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Stroke/TIA Flashcards

1
Q

Definition of stroke.

A

“An acute onset of focal neurology deficit or global neurological dysfunction leading to death, or lasting longer than 24 hours as a result of damage to the central nervous system that is vascular in origin”

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2
Q

Definition of TIA.

A

An acute onset of focal neurology deficit or global neurological dysfunction which resolves within 24hrs with no lasting effect - No death to CNS

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3
Q

What is the largest burden of stroke on the NHS?

A

The disability care and carers required post-stroke

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4
Q

How many people in the UK have a stroke each year?

A

152,000

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5
Q

What is the 4th leading cause of death in the UK?

A

stroke

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6
Q

What is the lifetime risk of having a stroke for men and women?

A

Men 1 in4

Women 1 in 5

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7
Q

What are the non-modifiable risk factors for stroke?

A 
Age 
Gender 
Genes 
Ethnicity 
Previous TIA/stroke
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8
Q

What are the modifiable risks for stroke/TIA?

A 
AF 
high BP 
high cholesterol 
vascular disease 
diabetes 
heart failure 
smoking/ recreational drug use 
physical inactivity/ obesity/ diet
Contraceptive pills
Thrombophilia 
OSA
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9
Q

How much of the cardiac output is to the brain?

A

20%

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10
Q

What is the normal cerebral perfusion rate?

A

50ml/100g/min

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11
Q

What perfusion rate can the brain compensate to?

A

about 20ml/100g/min

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12
Q

What perfusion rate does the brain become seriously affected?

A

10ml/100g/min

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13
Q

Why is the brain so dependent on glucose?

A

CAnt really respire anaerobically

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14
Q

Does everyone have co-dominant vertebral arteries?

A

No - one is normally dominant

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15
Q

What is the simplified purpose of the frontal lobe?

A

higher level cognition
language
Primary motor cortex

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16
Q

What are the simplified functions of the parietal lobe?

A

Reasoning tactile senses
verbal memory
expressive language
somatosensory cortex

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17
Q

What are the simplified functions of the temporal lobe?

A

speech perception, interpreting sounds/language

Hippocampus: memory – not often a key defining feature of a lot of stroke

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18
Q

What are the common symptoms of frontal lobe strokes?

A 
Disinhibition
Apathy 
Irritabilty/anger innapropriately
Innapropriate placidity
Obsessional behaviour
Distractability
Poor planning skills
Utilisation behaviour (see a tool- use it)
Release of primitive reflexes (pout, palmomental)
Gait apraxia
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19
Q

What are the main catergories of aetiologies of ischaemic stroke?

A

Carotid disease and verterobasilar disease
Embolic sources
Hypoperfusion
Inflammatory

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20
Q

What are some examples of carotid disease and vertebrobasilar disease?

A

Carotid stenosis- chronic atherosclerotic disease
Plaque rupture with either thrombosis (causing stenosis/occlusion) or embolism
Dissection- splits the blood vessel, blood flows into the slit instead of the vessel, blocks off vessel or causes thrombus. Typically painful. Usually history of trauma with neck pain and can be associated with Horner’s syndrome.

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21
Q

What are some examples of embolic sources of ischaemic stroke?

A

AF – static blood will clot
Paradoxical emboli and patent foramen ovale (25% of people have this)
SBE – subacute bacterial endocarditis – bacterial infection in heart, vegetation from growth of bacteria can dislodge
LV thrombus/post MI
Mechanical valves (usually with suboptimal anticoagulation) – metal valve can be traumatic and pro-thrombotic
Post operative carotid/peripheral vascular/valvular/cardiac surgery
Prothrombotic states – antiphospholipid syndrome, polycythaemias and hyperviscosity syndrome, cancer

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22
Q

What are some causes of hypoperfusion?

A

Sepsis, iatrogenic, hypovolaemia

Starotid stenosis

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23
Q

What is an example of an inflammatory disease that can cause ischaemic stroke?

A

Vasculitis

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24
Q

What is the aetiology of haemorrhagic stroke?

A

Rupture of vessels
Through excessive pressure (hypertension)
Or friable/damaged vessels:
Vasculitis
Amyloid angiopathy – blood vessel become weak leading to multiple small haemorrhages, can present similar to TIAs
Vascular malformations – cavernoma (benign vascular tumour) or arteriovenous malformations (generally present with epilepsy
Moyamoya
Trauma eg traumatic SAH
Malignancy – bleed due to abnormal vascular composition – weird to have a large haemorrhage further away from the centre – indicates cancer

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25
Q

What is the danger of blood in the ventricular system?

A

Blood in ventricular system – clot and block outflows of CSF = hydrocephalus

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26
Q

What is the common presentation of stroke of anterior circulation

A 
Hemiplegia
hemisensory loss
neglect/ inattention
Speech problems – dysarthria is slurred speech due to muscle problems, dysphasia is speech due to brain
Amarausis fugax
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27
Q

What are the common presentations of stroke of the posterior circulation?

A 
balance problems
visual field defects
swallowing problems
Poor co-ordination
Drowsiness – hypothalamus is key for keeping alert and awake 
cognitive issues (thalamic involvement)
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28
Q

What is haemorrhagic stroke commonly associated with that ischaemic stroke isnt

A

headache

drowsiness if a large bleed

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29
Q

What are common focal motor deficits

A

Patterns of motor weakness and examination
Hemiparesis
Focal single limb/facial weakness, could be proximal or distal, try and note if there is truncal weakness
Pyramidal in pattern (arms flexors>extensors, legs flexors

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30
Q

What are some motor symptoms that can lead to a wrong diagnosis of stroke?

A

Peripheral nerve distribution of weakness e.g. BELL’S PALSY IS NOT A STROKE SYNDROME. Bell’s palsy is LMN – effects whole face unilaterally, in stroke you generally have innervation to both sides of forehead still intact

Bilateral symptoms

Variable weakness during examination or fatiguability

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31
Q

What are some patterns of sensory loss associated with stroke?

