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A. NEUROLOGY REVISION > STROKE & TIA > Flashcards

STROKE & TIA Flashcards

1
Q

Definition of stroke

A

A clinical syndrome of presumed vascular origin characterised by rapidly developing signs of focal or global disturbance of cerebral functions with lasts >24 hours or leads to death

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2
Q

What is a TIA?

A

a transient (less than 24 hours) neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without evidence of acute infarctio
Most people have complete resolution of Sx and signs within 1 hour

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3
Q

What is a silent stroke?

A

radiological or pathological evidence of an infarction or haemorrhage not caused by trauma without an attributable history of acute neurological dysfunction attributable to the lesion

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4
Q

Epidemiology of stroke?

A

100,000 strokes every year in the UK
It’s a leading cause of death and disability - causes around 38,000 deaths a year in the UK

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5
Q

Non-modifiable risk factors for stroke?

A

Older age
Male
Race
Previous TIA or stroke
FHx - more common in black African or south Asian

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6
Q

Modifiable risk factors for stroke?

A

Hypertension
Diabetes
AF
CVD - valvular disease, CAD, CHF, MI, structural heart disease
Smoking
Hyperlipidaemia
Obesity
Poor diet and inactivity
Alcohol misuse
Drug abuse -cocaine and amphetamines
Migraines Hx
Other diseases - DM, sickle cell, APS, CKD, haemophilia, PCKD, connective tissue disorders, OSA, vascular malformations

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7
Q

What is the most important risk factor for cerebral haemorrhage?

A

Hypertension

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8
Q

Who is considered a young patient for a stroke?

A

<65

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9
Q

Risk factors specific for a “young stroke”?

A

Infarcts:
Arterial dissection
Heath abnormalities e.g. PFO or infective endocarditis
Vasculitis
Genetic e.g. CADASIL, MELAS
Illicit drug use

Haemorrhage:
AVMs
Aneurysms

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10
Q

Examples of stroke mimics?

A

Old stroke
Epilepsy
Todds paresis
Bell’s palsy
SOL
Head injuries
Delirium
Migraine
Mass lesion
MS
Encephalitis
Transient loss of consciousness
Hypoglycaemia
Hypoxia
Drug/alcohol use
Functional disorders

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11
Q

What are examples of stroke chameleons?

A

Acute confusional state e.g. receptive dysphasia
Abnormal movements / seizures
PNS symptoms e.g. pt presents with a wrist drop ans it actually turns out to be a stroke
Acute vestibular syndrome

(This are things commonly missed that are actually a stroke!!)

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12
Q

When does a CT scan have to be done if you suspect a stroke?

A

Within 1 hour of arrival to ED

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13
Q

Hyperacute findings on Non-contrast CT head after a stroke?

A

May directly visualise the clot immediately - hyper dense artery (white artery)
You may be able to see early parenchymal signs as early as 1 hour after onset. These may be loss of grey-white matter differentiation or cortical hypodensity with associated parenchymal swelling

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14
Q

Subacute findings on Non-contrast CT head after a stroke?

A

As time goes on, the swelling starts to subside and small amounts of cortical petechial haemorrhages (not to be confused with haemorrhagic transformation) result in elevation of the attenuation of the cortex. This is known as the CT fogging phenomenon 5. Imaging a stroke at this time can be misleading as the affected cortex will appear near normal.

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15
Q

Chronic findings on Non-contrast CT head after a stroke?

A

Later still the residual swelling passes, and gliosis sets in eventually appearing as a region of low density with a negative mass effect.
Cortical mineralisation can also sometimes be seen appearing hyperdense

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16
Q

Acute vs chronic CT head for a brain bleed

A

Acute - hyperdense i..e white
Chronic - hypodense i.e. black

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17
Q

What % of strokes are ischaemic?

A

85%

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18
Q

What are the 2 types of haemorrhagic strokes?

A

Remember 15% of all strokes are haemorrhagic…
10% of all strokes are intracerebral
5% are SAH

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19
Q

What causes an intracerebral haemorrhage?

A

Hypertension usually

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20
Q

What causes an subarachnoid haemorrhage?

