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► Med - Anatomy & Physiology > Neurology 4 > Flashcards

Neurology 4 Flashcards

1
Q

Are febrile fits epilepsy risk factors?

A

Yes

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2
Q

What can opiods, anti-emetics, antibiotics, analgesics (tramadol), amphetamines and aminophylline/theophylline all cause?

A

Epilepsy

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3
Q

What investigation is mandatory when approaching the fallen?

A

ECG

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4
Q

What investigation classifies epilespy, confirms non-epileptic attacks, surgical evaluation and confirms non-convulsive status?

A

EEG - electroencephalogram - recording brain activity

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5
Q

if you have had one seizure how long can you not drive a caqr for?

A

6 months

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6
Q

What is the definition of epileptic seizures?

A

Abnormal synchronisation of neuronal activity

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7
Q

In epiletpic seizures - why does abnornal synchronisation of neuronal activity happen?

A

Too much excitation
Too little inhibition
Changes

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8
Q

What is a partial simple epileptic seizure?

A

Without impaired consciousness

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9
Q

What is a partial complex epileptic seizure?

A

With impaired consciousness

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10
Q

What sensory semiology can partial seizures have?

A

Olfactory, gustatory, visual and auditory

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11
Q

Can generalised seizures start from a focal point?

A

Yes

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12
Q

What type of epilepsy: most have genetic predisposition, present in childhood and adolescence, generelaised spike wave abnormalities on EEG, tonic clonic, absence, myoclonic, clonic, tonic and atonic?

A

Generalised epilepsy

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13
Q

Wake up in morning and are stumbling and clumsy, dropping things?

A

Generalisd seizures

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14
Q

When does primary generalised epilepsy present?

A

Childhood or teens

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15
Q

What is treatment of choice for primary generalised epilepsy?

A

Sodium valproate - lamotrigine as alternative

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16
Q

Give a side effect of sodium valproate?

A

Teratogenic

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17
Q

What is juvenile myoclonic epilepsy an example of?

A

primary generalised epilepsy

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18
Q

Early morning jerks, generalised seizures, risk factosr are sleep deprivation, flashing lights?

A

Juvenile myoclonic epilepsy

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19
Q

When is the onset of focal onset epilepsy?

A

Any age - underlying structural cause

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20
Q

What is treatment for focal onset epilepsy?

A

Carbamazepine or lamotrigine

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21
Q

What can focal onset epilepsy frequently cause?

A

Complex partial seizures with hippocampal sclerosis

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22
Q

What do AEDs target?

A

Presynaptic excitability and neurotransmitter release

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23
Q

What do these drugs inhibit - carbamazepine, lamotrigine, oxcarbazepine, phenytoin?

A

Voltage gated sodium channels - influx increases excitability

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24
Q

K+ efflux reduces neuronal excitability, what increases channel activity?

A

Retigabine

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25
Q

What two drugs inhibit Ca2+ channel influx?

A

Pregablin and gabapentin

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26
Q

What AED binds to SV2A, interfering with synaptic vesicles and inhibiting neurotransmitter release?

A

Levetiracetam

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27
Q

What AED enhances GABA synthesis?

A

Sodium valproate

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28
Q

What AEDs target the GABAA receptor, reduce neuronal excitability and increases GABAA receptor activity?

A

Benzodiazepines, barbiturates, felbamate, topiramate

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29
Q

What drug targets GABA transaminase to stop degradation of GABA?

A

Vigabatrin (elevates GABA levels)

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30
Q

What does tiagabine target?

A

GABA transporter, removes GABA from synapse

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31
Q

What two AED should not be prescribed together?

A

Sodium valproate and lamotrigine

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32
Q

Give the initial treatment for partial seizures?

A

Carbamazepine

Lamotrigine

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33
Q

What treatment is for generalised seizures (absence)?

A
  1. Sodium valproate

2. Ethosuximide

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34
Q

What treatment is for generalised seizures (myoclonic)?

A
  1. Sodium valproate
  2. Levetiracetam
  3. Clonazepam
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35
Q

What treatment is for generalsied seizures (atonic, tonic, generalised tonic clonic)?

