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CBL > Neuro CBL > Flashcards

Neuro CBL Flashcards

1
Q

How should suspected stroke be evaluated in ED?

A

ABC, blood glucose

A good history is key - when were they last seen well or time of onset?

Did they have a seizure?

Medical history that may predispose to stroke

Medication e.g. oral anti-coags

IV access - blood tests

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2
Q

Diff dx of stroke?

A 
Migraine
Seizure
Hypoglycaemia 
Tumour or space occupying lesion
Peripheral neuropathy
Syncope
Functional weakness
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3
Q

Total anterior circulation syndrome (TACS)

A

Contra-lateral hemiparesis
Contra-lateral hemianopia
Higher dysfunction - e.g. dysphagia

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4
Q

Posterior anterior circulation stroke (PACS)

A

When 2 out of 3 of TACS present -
Contra-lateral hemiparesis
Contra-lateral hemianopia
Higher dysfunction - e.g. dysphagia

or isolated dysphagia

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5
Q

Different lacunar stroke presentations

A

Pure motor/hemiparesis
Ataxic hemiparesis
Dysarthria/clumsy hand
Pure sensory stroke

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6
Q

Posterior circulation stroke (POCS) symptoms

A

Cranial nerve palse with contralateral motor/sensory defect

Bilateral motor or sensory defect

Eye movement disorder

Cerebellar signs

Isolated homonymous hemianopia

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7
Q

Which tests requested in stroke?

A

FBC, UE, CRP, LFT, Lipid profile, glucose, coag profile

Exclusion of hypoglycaemia is mandatory - treatment of hyperglycaemic px with thrombolysis is detrimental!

12 lead ECG

Cranial imaging

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8
Q

Role of imaging in stroke?

A

To exlude mimics (tumours)
Distinguish ischaemic vs haemorrhagic
Identify site of thrombus

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9
Q

Which imaging used in stroke?

A

CT first line - non contrast CT can be supplemented by CT angiogram

MRI first line in advanced centres or for minor strokes where it wont be picked up by CT - MRI sequence known as diffusion weighted imaging is v. sensitive for detection of stroke

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10
Q

What should a px with acute stroke be managed with?

A CT scan showed occlusion

A

<4.5 hr time window for intra-venous thrombolysis

Alteplase is the licensed thrombolytic drug

If px presents early, could consider IVT followed by MT

Px should be admitted to stroke unit!! (easy marks)

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11
Q

Recombinant tissue plasminogen activator (rtPA) - effect?

A

Precipates reperfusion of a potentially salvageable tissue

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12
Q

Most feared complication of IVT?

A

Secondary haemorrhagic transformation

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13
Q

What are the cascade of events when blood flow to the brain drops below a critical threshold?

A

1) excitotoxity
2) peri-infarct depolarisation
3) oxidative stress
4) inflammation
5) apoptosis

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14
Q

Mechanism of cell death after stroke?

A

Tissue doesn’t immediately die - there is a time window when the tissue is compromised but is potentially salvagable.

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15
Q

Ischaemia vs infarction?

A

Hypoperfused and hypoxic tissue = ischaemic, doesn’t necessarily imply reverisble tamage

Only when infarction ensues is the ischaemic region irreversibly damaged

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16
Q

Day 2 after stroke - CT angiogram - calcified atheroma affecting carotid arteries and arch of aorta.

Echocardiogram showed left ventricular hypertrophy

Total cholesterol 6

What medications should now be commenced?

A

Antiplatelets -
evidence of aspirin being effective (not until 24hrs after IVT)
clopidogrel 75mg once daily
Aspirin 75mg and dipyridamole considered if px intolerant to clopidogrel

Statins - prevent further stroke - atorvastatin and simvastatin

Antihypertensives - not given in acute period, once px is stable - ACE inhibitor and thiazide diuretic

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17
Q

Which other therapies can be given after stroke?

A 
Physio
Occ health
Speech therapy
Smoking cessation
Dietician
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18
Q

Which other therapies can be given after stroke?

A 
Physio
Occ health
Speech therapy
Smoking cessation
Dietician
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19
Q

Uthoff’s phenomenon

A

Seen in demyelination - symptoms are worse with exercise (heat)

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20
Q

Significance of PMH of optic neuritis?

A

Inflammation of optic nerve presents with pain on eye movement and visual blurring

MS presents with optic neuritis in 20% of cases - 50% of those with MS will have it at some stage

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21
Q

Important history questions for MS diagnosis?

A

Tick bites? - lyme disease is an MS mimic
Illicit drugs
Do they drive? DVLA needs to be informed

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22
Q

Signs of optic neuritis?

A

Red desaturation
Relative afferent pupillary defect
Optic disc pallor (implies atrophy)

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23
Q

Hoffman’s sign

A

Upper motor neuron (UMN) sign - parallels the extensor plantar sign in the lower limb

It is positive when there is flexion of the ipsilateral thumb after tapping the nail bed of the third finger

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24
Q

UMN lesion signs?

A 
Increased tone 
Weakness
hyper-reflexia
Clonus
Extensor plantars
Positive hoffmans sign
25
Q

Dx of MS

A

Exlude mimics (bloods and MRI)

MS diagnosed based on clinical hx supported by findings and investigations

CSF

26
Q

signs and symptoms of MS

A

Can affect optic nerve (optic neuritis), brainstem (ataxia, swallowing), cord (bladder problems, constipation) and white matter (motor and sensory problems)

27
Q

What is found in the CSF of px with MS?

A

Positive oligoclonal bands (also seen in sarcoidosis)

Increase WCC

28
Q

Differential dx to exclude for MS?

