Cerebrovascular Disease & Stroke Flashcards
Deck copied directly from N&SS (with few added cards)
What else are strokes known as?
Cerebrovascular accidents
Remind yourself of the CHA2DS2VASc score
Calculates stroke risk for patients with atrial fibrillation
Remind yourself of the HASBLED score
Estimates risk of major bleeding for patients on anticoagulation to assess risk-benefit in atrial fibrillation care.
State some common stroke mimics
Stroke mimic is when pt presents with stroke-like symptoms but have alternative diagnosis e.g.
- Seizures
- Syncope
- Migraine with aura
- Bell’s palsy
- SOL
- Sepsis
- Hypoglycaemia
- Vestibular causes (e.g. vestibular neuronitis, BPPV etc..)
- Functional
NOTES from lecture:
Group 1 are readily identifiable with standard imaging. These include subdural haematomas, brain tumours, multiple sclerosis (MS), brain abscesses etc.
Group 2 are syndromically distinguishable from the stroke syndrome on clinical grounds after medical assessment. Examples include syncope syndrome, benign positional vertigo, vestibular neuronitis, transient global amnesia, Bell’s palsy etc. These “mimics” hugely benefit from a competent first assessment that allows clinical exclusion of stroke, reassurance where possible and institution of appropriate management.
Group 3 requires specialist stroke assessment including brain imaging to exclude the stroke syndrome. From time to time the difference with stroke syndrome can be finely balanced for all sorts of reasons. Included in this group are probably the commonest stroke mimics e.g. migraine with aura, focal seizures and functional syndrome. These are discussed further in a later slide.
For migraine with aura, discuss:
- Physiology behind migraine with aura (hint: key phrase)
- How it may present
The aura of migraine is physiologically characterised by cortical spreading depression (CSD) or aura activity. This nicely explains the typically gradual onset, migratory and sequential onset of migraine aura symptoms. Unlike in a TIA (where cessation of action potential activity applies), CSD involves altered but continuing brain cell activity. To a degree this explains the preponderance of “positive” symptoms as part of migraine aura.
In addition to looking for evidence of sequential onset, it is worth routinely looking for evidence of migration in all suspected stroke symptoms especially for visual and sensory disturbance. Please note headache may be absent or minimal in migraine episodes.
Although visual aura (occipital lobe) are commonest, other auras are possible and are explained by the brain location undergoing aura activity e.g. dysphasia and tinnitus (temporal lobe), pins and needles/transient cognitive disturbance (parietal lobe), unsteadiness/dizziness/collapse/hemiparesis (cerebellum, brainstem etc).
Trigger profile is worth exploring for those migraine patients with recurrent auras (and frequent attenders).
Define a stroke
- Stroke is a clinical syndrome of presumed vascular origin characterized by rapidly developing signs of focal or global disturbance of cerebral functions which lasts longer than 24 hours or leads to death. (CKS NICE)
- Neurological deficit lasting more than 24hrs caused by cerebrovascular aetiology (BMJ)
- Serious life threatening condition in which blood supply to part of brain is disrupted. Symptoms persist for more than 24 hours
Briefly outline pathophysiology of strokes (cellular level)
- “Dysfunction of neurovascular unit”
- Hypoperfusion leads to depletion of ATP
- Impairment of energy dependent cell processes
- Of the energy dependent cell processes that are impaired, impairment of membrane transport is responsible for stroke symptoms
- Impaired membrane transport → impaired generation of action potentials
- Action potentials are an example of binary system (on or off)
- Once available ATP in vascular territory drops below the threshold that can sustain action potential activity there is a phase transition from AP activity to AP cessation and subsequent absence of neuronal tramission
State, and describe, the two main types of stroke (include what % of strokes each accounts for) and any subtypes of each
-
Ischaemic stroke (85%)
- Thrombotic
- Embolic (important cause to remember is AF)
- Systemic hypoperfusion (e.g. due to cardiac arrest)
- Cerebral venous sinus thrombosis (causes back pressure which reduces perfusion)
-
Haemorrhagic stroke (10%)
- Intracerebral
- Subarachnoid
What are some key questions you must ask yourself when caring for a potential stroke pt? (Questions will help guide your management)
- Is it a stroke?