A

Soidum valproate

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36
Q

What AED causes gum hyperrophy?

A

Phenytoin

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37
Q

What drug should never bebn given in generalised epilepsy?

A

Carbamazepine

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38
Q

Give four side effects of sodium valproate?

A
  1. Weight gain
  2. Teratogenic
  3. Har loss
  4. Fatigue
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39
Q

What AED is for acute management only, rapid loading possible, enzyme enducer?

A

Phenytoin

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40
Q

What does levetiracetam cause?

A

Mood swings

41
Q

What AED causes sedation, dysphasia and weight loss?

A

Topiramate

42
Q

What do carbamazepine, oxcarbazepine, phenobarbitol, phenytoin, primidone, topiramate all induce?

A

Hepatic enzymes

COT3P

43
Q

What do carbamazepine, oxcarbazepine, phenobarbitol, phenytoin, primidone, topiramate all alter the efficacy of?

A

Combined oral contraceptive pill

COT3P

44
Q

What is not adequate if taking enzyme inducing AEDs (COT3P) and dose should be increased?

A

Morning after pill

45
Q

What is the term for recurrent epileptic seizures without full recovery of consciousness?

A

Status epilepticus - continuous seizure activity lasting more than 30 minutes

46
Q

Epilepsia partialis continua is a type of status epilepticus - what is it?

A

Continual focal seizures, consciousness preserved

47
Q

Sudden onset severe headache, collapse, vomiting, neck pain, photophobia?

A

SAH

48
Q

What focal neurological deficits are present in SAH?

A
  1. dysphasia
  2. hemiparesis
  3. 3rd nerve palsy
49
Q

What investigation is safe in alert patients with no neurological focal deficit and no papilloedema?

A

Lumbar puncture

50
Q

SAH lumbar puncture- what does it show?

A

Blood stained or xanthochromic CSF

51
Q

What is the gold standard for SAH?

A

Cerebral angiographt

52
Q

Give five complications of SAH?

A
  1. Re-bleeding
  2. Delayed ischaemic deficit
  3. Hydrocephalus
  4. Hyponatraemia
  5. Seizures
53
Q

Delayed ischaemic neurological deficit is a complication of SAH. How is it treated?

A

Nimodipine - CCB

High fluid intake tripe H therapy

54
Q

How do you treat hydrocephalus?

A

CSF drainage- LP, EVD, shunt

55
Q

How do you treat hyponatraemia caused by SAH?

A

Fludrocortisone

56
Q

What is bleeding into brain parenchyma?

A

Intracerebral haemorrhage

57
Q

What are 50% of intracerebral haemorrahges due to and what are 30% due to?

A

50% - hypertension

30% - aneurysm or AV malformation

58
Q

What shows Charcot Bouchard microaneurysms arising on small perforating arteries and basal ganglia haematoma?

A

Hypertensive Intracerebral Haemorrhage

59
Q

What are two investigations ofr ICH?

A

CT

Angiography

60
Q

What occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle?

A

Intraventricular haemorrhage

61
Q

What can cause intraventricular haemorrhage?

A

AV malformations - steal syndrome, headache

62
Q

What gies from motor cortex to anterior grey horn and decussates at medullary level?

A

Upper motor neurone

63
Q

What is the anterrior horn cell of corticospinal tract?

A

Lower motor neurone

64
Q

Is the corticospinal tract ipsilateral or contralateral?

A

Ipsilateral

65
Q

Give four features of Upper Motor Neurone Lesion?

A
  1. Increased tone
  2. Muscle wasting NOT marked
  3. No fasciculation
  4. Hyper - reflexia
66
Q

Give four features of Lower Motor Neurone Lesion?

A
  1. Decreased tone
  2. Muscle wasting
  3. Fasciculation
  4. Diminished reflexes
67
Q

Ipsilateral motor level
Ipsilateral dorsal column sensory level
Contralateral spinothalamic sensory level

A

Brown sequard syndrome

cord hemisection

68
Q

What causes central cord syndrome?

