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YEAR 3 & 5 CORE CONDITIONS > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

Define stroke and TIA - specifying the differences

A

Stroke = sudden onset of focal/global neurological disturbance lasting over 24 hours

TIA = less than 24 hour neurological dysfunction caused by ischaemia without evidence of acute infarction

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2
Q

What heart diseases particularly predispose you to ischaemic stroke?

A

AF
Infective endocarditis
Valve disease
Heart failure

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3
Q

What can cause a haemorrhagic stroke?

A

Rupture of an aneurysm
High blood pressure
Head injury

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4
Q

When do you anticoagulate after a stroke?

A

2 weeks after the stroke if they have AF

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5
Q

What is the mechanism of aspirin?

A

Inhibits COX1 which suppresses production of prostaglandins and thromboxane

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6
Q

What is the mechanism of clopidogrel?

A

It irreversibly binds to ADP which prevents platelet aggregation.

It is independent of COX so it is synergistic with aspirin

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7
Q

What is the most common cause of ischaemic stroke in young people?

A

Carotid artery dissection - usually caused by hitting their chin and hyperextending their neck, rupturing the carotid artery

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8
Q

What can cause a central venous thrombosis?

A

Pregnancy
Infection
Dehydration
Malignancy

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9
Q

How would an infarct of the superficial division of the middle cerebral artery present?

A
  • Expressive aphasia - Broca’s
  • Receptive aphasia - Wernicke’s
  • Face and arm motor weakness - motor cortex
  • face and arm sensory loss - sensory cortex
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10
Q

How would an infarct of the lenticulostriate branches of the left middle cerebral artery present?

A

Right upper-motor hemiparesis - damage to basal ganglia

Aphasia

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11
Q

How would an anterior cerebral artery infarct present?

A

Leg weakness - foot drop
Leg sensory loss
Frontal lobe behavioural abnormalities

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12
Q

What makes up the anterior circulation of the brain?

A

Internal carotid arteries
Middle cerebral artery
Anterior cerebral artery

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13
Q

How would a total anterior circulation infarct present?

A 
Hemiparesis (but with sparring of the forehead) 
Hemisensory loss 
Homonymous hemianopia 
Visuo-spatial deficit 
Dysphasia
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14
Q

What makes up the posterior circulation of the brain?

A

Vertebral arteries (branches from the subclavian arteries. In the cranium, the 2 vertebral arteries form the basilar artery)
Basilar artery
Posterior cerebral artery
Posterior communicating artery

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15
Q

How does a posterior circulation infarct present?

A

Cerebellar dysfunction
Homonymous hemianopia (superficial branch of posterior cerebral artery to occipital lobe)
Hemisensory loss
Hemiparesis

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16
Q

What percentage of strokes are due to infarction or haemorrhage?

A

85% - cerebral infarction
10% - primary haemorrhage
5% - subarachnoid haemorrhage

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17
Q

What symptoms point more towards a bleed than ischaemia?

A

Meningism
Severe headache
Coma
Seizure

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18
Q

What symptoms are in cerebellar dysfunction?

A

DANISH

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
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19
Q

Aside from stroke, what else can cause cerebellar syndrome?

A

PASTRIES

Posterior fossa tumour
Alcohol
MS
Trauma
Rare
Inherited
Epilepsy medication
Stroke
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20
Q

What is the first thing that should be done in suspected stroke?

A

CT head within 1 hour in order to rule out haemorrhage - don’t want to thrombolyse or anticoagulate if bleeding

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21
Q

What is the acute management of an ischaemic stroke?

A

Give alteplase within 4.5 hours once haemorrhage is excluded

If post-4.5 hours, given aspirin 300mg

Thrombectomy (particularly with large artery occlusion in proximal anterior circulation)

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22
Q

What is alteplase? When should it not be given?

A

Recombinant tissue plasminogen activator

Thrombolytic drug

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23
Q

When should alteplase not be given?

