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Finals - Neurology > Cerebrovascular accident (CVA) > Flashcards

Cerebrovascular accident (CVA) Flashcards

1
Q

What is some epidemiology for CVAs?

A 
More common in:
Black Africans (than caucasians) 
Men 
After the age of 40
The morning – blood pressure is lowered at night then rises upon waking and is more likely to dislodge any embolism
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2
Q

What are some risk factors for CVA?

A 
Age >65 
Hypertension 
Smoking 
DM 
Heart disease – valvular, ischemic, AF 
Peripheral vascular disease 
Past TIA 
Carotid bruit 
The pill 
Raised lipids 
Raised alcohol use Raised clotting (raised plasma fibrinogen, low anti-thrombin etc 
Syphilis
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3
Q

What are some common aetiologies for CVAs?

A

Small vessel occlusion/cerebral microangiopathy or thrombosis
Cardiac emboli - AF, endocarditis, prosthetic valve, post MI/mural thrombus Atherothromboembolism i.e. from carotids or vertebrals
CNS bleed - Raised BP, trauma, aneurysm rupture, anticoagulation, thrombolysis

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4
Q

What are some other aetiologies for CVAs?

A 
Sudden drop in blood pressure 
Carotid artery dissection – spontaneous or from neck trauma 
Vascultitis 
Subarachnoid haemorrhage 
Venous sinus thrombosis 
Antiphospholipid syndrome 
Thrombophilia
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5
Q

What is the pathophysiology of a CVA?

A

Ischemic infarction (80-90%) or haemorrhage (10-20%) into part of the brain
Infarct - Most commonly affected is the MCA or a branch of it
Haemorrhage - due to chronic HTN or AVM rupture

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6
Q

What is cell hypoxia and how does it cause damage in CVAs?

A

In either type of stroke there is a loss of blood to the tissues → Na/K pumps fail → Na accumulates in cells → upset in osmotic balance → cerebral oedema

i) → cells in area of infarct swell and burst → raised ICP → blood supply affected → vicious cycle
ii) → other local cells swell but do not burst, this area is called the penumbra and the point of treatment is to reduce further swelling and damage to these cells

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7
Q

What is excitotoxicity and how does it cause damage in CVAs?

A

Accumulation of Na within non lysed cells → continued depolarisation → damage via excitotoxicity
i) Also results in the failure of AMPA and NDMA receptors which allows excessive levels of Ca into the cells
→ release of free radicals → local necrosis.
→ production of cytokines → inflammation → increased oedema.
→ apotosis of cells in the penumbra.

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8
Q

What are some clinical pointers towards a haemorrhagic stroke?

A

(not necessarily reliable but…)
Meningism, severe headache and coma within hours
More likely to be progressive (whilst still having a sudden onset)
Nearly always due to uncontrolled chronic hypertension
i) Or cocaine, congenital aneurysm, AVM, clotting disorders or tumour

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9
Q

What are some clinical pointers towards an ischemic stroke?

A

Carotid bruit, AF, past TIA, IHD

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10
Q

What are some features of an MCA stroke?

A

Contralateral

Hemiplegia - initially flaccid then becoming spastic (as UMN lesion)

Dysphagia

Homonymous hemianopia, visuospatial deficit

Aphasia

Contralateral weakness in arm ± face

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11
Q

What are some features of an ACA stroke?

A

Dysarthria, aphasia
Unilateral contralateral motor weakness (leg/shoulder > arm/hand/face)
Minimal sensory changes (two-point discrimination) in the same distribution as above
Limb apraxia
Urinary incontinence

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12
Q

What are some features of a PCA stroke?

A

Visual disturbance

Cortical blindness

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13
Q

What are some features of a brainstem infarct?

A

Quadriplegia (Corticospinal tract)

Locked-in syndrome (aware but unable to respond) (upper brainstem infarct)

Disturbances of gaze/vision (Oculomotor nuclei)

Sensory loss (Spinothalamic tracts)

Facial weakness and numbness (5th and 7th cranial nerve nuclei)

Nystagmus and vertigo (Vestibular connections)

Dysphagia and dysarthria (9th and 10th cranial nerve nuclei)

Altered consciousness/coma (Reticular activating system)

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14
Q

What are some features of a lacunar infarct (basal ganglia, internal capsule, thalamus, pons)

A

May be asymptomatic.. otherwise 5x syndromes:

  1. Ataxic hemiparesis
  2. Pure motor stroke (only motor deficits)
  3. Pure sensory stroke
  4. Sensorimotor
  5. Dysarthria/clumsy hand

Cognition/consciousness is intact except in thalamic stroke

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15
Q

What do you expect to see on a CT/MRI head of an infarct?

A

Will always show up as a wedge shaped lesion

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16
Q

What do you expect to see on a CT/MRI head of a haemorrhage?

A 
Appears hyperdense (bright white) but the longer it has been the darker it gets, after a couple of weeks it will be indistinguishable from brain tissue - 
can use this to estimate the duration of time which the haemorrhage has been present

Hyperdense MCA sign = a direct visualisation of thromboembolic material within the lumen and is the earliest visible sign of the event, appearing 90 mins post

The MCA dot and hyperdense basilar tip signs are the longitudinal equivalents

17
Q

What are some general features of note when looking at a CT/MRI of a CVA?

