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Neurology > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What are the the features of fall onset to explore in history?

A 
What were they doing? Environment, etc
Light-head or other syncopal symptoms
What did they look like:
•	Pallor, breathing
•	Posturing of limbs, head turning
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2
Q

what are features of a fall itself to explore in the history?

A

Movement-Tonic phase, clonic movements, corpopedal spasms, rigor
Responsiveness and awareness throughout

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3
Q

what are features of a after a fall to explore in the history?

A

Speed of recovery, sleepiness/disorientation, deficits

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4
Q

what are the epilepsy risk factors to explore?

A

Birth, development, seizures in past (inc. febrile fits), head injury (inc. LOC), family history, drugs + alcohol misuse

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5
Q

what parts of the social history are important to explore in falls?

A

Driving, occupation

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6
Q

what other history is important in falls?

A

Collateral

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7
Q

which investigations are useful in falls?

A

ECG
Imaging - MRI CT
CT - acutely
EEG

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8
Q

what are the indications for CT in acute head injuries?

A 
Clinical or radiological skull fracture
Deteriorating GCS
Focal signs
Head injury with seizure
Failure to be GCS 15/15 4 hours after arrival
Suggestion of other pathology – eg SAH
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9
Q

What are the differentials of falls? (12)

A 
Syncope, Non-epileptic attack disorder
•	Panic attacks / Hyperventilation attacks
•	Sleep phenomena
•	TIAs
•	Migraine
•	Hypoglycaemia
•	Parasomnias
•	Paroxysmal movement disorders
•	Cataplexy
•	Periodic paralyses
•	Tonic spasms of MS
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10
Q

what are rules about driving and seizures?

A

o 1st seizure – car = 6 months, 5 years for HGV/PCV

o Epilepsy – car = 1 year or 3years during sleep, 10 years off medication for HGV/PCV

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11
Q

what is the mechanism of syncope?

A

decrease in blood flow to the brain due to autonomic nervous system

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12
Q

what are the causes of syncope?

A

AF, murmurs, PE, aortic dissection
Reflex - postural hypotension
Neural - exposure to blood, pain, strong feelings or specific activity such as urination, vomiting or coughing

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13
Q

what are the risk factors associated with syncope?

A

fasting long hours, taking in too little food and fluids, low blood pressure, low blood sugar, high g-force, emotional distress, and lack of sleep

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14
Q

what is the underlying mechanism of neural causes of syncope?

A

when blood vessels expand and heart rate decreases inappropriately

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15
Q

what are the clinical features of syncope?

A

Loss of consciousness and muscle strength
Fast onset, Short duration
Spontaneous and quick recover
Fall
Prior - yawn, sweat, fast breathing, confusion, lightheadness, blurred vision, spots, ringing in ears

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16
Q

what is the management of syncope?

A

o Put into recover position
o Treat underlying cause
o CVS examination and L+S BP important

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17
Q

what is a non epileptic event?

A

Looks like seizures but not caused by electrical activity in the brain

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18
Q

what are the clinical features of non-epileptic events?

A

o Compared to epileptic seizure – coordinated movements
o duration >2mins
o gradual onset, fluctuating course
o violent thrashing movement, side-to-side head movement
o asynchronous movements
o eyes closed
o recall for period of unresponsiveness.

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19
Q

what are the physiological causes of non-epileptic events?

A

Syncope, paroxysms of acute neurological insults, paroxysmal toxic phenomena, non-toxic organic hallucinosis, non-epileptic myoclonus, sleep disorders, paroxysmal movement disorders, paroxysmal endocrine disturbances and transient ischaemic attacks

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20
Q

what are the psychogenic causes of non-epileptic events?

A
  • Dissociative seizures
  • Psychiatric conditions e.g. panic attacks
  • Factitious seizures – e.g. Munchhausens sysndrome, fabricated or induced illness by carers
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21
Q

how are non-epileptic events investigated?

A

o EEG
o ECG
o MRI, Serum prolactin

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22
Q

what is the management of non-epileptic events?

A

treatment of underlying cause

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23
Q

what is the general mechanism of epilepsy?

A
  • Too much excitation or Too little inhibition

* Changes in cell numbers/types, connectivity, synaptic function, voltage gated ion channel function

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24
Q

What is the main clinical feature of epilepsy?

A

Seizures

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25
Q

what are the before, during and after features of seizures in epilepsy?

A

Prior - anxiety/dread spread through body
During - Lie on ground, jerky, tight = during
After - woozy and drowsy, longer to recover

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26
Q

what is the main investigation for epilepsy?