A 
Hemisensory loss    
Confined to one limb
Unilateral
Does not cross the midline
Generally mutlimodal
Look for cortical dysfunction such as stereognosis or graphaesthesia
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32
Q

What patterns of sensory loss could lead to wrong diagnosis of stroke?

A

Positive sensory phenomena generally do not occur in stroke – more likely to be lower motor neuron disorder
Peripheral nerve distribution
Sensory levels
Bilateral symptoms

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33
Q

What visual defects would a left TACS give you?

A

right homonymous hemianopia

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34
Q

What visual defect might a left superior parietal infarction give?

A

right inferior quadrantanopia

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35
Q

What are the symptoms needed to class a stroke as total anterior circulation syndrome or partial anterior circulation syndrome

A

Total anterior circulation syndrome (TACS)
All 3 of unilateral weakness/sensory deficit, homonymous hemianopia, higher cereberal dysfunction (dysphasia, inattention/neglect)
Partial anterior circulation syndrome (PACS)
Either 2 of the above or higher cerebral dysfunction alone

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36
Q

What are the symptoms needed to classify a stroke as posterior circulation syndrome?

A

Posterior circulation syndrome (POCS)
Any of: ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit; bilateral motor and/or sensory deficit; disorder of conjugate eye movement; cerebellar dysfunction; isolated homonymous visual field defect

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37
Q

What symptoms cause a stroke to be classed as a lacuna stroke?

A

Pure hemi-motor, pure hemi-sensory, pure sensori-motor, ataxic hemiparesis

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38
Q

What method is the classification of strokes based on?

A

Oxford Classification of stroke

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39
Q

What percentage of strokes are ICH?

A

10%

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40
Q

How does risk of an ICH alter with age?

A

It increases:

Incidence >55 yrs increases x2 with each decade
>80 yrs then x25

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41
Q

What are common causes of ICH?

A 
Acute and Chronic hypertension 
Increased cerebral blood flow:
Migraine, exercise, cold
Vascular anomalies:
AVM, venous angina 
Arteriopathies: 
Amyloid - 10% of ICH, Apolipoprotein Ee4 allele/ Down’s syndrome
Fibrinoid necrosis, lipohyalinosis, cerebral arteritis 
Tumours:
Coagulation disorders 
CNS sepsis
fungal , granuloma, herpes simplex 
Venous sinus thrombosis 
Drugs 
Cocaine 
Trauma
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42
Q

What does a AVM ICH look like? What does it cause? Where is it often?

A

Orange as the haemoglobin has stained it.
Causes epilepsy
Often in middle meningeal area?

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43
Q

What is the presentation of AVM?

A 
Haemorrhage:  40 - 60%
Less severe than SAH bleeds 
Epilepsy 
Neurological deficit 
Headache 
Cranial bruit - audible vascular sound
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44
Q

Should you immediately remove clot from a ICH?

A

Sucking out a clot will actually often kill the penumbra
Leave the clot in if it can be absorbed naturally, just relieve pressure
Quality of life rather than good surgical skills

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45
Q

What are the GCS guidelines for operating on a ICH?

A

If GCS of 14+ and the bleed is <4cm then treat medically

If GCS of 13 or lower and the bleed is larger than 4cm then treat surgically

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46
Q

Why is the threshold for operating on a clot that caused ICH lower if it is near the cerebellum?

A

In the cerebellum - lower threshold for as to operate as increased pressure = hydrocephalus

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47
Q

Describe decompressive craniectomies and why they are needed for ICH

A 
Most intracerebral strokes cause oedema
WO mortality is 80% 
Early intervention is better than late
Right side is better than left
There are predictors of early brain swelling on CT of more than 50% infarct
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48
Q

What is the most common cause of SAH?

A

trauma

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49
Q

What occurs in SAH?

A

Occurs when a blood vessels on the brain surface ruptures:
Aneurysm
Arteriovenous malformation (AVM) - arteries join directly to veins without capillary beds which means the blood moves into the vein quickly, without lowering the pressure from the artery. The veins are thin walled and leak blood.

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50
Q

What is the peak age for SAH?

A

55-60

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51
Q

What are the most common places for aneurysmal SAH?

A 
85-90% carotid system 
5-15% vertebrobasilar system 
30% AcommA 
25% PcommA 
20% MCA
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52
Q

What are the stats of fatality of SAH?

A

10% die before reaching hospital
Further 8% die before neurosurgical care
7% die with neurosurgery because of spasm

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53
Q

What are the symtpoms of SAH?

A 
Headache 
Nausea 
Vomiting 
Brief LOC 
Neck stiffness 
Hemiparesis 
Vertigo 
Faintness 
Confusion
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54
Q

What are 2 main factors that cause deteriation in hospital?

A

major rebleed

hydrocephalus

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55
Q

What are the risk factors for SAH?

A 
Hypertension 
Smoking 
OCP 
Cocaine - surge of BP 
Age 
LP/cerebral angiogram 
Pregnancy 
Diurnal variation in BP
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56
Q

What are the disease states associated with intracranial aneurysm formation?

A 
Increased BP 
Increased blood flow 
Blood vessel disorders 
Genetic 
Congenital 
Tumours metastatic to cerebral arteries 
Infectious
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57
Q

What are the non-aneurysmal causes of non-traumatic SAH?

A 
Arterial lesions
AV shunts 
Cardiac myxoma 
Sickle cell disease 
Vascularitis 
Infections 
Tumours 
drugs
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58
Q

Descibre the grading of SAH

A 
world federation of neurological societies 0-5. 
Based on GCS and deficit 
0 - normal baseline 
1 - GCS 15 
2 - GCS 13-14
3 - GCS 13-14 + deficit 
4 - GCS 7-12 +/- deficit 
5 - GCS 3-6 +/- deficit

4 and 5 are basically dead

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59
Q

What does the fisher grade assess?