A

Easier to see damage the longer it has been present i.e. 6-12hrs will be clearly visible (maybe not before)

Diffusion MRI scans are more sensitive than normal MRI/CT, especially with infarction - rely on the fact that the damaged cells are filled with water (at least in the early stages)

18
Q

What cardiac examinations are performed?

A

ECG for AF? (embolus)

CXR for LA hypertrophy?

Echo for mural thrombus or hypokinetic segment of muscle post MI?

19
Q

What vascular tests are performed?

A

Hypertension:
Retinopathy? Nephropathy? Cardiomegaly on CXR?

Carotid artery doppler USS
± CT/MRI angiography:
>70% stenosis is significant

20
Q

What blood tests are performed?

A

Hypo/hyperglycaemia

Hyperlipidaemia

Hyperhomocysteinaemia (elevated homocysteine = amino acid who’s increased levels are associated with certain disease states as well as nutrient deficiencies such as B12, B6 and folic acid)

Vascultits – raised ESR, ANA+ve

Prothrombotic states:
Thrombophilia

Hyperviscosity:
Polycythaemia
Sickle cell disease

Thrombocytopenia + other bleeding disorders

21
Q

What is the first stage of acute management?

A

Give aspirin 300mg PO once haemorrhagic stroke excluded

Protect the airway – to avoid hypoxia or aspiration

NBM
If swallowing attempts can lead to chocking

Hydrate with IVI: But don’t overhydrate – cerebral oedema

Pulse, BP:
Treating high BP may cause harm in this instance as too much of a drop can compromise cerebral perfusion as autoregulation is impaired

Stop HRT if on

Aim for glucose 4-11mmol/L

22
Q

What circumstances is a sub 1hr CT/MRI needed?

A

If thrombolysis is considered

High risk of haemorrhage: 
Low GCS 
Raised ICP 
Severe headache 
Meningism 
Progressive symptoms 
Known bleeding tendency or anticoagulated

Suspected haemorrhagic cerebellar stroke

Unusual presentation with alternative diagnoses likely: 
Head injury 
Hypo/hyperglycaemia 
SDH
Tumour 
Hepatic encephalopathy etc
23
Q

When is thrombolysis considered?

A

If found to be ischemic stroke with symptom onset <4.5hrs

Give alterplase 900 micrograms/kg over 60mins via IVI; first 10% of dose given IV injection

(fibrinolytic)

24
Q

What are some absolute contraindications to thrombolysis?

A

Previous intracranial haemorrhage

Seizure at onset of stroke

Intracranial neoplasm

Suspected SAH

Stroke or TBI in previous 3m

LP in past 7 days

GI haemorrhage in past 3w

Active bleeding

Pregnancy

Oesophageal varicies

25
Q

When is thrombectomy considered?

A

If found to be ischemic stroke within the proximal anterior circulation, with symptom onset <6hrs

Surgical extraction of clot
+
thrombolysis (within 4.5hr window)

26
Q

What other surgery may be indicated in the event of an ischemic stroke?

A

Carotid endarterectomy

If carotid Doppler shows stenosis >70% and patient has suffered a stroke or TIA in the carotid territory and is not severely disabled

27
Q

How do you manage a haemorrhagic stroke in a patient on anticoagulants?

A

Stop warfarin and give vit K

Stop heparin and give protamine sulphate

Seek specialist advice if on NOAC

28
Q

What pharmacological secondary prevention is recommended following an ischemic stroke?

A

1st line antiplatelet:
Clopidogrel

2nd line antiplatelet:
Aspirin + dipyridamole

If secondary to AF:
Warfarin - start 2wks post stroke

29
Q

What non pharmacological prevention is recommended following any kind of stroke?

A

Manage underlying pathology:
Hypertension
DM
Raised lipids – give statins

Exercise increase – increases HDL and glucose tolerance

Quit smoking

30
Q

What kind of rehab might be required after a stroke?

A

Physiotherapy:
Prevent spasticity and contractures and teaches patients to cope with current level of function

SALT:
Dysphagia
?PEG feeding if persistent
Dysphasia

OT:
Looks at level of function and makes home and lifestyle alterations

Optometry:
For any hemianopias etc

Psychiatry:
For any depression following – SSRIs/therapy

31
Q

What is the Bamford classification of stroke?

A

Classification system using clinical features only (and not imaging) to diagnose a stroke

4 clinical pictures: 
Total anterior circulation stroke (TACS)
Partial anterior circulation stroke (PACS)
Posterior circulation syndrome (POCS)
Lacunar syndrome (LACS)
32
Q

What is required for a TACS diagnosis?

A

A total anterior circulation stroke (TACS) involves a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.

All three of the following need to be present for a diagnosis of TACS:

Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)
33
Q

What is required for a PACS diagnosis?

A

A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised.

Two of the following need to be present for a diagnosis of PACS:

Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)
34
Q

What is required for a POCS diagnosis?

A

A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).

One of the following need to be present for a diagnosis of POCS:

Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

35
Q

What is required for a LACS diagnosis?

A

A lacunar syndrome (LACS) involves a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).

One of the following needs to be present for a diagnosis of LACS:

Pure sensory stroke
Pure motor stroke
Senori-motor stroke
Ataxic hemiparesis

36
Q

What territories do each of the cerebral arteries supply?

A

The anterior cerebral arteries supply the anteromedial area of the cerebrum

The middle cerebral arteries supply the majority of the lateral cerebrum

The posterior cerebral arteries supply a mixture of the medial and lateral areas of the posterior cerebrum

Finals - Neurology (30 decks)

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