74
Q

Identify the current commonly used AEDs, and older AEDs which are less used.

A

Current commonly used drugs:
• Lamotrigine
• Sodium Valproate
• Carbamazepine (good for temporal lobe attacks, but significant side effects)
• Oxcarbazepine (closely related to^, but less side effects)
• Levetiracetam
• Topiramat (significant side effects)

Older drugs, less used:
• phenytoin,
• ethosuxamide,
• Felbamate
• phenobarbitone, 
• vigabatrin,
• tiagabine
• Gabapentin and Pregabalin
75
Q

Identify AEDs that act primarily on Na+ channels. Briefly state the mechanism of action of each.

A

Generally, Sodium channel blockers reduce amount of Glutamate released

Phenytoin, Carbamazepine
– Block voltage-dependent sodium channels at high firing frequencies—use dependent

Oxcarbazepine (less side effects than Carbamazepine)
– Blocks voltage-dependent sodium channels at high firing frequencies
– Also effects K+ channels

Zonisamide
– Blocks voltage-dependent sodium channels and T-type calcium channel

Lamotrigine

76
Q

Describe mechanism of action, dose, side effects of Lamotrigine.

A

LAMOTRIGINE

– acts by inhibiting sodium channels
– Twice a day
– broad therapeutic profile
– main side-effects are hypersensitivity reactions (especially skin rashes) (so build up dose over few weeks to avoid)

77
Q

Describe mechanism of action, side effects of Sodium Veloproate.

A

SODIUM VALPROATE

– mechanism of action not clear. It causes a significant increase in the GABA content of the brain. It is a weak inhibition of GABA transaminase. It has some effect on sodium channels
– Relatively few unwanted effects: hair loss, teratogenicity and foetal syndrome (avoid in pregnancy), liver damage (very rare, but serious)

78
Q

Is Sodium Valproate chemically related to other AEDs ?

A

No, Sodium Valproate chemically unrelated to other antiepileptic drugs.

79
Q

CARBAMAZEPINE

  • Class of drug
  • Indications
  • Side effects
A

CARBAMAZEPINE

– derivative of tricyclic antidepressants
– effective particularly in partial seizures; also useful in trigeminal neuralgia.
– unwanted effects; principally sedation, ataxia, mental disturbances (feeling doped up), water retention (leading to low sodium) (strong enzyme-inducing agent, so many drug interactions such as interaction with the pill making it less effective or ineffective)

80
Q

OXCARBAZEPINE

  • Mechanism of action
  • Indications
  • Side effects
A

OXCARBAZEPINE

  • Mechanism of action: May also augment K+ channels*
  • Indications: monotherapy, or add-on therapy in partial seizures
  • Side effects: Sedating but otherwise less toxic than Carbamazapine (some induction of P450 but much less than that seen with CBZ, so less drug interactions)
81
Q

LEVETIRACETAM

  • Mechanism of action
  • Indications
  • Side effects
A

LEVETIRACETAM

  • Mechanism of action: mechanism of action unknown, probably inhibits presynaptic Ca+
  • Indications: Useful in partial seizures and generalised seizures now
  • Side effects: Can cause psychiatric side effects (people feel quite depressed)
82
Q

TOPIRAMATE

  • Mechanism of action
  • Side effects
A

TOPIRAMATE

  • Mechanism of action: complex actions, not fully understood
  • Side effects: risk of teratogenesis + need slow titration to avoid cognitive side effects (i.e. feeling doped up)
83
Q

TIAGABINE

  • Mechanism of action
  • Indications
  • Side effects
A

TIAGABINE

  • Mechanism of action: GABA-uptake inhibitor
  • Indications: Licensed for partial seizures
  • Side effects: dizziness and confusion
84
Q

ZONISAMIDE

  • Mechanism of action
  • Side effects
A

ZONISAMIDE

  • Mechanism of action: blocks sodium channels
  • Side effects: may cause anorexia, and somnolence
85
Q

PHENYTOIN

  • Dose
  • Mechanism of action
  • Indications
  • Side effects
A

PHENYTOIN
-Dose: once a day
-Mechanism of action: acts mainly by use-dependent block of sodium channels
-Indications: widely used in treatment of epilepsy (effective in many forms of epilepsy, but not absence seizures); also used as antidysrhythmic agent
-Side effects: common drug interactions, main unwanted effects are confusion, gum hyperplasia, skin rashes,
anaemia, teratogenesis, cerebellar syndrome, osteoporosis

86
Q

Describe the metabolism of Phenytoein.

