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Module 202 Neuroscience & behaviour > Seizures symposium > Flashcards

Seizures symposium Flashcards

1
Q

What is epilepsy?

A

Recurring, unprovoked seizures

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2
Q

What are some acute insults that can provoke acute symptomatic seizures?

A 
Stroke
Alcohol withdrawal
Infections
High fever
Metabolic disturbance
Recreational drugs
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3
Q

What does a generalised onset mean?

A

Electrical discharges appear to start over the whole brain at the same time

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4
Q

What does a partial / focal onset mean?

A

Electrical discharges appear to start in one cortical region & then may remain localised or spread over whole brain

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5
Q

What are the 6 types of idiopathic generalised seizures?

A 
Tonic-clonic
Tonic
Clonic
Atonic
Myoclonic
Absences
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6
Q

Describe idiopathic generalised seizures

A 
Onset in childhood or adolescence
Usually no focal symptoms / signs
Often a cluster of seizures
Generalised (all leads) spike & wave dischargers on EEG
Photosensitivity may be present
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7
Q

Describe Juvenile myoclonic epilepsy

A

Commonest form of primary generalised epilepsy
3-12% of all epilepsy
Begins in adolescence
Early morning myoclonic jerks
Photosensitive, sleep deprivation triggers
Possible absences
Generalised tonic-clonic seizures which occur without warning

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8
Q

Describe the tonic phase in a tonic-clonic seizure

A 
Continuous muscle spasm
Will fall
May have cyanosis due to thorax muscles contracting
Tongue biting
Incontinence
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9
Q

Describe the clonic phase in a tonic-clonic seizure

A

Rhythmic jerking slows & gets larger in amplitude as the seizure ends

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10
Q

Describe the postictal phase in a tonic-clonic seizure

A 
Coma
Drowsiness
Confusion
Headache
Muscle aching
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11
Q

Describe an absence seizure

A

Abrupt
5-20 seconds
Multiple times a day, can lead to learning difficulties
Unresponsive, amnesia for the gap, rapid recovery
Tone preserved or mildly reduced
Eyelid flickering
Tend to stop in adulthood

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12
Q

What are the types of partial seizures?

A

Simple partial seizure - patient is aware

Complex partial seizure - aura / warning with reduced awareness

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13
Q

What is the frequency of partial seizures in each lobe?

A

Parietal - 1%
Occipital - 4%
Frontal - 25%
Temporal - 70%

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14
Q

Describe a secondary generalised tonic-clonic seizure

A

Warning / aura
Can’t abort attack
Sudden onset
Last 1-3 minutes
Falls, loses consciousness as seizure generalises
Rigidity, convulsive jerks, excessive salivation
Incontinence, tongue biting

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15
Q

What is the aetiology of temporal lobe seizures?

A 
Hippocampal sclerosis - 50%
Tumour - 18%
Birth hypoxia - 10%
Vascular - 10%
Post-traumatic - 8%
Other - 4%
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16
Q

What are the risk factors for epilepsy in those with temporal lobe seizures?

A 
Febrile convulsions below 6 months
Duration greater than 15 minutes
Recurrence within 24 hours
Focal features
Developmental delay
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17
Q

What are the physical symptoms of temporal lobe epilepsy?

A 
Hallucination of taste, speech, smell, visual distortion
Epigastric rising sensation
Pallor, flushing, heart rate changes
Automatisms - semi-purposeful movements
Oral - lip smacking, chewing movements
Dystonic posturing
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18
Q

What are the cognitive symptoms of temporal lobe epilepsy?

A

Deja vu
Speech arrest
Formed words during the seizure implies a non-dominant hemisphere focus

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19
Q

Describe frontal lobe seizures

A 
Brief: 10-30 seconds
Rapid recovery
Frequent
Predominantly nocturnal
Forced head / eye deviation to contralateral side
Motor activity described as bizarre. thrashing
EEG during the seizure is often normal
Jacksonian spread with Todd's paresis
Automatisms, dystonic posturing
20
Q

Describe the symptoms of parietal lobe epilepsy

A

Positive sensory symptoms
Tingling, pain
Distortion of body shape / image
Jacksonian march of positive sensory symptoms

21
Q

Describe the symptoms of occipital lobe epilepsy

A

Typically simple visual hallucinations

Amaurosis at onset

22
Q

What patients should be scanned?

A

New onset of Jacksonian motor or sensory seizures
Patients with focal neurological deficit
Alcohol withdrawal seizure if haematoma is suspected

23
Q

What is the definition of epileptogenesis?

A

Process by which parts of a normal brain are converted to a hyper excitable brain

24
Q

What is an epileptic seizure?

A

Explosion of synchronous activity by lots of neutrons at once which has a tendency to spread throughout the cerebral cortex causing an electrical-brain storm

25
Q

Why is the brain prone to seizure activity?

