Stroke Flashcards

1
Q

What is the neurovascular unit?

A
  • Broadly describes the relationship between brain cells and their blood vessels
  • Functional unit of the CNS
  • Functional & structural interplay between/ among neurones, glial cells (metabolic support cells- homeostasis) and endothelial lumens (including the dynamic of the BBB)
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2
Q

How do stroke symptoms occur (physiology)?

A
  • Dysfunction of the neurovascular unit…
  • Hypoperfusion in the endothelial lumen
  • This leads to ↓ O2 & glucose
  • This leads to ↓ ATP synthesis, impairing energy dependent cell processes
  • Consequent action potential arrest
  • Leading to absence of neuronal transmission
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3
Q

What are the typical stroke syndrome features?

A
  1. Sudden onset – clarify w/ pt that from a medical perspective ‘sudden’ means seconds
  2. Focal – hypoperfusion occurs only in a branch of cerebrovasculature hence only the neurovascular units in the concerned vascular territory are affected
  3. Predominantly negative neurological symptoms – dysfunction of the neurovascular unit is mediated by cessation of action potentials hence typical stroke symptoms reflect loss of function
  4. Vascular territory hypoperfusion can explain collection of symptoms

+ 2 additional considerations:

  • Symptoms do not typically migrate – slow migration can occur in migranous sensory & visual aura, rapid migration in focal seizures (Jacksonian march)
  • Episodes do not stereotype – stereotyping is defined as episodic recurrence of symptoms in an identical fashion with complete resolution in between, so in a stroke repeat embolisation of the same blood vessels
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4
Q

What is capsular warning syndrome?

A
  • Recurrent stereotyped lacunar transient ischaemic attacks (TIAs)
  • This is not true stereotyping but fluctuation of symptoms with episodes recurrent over minutes to hours
  • Lenticulostriate arteries are deep branches of the middle cerebral artery
    • Supply deep grey matter structures including lentiform nucleus, caudate nucleus, internal capsule, basal ganglia
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5
Q

What is the basal ganglia?

What is the function of the basal ganglia?

Where does the basal ganglia receive its blood supply from?

A
  • Basal ganglia refer to 4 main subcortical nuclei that regulate and coordinate movement
  1. Striatum = caudate nucleus + putamen
    1. Caudate nucleus- lateral wall of lateral ventricle, separated from putamen by internal capsule (descending white matter fibres)
  2. Globus pallidus- externa and interna
  3. Subthalmic nucleus
  4. Substantia nigra
  • Main purpose of basal ganglia- stimulate motor cortex, fine-tune the voluntary movements
    • Receives information from several sources including cerebral cortex
    • Basal ganglia feeds info back to the cortex via the thalamus
  • Globus pallidus + putamen = lentiform nucleus
  • Thalamus- stimulates basal ganglia
  • Blood supply comes from middle cerebral artery
    • Lenticulostriate artery
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6
Q

Label the following parts of the basal ganglia

A
  1. Caudate nucleus
  2. Putamen
  3. Globus pallidus
  4. Thalamus
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7
Q

What is the blood supply to the thalamus?

A
  • Posterior cerebral artery
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8
Q

What is the blood supply of the cerebrum?

A
  • The internal carotid gives rise to the anterior and medial cerebral artery
  • The anterior cerebral arteries: anteromedial area of cerebrum
    • Runs within interhemispheric fissure
  • Middle cerebral arteries: majority of lateral cerebrum
    • Runs within lateral sulcus (separates frontal & parietal above from temporal lobe below = lateral fissure)
    • Within this fissure some small branches are given off called striate arteries which supply the basal ganglia
  • The vertebral arteries unite and form the basilar artery at the bottom of the pons, when it reaches the midbrain it terminates by splitting into the posterior cerebral arteries
  • Posterior cerebral arteries: supply a mixture of the medial and lateral areas of the posterior cerebrum
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9
Q

What 2 arterial sources of the circle of Willis?