A

Do not give after 4.5 hours since onset of stroke or if there is no clear onset time

Contraindications:

  • Previous haemorrhage
  • Aneurysm
  • Recent head injury
  • Known clotting disorder
  • Intracranial cancer
  • Acute pericarditis
  • Seizure at onset of stroke (suggests haemorrhage or tumour)
  • Recent lumbar puncture
  • Systolic BP > 185 mmHg
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24
Q

What causes a unilateral progressive vision loss ‘like a curtain descending’?

A

Amaurosis fugax = TIA of a retinal artery

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25
Q

If carotid stenosis is > 70% what do you do?

A

A carotid endarterectomy = removal of material on inside of artery

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26
Q

What is the long term management post-stroke?

A

Clopidogrel 75mg daily
If they cannot tolerate clopidogrel, give aspirin 75mg + modified-release dipyridamole 200mg bd (inhibits phosphodiesterase to block platelet aggregation)

Statins
Blood pressure control

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27
Q

Diagnose: Thunderclap headache/worst headache ever

A

Subarachnoid haemorrhage

28
Q

What usually causes a SAH?

A

Rupture of a Berry aneurysm in Circle of Willis.

Most are saccular aneurysms (i.e. not congenital) - elastic lamina damaged by stressors such as hypertension and smoking

29
Q

What is the second most common cause of SAH?

A

Arterio-venous malformations

30
Q

What is the most common cause of blood in the subarachnoid space?

A

Traumatic injury

spontaneous SAH is aneurysm though

31
Q

Name some genetic disorders that can predispose you to a subarachnoid haemorrhage

A

Marfan’s syndrome
Autosomal dominant polycystic disease
Ehlers-Danlos syndrome
Neurofibromatosis

32
Q

What can come on 6 hours after onset of SAH?

A

Neck stiffness
Kernig’s sign - positive when thigh is flexed at hip and knee is at 90 degrees, then subsequent extension of knee is very painful

33
Q

How would an aneurysm in the posterior communicating artery present?

A

Pupil dilatation due to CNIII palsy (compression)

34
Q

What is the most common cause of a CNIII palsy?

A

Diabetes

Down and out pupil

35
Q

What usually causes a CNVI palsy?

A

Raised intracranial pressure

36
Q

Why might there be hypertension in SAH?

A

Sympathetic reflex to intracerebral haemorrhage

37
Q

What investigations should be done in suspected SAH?

A

Urgent CT head - detects >95% of SAH within 24 hours
LP - if CT head negative but history is suggestive - yellow CSF due to bilirubin
Angiography - to identify aneurysms

38
Q

How do you manage a subarachnoid haemorrhage?

A

Prevent vasospasm
- Calcium channel blockers - nimodipine

Prevent rebleeding

  • Clipping = craniotomy with clips around neck of aneurysm
  • Coiling = obliterate aneurysm by causing clot to form in it
39
Q

What does blood look like on a CT head?

A

Hyperdense = white - recent blood

Hypodense = dark - old blood

40
Q

How do you differentiate between extradural and subdural haematoma on CT head?

A

Extradural haematoma

  • lens shape of bleeding
  • can’t cross sutures of skull
  • can cross midline

Subdural haematoma

  • crescent shape of bleeding
  • can cross sutures of skull
  • can’t cross midline
41
Q

How do you differentiate between extradural and subdural haematoma with symptoms?

A

Extradural haematoma - LOC then lucid interval then 2nd LOC

Subdural haematoma - slow progression + confusion

42
Q

What most commonly causes peripheral neuropathy?

A

Diabetes - poor glycaemic control

43
Q

What is Guillan-Barré syndrome?

A

Autoimmune disorder that causes acute demyelination.

75% had prior infection usually of GI or respiratory systems e.g. Mycoplasma, EBV, Campylobacter

Presents with muscle weakness starting in feet and hands

44
Q

What are some complications of Guillan-Barré syndrome? What investigation must be done?

A

It can affect proximal muscles e.g. trunk, respiratory and cranial nerves (progressive facial drooping)

Respiratory depression - check vital capacity (it is likely to get worse before ABG shows signs of hypoxia)

45
Q

How do you treat Guillan-Barré syndrome?

A

IV immunoglobulins for 5 days

46
Q

What should you investigate in peripheral neuropathy?