A

The amount of haemhorrage on CT scans - blood loss and severity

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60
Q

Describe the management of SAH

A

Day 3 - 21: major arteries go into spasm so try to keep BP normal:
Treat with lots of fluids
If you can drop normal osmolarity of blood by 1/3rd increases blood flow and decreases the likelihood of another bleed
Loss of Na+ due to BNP:
Need to monitor fluid and salts to keep level
Vasospasm monitored on angiogram/dopplers
Nimodopine - Blocks calcium dumping at end of apoptosis to keep cells alive:
Doesn’t reverse vasospasm

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61
Q

What is the treatment for SAH from an aneursym?

A

Radiologist can coil aneurysms- not invasve, has massively overtaken clipping:
Surgeons can clip any aneurysm but requires surgery - can be done with hypothermic circulatory arrest to increase time
Gamma knife treatment - slow to work but works really well in long run to prevent long term problems

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62
Q

What are the complications of SAH?

A 
Rebleeding
Hydrocephalus 
Vasospasm
Hyponatremia 
Infarction
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63
Q

What are the risk factors for vasospasm?

A 
Younger
Smoking
Hyponatremia 
Hyperthermia 
Dehydration 
Hypotension 
Hypoxia
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64
Q

What are the advantage of early surgery following stroke?

A 
Prevention of rebleeding 
Aggressive management of vasospasm 
Removal of sub arachnoid blood 
Early ambulation 
Reduced medical complications
Shorter hospital stay
Pyschosocial reassurance
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65
Q

What are the disadvantages of early surgery following stroke?

A

Swollen brain
Unstable patient
Scheduling difficulties
Inexperienced operating team

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66
Q

What are the advantages of delaying surgery following stroke?

A 
Slack brain 
Stabilised patient 
Esaier dissection 
Flexibility in scheduling 
Experienced operative team
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67
Q

What are the disadvantages of delayed surgery following stroke?

A

Rebleeding
Delayed ambulation
Longer hospital stay
Psychosocial stress

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68
Q

How is the risk of stroke following a TIA assessed?

A

ABCDD score

Brain imaging - DW MRI

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69
Q

What ABCDD puts a patient at high risk of having a stroke? What does this result in?

A

> 4 – high risk, seen in 24 hrs

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70
Q

What ABCDD puts a patient at low risk of having a stroke? What does this result in?

A

<4 – low risk, seen in clinic within 1 week

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71
Q

Why is diagnosing TIA difficult?

A

• Diagnosing is difficult: post presentation, relying on history

Variety of symptoms - depends where

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72
Q

What are the high risk TIAs

A

o Crescendo
o Anti-coagulants
o AF
o Known carotid stenosis

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73
Q

What is emergency treatment for a TIA?

A

o Aspirin 300mg stat – 75mg od
o If on warfarin – test INR and see if the response is good
o Clopidogrel monotherapy

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74
Q

What is the early secondary prevention for TIA?

A

o BP, DM, cholesterol, smoking, alcohol, weight, exercise
o Warfarin/DOAC for patients in AF
o Statin

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75
Q

What are amyloid spells?

A

transient neurological phenomena which leaks small amount of blood onto the surface of the brain

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76
Q

What percent of strokes are ischaemic and of them what percent are the different causes?

A

85%:

25% large vessel disease
25% small vessel disease
25% cardioembolic stroke
25% other/obscure

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77
Q

What is key for atherosclerois (large vessel disease)?

A

Inflamamtion

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78
Q

Describe the mechanism of formation of atheroma.

A

o Thrombus on lesion causing local occlusion
o Embolism of plaque debris or thrombus in distal vessel
o Small vessel origin occlusion by growth of plaque
o Severe reduction in diameter of vessel lumen leads to hypoperfusion and infarction of distal “watershed” areas

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79
Q

Why do you not know about carotid stenosis until you have a TIA/stroke?

A

the cerebro-automatory mechanisms are too good, not like heart where you get angina

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80
Q

What is indications for carotid endarterecteomy or carotid artery drug eluting stent?

A

if you see severe carotid stenosis with symptoms

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81
Q

What are the risks of CEA?

A

3-6% of stroke

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82
Q

Where does a carotid bifurcation emboli usually go?

A

eye or anterior 2/3rds of cerebral hemisphere

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83
Q

What are some examples of antiplatelet treatments?

A

Clopidogrel, ticagrelor, aspirin

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84
Q

What is lacunar stroke?

A

occlusions of small penentrating arteries

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85
Q

What causes lacunar strokes?

A

• Small vessel arteriopathy -hyaline arteriosclerosis:
o Muscle and elastin in arterial wall replaced by collagen
o Wall thickening with subsequent lumen narrowing
o Diabetes, hypertension, age

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86
Q

What are the causes of cardioembolic stroke?

A
  • AF
  • Myocardial infarction (anterior wall) with hypokinetic wall segment)
  • Infective endocarditis
  • Diseased valves
  • Non-bacterial thrombotic endocarditis
  • Paradoxical embolus –
87
Q

Why can prosthetic valves cause stroke?

A

prosthetic heart valves are metal and pro-thrombotic

88
Q

What is paradoxial embolus?

A

• Paradoxical embolus – (emboli from venous to arterial blood) passes through patent foramen ovale

89
Q

What are some other/obscure causes of ischaemic stroke?

A
  • Antiphospholipid syndrome or any inflammatory vascular disease
  • Cancer
  • Anything that makes bloody more sticky
  • Arterial dissections – spontaneous or trauma
  • Recreational drugs – vasospasm due to cocaine, amphetamines
  • Peri-operative
90
Q

What are the 4 types of intracranial haemorrhage?