A
  • Internal carotid – divides to form middle and anterior cerebral artery
  • Vertebral arteries (from first part of subclavian, run up through transverse foramen of cervical vertebrae) – provides the posterior circulation
  • The circle of Willis is at the base of the brain around the optic chiasm and hypothalamus
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10
Q

Where does the ophthalmic artery come from?

A
  • Internal carotid artery
  • Arise immediately after ICA passes through the cavernous sinus to enter the cranial cavity
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11
Q

Describe the blood supply to the cerebellum?

A
  • Branches of basilar artery-
    • Superior cerebellar artery
    • Anterior inferior cerebellar artery
  • Branch of vertebral artery-
    • Posterior inferior cerebellar artery
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12
Q

What signs and symptoms can dysfunction of the cerebellum produce?

A

DANISH

  • Dysdiadochokinesia (difficulty carrying our rapid, alternating movements)
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurring speech
  • Hypotonia
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13
Q

Describe the blood supply of the brainstem?

A
  • Midbrain
    • From basilar artery and its branches- posterior cerebral artery, superior cerebellar artery, posterior choroidal artery, interpeduncular branches of basilar artery
  • Pons
    • Pontine arteries from basilar artery
    • Anterior inferior cerebellar artery and superior cerebellar artery
  • Medulla
    • Anterior spinal, posterior spinal, posterior inferior cerebellar, anterior inferior cerebellar, vertebral arteries
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14
Q

What is the Oxford Community Stroke Project Classification (OCSP)? (also known as Bamford classification of ischaemic stroke)

A
  • A simple clinical assessment that finds utility in assessing stroke type ie vascular territory involved, severity, aetiology & prognosis
  • Imaging is not necessarily required to complete the OCSP classification
  • The following criteria should be assessed:
    • Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
    • Homonymous hemianopia
    • Higher cognitive dysfunction eg dysphasia
  • Dysarthria doesn’t count in OCSP
  • Impairment of motor and sensory function is divided into the somatic distributions of face, arm and leg
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15
Q
  1. What is dysphasia and what is dysarthria?
  2. Suggest some causes of isolated dysarthria (slurred speech)?
A

1.

  • Dysphasia- difficulty understanding or speaking language
  • Dysarthria- slurring of speech

2.

  • Alcohol intoxication
  • Sepsis
  • Lack of sleep
  • Post-ictal phase
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16
Q

What is a total anterior circulation stroke (TACS)?

A
  • Large cortical stroke affecting the areas of the brain supplied by both middle & anterior cerebral arteries
  • All 3 of the following need to be present-
    1. Unilateral weakness +/- sensory deficit, of the face, arm and leg
    2. Homonymous hemianopia
    3. Higher cerebral dysfunction (dysphasia, visuospatial disorder)
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17
Q

What is a partial anterior circulation stroke (PACS)?

A
  • A less severe form of TACS, in which only part of the anterior circulation has been compromised
  • 2 of the following need to be present:
    • Unilateral weakness +/- sensory deficit, of the face, arm and leg
    • Homonymous hemianopia
    • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
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18
Q

What is a posterior circulation syndrome (POCS)?

A
  • Involves damage to the area of the brain supplied by the posterior circulation (eg cerebellum and brainstem)
  • 1 of the following need to be present:
    • Cranial nerve palsy and a contralateral motor/sensory deficit
    • Bilateral motor/ sensory deficit
    • Conjugate eye movement disorder eg horizontal gaze palsy
    • Cerebellar dysfunction eg vertigo, nystagmus, ataxia
    • Isolated homonymous hemianopia
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19
Q

What is a lacunar stroke (LACS)?

A
  • Subcortical stroke that occurs secondary to small vessel disease
  • No loss of higher cerebral functions eg dysphasia
  • 1 of the following need to be present:
    • Pure sensory stroke
    • Pure motor stroke
    • Sensori-motor stroke
    • Ataxic hemiparesis
    • Clumsy hand dysarthria (internal capsule)
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20
Q

Suggest some stroke mimics?

