Stroke Flashcards
1
Q
What are the two types of cerebrovascular accident?
A
Ischaemia or infarction of the brain tissue secondary to inadequate blood supply
Intracranial haemorrhage
2
Q
What can cause disruption of the blood supply leading to a stroke or TIA?
A
Thrombus formation or embolus, for example in a pt with AF
Atherosclerosis
Shock
Vasculitis
3
Q
What is a TIA?
A
Transient ischemic attack is transient neurological dysfunction secondar to ischemia without infarction (previously definied as symptoms of a stroke resolving within 24hrs)
They often precede a full stroke
4
Q
What is a cresendo TIA?
A
A crescendo TIA is where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.
5
Q
Presenting features of a stroke?
A
Sudden weakness of limbs
Sudden facial weakness
Sudden onset dysphasia (speech disturbance)
Sudden onset visual or sensory loss
6
Q
Stroke risk factors?
A
Cardiovascular disease such as angina, myocardial infarction and peripheral vascular disease
Previous stroke or TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
Combined contraceptive pill
7
Q
What tool is used in A&E to identify stroke and what score indicates stroke is likely
A
ROSIER anything above 0
8
Q
Mgx stroke
A
Admit patients to a specialist stroke centre
Exclude hypoglycaemia
Immediate CT brain to exclude primary intracerebral haemorrhage
Aspirin 300mg stat (after the CT) and continued for 2 weeks
Once intracranial haemorrhage excluded thrombolysis or thrombectomy
9
Q
What is used in stroke management for thrombylsis?
A
Alteplase (a tissue plasminogen activator that rapidly breaks down clots)
10
Q
When should alteplase be given by to reverse the effects of a stroke?
A
Within 4.5 hours
11
Q
What is thrombectomy?
A
Mechanical clot removal, which may be offered within 24 hours of the honest of symptoms (depending on the location) if an occlusion is confirmed on imaging
12
Q
Why should blood pressure not be lowered during a stroke?
A
Risk of reduced perfusion to the brain
13
Q
TIA management
A
Start aspirin 300mg daily.
Start secondary prevention measures for cardiovascular disease.
They should be referred and seen within 24 hours by a stroke specialist.
14
Q
What is used as secondary stroke prevention
A
Clopidogrel 75mg OD
Atorvastatin 80mg should be started but no immediatley
Carotid endarterectomy or stenting in patients with carotid artery disease
Treat modifiable risk factors such as hypertension and diabetes
15
Q
What specialist imaging can be used to establish the vascular territory involved in a stroke?
A
Diffusion weighted MRI/CT
Carotid ultrasound can be used to assess for carotid stenosis
16
Q
What is the gold standard stroke imaging?
A
Diffusion weighted MRI
17
Q
Once patients have had a stroke they require a period of adjustment and rehabilitation. This is essential and central to stroke care. Who is involved as part of the MDT?
A
Nurses
Speech and language (SALT)
Dieticians
Physiotherapy
Occupational therapy
Social services
Optometry and ophthalmology
Psychology
Orthotics
18
Q
How does an infarct appear on CT head?
A
Hypodense
19
Q
How does cerebellar dysfunction present?
A
DANISH:
Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
Ataxia (a broad-based, unsteady gait)
Nystagmus (involuntary eye movements)
Intention tremor (seen when the patient is asked to perform the ‘finger-nose test’)
Slurred speech
Hypotonia
20
Q
Causes of cerebellar dysfunction?
A
Most common: Stroke (ischemic more commonly than haemorrhagic, affecting the POSTERIOR CIRCULATION), multiple sclerosis
Other: Lyme disease, trauma to posterior fossa, alcoholism, drugs such as phenytoin or carbamazepine, primary tumors (e.g. cerebellopontine anfle tumours, acoustic neuroma), metastases - e.g. breast cancer, lunge cancer, congenital causes such as Friedrich’s ataxia, and the spinocerebellar ataxias.
21
Q
What does dysphagia suggest about the nature of a stroke?
A
Dominant cortex involvement
22
Q
Most common type of ischemic stroke?
A
Middle cerebral artery territory infarcts are the most common of the thromboembolic strokes.
23
Q
The presence of isolated monoparesis (pure motor stroke) suggests what classification?
A
Lucanr strokes (LACS)
24
Q
TACS
A
A total anterior circulation stroke (TACS) is 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 a TACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)
25
PACS
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 a PACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
*Higher cerebral dysfunction alone is also classified as PACS.
26
POCS
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 a 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
27
LACS
A lacunar stroke (LACS) is 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 a LACS:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
28
What does the ACA supply
The anterior cerebral arteries supply the anteromedial area of the cerebrum.