- What is the cause?
- Are they are complications or any likely complications?
- What treatment/intervention & information does the patient need & when?
- How well is the patient likely to do?
- When can they safely leave our care?
Comparison of ischaemic and haemorrhagic strokes
Remind yourself of the blood supply to the brain
- Anterior cerebral artery: medial aspect of frontal lobe, medial aspect of parietal lobe, corpus callosum
- Middle cerebral artery: lateral parts of frontal & parietal lobe, superior temporal lobe, deep grey matter structures via lenticulostriate arteries
- Posterior cerebral artery: occipital lobe, inferior temporal lobe, thalamus, midbrain
-
Cerebellum:
- Superior: superior cerebellar artery
- Anterior inferior: anterior inferior cerebellar artery
- Posterior inferior: posterior inferior cerebellar artery
-
Brainstem:
- Midbrain: superior cerebellar artery & branches from PCA
- Pons: anterior inferior cerebellar artery & pontine arteries from basilar artery
- Medulla: posterior inferior cerebellar artery
State some risk factors for ischaemic strokes
- Increasing age
- Previous stroke or TIA
- Cardiovascular disease
- Hypertension
- Smoking
- Hyperlipidaemia
- Diabetes
- AF (for embolism)
- Carotid artery disease
- Vasculitis
- Thrombophilia
- COCP
State some risk factors for haemorrhagic strokes
- Increasing age
- Hypertension
- Anticoagulation
- Coagulation disorders
- AV malformations
State some characteristics of stroke syndrome
- Sudden onset
- Focal
- Predominantly negative
- Set of symptoms should fit into a vascular territory
Outline possible features of a stroke
Sudden onset of:
- Weakness of limbs
- Facial weakness
- Dysphasia
- Visual disturbance
- Sensory disturbance
- Balance problems
Symptoms & signs depend on where in brain the stroke is
What is stereotyping?
Stereotyping over weeks, months and years is a strong indicator of…?
- Stereotyping is the episodic recurrence of neurological disturbance in an identical fashion with complete resolution in between
- Strong indicator of stroke mimics (however, stereotyping can also occur in stroke syndromes e.g. capsular warning syndrome)
State some potential sites of strokes and features of each
- Lacunar strokes: stroke affecting lenticulostriate arteries supplying deep grey matter structures e.g. basal ganglia, thalamus, internal capsule. Strong association with hypertension. Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
Ischaemic strokes can be classified using two systems/classifications; state these
- Oxford Community Stroke Project classification system (also known as the Bamford or Oxford classification): classifies based on symptoms
- TOAST Classification: classifies based on pathophysiology
State the classes of stroke based on the Oxford/Bamford stroke classification
- Total anterior circulation infarct (TACI) 15%
- Partial anterior circulation infarct (PACI) 25%
- Posterior circulation infarct (POCI) 25%
- Lacunar infarct (LACI) 25%
For a total anterior circulation infarction (TACI), discuss:
- Which artery commonly involved
- Features
- Middle & anterior cerebral arteries resulting in large cortical stroke
-
ALL THREE OF THE FOLLOWING:
- Unilateral hemiparesis and/or hemisensory loss of face, arm & leg
- Homonymous hemianopia
- Higher cognitive dysfunction (e.g. dysphasia, neglect/inattention, visuospatial abnormalities)
For a partial anterior circulation infarct (PACI), discuss:
- What artery usually involved
- Features
- Only part of anterior circulation compromised e.g. could be upper or lower division of MCA
-
TWO OF THE FOLLOWING MUST BE PRESENT:
- Unilateral hemiparesis and/or hemisensory loss of face, arm & leg
- Homonymous hemianopia
- Higher cognitive dysfunction (e.g. dysphasia)
- OR higher cerebral dysfunction alone
- OR a motor/sensory deficit more restricted than those classified as LACI (e.g. confined to one limb)
For a lacunar infarct (LACI), discuss:
- Which artery commonly involved