A
  • Extradural
  • Subdural
  • Subarachnoid
  • Primary intracerebral haemorrhage
91
Q

What are risk factors of a primary intracerebral haemorrhage?

A 
o	Intracranial small vessel disease 
o	Cerebral amyloid angiopathy 
o	AVMs 
o	CNS neoplasms (cancer) 
o	Anticolagulation
92
Q

What does the location of an intracerebral haemorrhage tell you?

A

o Deep – susceptible to hypertension

o Surface – amyloid angiopathy, neoplasm

93
Q

What do the clinical features of a stroke depend on?

A

o Pathological type of stroke
o Position of lesion in the brain
o Size of lesion
o Arterial supply to the brain

94
Q

What is the national cost of stroke?

A

o £2.8 billion direct care costs
o £1.8 billion lost productivity and disability
o £2.4 billion informal care costs
o At least £7 billion per year

95
Q

What is the 30 day mortality rate of stroke?

A

20%

96
Q

How does stress increase risk of stroke?

A

o Data to prove for it – chronic stress increases atherosclerosis, acute stress can cause plaque rupture
o No data that relaxation can reverse it yet
o Little bit of alcohol is good, helps relax

97
Q

WHat is the relationship between stroke and hypertension?

A

for every 10 deaths from stroke 4 are preventable if BP treated
o Linear relationship between risk of stroke and increasing BP

98
Q

What are some ways to reduce BP without pharmacological intervention?

A 
	Increased exercise 
	Lower salt intake 
	More fruit and veg
	Reduced cholesterol intake 
	Reduced alcohol 
	Smoking Cessation§
99
Q

How does smoking increase risk of stroke?

A

smoking doubles risk of stroke (damages endothelial lining, enhances clotting, raises LDL cholesterol, lowers HDL cholesterol, raises BP)

100
Q

What waist to hip ratios and BMIs are considered overweight and increase risk of stroke

A

o BMI >25 overweight and >30 obese

101
Q

How does social deprivation effect risk of stroke?

A

o People in deprived areas are 3 times more likely to die from stroke than the least deprived

102
Q

What is the increased risk of stroke with AF?

A

6 fold

103
Q

What scores predict risk of stroke in people with AF and individual risk of haemorrhage on treatment?

A

o CHADS2VASC score predicts risk of stroke

o HASBLED score predicts individual risk of haemorrhage on treatment

104
Q

What are the 3 causes of TIA?

A

Atheroma
Embolism
Hypoperfusion

105
Q

Basically describe formation of an atheroma

A

Lipid deposition
Fatty plaque
Rupture causing increase in inflammatory cytokines
Emboli

106
Q

Why is the ABCDqaured scheme not used anymore?

A

However its biased to age - missing younger group

Edinburgh did research and found it not useful so not used anymore

107
Q

What is the current NICE guidance for suspepted TIA presentation? Why is it difficult?

A

NICE guidance now that anyone who has sudden neurological symptoms to been seen in emergency clinic in next 24 hrs - logistically difficult as at least 1/3rd of patients in TIA clinic is mimics (gone up to 50% since the pressure to see everyone within 24hrs)
A and E don’t have time to work out diagnose in detail - anyone with sudden neurological deficit referred to TIA clinic

108
Q

What investigations will be done at a TIA clinic?

A 
Carotid Doppler 
MRI/CT of brain 
MR/CT angiogram if doppler indicates need 
Blood Test 
ECG
109
Q

What does the doppler of carotids in TIA clinc look for?

A

If show stenosis, have an angiogram at same time as MRI

Doppler might overcall - suggest larger stenosis than MRI so need 2 modalities

110
Q

What is the standard investigation for AF here? what others are used around the world?

A

Standard 72 hr ECG will be done later, other parts of world do 7 day ECG, new technology uses bluetooth to send results to a central recording assessment centre where someone continuously monitors them - expensive and issue with data protection

111
Q

What do you expect to see on a scan of TIA?

A

normal scan

112
Q

What are the differences in ischaemia on DWI, ADC and FLAIR MRI?

A

DWI - see bright white spots for ischaemia
FLAIR - becomes positive at different time point so can pin down time
ADC - dark spots for ischaemia

113
Q

When would intervention for TIA be advised?

A

American trial found that carotid narrowing of more than 70% would benefit from intervention, such as carotid endarterectomy or stenting (endarterectomy is better)
Sometimes treat patients with lower degree of stenosis:
Shape of plaque
Retinal transient ischaemia
CART score - developed by Oxford to work out whether to intervene

114
Q

What angiography is done for TIA patients where doppler indicates use of angiography?

A

Used to do a formal catheter angiogram in all patients, but its invasive and expensive
MR angiography has increased resolution greatly
CT angiogram if patient cant tolerate MRI

115
Q

What indicates cardioembolic source of TIA?

A

Slightly more likely to be in posterior circulation

Multi-territories affected - strong likelyhood of heart source

116
Q

What are some examples of cardiac sources of TIA?

A 
AF 
Mural thrombosis 
Septic embolis 
Myxoma 
endocarditis 
Heart valve thrombosis 
PFO - patent foramen ovale 
Calcific embolis from aortic valve
117
Q

What investigations would be done to look for cardiac sources of emboli?

A

Use transthoracic echo, transcranial doppler (for PFO), holter monitor (72 hr ECG)

118
Q

Why do cardiologists meet with neurologists monthly?

A

Meet with cardiologists monthly:
Determine treatment plan
Hot topic is PFO - young people in particular, present in 25% of population
Also how much AF warrants anti-coagulation - cardiologists have higher threshold than neurologists, dont want to put young people of anti-coagulation for life

119
Q

What does a transcranial doppler look at?

A

look at blood flow through MCA by looking through bony window in temporal bone, agitate with bubbles of saline to look for microemboli

120
Q

What evidence is there for PFO closure devices? Are they good?