29
What does the MCA supply
The middle cerebral arteries supply the majority of the lateral cerebrum.
30
What does the PCA supply
The posterior cerebral arteries supply a mixture of the medial and lateral areas of the posterior cerebrum.
31
What is CPP
Cerebral perfusion pressure (CPP) drives oxygen and nutrient supply to brain tissues.
The brain can autoregulate blood flow in order to ensure constant flow that is isolated from fluctuations in systemic blood pressure.
This microcirculation is regulated by cerebral vessel constriction and dilatation.
Most of the blood within the cranial cavity is contained within the low-pressure venous system. Venous compression is the main method of displacing blood volume in the aforementioned mechanism.
This is the mechanism that is frequently lost secondary to head trauma, leading to cerebral ischaemia and neuronal death (secondary brain injury). CPP can be calculated using the following formula
CPP = MAP – ICP
32
From which arteries is the anterior circulation of the brain derived?
Internal carotid artery, left and right
33
From which arteries is the posterior circulation of the brain dervived?
Left and right vertebral arteries
34
What is the anterior circulation of the brain responsible for supplying?
Cerebrum
Opthalmic artery
35
ICA - course and branches
The left and right common carotid arteries bifurcate at the level of C3/C4 to give off the internal carotid arteries (ICA) within the carotid sheath.
The internal carotid arteries then proceed through the respective carotid canal, within the petrous portion of the temporal bone.
Once in the cranial cavity, the internal carotid arteries pass anteriorly through the cavernous sinus.
Once the internal carotid arteries are distal to the cavernous sinus, each gives rise to the following branches:
Ophthalmic artery: Supplies all the structures in the orbit as well as some structures in the nose, face and meninges.
Posterior communicating artery:
Anteriorly connects to the internal carotid artery prior to the terminal bifurcation of the ICA into the anterior cerebral artery and middle cerebral artery.
Posteriorly, it communicates with the posterior cerebral artery.
Anterior cerebral artery: Supplies oxygenated blood to most midline portions of the frontal lobes and superior medial parietal lobes.
The internal carotid arteries then continue as the middle cerebral arteries. The middle cerebral arteries supply the lateral cerebral cortex, in addition to the anterior temporal lobes and the insular cortices.
36
The left and right common carotid arteries bifurcate at what level to give off the internal carotid arteries (ICA) within the carotid sheath?
C3/C4
37
ICA segments
C1 – Cervical
C2 – Petrous
C3 – Lacerum
C4 – Cavernous
C5 – Clinoid
C6 – Ophthalmic (supraclinoid)
C7 – Communicating (terminal)
38
What is the posterior circulation responsible for supplying?
Occipital lobes
Cerebellum
Brainstem
39
Vertebral arteries - course and branches
The left and right vertebral arteries arise from their respective subclavian arteries, on the posterosuperior aspect.
The vertebral arteries then proceed to enter the transverse foramina of the spine at level C6 and continue superiorly.
After passing through the transverse foramen of C1, the arteries traverse the foramen magnum.
Once inside the cranial vault, the vertebral arteries give off the following branches:
Posterior inferior cerebellar artery (PICA) – this is the largest branch of the vertebral artery and is one of three main arteries supplying the cerebellum
Anterior and posterior meningeal arteries – supply the dura mater
Anterior and posterior spinal arteries – supply the spinal cord along its entire length
The vertebral arteries then converge to form the basilar artery at the base of the pons, inside the cranium.
40
Segments of the vertebral artery
V1 – preforaminal
V2 – foraminal
V3 – atlantic, extradural, or extraspinal
V4 – intradural, intracranial
41
Basilar artery: course and branches
The basilar artery runs superiorly within the central groove of the pons, giving off a number of branches including the pontine arteries, which supply the pons.
The basilar artery eventually anastomoses with the circle of Willis via the posterior cerebral arteries and posterior communicating arteries.
42
Locked in syndrome
Pontine infarcts cause an interruption in the myriad of neuronal pathways enabling communication between the cerebrum, cerebellum and spinal cord. This can result in complete paralysis of all voluntary muscle groups, sparing those controlling the eyes. Individuals suffering from damage to the pons are fully conscious and cognitively intact.
43
Circle of Willis
the terminal branches of the anterior and posterior circulation form an anastomosis to create a ring-like vascular structure known as the circle of Willis, within the base of the cranium (highlighted in pink below).