A

Lyme disease
B12 deficiency
Vasculitis
PML

29
Q

What are VERS and what do they show?

A

Visual evoked responses - the speed at which impulses travel along the optic nerve.

30
Q

Role of MRI in dx of MS?

A

Can detect a lesion of MS - demonstrated as bright with lesions on T2-weighted MRI

31
Q

McDonald criteria require dissemination in space, a lesion in at least two of:

A

Periventricular
Juxtacortical
Infratentorial
Spinal cord

Dissemination in time - 2 clinical attacks or MRI lesions of different ages

32
Q

Acute tx options for an MS relapse?

A

IV steroids - do not affect long term tissue damage

PPI given with steroids

Physiotherapists and occupational therapists

Disease modifying therapies

33
Q

Aetiology of MS

A

Exercise can worsen symptoms - heat - also hot showers? (uhthoff’s phenomenon)

Multi-factorial

Vit D deficiency, low levels of sunlight, viral infections (EBV?), genetics, smoking

34
Q

First line disease modifying treatments for MS?

A

Injectable tx -
Beta interferons and glatiramer acetate

Oral -
Dimethyl fumerate suppresses the immune system and reduces lymphocyte counts
Teriflunomide suppresses immune system

Induction therapy -
Alemtuzumab

35
Q

Tx for progressive MS?

A

Targeted at symptom control -

Fatigue - Antidepressant or modafinil?

Urinary - tamsulosin?

Spasticity - physio/OT, baclofen, benzodiazepines, gabapentin, botox?

36
Q

Components of history with a headache?

A 
Aura 
Location 
Onset
Severity
Associated symptoms - nausea, photophobia
Exacerbating/relieving factors
37
Q

Red flag symptoms in headache?

A 
Age <5 or >50
Thunderclap headache
Focal/non-focal neuro deficits
Worsening with posture or coughing 
Previous hx of cancer 
Fever
Weight loss 
Early morning headaches
38
Q

Thunderclap headache

A

High intensity headache which reaches maximal intensity in <5 minutes

In most cases of SAH it only takes few seconds

39
Q

Visual aura

A

1/3 of px with migraines experience this

Symptoms may be positive (flickering lights, spots) or negative (loss of vision, numbness)

40
Q

Triggers of migraine

A

Menstrual period, stress, caffeine, hunger, sleep deprivation

41
Q

Features to examine for raised intracranial pressure

A

Papilloedema on fundoscopy
Constriction of visual fields
Enlargement of blind spots
Unilateral or bilateral VIth nerve palsy

42
Q

Investigations of a migraine?

A

ESR/CRP may be useful if px has features suggestive of temporal arteritis

43
Q

Cluster headache other name?

A

Trigeminal autonomic cephalgias - unilateral and associated with prominent ipsilateral cranial autonomic features

44
Q

Pathogenesis of migraine

A

Pain results from interactions between components of the trigeminovascular system

1) pain sensitive cranial blood vessels
2) trigeminal nerves which innervate them
3) cranial parasympathetic outflow

45
Q

Mx of migraine

A

Lifestyle - reduce alcohol and caffeine, good sleep pattern and regular meals

Acute tx - anaglesia, triptans (highly selective 5-HT1 agonists), Antiemetics (prochloperazine, metoclopramide)

Prophylaxis - B blockers, tricyclics, anti-epileptic drugs

46
Q

Differential dx for thunderclap headache?

A 
SAH
Intercerbral haemorrhage
Arterial dissection
Bacterial meningitis
Exertional headache
47
Q

Risk factors for subarachnoid haemorrhage?

A

Modifiable - smoking, hypertension, alcohol

Non modifiable - previous SAH, polycystic kidney disease, strong family hx

48
Q

Kernig’s sign

A

Positive when the hip and knee are flexed to 90 degrees and subsequent extension of knee is painful

49
Q

Which symptoms suggest meningism?

A

Headache, photophobia, neck stiffness and a positive kernig;s sign

50
Q

3rd nerve palsy with dilation of the pupil?

A

Surgical 3rd nerve palsy

Parasympathetic fibres that supply pupillary constrictor muscles run on outside of 3rd nerve and are subject to compression (e.g. tumour or aneurysm)

51
Q

Isolated, complete 3rd nerve palsy with dilation of pupil?

A

Aneurysm of posterior communicating artery until proven otherwise

52
Q

Isolated, pupil-sparing, complete 3rd nerve palsy?

A

Small vessel ischaemia

53
Q

Inv for suspected SAH?

A

Bloods - FBC, UE, LFT, coag screen, CRP

ECG - ischaemic changes

Imaging - Non contrast CT

Lumbar puncture

54
Q

What would be seen in a lumbar puncture with SAH?

A

Xanthochromia - billirubin in CSF as blood breakdown product

Red blood cells

Opening pressure elevated

55
Q

Pathogenesis of SAH

A

SAH occurs when blood extravasates into the space between the arachnoid membrane and the pia mater

Most common cause is trauma

Non traumatic are due to saccular or berry aneurysms

Polycystic kidney disease may be a cause

90% of aneurysms develop in the anterior cerebral circulation

56
Q

Perimesencephalic SAH

A

Non traumatic SAH in which aneurysms can’t be found

57
Q

What are berry aneurysms?

A

Out-pouchings of the intimal layer through the muscular wall of the artery

Can be due to smoking or hypertension

58
Q

Mx of SAH

A

Fluid resuscitation
Analgesia
Calcium antagonist (nimodipine) prevents focal cerebral ischaemia

Endovascular coiling

59
Q

Complications of SAH

A

Rebleeding

Hydrocephalus

Seizure

Vasospasm

CBL (9 decks)

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