A

Action potentials rely on positive feedback & are unstable
Single neuron can fire spontaneously without external stimulation
Network of excitatory neurons connected in a convergent or divergent pathway can be explosive. Stimulation of any one cell can lead to a chain reaction due to the progressive spread of activity over a large area
Brain requires at least as much inhibition as excitation to avoid this
Epilepsy represents a failure of inhibitory regulation, either focally or generally

26
Q

Describe the link between ion channels and epilepsy

A

Point mutation in Na+ channel (beta subunit) –> abnormally slow inactivation –> repolarisation is impaired. Example is generalised epilepsy with febrile seizures in infants

Defect in KCNQ2 or KCNQ3 channel subunit –> impaired activation –> impaired action potential repolarisatin. Example is benign familial neonatal convulsions

27
Q

What is an electroencephalogram (EEG)?

A

Array of electrodes on the scalp which gives information about the electrical activity of a large number of neurons in the cerebral cortex
Help determine location of a seizure
Rhythmic oscillations - without sensory inputs the various neural networks feedback upon themselves
When aroused, neuronal activity becomes desynchronised
Hyperexcitation of a seizure –> synchronous activity on EEG

28
Q

Describe the origin of focal (partial) seizures

A

Originate within a small group of 1000 neutrons
Synchronised paroxysmal depolarising shift overcomes inhibition
Increased extracellular K+ due to neuronal damage or reduced uptake by astrocytes, plus glutamate release from neurons or astrocytes
During PDS, trains of action potentials occur

29
Q

Describe the spread of focal seizures

A

Spread to other brain regions along normal neuronal pathway & may show secondary generalisation if activity spreads to thalamus

30
Q

Describe the origin of primary generalised seizures

A

Reach cerebral cortex via normal neuronal pathways from thalamus
Pathways originate in brainstem & are normally involved in regulating sleep/wake cycle & arousal of cerebral cortex
Ca2+ channels & inhibitory GABA receptors in thalamic neutrons have been implicated in spike & wave seizures showing inhibition is preserved

31
Q

What causes increased activity in the brain?

A

Increased membrane excitability
Increased efficiency of excitatory synaptic transmission (glutamate)
Decreased efficiency of inhibitory synaptic transmission (GABA)

32
Q

Give examples of Na+ channel blocker anticonvulsant drugs

A 
Phenytoin
Lamotrigine
Carbamazepine
Zonisamide
Lacosamide
33
Q

What is perampanel and how does it work?

A

AMPA receptor antagonist
Non-competitive blockade of AMPA glutamate receptor
Reduce spread / generalisation of seizure
Well tolerated with improved alertness

34
Q

What does Ethosuximide do?

A

Blocks T-type calcium channels in the thalamus, which are involved in bursting & intrinsic oscillations

35
Q

Give some examples of anticonvulsant drugs that facilitate GABAergic transmission

A 
Sodium valproate
Benzodiazepines - lorzepam
Barbiturates
Tiagabine
Vigabatric
36
Q

What is Levetiracetam?

A

High affinity synaptic vesicle protein 2A ligand
Modulates neurotransmitter release
Rapidly titrated & effective
Mood lowering / agitation side effects

37
Q

What is an ideal antiepileptic agent?

A 
Good efficacy, easy & rapid to titrate
No drug-drug interactions
No cognitive side effects
No bone marrow suppression
No affective / drowsy side effects
Different routes of administration
Cost effective
38
Q

Describe established drugs

A 
Single mode of action
Less selective effects
More side effects in cognition / sedation
More drug interactions
Kinetics / narrow therapeutic range
Cheaper
39
Q

Describe modern drugs

A 
Broad spectrum
More selective actions
Less sedating side effects
Psychiatric side effects
Less long-term toxicity
Fewer drug interactions
Easier titration
10 X more expensive
40
Q

What is the first line treatment for primary generalised epilepsy?

A

Sodium valproate

Iamotrigine

41
Q

What is the first line treatment for partial epilepsy?

A

Carbamazepine

Iamotrigine

42
Q

What drugs exacerbate generalised seizure types such as myoclonus and absences?

A

Phenytoin
Carbamazepine
Gabapentin / pregabalin

43
Q

What are the side effects of benzodiazepines?

A 
Drowsiness
Ataxia
Hyperactivity
Personality change
Cognitive impairment
Tolerance / dependence
44
Q

What are the side effects of phenytoin?

A 
Ataxia
Diplopia
Nystagmus
Gingival hyperplasia
Osteomalacia
Cerebellar atrophy
45
Q

What are the side effects of sodium valproate?

A 
Sedation
Nausea / vomiting
Tremor
Hair thinning
Weight gain
Menstrual irregularities
Encephalopathy

Module 202 Neuroscience & behaviour (39 decks)

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