The left and right internal carotid arteries continue as the middle cerebral arteries (MCA), after each giving off a branch to supply the anterior cerebral arteries (ACA). The anterior communicating artery links the two anterior cerebral arteries together.
The internal carotid arteries also give off the posterior communicating arteries (PCoA), linking the middle cerebral arteries (MCA) with the posterior cerebral arteries
44
Berry aneurysms in the circle of Willis are a common cause of non-traumatic subarachnoid hemorrhage - how are they managed?
45
An anyeurysm where is associated with CN3 nerve palsy?
The third cranial nerve is commonly affected by aneurysms in the circle of Willis, particularly those involving the posterior communicating artery (PoCA) due to its close anatomical relationship.
46
CN3 palsy - medical vs surgical?
Clinically, “surgical” third nerve palsy can be differentiated from “medical” third nerve palsy by evidence of pupillary involvement.
External compression of the third nerve affects parasympathetic fibres surrounding the outermost region of the third nerve. This compression results in an inability to constrict the pupil, making it appear fixed and dilated (often referred to as a ‘blown pupil’).
“Medical” third nerve palsy results from involvement of the vaso vasorum, which is involved in supplying the central area of the third cranial nerve. This results in pupillary involvement arising much later. Common causes of “medical” third nerve palsy include those affecting microvasculature, such as diabetes and atherosclerosis.
47
Most common causes of large artery occlusion (ie. TACS, PACS)
The two most common causes of large artery occlusion are cardioembolic (e.g. from AF), or plaque embolization (e.g. from significant carotid disease).
48
What test rules out carotid artery disease as a cause of stroke?
Carotid dopplers
In this case, carotid dopplers were normal, this rules out carotid artery disease, as you would still be able to see a ruptured plaque had that embolised previously.
49
Where is Wernicke's area located?
Left temporal lobe
50
Damage to Wernicke's area results from occlusion of which artery?
MCA
51
Consequence of damage to Wernikes area
Damage caused to Wernicke's area results in receptive, fluent aphasia. This means that the person with aphasia will be able to fluently connect words, but the phrases will lack meaning. This is unlike non-fluent aphasia, in which the person will use meaningful words, but in a non-fluent, telegraphic manner.
52
What is receptive aphasia and what causes it?
Patients will not be able to respond to questions asked of them and will respond with fluent sentences that do not make sense
Patients are not aware that their speech does not make sense
Patients will be repetitive in their speech
Damage to Wernicke's area - area located in the left temporal lobe and is responsible for the ability to understand speech. It is supplied by the left middle cerebral artery and therefore strokes that affect this vascular territory can result in receptive aphasia.
53
Where is Broca's area and what is it involved in?
The left frontal lobe is the location of Broca's area, which is involved in the expression of speech (written and spoken word).
Damage to Broca's area results in expressive aphasia, in which the patient can understand speech but is unable to communicate their own thoughts.
54
What is expressive aphasia and what causes it?
Damage to Broca's area results in expressive aphasia, in which the patient can understand speech but is unable to communicate their own thoughts.
Non fluent type
MCA stroke
55
What do strokes affecting the left occipital lobe typically cause and why?
The right occipital lobe is involved in the processing of visual stimuli and strokes affecting this region would typically result in isolated homonymous hemianopia.
56
Lesion of left vs right hemisphere
As a general rule, a lesion of the left hemisphere will cause dysphasia whilst, in the right hemisphere, it will cause neglect, visuo-spatial and cognitive problems.
(99% right handed patients and 30% left handed)
57
Alteplase is recommended for treating acute ischaemic stroke in adults in what circumstances?
Alteplase is recommended for treating acute ischaemic stroke in adults if:
treatment is started as soon as possible within 4.5 hours of the onset of stroke symptoms and
intracranial haemorrhage has been excluded by appropriate imaging techniques
58
Management of warfarin-associated intracerebral haemorrhage?
Immediate warfarin reversal with prothrombin complex concentrate is required to limit haematoma expansion, which is also associated with a poor prognosis.
59
ACA stroke: presentation and explanation
An anterior cerebral artery stroke is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel:
the medial aspects of the frontal and parietal lobes,
basal ganglia, anterior fornix and anterior corpus callosum.
This comprises 2% of ischaemic strokes.
This causes contralateral motor and sensory loss, involving primarily the lower limbs and pelvic floor muscle/perineum (sparing the face and upper limbs), apraxia (individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task), behavioral issues (frontal cortex), anosmia etc.
60
Symptoms of ACA stroke
Contralateral motor and sensory loss, involving primarily the LOWER LIMBS, PELVIC FLOOR MUSCLES, PERENIUM (sparing the face and upper limbs),
Apraxia (individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task),
Behavioral issues (frontal cortex),
anosmia etc.