A

Most common cause is head injury

80% of non-traumatic SAH are caused by rupture of an intracranial saccular ‘berry’ aneurysm
20% are due to AVMS, arterial dissections and use of anticoagulants

21
Q

Conditions associated with berry aneurysms and therefore SAH?

A

Hypertension
Adult PCKD
Ehlers danlos syndrome
Coarctation of the aorta

22
Q

Whats the prognosis of a stroke?

A

1 in 7 pts with acute stroke die in hospital
30 day mortality for ischaemic stroke is 12% and haemorrhagic is 30.5%
Of people with SAH, up to 15% will die before hospital
Disability following stroke is very common - at 6 months after haemorrhagic stroke only up to 30% will live independantly
Falls occur in up to 73% of pts within the first year after severe stroke

23
Q

Investigations for ?stroke

A

FBC, ESR
Blood glucose
Choleserteol
U&Es
12 lead ECG to exclude arrhythmias
Non-contrast CT head
Carotid Doppler

Consider: CT angiogram, 24 hour tape for paroxysmal AF, ECHO for IE, thrombophilia screen (protein C, protein S, leiden 5 factor),

24
Q

What causes an ischaemic stroke?

A

50% thrombosis and embolism from atherosclerosis
25% intracranial small vessel disease - often related to hypertension and diabetes
20% cardiac source of embolism e.g. AF, IE, atrial myxomas
5% rarer causes e.g. hypercoagulable states, vasculitis, arterial dissection, genetic causes

25
Q

What classification do we use for strokes?

A

Bamford classification of stroke

26
Q

Outline Bamford classification of stroke

A

Use these criteria:
1. U/L hemiparesis and/or hemisensory loss of face, arm & leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphasia

TACI - all 3 of above criteria
PACI - 2 of above criteria
LACI - presents with 1 of the following: U/L weakness and/or sensor deficit of face & arm, arm &leg or all 3, pure sensory stroke or ataxic hemiparesis
POCI - presents with 1 of the following: cerebellar/brainstem syndrome, LOC, isolated homonymous hemianopia

27
Q

Which arteries are affected in a total anterior circulation infarct?

A

MCA and ACA

28
Q

Which arteries are affected in a partial anterior circulation infarct?

A

Smaller arteries of anterior circulation e.g. upper or lower division of MCA

29
Q

Which arteries are affected in a lacunar infarct?

A

The small deep perforating arteries around the internal capsule, thalamus and basal ganglia

30
Q

Which arteries are affected in a posterior circulation infarct?

A

Vertebrobasilar arteries

31
Q

If a pt wakes with Sx, how do you define onset of stroke?

A

You would use the last time the pt was awake and symptom free

32
Q

How should you examine a pt with a stroke?

A

Upper and lower limb neuro
Cranial nerves
Cardiovascular examination

33
Q

How does cerebral amyloid angiography present on a CT head?

A

Lots of cerebral microhaemorrhages

34
Q

Management of cerebral haemorrhage treatment?

A

Basic care - bed rest, analgesia, DVT prophylaxis
Rapid BP lowering if systolic BP is 150-220 and they are not going to have early neurosurgery. Aim for systolic <140
Immediate referral for a neurosurgical assessment - if raised ICP they will require neurosurgery e.g. burr hole or craniotomy
Anticoagulant reversal

If SAH - oral nimodipine is used to prevent vasospasm & then interventional neuroradiology with coil within 24 hours. A minority require a craniotomy and clipping

35
Q

Complications of stroke?

A

Urinary incontinence
Malnutrition
Acute confusion
Pain
Chest infections
VTE
Epilepsy
Depression

36
Q

How do we avoid complications after stroke?

A

Discharge with a comprehensive health and social care plan!
Swallow assessment for dysphagia and management of this
Early sitting out and mobilisation - PT assessments every day
Careful handling and positioning
Prevent pressure sores
Avoid urinary catheters if possible
DVT prevention
Psych review

37
Q

Secondary prevention of stroke?