A

Metabolism shows saturation kinetics (zero order kinetics, as increase drug dose, plasma concentration increases logarithmically); therefore, plasma concentration can vary widely and monitoring is needed

87
Q

ETHOSUXIMIDE

  • Mechanism of action
  • Indications
  • Side effects
A

ETHOSUXIMIDE

  • Indications: was the main drug used to treat absence seizures in children, may exacerbate other forms
  • Mechanism of action: blocks T-type Calcium channels
  • Side effects: relatively few unwanted effects, mainly nausea and anorexia
88
Q

PHENOBARIBITONE

-Side effects

A

PHENOBARIBITONE (rarely used but people still on it)
-Side effects: (enzyme inducing, very long half life) osteporosis, reactive seizures if abruptly stopped (must decrease dose gradually if need)

89
Q

Describe treatment of status epilepticus.

A

Lorazapam and Diazepam (Benzodiazepines), delivered IV (fast, short-acting, sedating)

Followed by phenytoin (can be given IV), fosphenytoin, or phenobarbital (longer acting) when control is established

If that doesn’t work, need to sedate, paralyse them, and put them on ventilator

90
Q

FELBAMATE

  • Mechanism of action
  • Side effects
  • Indications
A

FELBAMATE

  • Mechanism of action: unknown
  • Side effects: possible severe hypersensitivity reactions, aplastic anaemia
  • Indications: use limited to intractable disease because of risk of^
91
Q

To what extent does Felbamate have a broad therapeutic profile ?

A

Broad therapeutic profile

92
Q

VIGABATRIN

  • Mechanism of action
  • Indications
  • Side effects
A

VIGABATRIN

  • Mechanism of action: acts by inhibiting GABA transaminase
  • Indications: effective in patients unresponsive to conventional drugs
  • Side effects: drowsiness, behavioural and mood changes, retinal loss (i.e. going blind), now rarely used
93
Q

GABAPENTIN and PREGABALIN

  • Mechanism of action
  • Indications
  • Side of effects
A

GABAPENTIN and PREGABALIN

  • Mechanism of action: Act specifically on calcium channel subunits called a2d1. It is unclear how this action leads to their antiepileptic effects, but inhibition of neurotransmitter release may be one mechanism
  • Indications: Used in add-on therapy for partial seizures and tonic-clonic seizures (but main uses in neurophatic pain)
  • Side of effects: Less sedating than classic AEDs
94
Q

What are the main AED treatment options for partial seizures ?

A

Lamotrigine (first choice)
Oxcarbazepine (second choice)

Possibly:
Carbamazepine
Sodium valproate
Levetiracetam

95
Q

What are the main AED treatment options for absence primary generalised seizures ?

A

Ethosuximide

96
Q

What are the main AED treatment options for primary generalised seizures ?

A

Lamotrigine, valproic acid

97
Q

Most seizures last how long ?

A

Couple of minutes

98
Q

Identify a treatment option for patients with epilepsy who do not respond to AEDs.

A

Neurosurgery for Epilepsy

99
Q

What are the main indications for neurosurgery for epilepsy ?

A
  • Most common for partial seizures

* When you’ve tried at least 3 AEDs

100
Q

How is neurosurgery for epilepsy prepared ?

A
  • Work-up includes detailed electrophysiology
  • Functional MRI, specialist centre (to detect where abnormal activity coming from)
  • Best results when lesion (through MR scan) correlates with EEG
  • Ideally non-dominant hemisphere (to spare for instance area for language)
101
Q

Identify a GABA agonist.

A

BACLOFEN

102
Q

BACLOFEN

  • Mechanism of action
  • Indications
  • Side effects
A

BACLOFEN

  • Mechanism of action: Selective agonist on GABAB-receptors, action exerted mainly at the level of the spinal cord to inhibit motoneurons.
  • Indications: Effective orally and is given widely for the treatment of spasticity associated with multiple sclerosis or spinal injury. Ineffective for cerebral spasticity caused by birth injury. Not useful in epilepsy.
  • Side effects: drowsiness, motor incoordination and nausea. Many behavioural effects (need to build up dose slowly)

MD4001 (74 decks)

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