61
What is Wallenberg’s syndrome?
This is caused by injury to the lateral part of the MEDULLA OBLONGATA
It causes a range of symptoms, but typically
ipsilateral cranial nerve involvement (loss of facial sensation and dysphagia),
with contralateral sensory loss to the limbs and trunk.
Damage to the hypothalamospinal fibres can cause an ipsilateral Horner’s syndrome-like picture (ptosis and miosis).
62
What is West's syndrome charecterised by?
West’s syndrome is characterised by ipsilateral oculomotor nerve palsy and contralateral weakness.
63
What is Brown-Sequard syndrome
Brown-sequard syndrome is caused by damage to one half of the spinal cord. It results in paralysis and loss of proprioception on the same (ipsilateral) side as the injury, and loss of pain and temperature sensation on the opposite (contralateral) side to the lesion.
64
What is Gerstmann's syndrome?
Gerstmann’s syndrome is caused by a dominant middle cerebral artery stroke, with weakness, sensory loss, hemianopia and aphasia.
65
MCA stroke - presentation and explanation
The middle cerebral artery supplies the majority of the lateral surface of the cerebral hemisphere.
Infarction leads to contralateral hemiplegia and hemiparesis mainly of the face and upper limb,
in addition to contralateral homonymous hemianopia.
Global aphasia can occur if the stroke affects the dominant hemisphere.
66
MCA vs ACA - distribution of weakness
ACA - lower limb
MCA - upper limb and face
67
How would a basilar artery occlusion present?
Occlusion of the basilar artery would cause, vertigo, ataxia, bilateral motor and sensory dysfunction, lower cranial nerve deficits and impaired consciousness.
68
Posterior cerebral artery occlusion
The posterior cerebral artery supplies the occipital lobe. Occlusion typically leads to homonymous hemianopia with macular sparing, and the patient may have difficulty in naming objects.
69
What should immobile stroke patients be offered as VTE prophylaxis
Based on Royal College of Physicians guidance, patients with immobility after acute stroke should be offered intermittent pneumatic compression (IPC - e.g. Flowtrons) within 3 days of admission to hospital for the prevention of deep venous thrombosis (DVT). IPC should be continued for 30 days or until the patient is mobile or discharged.
70
What is lateral medullary syndrome, what might cause is and how might it present?
a clinical entity arising from the infarction of a portion of the medulla oblongata.
The most common cause is an occlusion of the posterior inferior cerebellar artery which supplies this part of the brain, although other rarer causes of stroke (carotid artery dissection, vasculitis etc...) are also possible.
The condition results in a complex neurological presentation due to the many functions of the medulla:
-Ipsilateral Horner's syndrome (miosis, ptosis, anhidrosis)
-Ipsilateral loss of pain and temperature sensation on the face
-Contralateral loss of pain and temperature sensation over the contralateral body.
-Hiccups
-Past finger pointing
-Nystagmus
71
What post thrombylsis complications should patients be monitored for?
Intracranial hemorrhage
System hemorrhage
72
When should a vascular cause of neurological symptoms be suspected?
Sudden onset of symptoms
73
What is a cryptogenic stroke?
A stroke of unknown cause is called a “cryptogenic stroke. ... It's estimated that about 1 in 3 ischemic strokes are cryptogenic.
74
A PACS typically presents from what aetiology
Embolism
75
Fibrinolytic necrosis can be suspected in hypertensive or diabetic patients presenting with what type of stroke?
LACS
76
What aetiology might you suspect in the pregnant stroke patient or the patient with a history of venous thromboembolism (VTE), multiple miscarriages or active cancer
Underlying thrombophillia
77
What does watershed ischaemia on neuro imaging suggest about the aetiology of a stroke?
Carotid disease, or intracranial stenosis
78
What does an embolisation pattern of ischema on neuro imaging suggest about the aetiology of a stroke?
cortical infarcts from distal vessel hypoperfusion
79
What does cardio-embolisation pattern of ischema on neuro imaging suggest about the aetiology of a stroke?
multifocal/bilateral embolic infarcts
80
What does lacunar topography seen on pattern of ischema on neuro imaging suggest about the aetiology of a stroke?
lacunar infarction, which is usually <15mm in size
81
Deep vs lobar bleeds - primary or secondary?