A

Clopidogrel 75mg OD (second line is aspirin)
Atorvastatin 80mg ON
Treat hypertension
If pt has AF treat immediately after excluding a haemorrhage in a TIA OR if debilitating ischaemic stroke wait 14 days
Lifestyle - physical activity, stop smoking, healthy balanced diet, lower alcohol
Optimise management of comorbidities
Consider women on COCP and HRT
Annual influenza vaccines
Driving rules
Travel - wait 10 days after stroke for a flight

38
Q

Stroke rehabilitation

A

Swallowing
Pressure sore risk
Nutrition
Cognitive impairment
SALT
Depression and anxiety
PT
OT with ADLs
Carers training and equipment to handle pt at home

39
Q

When must you assess a pt and what imaging modality is best for TIA

A

Assess urgently within 24 hours by a stroke specialist clinician. (If TIA occurred >1 week ago then this is within 7 days)
MRI is the preferred imaging

40
Q

Management of TIA?

A

As soon as haemorrhage is excluded - 300mg aspirin
Assess urgently within 24 hours by a stroke specialist clinician (if they have presented after 7 days then see them within 7 days)
Start secondary prevention as soon as diagnosis is confirmed
Start clopidogrel (300mg loading dose followed by 75mg daily) & aspirin (300mg loading dose followed by 75mg daily) for 21 days followed by monotherapy with clopidogrel OD
Start atorvastatin 80mg ON
If they have AF then anticoagulate as soon as bleed has been excluded
If considered candidates for carotid intervention then do carotid imaging within 24 hours & if stenosis >=50% then perform a carotid endarterectomy within 7 days of Sx onset

41
Q

What imaging options are there for determining carotid stenosis?

A

carotid duplex ultrasound
CT angiography
MR angiography

42
Q

What is virchows triad?

A

Stasis of blood flow
Endothelial injury
Hypercoagulabiloty

43
Q

what is the ischaemic penumbra

A

the part of an acute ischaemic stroke that is at risk of progressing to infarction but is still salvageable if reperfused. It is usually located around an infarct core

44
Q

Pathophysiology of ischaemic stroke?

A

Embolism or thrombosis cuts off oxygen to a part of the brain. This causes an ischaemic core and the penumbra around it.
Without oxygen brain cells lose their energy source which is needed to pump ions in and out of cells. This causes Na+ and water to flood into cells = this is cytotoxic oedema
Starving brain cells release too much glutamate which overstimulates nearby cells causing them to take in too much Ca and eventually die
Evenrutally the brains immune response kicks in and the blood brain barrier becomes leaky = vasogenic oedema
When blood flow is restored it can sometimes cause additional damage due to a sudden rush of oxygen which generates ROS = reperfusion injury

45
Q

Management of acute ischaemic stroke?

A

Admit directly to a hyperacute stroke service and recieve brain imaging within 1 hour of arrival to hospital - if potentially eligible for mechanical thrombectomy this should be a CT angiogram

As soon as haemorrhage is excluded give 300mg aspirin (continue this daily for 2 weeks)
Thrombolysis if it can be administered within 4.5 hours of stroke Sx onset (or 4.5-9 hours if they have evidence from imaging of the potential to salvage brain tissue)
Mechanical thrombectomy - if within 6 hours of Sx onset if confirmed occlusion of Procimal anterior circulation demonstrated by CTA or MRA (6-24 hours/wake-up stroke if potential to salvage brain tissue is shown via brain imagine)
Consider thrombectomy if pt is last known to be well up to 24 hours previously and have confirmed occlusion of proximal posterior circulation and there is potential to salvage brain tissue as shown by imaging

Consider carotid endarterectomy
Dont lower bp in acute phase unless there are complications. Note bp should be lowered to 185/110 before thrombolysis however
Dont start anticoagulants for AF until at least day 14
Dont start statin treatment until after at least 48 hours due to risk of haemorrhagic transformation

46
Q

What drugs can we use for thrombolysis?

A

Alteplase and tenecteplase

47
Q

What imaging can be used to determine if there is potential to salvage brain tissue after a stroke?

A

CT or MR perfusion scan (core-perfusion mismatch)
MRI (DWI-FLAIR mismatch)

48
Q

If a pt is going for thrombolysis what should their bp be?

A

<=185/110

A. NEUROLOGY REVISION (3 decks)

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