A

Original research by industry - potentially biased and had low threshold for inclusion
Data from confirmed TIA/stroke patients does suggest that PFO closure can help - going through NICE appraisal
No surgeons in Sheffield, go to LEeds but no funding to do it at Leeds - instead using anticoagulation for patients with PFO and confirmed microemboli

121
Q

What are the drugs given for TIA?

A

Give antiplatelet, statin and antihypertensive to all indicated, prescription on day
Anticoagulants only for those with AF

122
Q

Which anti-platelet drugs is first choice for TIA?

A

aspirin (start immediately, well tolerated), clopidogrel (some patients are resistant but have no tests so make decision next day in clinic whether to swap as clopidogrel is the first line choice now),

123
Q

Why are strronger antiplatelets not used yet for TIA?

A

new stronger antiplatelets such as prasergel emerging but haven’t been researched for TIA/stroke, may cause excess risk of bleeding as brain circulation more susceptible than heart circulation

124
Q

Which statins are first choice for TIA?

A

Statins - huge evidence that they reduce chance of stroke in TIA patients, torvostatin favoured over simvastatin now price has equalled

125
Q

What are some effects statins have as to why they could be beneficial for TIA?

A 
Decrease CRP 
Reduce cytokines 
Reduce chemokines 
Reduce adhesion molecules 
Increased endothelial NO 
Antioxidant 
Cytoprotection
126
Q

Which antihypertensives are first line treatment for TIA?

A

type of antihypertensive depends on ethnicity and age:
Under 55 - ACE inhibitor or ARB such as candesartan
Over 55 or Afro-Caribbean - calcium channel blocker such as amlodipine

127
Q

What are the pros and cons of warfarin and DOACs for AF causing TIA?

A

all have 2% risk of bleeding intra or extracranial, need to assess risk against risk of further stroke
DOAC - can give prescription there and then, GPs/doctors not familiar with them, don’t get information leaflet, which one used depends on age:
Younger - dogibitran, slightly higher risk of intracranial hemorrhage but have a reversal agent for it
Older - epixiban - lower risk of intracranial hemorrhage
Warfarin - need blood monitoring which is inconvenient, huge amount for safety data, works well, people know more about it, patients get safety card to always carry

128
Q

What lifestyle advice would be given for TIA?

A

smoking cessation, exercise, can’t drive after TIA for a month

129
Q

What is hte gold standard imaging for assessing stroke treatment?

A

CT perfusion - shows the penumbra

130
Q

How long has thrombolysis been lisenced in the UK now?

A

since 2003

131
Q

Describe the NINDS study

A

NINDS Study - IV thrombolysis up to 3 hrs
624 patients given thrombolysis within 3 hours of onset
At 3 months, treatment with IV thrombolysis increase the chance of an excellent recovery by 30%
Ordinal shift analysis of the NIHSS scores show better outcomes
Ordinal shift analysis of the modified Rankin score too
Number needed to treat - 8 to get one additional patient with near complete recovery,

132
Q

Describe the ECASS III trial

A

ECASS III trial - IV thrombolysis up to 4.5 hrs
Investigated for 4.5 hours post onset
821 patients given IV thrombolysis between 3 - 4.5 hours of onset
Significantly better outcomes
Not as good as 3 hours
NNT - 14 (was 8 at 3 hours)
Mortality rates are similar - no increase risk of death

133
Q

What are the limitations of IV thrombolysis?

A

TIme window is small
Many contraindications - warfarin etc.
Only about 12% of stroke patients receive IV thrombolysis
Bigger blood vessel clots don’t recanalise as well e.g. ICA is 8% in one hour, distal MCA branches are 40%

134
Q

What is the NHS 10 year plan with regards to stroke treatment?

A

Dedicated bullet point in NHS 10 year plan - want to get 20% rate of thrombolysis from 12% and 10% thrombectomy rate from 1% by 2024

135
Q

What is intra-arterial treatment for acute stroke?

A

Squirt the thrombolysis directly on the clot via guideline into the femoral artery
Goals:
Can we increase the time window?
Can we increase the safety? - directly at blood clot

136
Q

Describe the PROACT II trial

A

Proact II - IA thrombolysis
1999 - 180 patients intra arterial thrombolysis within 6 hours from onset
Favourable outcomes increase at 3 months
Haemorrhage rates slightly higher than placebo
No difference in mortality
Better recanalisation rates (TIMI score - measure of recanalisation)
Dosage used varied at different centres - not good

137
Q

What was the general concensus regarding the first generation mechanical devices?

A

Original devices weren’t very safe, didn’t work very well, often lead to blood clots coming away
Thrombolysis was still favoured

138
Q

Describe the IMS III study

A

IMS III study - IV and IA thrombolysis together
Better recanalisation
Mortality rates a bit lower
But study stopped early as thought they had proved it right
However 2 other trials (synthesis expansion and MR-rescue) that completed at the time found the IV and IA combination to not be of better use

139
Q

describe the MR RESCUE trial

A

MR - Rescue
8 hours post onset, thrombolysis vs endovascular therapy
Separate patients into those with penumbra and those without
Not much difference

140
Q

How did the 2nd generation devices for thrombectomy compare against 1st generations

A

2nd gen devices (solitaire is brand name) had much better outcomes than 1st gen (merci)

141
Q

Describe the MR CLEAN trial

A

MR CLEAN - IV thrombolysis + IA therapies
6 hours post onset
Had to have occlusion of major branch vessel
NIHSS score of 2 or higher - enhanced patient selection (significant deficit)
Average time between onset and groin puncture was 260
Functional independence in favour of the intervention
No difference in mortality or bleeding
Ordinal shift showed better outcomes for the more severe strokes

142
Q

Describe the EXTEND IA trial

A

EXTEND IA - IV thrombolysis vs endovascular therapies
6 hours
First trial to start using CT perfusion imaging to look at the size of core for selecting patients
Trial was stopped early because reperfusion rates were better in the IA group

143
Q

Describe the ESCAPE trial

A

IV vs IV and IA
Excluded large infarct core, used ASPECTS score to assess which patients have penumbra which is likely to have better chance for salvaging brain
Stopped early because of dramatic improvements in those with the IA therapy
Primary outcome favoured intervention
Mortality reduced
Median time from onset to reperfusion was 4 hours

144
Q

What has meta analysis of stroke treatment trials shown?