Deep bleeds are typically primary due to hypertension. Lobar bleeds tend to be secondary
82
Why might a lobar bleed occur
Secondary causes
Causes include underlying vascular anomalies, mass lesions, and cerebral amyloid angiopathy. Venous infarction is worth considering in some cases of lobar haemorrhage. Interval imaging is sometimes required to clarify the cause of haemorrhage. Appraisal of stroke aetiology has major implications in
83
A strategy of anticipation (to pre-empt preventive measures) and surveillance (to allow early recognition and intervention) is central to the management of stroke patients, what does routine review include?
Routine review of EWS (early warning score) observations, mood, bowel & urine function, progress of stroke impairments, sleep, legs/calves (?DVT) and monitoring bloods should be part of this surveillance.
84
What is extension of a stroke?
Extension of stroke is due to loss of the ischaemic penumbra resulting from suboptimal physiology
85
Why might raised intracranial pressure occur in a stroke patient?
This can be due to haematoma expansion, malignant oedema, haemorrhagic transformation or hydrocephalus
86
Potential stroke complications?
Raised intracranial pressure
Recurrent stroke
Extension of stroke
Infections
Complications of immobility
Mood and cognitive dysfunction
Post stroke pain and fatigue
Spasticity, contractures and secondary epilepsy
Disability
Death
87
What are the interventions used to manage stroke?
Admission to the stroke unit
Revascularisation therapy
Optimising physiology (via surveillance, prevention and early intervention of
complications) and nutritional support
Secondary prevention
Rehabilitation and reablement
88
Stroke prognosis can be guided by recovery trajectories. What time Broadly speaking recovery trajectories and their corresponding functional plateaus can be divided into three groups into groups?
* Early, high functioning plateau – the extreme version of this is a TIA or minor stroke,
signifying excellent functional prognosis.
* Early, low functioning plateau – the extreme version of this is a TACS with no
meaningful improvement in function as time passes, signifying poor functional
prognosis.
* Delayed and medium functioning plateau – this will likely define recovery in most
moderate strokes. These patients will benefit from a chance at sustained rehabilitation
efforts until a functional plateau is achieved.
89
Revascularisation therapies and relevant investigations are CT scan, CT angiogram and associated assessment tools
Modalities are IV alteplase and mechanical thrombectomy.
IV alteplase applies to non-contraindicated patients with disabling stroke presenting within 4.5 hrs.
Mechanical thrombectomy applies for patients with large vessel occlusion (LVO) and should be executed within 6 hrs of symptom onset.
Relevant investigations are CT scan, CT angiogram and associated assessment tools include FAST test, NIHSS, mRS (modified Rankin score) and ASPECTS score
90
Decompressive Hemicraniectomy (DHC)
Indicated for the management of malignant oedema in younger (<60 yrs. old) but can
be considered in otherwise biologically fit stroke patients above this cut off. Referrals
to neurosurgical units should be made within 24 hrs and surgery completed within 48
hrs. The procedure in most cases preserves life in the context of significant dependency
30 by virtue of being required in patients with major strokes.
91
Interventions for intracerebral haemorrhage (ICH)
Development of raised intracranial pressure is the most worrisome concern in ICH (and
the reason for the higher early mortality relative to ischaemic stroke. This can be due
to haematoma expansion or hydrocephalus. Non-surgical strategies to address this are
blood pressure control and correction of clotting abnormalities. Evacuation of
haematoma and ventricular drains are surgical options in selected patients.
92
Antithrombotic therapy (Anticoagulation and antiplatelet therapies)
* Anticoagulation options include iv or subcut heparin, warfarin, and direct oral
anticoagulants (DOACS). Applies in patients with AF, severe left ventricular
dysfunction, thrombophilia, and venous sinus thrombosis. Relevant investigations are
ECG, MRV/CTV, Holter monitor, Echocardiogram, and thrombophilia screening. Risk
stratification for primary prevention in AF utilises CHA2DS2VASc and HASBLED tools.
Remember patients with high HASBLED scores (whose impact can be modified) are
usually also the most to gain from anticoagulation.
* Immediate administration of antiplatelet agent is standard practice in all suspected
TIAs, on confirmation of ischaemic stroke and 24 hrs after thrombolysis. See CEA
section for role of dual antiplatelet therapy.
93
Carotid endarterectomy (CEA)
Mainstay intervention for managing symptomatic carotid disease (after TIA or stroke
with good recovery) of more than 50% (NASCET method) lumen reduction on carotid
ultrasound.
Surgery is scheduled as soon as possible following symptoms.
Reduction of recurrent stroke is optimised by aggressive medical therapy (BP control [<130/80], high dose statin therapy, and dual antiplatelet therapy) before surgery or if surgery not an
option.