A

Hyperflexion or extension injury to already stenotic neck

69
Q

What gets weakness in central cord sybndrome?

A

Distal upper limb weakness - wrists and elbows

70
Q

Cape like spinothalamic sensory loss?

A

Central cord syndrome

71
Q

What colums are preserved in central cord syndrome?

A

dORSAL

72
Q

how do you treat spinal cord metastatic tumours?

A

Dexamethasone
Radiotherapy
Surgery

73
Q

What part of brain is affected in ataxia?

A

Cerebellum

74
Q

In upper motor neuron pattern there is pyramidal/corticospinal patter nof weakness - whjat does it involve?

A

Weak extensors of arm

Weak flexors of leg

75
Q

What lobe enables self critisism and trying again?

A

Frontal lobe

76
Q

What lobe is affected in brocos dysphasia?

A

Dominant frontal lobe

77
Q

Memory dysfunction nad difficulty recognising things?

A

Temporal lobe lesion

78
Q

What lobe is affected iun Wernickes disorder?

A

Temporal

79
Q

What lobe in congruous upper homonymous quadrantanopia?

A

Temporal lobe

80
Q

Visual field defect (congruous lower homonymous quadrantanopia)

A

parietal lobe

81
Q

Gerstmann’s syndrome (disease of the dominant angular gyrus, part of the inferior parietal lobe): Dysgraphia, left-right disorientation, finger agnosia, acalculia

A

Parietal lobe

82
Q

What lobe in inattention and denial?

A

Parietal

83
Q

What condition are COMT inhibitors such as entacapone and tocapone used for?

A

Parkinsons

84
Q

The mainstay treatment of PD is levodopa which can lead to what?

A

Dyskinesias

85
Q

Visual compromise, stiffness and weakness ?

A

MS

86
Q

nAME A Pure upper motor neurone syndrome of MND?

A

Primary lateral sclerosis

87
Q

What stroke related syndrome - no visual field defect, pure motor hemiparesis, or pure sensory deficit on one side of body, clumsy hand syndrome?

A

Lacunar syndromes

88
Q 
Cranial nerve palsy
Unilateral or bilateral motor or sensory deficit
Disorder of conjugate eye movements
Cerebellar dysfunction
Homonymous hemianopia
Cortical blindness
A

posterior circulation syndrome

89
Q

where is stroke lesion?
Hemiplegia and homonymous hemianopia contralateral to the lesion, and
Either aphasia or visuospatial disturbances
+/- sensory deficit contralateral to the lesion

A

Total anterior circulation syndromes

90
Q

where is stroke lesion?
One or more of unilateral motor or sensory deficit, aphasia or visuospatial neglect (with or without homonymous hemianopia)
Motor or sensory deficit may be less extensive than in lacunar syndromes

A

Partial anterior circulation syndromes

91
Q

What term is given to glove and stocking type peripheral neuropathy with weakness and or loss of sesnation?

A

Length dependant peripheral neuropathy

92
Q

Name an acute condition of demyelinating neuropathy?

A

Guillaine barre syndrome

93
Q

Name a chronic demyelinating neuropathy?

A

CIDP

Hereditary sensory motor neuropathy = charcot marie tooth disease

94
Q

Progressive paraplegia over days, pain common, post infection campylobacter?

A

Guillain Barre Syndrome

95
Q

Pure motor, sensory, sensorimotor, small fibre (congenital insensitivity to pain syndrome) and autonomic variants.
Demyelinating and axonal varieties.
Genetic testing available for the most common mutations (eg CMT1a)

A

Hereditary neuropathy

96
Q

Treatment of peripheral neuropathy - axonal vasculitic?

A

Pulsed IV methylprednisolone and cyclophosphamide

97
Q

Treatment of peripheral neuropathy demyelinating?

A

IVIg pooled immunoglobulin
Steroids
Azathioprine, mycophenalate and cyclophosphamide

98
Q

What nerve fibres are damaged in muscle control, touch vibration, position, perception?

A

Large

99
Q

What nerve fibres are damaged in cold, perception and pain?

A

Small

► Med - Anatomy & Physiology (130 decks)

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