A

Overall results now in favour of thrombectomy with second generation devices.

145
Q

What does the HERMES trial, collating data from 5 stroke treatment studies conclude?

A

Across the board improvement with endovascular thrombectomy
NNT = 2.6 - more effective than IV thrombolysis
Mortality and bleeding didn’t differ
Effects favour populations of interest: older people, post 300 mins onset (later than IV thrombolysis), brain imaging will hopefully in future allow the cutoff to be less important, allowing treatment of more people, and those not eligible for IV alteplase
Trials only for anterior circulation, much more difficult to get basilar artery occlusions in studies, very different presentation

146
Q

Why does the NICE guidelines differ with regards to stroke treatment for basilar artery stroke

A

Consider thrombectomy for basilar artery clot up to 24hrs, 90% risk of death if do nothing, so very little to lose to lose
Get IV thrombolysis if eligible and also get thrombectomy if can too

147
Q

What does normal clotting depend on?

A

Virchow’s triad:
Blood coagulability
Changes in vessel wall
Changes in blood flow

148
Q

Which thrombotic disorders can cause stroke?

A

Protein C and S deficiency
Factor V Leiden deficiency
Antiphospholipid antibody syndrome

149
Q

Which bleeding disorders can cause stoke?

A

Von Willebrand disease
Haemophilia
Hereditary platelet disorders

150
Q

What types alteration in the arterial structure cause stroke?

A

Split in blood vessel
External damage - trauma that cuts across vessel or compresses
Inflammation of vessel wall
Internal blockage due to local thrombus or embolus
Infection
Toxic insults
Post radiation

151
Q

Describe the mechanisms by which vascularitis can cause stroke

A

Can get primary CNS associated vascularitis - just brain blood vessels
Autoimmune so sets of inflammation cascade which triggers thrombosis - local occlusions or disruption of the blood vessel wall which leads to hemorrhagic stroke - see both ischaemic and haemorrhagic stroke in these patients and rapid deterioration
Increase in autoimmune markers such as CSP and ESR help diagnosis of vasculitis
Particularly helpful in temporal arteritis, which presents with transient loss of vision, jaw pain, temporal artery tenderness, diagnosed with biopsy of temporal artery showing raised ESR

CSF - look at inflammatory markers in CSF

152
Q

Why is it difficult to diagnose vascularitis?

A

Difficult to make diagnosis in general - often tests are inconclusive, normally biopsied to make diagnosis elsewhere but can be patchy and also risky to biopsy in brain

153
Q

What is the primary treatment for vascularitis?

A

Primary treatment is high dose steroids initially and following cyclophosphamide

154
Q

Describe the mechanisms by which arterial dissection can cause stroke

A

Split in blood vessel wall
Cause flow to go down a false lumen and compresses actual lumen causing hypoxia
Or can cause microemboli to form on the dissection flap

155
Q

What can cause arterial dissections?

A

Can occur spontaneously or have an underlying collagen vascular disorder e.g. Erlers-Danlos syndrome
Also minor trauma - hairdressers

156
Q

How do dissections often present?

A

Often present as painful Horner’s or painful neck - urgent scanning needed to confirm dissection diagnosis and start on dual antiplatelets to prevent stroke or TIA

157
Q

What is the best treatment for dissections

A

Best treatment is disputed - used to anticoagulate but study found that anticoagulant and anti-platelet is equally effective
At three months decide if need constant anticoagulants - depends on vascular conditions, how the dissection occurred

158
Q

How can infection cause stroke in patients

A

HIV - trophic for endothelial cell, can cause inflammatory cytokines to be released, can make patients more susceptible to other infection e.g. VZV (chicken pox) which often targets MCA area.
VZV also seen in elderly patients with shingles
Primary vasculopathy
Altered lipid status
Syphilis often co-exists with HIV, but can cause stroke on its own by causing aortitis and inflammation

159
Q

How can venous sinus thrombosis present?

A

Can just present with headache or seizure or with neurological deficit

160
Q

When might you suspect venous sinus infarct

A

If the appearance of infarct looks abnormal on CT

161
Q

What are some risk factors that patients with CVT often have?

A

Infection (often of middle ear)
Thrombophilia
Chronic inflammatory conditions (IBD, lupus)
Pregnancy and shortly post-delivery
Blood disorder with hyperviscosity, polycythemia
Direct injury/trauma to venous sinuses

162
Q

How can antiphospholipid syndrome present as stroke? What is the treatment?

A

Antibodies against phospholipids
Arterial and venous thrombosis or arterial stroke
Treatment - anticoagulation, heparin and warfarin
Venous thrombosis - anticoagulants
Arterial thrombosis - no evidence for or against anticoagulants
Antibodies can be transiently upregulated in normal populations so need 3 months between blood tests for them

163
Q

How can drugs cause stroke?

A

Cocaine can cause primary vasculitis and vasospasms
Amphetamines can cause surges of BP
IV drug users can get bacterial infection from dirty needles that travel to heart - endocarditis that cause microemboli

164
Q

What is edinburgh researching with regards to drugs?

A

Edinburgh is researching a breath test to determine drug levels in A and E

165
Q

What is amyloidosis and how does it cause stroke?