- Features
- Subcortical stroke due to small vessel disease involving perforating/lenticulostriate arteries (which supply deep grey matter structures e.g. internal capsule, thalamus, basal ganglia)
-
ONE OF THE FOLLOWING:
- Unilateral weakness and/or sensory deficit of face & arm, arm and leg or all three
- Pure sensory stroke
- Ataxic hemiparesis
- NOTE:for a LACS motor and/or sensory must involve at least 2 contiguous areas or all three (e.g. face/arm/leg or face/arm or arm/leg). If distribution is restricted to one somatic area (e.g. face or arm or leg) then it is a PACS*
- Lacunar infracts can be:*
- Pure sensory stroke
- Pure motor stroke
- Sensori-motor stroke
- Ataxic hemiparesis
For a posterior circulation infarct (POCI), discuss:
- Which artery commonly involved
- Features
- Disruption to posterior circulation (posterior cerebral artery, vertebral artery, basilar artery)
-
ONE OF THE FOLLOWING:
- Cerebellar or brain stem syndromes
- Loss of consciousness
- Isolated homonymous hemianopia
*NOTE: brainstem or cerebellar syndromes could include:
- 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)
Summary of OCS classification and the notes form lecture slides
This is a simple clinical assessment that finds utility in assessing stroke type (i.e. vascular territory involved), severity, aetiology and prognosis. It should form part of every stroke assessment. The table above does include corresponding imaging characteristics although you do no need imaging to complete the OCSP classification. On occasion the exact vascular territory may be revised by imaging (example is thalamic ischaemia which can present on clinical picture as a PACS or even a TACS. The thalamus is however supplied by the PCA which is part of the posterior circulation). This however does not change the usefulness of the OCSP as a clinical tool in the assessment of stroke patients.
As a rule, in the OCSP;
- Dysarthria does not count
- Impairment of motor and sensory function is divided into the somatic distributions of face, arm and leg
The first question by way of attaching OCSP class should be Is there any cortical dysfunction or hemianopia? If the answer is YES then the OCSP class cannot be a LACS. If the answer to this is NO then next question should be Does pure motor/sensory (or combination of two) involve at least 2 contiguous somatic areas or all 3? (i.e. face/arm/leg or face/arm or arm/leg). If answer is YES then OCSP class is a LACS. Other LACS criteria are noted in slide.
If isolated motor/sensory (or combination of two) is restricted to one somatic area i.e. face or arm or leg, then OCSP class is a PACS. Appreciating cortical functional representation (the homonculus) is handy here. Essentially axons from cortical neurones narrow together into bundles in the white matter. Blood vessels supplying the white matter are typically end arteries (lenticulostriate, thalamogeniculate arteries etc). Hypoperfusion of these arteries (as happens in lacunar infarcts) would take out axons from at least two somatic areas leaving the only place you can get motor/sensory limited to one somatic distribution being the cortex, hence the OCSP class being a PACS.
If there is cortical dysfunction, conclusion to a TACS classification is easy if all three are involved i.e. motor/sensory plus hemianopia plus higher cortical dysfunction. Any other combination equates to a PACS with the exception of ISOLATED homonymous hemianopia (HH) which is a POCS since this can only be explained by ischaemia in the occipital lobe (PCA territory) hence a POCS as noted in above slide. Although isolated quadrantanopias may result from small occipital lobe infarcts, thought should be given that these may actually be PACS events involving either the parietal (lower quadrant) or temporal (upper quadrant) lobes with any expected associated signs (eg sensory inattention or other cognitive dysfunction) being subtle or resolve early.