A
  • Classify them in 3 groups
  1. Readily identifiable on brain imaging
    1. SoL- brain tumour, abscess
    2. Subdural haematoma
    3. Multiple sclerosis
  2. Syndromically distinguishable from the stroke syndrome – there are secure clinical features to distinguish from typical stroke syndrome
    1. Syncope syndrome
    2. BPPV
    3. Vestibular neuronitis
    4. Transient global amnesia
    5. Bell’s palsy
  3. Exclusion of stroke syndrome requires specialist stroke assessment including brain imaging (there may be clues if you have recurrent episodes)
    1. Migraine with aura
    2. Focal seizures
    3. Functional syndrome
    4. Hypoglycaemia
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21
Q

How to describe the causes of stroke?

A
  • Type of brain parenchymal damage
    • Infarct vs bleed
  • Mechanism causing hypoperfusion
    • Eg embolization from carotid artery vs thrombosis vs vasoconstriction
  • Disease/ pathology process primarily responsible for mechanism of hypoperfusion
    • Antiphospholipid syndrome, thyroid disease, AF, infective endocarditis, brain aneurysm, thrombophilia, carotid disease, fibrinolytic necrosis
  • Climate in which disease process has thrived
    • Eg smoking causing carotid disease, uncontrolled htn causing end artery arteriosclerosis eventually culminating into fibrinolytic necrosis, or obesity as part of metabolic syndrome
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22
Q

What is the commonest cause of stroke?

A
  • Atrial fibrillation
  • Tend to be more severe by virtue of the larger size clots from the heart in addition the dynamic of poor mobilisation of collateral circulation relative to large vessel embolization
  • Risk of stroke assessed with CHA2DS2VASc score (primary prevention only)
  • HASBLED to assess bleeding risk
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23
Q

If AF is the cause of a patient’s stroke in whom anticoagulation is contraindicated, what other treatment options are there?

A
  • Left atrial appendage closure
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24
Q

What are the causes of intracranial haemorrhage?

A
  • Primary (small vessel) haemorrhage
    • Hypertension
    • Cerebral amyloid angiopathy
  • Secondary haemorrhage
    • Haemorrhagic transformation infarct
      • Venous sinus thrombosis and venous infarction
    • Tumour- glioblastoma multiforme, anaplastic astrocytoma, metastasis
    • Vascular- aneurysm, AVM, vasculitis
    • Coagulopathy, warfarin, aspirin
    • Cocaine, alcohol
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25
Q

What is cerebral amyloid angiopathy (CAA)?

A
  • Amyloid build up on walls in the brain
  • Causes Alzheimer’s dementia, stroke
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26
Q

What is the TOAST classification of stroke?

A
  • Denotes 5 subtypes of ischaemic stroke, based on clinical symptoms as well as radiological and other investigation results
  1. Large-artery atherosclerosis
  2. Cardio-embolic
  3. Small-vessel occlusion (lacunae)
  4. Stroke of other determined aetiology
  5. Stroke of undetermined aetiology
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27
Q

What is the FAST screening tool?

A
  • Face Arm Speech Test- positive if any of the following are met
    • NEW FACIAL WEAKNESS: Can pt smile/ has face fallen to one side
    • NEW ARM WEAKNESS: Can pt raise both arms and keep them there
    • NEW SPEECH DIFFICULTY: Can pt speak clearly & understand what you say, is their speech slurred
  • Used outside hospital to screen people with sudden onset of neurological symptoms for a diagnosis of stroke or TIA
  • Well known within the community
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28
Q

What is the ROSIER score?

A
  • A variant of the FAST screening tool
  • Used by medical professionals to establish the diagnosis of a suspected stroke or TIA when pts are admitted into ED
  • Looks at: LoC or syncope, seizure activity, asymmetric facial weakness, arm weakness, leg weakness, speech disturbance, visual field defect
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29
Q

What is the initial mx of suspected TIA?