The latter strategy aims to achieve “plaque stabilisation”.
The unstable plaque serves as embolic source and facilitates acute stroke in carotid disease.
Selected patients can be considered for surgery outside of symptomatic carotid disease.
94
Optimisation of vascular risk factors
Applicable are smoking cessation, maintaining average BP <130/80, glycaemic control
to HbA1c<7, total cholesterol <4 and LDL cholesterol <2 and weight loss towards BMI
25 and promotion of exercise. Weight loss (emphasizing reduction in “visceral” fat)
becomes even more important for those patients satisfying the criteria for metabolic
syndrome. This can be complicated by obstructive sleep apnoea, which is an independent vascular risk factor.
95
Left atrial appendage closure
This is an option for stroke secondary prevention in patients with AF in whom anticoagulation is contraindicated.
96
Nasogastric and PEG (Percutaneous endoscopic gastrostomy) tube feeding
Nutritional support is important for recovering stroke patients. In the majority of
stroke patients with unsafe swallow function, tube assisted enteral feeding is
temporary pending return of safe swallow function. In addition to bedside
assessments, swallowing can be assessed instrumentally with Video fluoroscopy and
Flexible endoscopic evaluation of swallowing (FEES). Commencement (or prolonged
use) of parenteral feeding is best avoided in patients at the end of life. Such patients
are subjected to the risks of tube feeding without any meaningful gains in the goals of
minimising symptoms, improving quality of life, and preventing death.
97
What does stroke rehabilitation involve
This is a goal-oriented exercise.
Mobility, ADL (activities of daily living), speech and cognitive therapy are the mainstays of stroke rehabilitation.
Other interventions in the rehabilitation setting include those for managing spasticity (including orthotic prostheses and botulinum toxin therapy), and environmental modifications
98
What is the National Institutes of Health Stroke Scale (NIHSS)?
The NIHSS is a systematic assessment tool that provides a quantitative measure of stroke-related neurologic deficit.
Used in assessing stroke severity, patient selection for various acute therapies, estimating prognosis and charting stroke recovery.
99
What is The Alberta Stroke Programme early CT score (ASPECTS)?
ASPECTS is a 10-point quantitative topographic CT scan score used in patients with middle cerebral artery (MCA) stroke.
Segmental assessment of the MCA vascular territory is made, and 1 point is deducted from the initial score of 10 for every region involved.
Used in revascularisation therapies for patient selection and outcome prediction.
100
What is the Modified Rankin Scale?
measure of global disability used to assess baseline function and evaluate outcomes and treatment impact after interventions
0 - No symptoms.
1 - No significant disability. Able to carry out all usual activities, despite some symptoms.
2 - Slight disability. Able to look after own affairs without assistance, but unable to
carry out all previous activities.
3 - Moderate disability. Requires some help, but able to walk unassisted.
4 - Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk without assistance.
5 - Severe disability. Requires constant nursing care and attention, bedridden, incontinent.
6 – Dead.
101
CHA2DS2-VASc and HAS-BLED tools to guide anticoagulation in patients with AF
102
TOAST classification
The TOAST classification denotes five subtypes of ischemic stroke:
1) large-artery atherosclerosis,
2) cardioembolism,
3) small-vessel occlusion
, 4) stroke of other determined etiology, and
5) stroke of undetermined etiology
103
TOAST stroke classification
Large-arteryatherosclerosis(embolus/thrombosis)
Cardioembolism (high-risk/medium-risk)
Small-vessel occlusion (lacune)
Stroke of other determined etiology
Stroke of undetermined etiology
- Two or more causes identified
- Negative evaluation
- incomplete evaluation
104
Toast classification - large artery sclerosis
Clinical: signs of lesion in cortex (aphasia, apraxia, neglect), subcortex, cerebellum, or brainstem
Radiological: CT/MRI shows lesion >1.5cm in cortex, subcortex, cerebellum, or brainstem. CT scan negative when performed shortly after onset
Other: Color duplex images of precerebral arteries shows stenosis is greater than or equal to 50% or occlusion in symptomatic major intracranial extra cranial artery
105
Toast classification - cardioembolic
Clinical: signs of lesion in cortex (aphasia, apraxia, neglect), subcortex, cerebellum, or brainstem
Radiological: CT/MRI shows lesion >1.5cm in cortex, subcortex, cerebellum, or brainstem. CT scan negative when performed shortly after onset
Other: ECG/TTE confirm high risk of cardioembolic source
106
TOAST classification - small vessel disease
Clinical: clinical signs of lacunar syndrome (pure motor, pure sensory, sensorimotor, ataxic hemiperisis or dysarthria-clumsy hand syndrome)
Radiological: CT/MRI shows lacunar infarction (lesion <1.5cm) compatible with the symptoms.