A

Glucose levels
B12 levels
Folate levels
Neuro-conduction studies

47
Q

What is Romberg’s sign?

A

Sensoriataxia - when patient closes their eyes they wobble.

NOT a cerebellar test because they would wobble even with their eyes open

48
Q

What drug can cause peripheral neuropathy?

A

Nitrofurantoin
Phenytoin
Amiodarone
Metronidazole

49
Q

What congenital conditions can cause peripheral neuropathy?

A

Charcot-Marie-Tooth syndrome

Freidrich’s ataxia

50
Q

Name some LMN signs

A
  • Muscle paralysis
  • Fasciculations - spontaneous involuntary twitching
  • Hypotonia
  • Reduced reflexes
  • Muscle wasting
51
Q

Name some UMN signs

A
  • Spasticity - increased tone that is velocity dependent (the faster you move the muscle, the greater the resistance until it gives way like a clasp-knife)
  • Pronator drift
  • Babinski’s sign - dorsiflexion of foot
  • Clonus - rapidly dorsiflexing the foot then many downbeats of the foot
  • Hyper-reflexia
  • Reduced power
52
Q

What drugs can be given for peripheral neuropathy?

A

Tricyclic antidepressants e.g. amitryptiline

Gabapentin

53
Q

What is epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures

54
Q

Describe the different elements of a seizure

A

Prodrome (hours/days) - change in mood/behaviour
Aura - focal seizure (often from temporal lobe), deja vu, strange smells, flashing lights
Post-ictal phase - headache, confusion, myalgia, temporary weakness, dysphasia

55
Q

What causes epilepsy?

A

2/3rd = idiopathic

Space-occupying lesion e.g. neoplasm
Head injury or cortical scarring from previous head injury
CNS infections
Stroke
Hippocampal sclerosis after febrile convulsion
Vascular malformations

56
Q

Name some triggers for a seizure in epilepsy?

A

Alcohol
Stress
Flashing lights

57
Q

What is a sign of neurofibromatosis?

A

Café au lait spots

58
Q

What is a focal seizure?

A

Start in one area of one side of the brain

Often seen with underlying structural disease

59
Q

What are generalised seizures? Name some different types

A

Involve both hemispheres of the brain

  1. Absence seizures - brief (less than 10 sec) pauses e.g. stares into space for 5 seconds then resumes talking
  2. Tonic-clonic - LOC, stiff limbs (tonic) then jerk (clonic). Tongue biting, incontinence. Post-ictal confusion and drowsiness
  3. Myoclonic - sudden jerk of a limb/trunk/face
  4. Atonic - all muscles relax and drop to floor, no LOC
60
Q

What investigations should you do in epilepsy?

A

Anti-epileptic levels - check compliance
EEG
MRI - if focal onset or if seizures continue with medication
ECG - in all patients with altered consciousness
LP - if infection suspected

61
Q

What are 1st and 2nd line treatments for focal/partial seizures?

A

1st line - carbamazepine or lamotrigine

2nd line - sodium valproate

62
Q

What are 1st line treatment for all generalised seizures

A

Sodium valproate

63
Q

What type of seizures should you avoid carbamazepine in ?

A

Myoclonic seizures - may worsen them

64
Q

What are some side effects of sodium valproate?

A

Hair loss due to hypersensitivity - regrowth is curly hair
Nausea (always take with food)
Thrombocytopenia
Tremor

65
Q

Which drug should you avoid if someone is taking sodium valproate?

A

Aspirin - it displaces sodium valproate from its binding sites which increases the adverse effects

66
Q

Why is phenytoin no longer first line treatment for epilepsy?

A

Risk of toxicity –> nystagmus, diplopia, tremor, ataxia

Side effects –> reduced cognition, depression, acne, gum hypertrophy, polyneuropathy

67
Q

Which anti-epileptic drug must be strictly avoided in pregnancy? Which is preferred? What must be thought about in terms of contraception?

A

Sodium valproate is the most teratogenic

Lamotrigine is preferred

Anti-epileptic drugs are P450 enzyme inducers so they make progesterone-only contraception unreliable.
Oestrogen-containing contraceptives lower lamotrigine levels so need increased dose.

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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