A

Blood vessels with amyloid in walls are more stiff and leak easier - often lobar bleeds which tend to be peripheral and look more dramatic compared to the symptoms the patient is presenting with.
Amyloid spells - transient symptoms, can be like migraine, like seizure, tingling

166
Q

What is the UCL trial COMOS researching?

A

UCL trial (COMOS) to decide what to do in patients with AF and amyloidosis as anticoagulation may cause an increase in bleeding from amyloidosis. Think anticoagulant is still better overall though (risk of ischaemic stroke is higher than the risk of bleeding)

167
Q

Describe moya moya syndrome and how it can cause stroke

A

Premature arteriopathy affecting terminal carotids
Prominent in Asian populations
Appearance on angiograms looks like smoke as lots of collaterals are formed
These collaterals are more susceptible to bleed
Ischaemia, seizures, haemorrhage

168
Q

What treatment can be given for moya moya syndrome in children?

A

Common in children - can bypass procedures from carotid onto the surface of brain but are not funded by NICE for adults

169
Q

What are some metabolic causes of stroke?

A

Mitochondrial disease
MELAS is episodes that look like stroke due to mitochondrial dysfunction
Homocysteinuria - can cause arterial stroke

170
Q

What is Fabry’s disease? What is the treatment?

A

Results from x-linked recessive inherited deficiency of the enzyme which breaks down fatty substance which results in abnormal deposits of a fatty substance in blood vessel walls throughout the body
Enzyme replacement therapy is a treatment

171
Q

What is CADASIL? Presentation and treatment?

A

Inherited form of cerebrovascular disease which leads to accumulation of tissue under blood vessels - causes thicker and stiffer blood vessels
Presents as young onset stroke, migraine, seizures or memory
Statins, antihypertensives, antiplatelet and lifestyle changes - has an affect

172
Q

What are some common causes of endocarditis?

A

Usually bacterial infection but sometimes fungal
Dental/mouth injuries or IV drugs are common causes of introduction of bacteria/fungi
Immunocompromised have higher rate of different bugs
Valve material can break off too

173
Q

How can cancer cause stroke?

A

Induces a pro-thrombotic state

174
Q

How can stroke cause global symptoms?

A

if it affects the brainstem/thalamus or is particularly large

175
Q

Describe the study by Hand et al. in 2006 into stroke mimics

A

350 presentations in stroke clinic
Final diagnosis of stroke in 241 (69%), mimic in 109 (31%)
Predictors of mimic
Cognitive impairment
Not knowing time of onset exactly (unless sleeping)
Predictors of stroke
Precise onset of time - what exactly were they doing during it
Focal symptoms
Abnormal vascular signs - hypertensive, overweight, male
Lateralizing neurological signs
Known cause - AF, PFO, hypercoagulable

176
Q

What are some common stroke mimics

A 
Seizures - epilepsy in past medical history, positive symptoms, synchronous jerks, pins and needles, if they have extreme difficulty explaining what happened 
Sepsis 
Toxic/metabolic - renal failure 
Migraine - common one 
Space occupying lesion 
Syncope/presyncope - less so nowadays 
Acute confusional state 
Vestibular dysfunction - very uncomfortable, difficult to distinguish between peripheral or central problems 
Acute mononeuropathy 
Dementia 
Medial unexplained symptoms
177
Q

Is it safe to give thrombolysis to patients with stroke mimic?

A

RTC - 512 patients thrombolysed, 21% found not to have an infarct
No cases of intracerebral bleeding
No cases of angio-oedema
Cerebrovascular system more intact and healthier so less likely to have adverse effect

178
Q

What are some of the most common stroke chameleons?

A

Stroke in contralateral subthalamic nucleus give hemi-balismic movement which looks like acute movement disorders
Strokes of the thalamus are often missed as confused state
Bilateral frontal lobe infarct also present as confused state - aphasic symptoms often missed, receptive more often
Cortical blindness - infarct of the occipital cortex, patient can’t see but believes they can by confabulation
Rarely strokes are missed as expected seizures - normally amyloidopathy, amyloid spells of mini infarcts often give positive symptoms which are more in concurrence with seizures - find on MRI

179
Q

What investigations would be carried out in young patients/atypical stroke?

A 
Bloods
HIV and vasculitic screen
Thrombophilia screen 
Homocysteine 
Cardiac investigations
7 day Holter recorder/implantable loop recorder
Transcranial dopplers
Transoesophageal echo
Vascular imaging
CT angiography
MR angiography
180
Q

What are the pros and cons of CT in acute stroke?

A 
Pros: 
Quick 
Readily available 
Sensitive to haemorrhage 
May see a ‘hyperdense vessel’ 
Cons: 
Cannot usually diagnose an infarct in the acute phase 
Less sensitive than MRI for picking up other abnormalities (demyelination, mass lesions, microhaemorrhages) and for lacunar and posterior circulation infarcts.
181
Q

What is the needed post-thrombolysis care?

A

BP:
Monitored really aggressively if had hemorrhagic stroke but normally with ischaemic stroke allow up to 220/110
With thrombolysis 185 is the cutoff, ideally under 180 systolic
Constant vigilance for bleeding
24hr CT head to check for hemorrhagic transformation

182
Q

What are the components of a multi-disciplinary stroke team for rehab?

A 
Nurses
Physiotherapists 
OT 
Speech and language therapists 
Dieticians 
Orthoptics
183
Q

What lifestyle changes need to be made post stroke?

A 
Smoking cessation 
Drug and alcohol cessation 
Dietary modifications 
Exercise 
Driving advice
184
Q

What medical management is needed post stroke?

A

VTE assessment
Hydration
NG feeding
Spasticity – botox
Monitoring for infection
Seconardy prevention:
Antiplatelets – aspirin/ clopidogrel for life
Anticogaulation – if AF, use the HASBLED and CHADSVASC to determine risk of haemorrhage and AF stroke risk
Hypertension – target of <130/80
Cholesterol – statin therapy, aim for 40% reduction in non-HDL cholesterol

185
Q

When might surgical management be needed post stroke?