In addition to isolated HH, POCS class is reached by demonstrating brainstem or cerebellar stroke syndromes. Helpful are demonstrations of typical cerebellar features (ataxia, vertigo etc), crossed involvement of cranial nerves versus somatic motor/sensory dysfunction etc.
Other than those included in the Oxford/Bamford stroke classification there are other recognised patterns of stroke; state 2
- Lateral medullary syndrome/Wallenberg’s syndrome
- Weber’s syndrome
For lateral medullary syndrome/Wallenberg’s syndrome, discuss:
- Which artery is affected
- Features (and why these features are seen)
- Posterior inferior cerebellar artery (supplies lateral medulla
- Features:
- Ipsilateral limb ataxia (inferior cerebellar peduncle)
- Nausea, vomiting, vertigo, nystagmus (CNVIII nuclei)
- Dysphagia, dysarthria, loss of gag reflex (nucleus ambiguus)
- Contralateral pain/temp loss on body (spinothalamic- remember decussate at level they enter spine)
- Ipsilateral pain/temperature loss on face (spinal trigeminal tract)
- Ipsilateral Horner’s syndrome (descending hypothalamics)
For Weber’s syndrome, discuss:
- What artery is affected
- Features (and why these features are seen)
- Branch of posterior cerebral artery interrupting blood supply to the part of midbrain (crus cerebri and CNIII)
- Features:
- Ipsilateral CNIII palsy
- Contralateral weakness (motor fibres run in crus cerebri then decussate at medulla)
Briefly outline TOAST classification for ischaemic strokes (focus on naming 5 subtypes)
What tool is used for recognition of stroke in the emergency room?
Briefly outline this tool
Rosier score
Stroke is likely is >0
What might you see on non-contrast CT head In:
- Acute ischaemic strokes
- Acute haemorrhagic strokes
Acute ischaemic stroke:
- Low density/hypodensity (dark)
- Hyperdense artery sign (corresponding with the responsible arterial clot)
Acute haemorrhagic stroke:
- Hyperdense (bright) material (blood) surrounded by low density (oedema)
- *May also see effacement & loss of grey/white matter differentiation*
State some absolute contraindications to thrombolysis
PassMed differs slightly from slides. Slides say some absolute contraindications are:
- Active internal bleeding
- Stroke in last 14 days
- Surgery or trauma last 14 days
- LP in last 7 days
- Childbirth in previous 4 weeks
- Acute pancreatitis
- INR >1.7
- BP >185/110 after 2 attempts to reduc elevels
What score is used to risk stratify patients with a suspected TIA?
ABCD2 prognostic score (estimates risk of stroke after suspected TIA)
Score 0-3 is low risk, 4-5 is moderate risk, score 6-7 is high risk
**NOTE: PassMed says no longer recommended by NICE as it performs poorly
What scores can be used to measure disability post-stroke?
Barthel index (BI) or modified Rankin Score (mRS)
- **Barthel index: 10 tasks/ADLs scored according to amount of time or assistance required. Score is from 0 to 100 (worst). Should be used post-stroke and during ongoing rehabilitation to monitor improvement*
- **Modified Rankin Score= 0-6 points looking at how much assistance they need. 6 is dead (measure of global disability used to assess baseline function and evaluate outcomes & treatment impacts after intervention)*
What is the stroke pathway?
Document that details the core components of optimal service for someone who has suffered a stroke
What is loss of grey-white matter differentiation and what does it suggest?
- Loss of distinction between grey & white matter
- Suggests oedema which may be secondary to hypoxic brain injury, infarction, tumour or cerebral abscess
How can you distinguish between a T1 and T2 weighted head MRI?
Based on density of grey and white matter you expect white matter to appear darker (as it is hypodense) and grey matter to appear lighter (hyperdense):
- T1: grey matter darker than white matter
- T2: grey matter is lighter than white