A

EEG

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27
Q

what drugs worsen symptoms of epilepsy?

A

aminophylline/theophylline, analgesics e.g. tramadol, antibiotics e.g. penicillins, cephalosporins, quinolones, anti-erretcics e.g. procholrperazine, opioids e.g. diamorphone, pethidine

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28
Q

what are the two types of epilepsy?

A

Focal and Generalised?

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29
Q

what are the causes of focal epilepsy?

A
  • trauma (penetrating head injuries)
  • CNS infection
  • Brain tumours
  • stroke
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30
Q

what are the mechanisms of focal epilepsy?

A

structural abnormality
Imbalance of excitatory and inhibitory neurotransmitters and channels
Newer potential mechanisms

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31
Q

what is the consequence of a structural abnormality in focal epilepsy?

A

CNS insult sets up epileptogenic focus

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32
Q

what is the route of a focal seizure?

A

initiates as a focal seizure then evolves through the ipsilateral hemisphere. The ictal activity crosses the corpus callosum and then continues in the contralateral hemisphere (in addition to ipsilateral hemisphere)

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33
Q

what is involved in the neural imbalance in focal epilepsy?

A

imbalance between gamma-aminobutyric acid (GABA)-ergic (inhibitory) and glutaminergic (excitatory) neurotransmitters, voltage-gated sodium channels, T-type voltage-gated calcium channels, and an alpha-2-delta subunit of voltage-gated calcium channels.

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34
Q

what are the newer potential mechanisms involved in epilepsy?

A

alterations in gap junctions (connexins), SV2A synaptic protein vesicles, G-protein-coupled receptors, A or M voltage-gated potassium channels, and ionotropic glutamate receptors, among others.

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35
Q

what are the 2 types of seizure types?

A

Simple

Complex

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36
Q

what is a simple seizure?

A

seizure without impaired consciousness

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37
Q

what is a complex seizure?

A

seizure with impaired consciousness

38
Q

what are the motor symptoms of focal epilepsy?

A

rhythmic jerking, posturing, head and eye deviation, automatisms, vocalisation. part of your body going stiff or limp, irregular jerks, Lip smacking, swallowing chewing, progression of jerking movements, repeated movements such as rocking, pedalling or pelvic thrusting

39
Q

what are the Psychic symptoms of focal epilepsy?

A

memories, déjà vu, jamais vu, depersonalisation, aphasia, complex visual hallucinations, processing language

40
Q

what are the sensory symptoms of focal epilepsy?

A

changes to somatosensory, olfactory, gustatory, visual, auditory, thermosensory, propioception

41
Q

how else are focal seizures classified?

A

frontal, temporal, parietal or occipital

42
Q

what often precedes a focal seizure?

A

an aura

43
Q

what is the term Jacksonian mark?

A

seizures initiated and works down primary motor cortex

44
Q

what are the features of EEG of focal seizures?

A

have only intermittent abnormalities

45
Q

what is the 1st Line management of Focal Epilepsy?

A

Carbamazepine or Lamotrigine

46
Q

what are the non first line drugs for focal epilepsy?

A

o Oxcarbazepine
o Levetiracetam
o Topiramate
o Sodium valproate

47
Q

what are the add on drugs for focal epilepsy management?

A

Gabapentin, Tiagabine, Pregabalin, Zonisamide, Vigabatrin, Clonazepam, Clobazam

48
Q

what are the older drugs used in focal epilepsy management?

A

o Phenytoin
o Phenobarbitone
o Primidone

49
Q

what are the causes of generalised epilepsy?

A

genetics
metabolic
toxic and environmental factors

50
Q

what part of the brain is affected in generalised epilepsy?

A

Global

51
Q

what is the mechanism of global seizures?

A

o effects pathways that interconnect – corticothalamic circuitry
o thalamic generator source?
o begins immediately with hemispheric electrical discharges

52
Q

what are the different types of generalised seizures?

A 
absence
myoclonic
atonic
tonic
tonic clonic
53
Q

what are the features of absence seizures?

A

long periods of clouding of consciousness with continuing ‘spike and wave’ activity on EEG

54
Q

what are the features of myoclonic seizures?

A

sudden, brief, generalised muscle contractions

55
Q

what are the features of tonic seizures?

A

body goes rigid

 sudden sustained muscular contraction associated with immediate loss of consciousness

56
Q

what are the features of tonic clonic seizures?

A

epileptic cry
tonic phase – rapid neuronal discharge
clonic phase – neuronal discharge slows

57
Q

what is the EEG feature in generalised epilepsy?

A

more widespread than focal

58
Q

what is the 1st line management of absence seizures?