CT scan negative with performed shortly after onset
Other: no large vessel disease or cardioembolic disease dentifrice in colour duplex images of pre cerebral arteries or in ECG/TTE
107
What is the ABCD2 score risk assesment
ABCD2 score for stroke risk assessment after a TIA
High risk groups (ABCD2>4, multiple TIAs
[>2 in previous 7 days], patients in AF or
on anticoagulants) will require urgent
review, i.e. within 24 hrs
In principle all TIA patients should be
seen urgently wherever possible since as
noted earlier the TIA scenario is loaded
with opportunities for secondary
prevention when a TIA is diagnosed
108
Example of stroke mimics readily recognised on imaging?
brain space occupying lesions,
MS,
subdural haematoma
109
Examples of stroke mimics that that have distinct non-stroke syndrome features which allow a secure diagnosis on clinical grounds
BPPV
Vestibular neuornitis
Syncope syndrome
Transient global amnesia
110
Stroke mimics where recognition is also clinical but features can be subtle and justify specialist assessment including clinical opinion and additional investigations e.g. MRI scan for prolonged (> 1 hr) episodes, EEG.
Complicated migraine with aura
Focal seizure
Functional syndrome
Amyloid spells
111
What is meant by “apparent neurological deficit”
This refers to neurological dysfunction in patients with chronic stroke (but seemingly good recovery) and residual areas of scar tissue (gliosis) at the site of previous brain damage. Symptoms can return (i.e. become “apparent”) due to underperformance of the gliotic tissue in the context of suboptimal physiology as in infection, low blood pressure, hypoglycaemia, hypoxia, fatigue etc. Correction of the culprit disturbance applies, with return of baseline function.
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Neuro imaging in stroke
Non contrast CT
MRI
Comprehensive (“multimodal”) brain imaging may also involve angiography and perfusion studies
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Why are effacement and loss of grey/white matter distinction seen on neuro imaging in cerebral ischemia
Ischemia
Failure of membrane transport
Consequent intracellular fluid and electorlyte shift
Brain cell swelling
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Hallmarks of early cerebral ischemia on CT scan?
Effacement
Loss of grey/white matter distinction
Increased density of the relevant blood vessels (due to the presence of clotted blood)
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Hallmark of intracranial haemorrhage
Area of increased attenuation
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Hypertensive bleeds tend to be shallow or deep?
Deep
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Do hypertensive bleeds benefit from surgery
Not usually, unless there is a presence of hydrocephalus
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Causes of peripheral/lobar haemorrhage
Underlying tumour
Vascular abnormality
Vascular degeneration (e.g. cerebral amyloid angiopathy)
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Ischemic stroke can appear normal on CT - why is it still performed
Rule out haemorrhagic stroke
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Timeline of IV alteplase for stroke thrombolysis
Within 4.5 hours of onset of symptoms
Initial bolus
One hour IV infusion
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Aspirin and clopidogrel in secondary stroke prevention
2 weeks aspirin:
- If hyper-acute treatments are not offered, patients should receive aspirin 300 mg orally once daily for two weeks.
- If hyper-acute treatments are offered, aspirin is usually started 24 hours after the treatment following a repeat CT Head that excludes any new haemorrhagic stroke.
Then switch to clopidogrel long term (risk of haemorrhagic transformation)
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Risk factors for haemorrhagic stroke
Increasing age
Male sex
Family history
Haemophilia
Cerebral amyloid angiopathy/hypertension
Anticoagulation therapy
Sympathomimetic drugs (cocaine, amphetamines)
Vascular malformations (particularly in younger patients)
Weaker risk factors: NSAID use, heavy alcohol use, thrombocytopenia
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Why might a patient with a haemorrhagic stroke require ICU input
May require intubation
May require invasive monitoring of ICPs
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To avoid poorer outcomes, under what BP should be aimed in a patient with a haemorrhagic stroke?
Under 140/80
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Causes of ischemic stroke (in order of how common to rare they are)
(Most common to least common)
1. Large vessel atherosclerosis (e.g. carotid artery stenosis) ~ 50%
2. Intracranial Small Vessel Atherosclerosis ~ 25%
3. Cardioembolic (AF) ~ 20%
4. Primary vascular causes (vasculitis, arterial dissection) ~ rare
Haematological causes (prothrombotic states) ~ rare
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Briefly describe the most common pathological process leading to ischemic stroke
Atherosclerosis of large vessel (e.g. carotid artery)
Thrombus formation of atherosclerotic plaque
Subsequent embolism of thrombus to smaller cerebral artery
Occlusion of the cerebral artery leading to cerebral ischemic and then infarction
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How can atrial fibrillation lead to a stroke?
Disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node
Uncoordinated, irregular and rapid contraction of atria
Stasis of blood flow in the left atrium
Predisposes to thrombus formation in the left atrium
Subsequent embolisation to the brain
Occlusion of cerebral arteries
Cardioembolic ischemic stroke
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Ischemic stroke - post-acute investigations
Carotid ultrasound (to identify critical carotid artery stenosis)
CT/MR angiography (to identify intracranial and extracranial stenosis)
Echocardiogram (if a cardio-embolic source is suspected).
In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.
Further investigations to quantify vascular risk factors include:
serum glucose (all patients with stroke should be screened for diabetes with a fasting plasma glucose or oral glucose tolerance test),
serum lipids (to check for raised total cholesterol/LDL cholesterol).
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When investigating post-acuteley in a patient who has had a haemorrhagic stroke, what screen might you perform and why?
Serum toxicology screen (sympathomimetic drugs e.g. cocaine are a strong risk factor for haemorrhagic stroke)
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Stroke management (chronic) - HALTSS
H- HYPERTENSION
A- ANTIPLATELET THERAPY patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
L-LIPID LOWERING THERAPY patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
T-TOBACCO offer smoking cessation support.
S- SUGAR screen for diabetes and manage appropriately
S- patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy
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When should patients with ipsilateral carotid artery stenosis be referred for surgery - and which surgery should they be referred for?
Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
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Post ischemic stroke pharmacological therapies (x3)
1. Antiplatelet therapy:
ASPIRIN
Aspirin 300mg for two weeks - if hyperacute treatment has been offered then commence after 24 hours following treatment - following a repeat CT Head that excludes any new haemorrhagic stroke. If hyperacute treatment wasn't offered commence straight away.
CLOPIDOGREL
Patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy following 2 weeks of aspirin therapy.
2. Anticoagulant therapy:
DOAC or WARFARIN
In patients with ischemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
3. Lipid lowering therapy:
STATIN
Patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
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What is the most sensitive test for confirming ischemic infarct? Why might it be used/not used?
The most sensitive test for confirming ischaemic infarct is a diffusion weighted MRI.
This is generally used if the diagnosis is unclear but is
not normally possible in the emergency setting due to logistical challenges.
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How should statins be prescribed post ischemic stroke?
Atorvastatin 20-80 mg once nightly
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How should clopidogrel be prescribed post ischemic stroke?
75mg OD
To be commenced following 2 weeks of therapy with 300mg aspirin OD
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Which patients might be suitable for mechanical thrombectomy and under which timeframe?
Mechanical Thrombectomy can be performed in patients with anterior circulation strokes within 6 hours of symptom onset, provided that they have a good baseline functional status and lack of significant early infarction on initial CT scan.
Mechanical Thrombectomy can also be performed in posterior circulation strokes up to 12 hours after onset.
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Thrombolysis contraindications
Recent head trauma
GI or intracranial hemorrhage
Recent surgery
Systolic blood pressure (BP) of more than 185 mmHg on presentation
Diastolic blood pressure of over 110 mmHg on presentation
History of chronic, severe, or poorly controlled HTN
Platelet count (<100 000/mm 3)
INR >1.7
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Posterior Stroke Syndromes
Locked in syndrome
Lateral pontine syndrome
Wallenberg's syndrome (lateral medullary syndrome)
Weber's syndrome/medial midbrain syndrome
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What complications/syndromes are more likely to present in a patient who has suffered occlusion of the basilar artery?
Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death
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What is locked in syndrome?
Quadriparesis with preserved consciousness and ocular movements
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What is Weber's syndrome/medial midbrain syndrome?
Weber's syndrome/medial midbrain syndrome is a posterior stroke syndrome
Occlusion of paramedian branches of the upper basilar and proximal posterior cerebral arteries)
Causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.
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Occlusion where can cause an ipsilateral oculomotor nerve palsy and contralateral hemiparesis? What is this known as?
Paramedian branches of the upper basilar and proximal posterior cerebral arteries
Weber's syndrome/medial midbrain syndrome
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Occlusion of which artery can cause lateral medullary syndrome (Wallenberg's syndrome)
Posterior inferior cerebellar artery
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Pupil changes in horners syndrome?
anisocoria - unequal pupils
miosis of affected pupil - small pupil