A

Extracranial carotid stenosis: 70-99% stenosis recommended carotid endarterectomy (awake during surgery to make sure don’t give another stroke), alternative if lower is cartid artery stenting
Malignant MCA syndrome – decompressive hemicraniectomy
Posterior circulation infarct:
Risk of hydrocephalus – shunt
EVD/posterior fossa decompression

186
Q

What is the definition of recovery?

A

Improvements across a variety of outcomes in performance in activity based behavioural measures

187
Q

What is the definition of rehabilitation?

A

stroke care to reduce disability and promote active particiaption in ADL, to prevent deterioration, preserve remaining function and train patients to achieve their goals

188
Q

what are the 3 key mechanisms for stroke rehab?

A

adaptation
regeneration
neuroplasticity

189
Q

What is adaptation? Give some examples

A

the reliance on alternative physical movements or devices to compensate for post stroke deficits:
• Becoming left hand dominant post stroke
• Shower chairs
• Prisms for diplopia

190
Q

What is regeneration?

A

damaged tissue grows back in the brain

191
Q

What are the inhibiting factors of regeneration?

A
  • Limited - not much neurogenesis
  • Gliosis and scarring prevent dendrites forming
  • Oligodendrocytes incomplete myelination and production of inhibitory factors
  • Low production of growth factors
192
Q

What is neuroplasticity?

A 
Neuroplasticity – the dynamic potential of the brain to reorganise itself in response to:
•	Training 
•	Injury
•	Rehabilitation
•	Pharmacotherapy 
•	Electrical and magnetic stimulation
•	Stem cell and gene therapy
193
Q

What are 4 key mechanisms in neuroplasticity?

A

Vicariation
Collateral Sprouting
Synaptic Plasticity
Diachisis

194
Q

What is vicariation?

A

When a different area of the brain takes over a function

195
Q

What is collateral sprouting?

A

reciveing new synaptic dendritic input from sprouting neurons

196
Q

What is synaptic plasticity?

A

The ability of synapses to alter their reposne to stimuli, cells that fire together wire together

197
Q

What is diaschisis?

A

A focal lesion can lead to changes in brain function far away from the lesion e.g. enhanced activity contralesional or cerebellar

198
Q

What is learned disuse phenomenon?

A

Harmful to the recovery process, this is when the patients do no use their affected limb even though they have to capacity to just because it is easier – need to still use the other hand as much as possible to keep mobile

199
Q

What are the key properties of a goal for rehabilitation

A

task specific and goal directed
challenging and interesting
allow repetition

200
Q

How can you predict stroke recovery in the upper limb?

A

based on shoulder abduction and finger extension
if present at 48hrs good outcome in 98%
If not present by day 9 only 14% good outcome

201
Q

Which out of swallowing
facial movement
language
spatial attention and gait are likely to have better outcome? Why?

A

• Bilateral represented actions have better outcome:
o Swallowing
o Facial movement
o Gait

202
Q

What hinders recovery from stroke?

A
  • Natural history of stroke recover – tends to plateau at 3-6 months
  • Depression
  • Medication – BZD
  • Comorbidities e.g. C spine disorders
203
Q

When is best to start rehab?

A
  • Early but gentle and gradual
  • Depends on severity of the stroke
  • If push too much you can increase size of stroke – animal models - NICE dont recommend immediate strong rehab.
204
Q

What evidence is there that a multi-disciplinary stroke specialist unit is better?

A

• Meta -analysis: for every 100 patients you get an extra 5 patients that reach independency in a stroke unit (save money and better for patients)

205
Q

Give 5 examples of techniques for rehab?

A

• Gait training with rhythmic acoustic pacing:
o Better stride length and speed
• Mirror therapy:
o Patient gets the visual impression that the limb in the mirror if fully functioning
• Repetitive training, aerobic exercises and muscle strength training
• Constraint induced therapy – constrain unaffected extremity to force the patient to use affected one
• Electric stimulation technique – improves motor function, portable and can be used at home

206
Q

What is a technique that can be valuable for expressive dysphasia?

A

• Melodic intonation therapy – singing and melody is in the non-dominant hemisphere, can use this to try and get reorganisation of the networks – most helpful in expressive aphasia

207
Q

What is the dysphagia? Why is it important to pick up?

A

Inability to swallow properly. Because aspiration pneumonia is the leading cause of mortality in acute stroke

208
Q

What is spatial neglect caused by?

A

Non-dominant parietal hemisphere (normally right)

209
Q

What is apraxia?

A

• Lost information about how to perform skilled movements e.g. brushing hair

210
Q

What pharamacological advances may be used post stroke?

A
  • Push for antidepressants if showing signs of depression – fluoxetine over sertraline
  • Neuromodulation improves aphasia- cholinesterase inhibitors and glutamatergic agents
  • Don’t give diazepam
  • Avoid codeine/opioids
  • Avoid dopamine blockers like typical antipsychotics
211
Q

How common is depression post stroke?

A

30%

Inhibits rehab process

212
Q

What are some treatments for spasticity post stroke?

A
  • Conservative PT and casting
  • Baclofen orally
  • Botulinum toxin
  • Intrathecal Baclofen pumps in severe spasticity (targeted with fewer SE)
213
Q

What are some recent advances in stroke rehab?

A
  • Telerehab for patients that can’t access rehab
  • Stem cells and growth factors
  • Develop biomarker to help patient tailor rehab techniques depending on stroke type
214
Q

What are the qualifying features for driving post stroke?

A
  • 4 weeks off
  • Need to see GP
  • No seizures
  • No cardiac conditions
  • Can go to functional driving assessments at specific centres

627 (10 decks)

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