A

sodium valproate or ethosuximide

59
Q

what other drugs are used in management of absence seizures?

A

topiramate, levetiracetam

60
Q

what is the 1st line management of myoclonic seizures?

A

sodium valproate, Levetiracetam, clonazepam

61
Q

what other drugs are used in management of myoclonic seizures?

A

lamotrigine, topiramate

62
Q

what is the 1st line management of Atonic, Tonic, Generalised tonic clonic seizures?

A

sodium valproate

63
Q

what other drugs are used in the management of Atonic, Tonic, Generalised tonic clonic seizures?

A

levetiracetam, topiramate, lamotrigine

64
Q

which drug should never be used in management of generalised epilepsy?

A

CARBAMAZEPINE

65
Q

what are the risk factors to triggering seizures in juvenile myoclonic epilepsy?

A

sleep deprivation

flashing lights

66
Q

what are the clinical features of juvenile myoclonic epilepsy?

A

early morning jerks

generalised seizures

67
Q

what is the management of juvenile myoclonic epilepsy?

A

Sodium Valproate

Lamotrigine

68
Q

what are the causes of status epilepticus?

A 
o	Severe metabolic disorders
o	Infection
o	Head trauma
o	Sub-arachnoid haemorrhage
o	Abrupt withdrawal of anti-consultants
o	Treating absence seizures with CBZ
69
Q

what is the underlying mechanism of status epilepticus?

A

occurs when mechanisms that abort seizure activity fail. This failure can arise from excessive and abnormally persistent excitation or ineffective inhibition

70
Q

what is the consequence of status epilepticus?

A

cerebral injury
o due accumulation of excitatory neurotransmitters, i.e. glutamate
o Other mechanisms include hyperthermia, hypoxia, lactic acidosis, and hypoglycaemia

71
Q

what is the clinical feature of status epileptics?

A

o Recurrent epileptic seizures without full recover of consciousness
o Continuous seizure activity lasting more than ?30 minutes

72
Q

what are the different types of status epileptics?

A

o Generalised convulsive
o Non Convulsive Status
o Epilepsia partialis continua

73
Q

what are the features of Generalised convulsive status epileptics?

A

Can cause respiratory insufficiency and hypoxia
Hypotension Hyperthermia
Rhabdomyolysis

74
Q

what are the features of non convulsive status epileptics?

A

conscious but in altered state

75
Q

what are the features of Epilepsia partialis continua status epileptics?

A

continual focal seizures, consciousness preserved

76
Q

what is the management of status epileptics?

A

ABCDE
Identify cause - bloods and CT
Anti Convulsant - Phenytoin, Keppra, Valproate, Benzodiazepines
ITU transfer within 1 hour

77
Q

what are the channels involved in pre-synaptic excitability and neurotransmitter release?

A 
voltage-gated Na+ channels 
voltage-gated K+ channels 
N-type voltage-gated Ca2+ channels
T-type Ca2+ channels 
 SV2A
78
Q

what drugs inhibit voltage-gated Na+ channels in epilepsy management?

A

carbamazepine, oxcarbazepine, eslicarbazepine, phenytoin, felbamate, lacosamide, lamotrigine, rufinamide, topiramate, and zonisamide

79
Q

what drugs inhibit voltage-gated K+ channels in epilepsy management?

A

retigabine

80
Q

what drugs inhibit N-type voltage-gated Ca2+ channels in epilepsy management?

A

gabapentin and pregabalin

81
Q

what drugs inhibit T-type Ca2+ channels in epilepsy management?

A

ethosuximide

82
Q

what drugs inhibit SV2A in epilepsy management?

A

levetiracetam

83
Q

what are the components of the GABA system?

A

the GABA system is made up of receptors, transporters and GABA transaminase

84
Q

what drugs enhance the GABA receptor response in epilepsy management?

A

benzodiazepines, barbiturates, felbamate, topiramate

85
Q

which drugs inhibit the GABA transporter in epilepsy management?

A

tiagabine

86
Q

which drugs inhibit the GABA transaminase in epilepsy management?

A

vigabatrin

87
Q

what are the side effects of sodium valproate?

A

weight gain, teratogenic, hair loss, fatigue

88
Q

what is a side effect of topiramate?

A

Sedation, dysphasia, pyscosis, weight loss

89
Q

which anti-convulsants induce hepatic enzymes?

A

Carbamazepine, oxcarbazepine, phenobarbital, phenytoin, primidone, topiramate

90
Q

what is the effect of anti-convulsant on oral contraception?

A

reduce efficacy

Neurology (18 decks)

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