A
  • Aspirin 300mg daily
  • Supplemental O2 if their O2 sats <95%
  • Offer secondary prevention in addition to aspirin as soon as TIA diagnosis is confirmed
  • Refer to TIA clinic
  • After specialist assessment in TIA clinic, consider MRI to determine territory of ischaemia, or to detect haemorrhage or alternative pathologies- perform on same day as assessment
  • Immediate statin treatment not recommended; continue statins if they were already receiving them
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30
Q

What are the indications for a head CT scan in suspected stroke?

A
  • Indications for thrombolysis or thrombectomy
  • On anticoagulant therapy
  • Known bleeding tendency
  • Depressed GCS <13
  • Unexplained progressive or fluctuating symptoms
  • Papilledema, neck stiffness, fever
  • Severe headache at onset of stroke symptoms
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31
Q

What sort of things comprise a care bundle for stroke patients?

A
  • Admission to stroke unit
  • Revascularisation therapy (IV alteplase, within 4.5 hrs, or thrombectomy for patients with large vessel occlusion, 6hr therapy window)
  • Optimising physiology and surveillance, prevention and early intervention of complications
  • Nutritional support
  • Secondary prevention (antiplatelet therapy, anticoagulation, carotid endarterectomy (CEA), BP, lipid control)
  • Rehabilitation
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32
Q

Describe the current pathway for emergency stroke assessment in Leicestershire?

A
  • 999 call
  • Urgent paramedic assessment
  • FAST +ve
  • LRI ED- core stroke team alerted- Rapid Assessment Protocol (RAP)
  • The RAP team have 5 priorities
  1. Clinically confirm diagnosis, that thrombolysis is indicated, get venous access, do bloods, obs, weigh, request CT scan
  2. Identify contraindications (outside of imaging)
  3. Complete consent/ assent (or best interest)
  4. Imaging
  5. Bolus and infusion
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33
Q

What is the role of the CT during assessment for thrombolysis?

A
  • Exclusion of intracranial haemorrhage
  • Early changes diagnostic for ischaemic stroke-
    • Evidence of thrombus in vessels- clotted blood is white on CT hence vessels become white
    • Effacement (swelling of brain cells) & loss of grey and white matter distinction
      • The failure of membrane transport à consequent intracellular fluid and electrolyte shifts results in brain cell swelling
      • Normally white matter has darkish hue on CT due to myelin, when grey matter cells absorb excess water the attenuation changes and resembles white matter à loss of grey and white matter distinction
      • Quantifying effacement & obscuration is the basis of the ASPECTS score
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34
Q

Thrombolysis with alteplase is recommended for treating acute ischaemic stroke if what criteria is met?

A
  • Treatment is started as soon as possible within 4.5 hrs of onset of stroke symptoms
  • Intracranial haemorrhage has been excluded by appropriate imaging techniques
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35
Q

Alteplase indications and contraindications?

A
  • Indications:
    • Administered within 4.5 hours from onset of stroke symptoms
    • Disabling impairments (NIH>4, dysphasia, inability to self-care or mobilise independently, visual field defect, dysphagia)
    • No contraindication
  • Contraindications: see table in image attached
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36
Q

What is the ASPECTS score?

A
  • (Alberta Stroke Programme Early CT Score)
  • 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
37
Q

When is thrombectomy used to treat stroke?

A
  • Combination with thrombolysis (if not contraindicated & within the time window)
  • For ischaemic stroke
  • Thrombectomy involves removal of thrombus from vessel
  • NICE set out specific criteria for use of thrombectomy- Offer as soon as possible to people who were last known to be well between 6 and 24 hrs previously:
    • Who have acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation determined by CT or MRI, AND
    • If there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume
38
Q

How to decide the optimal imaging for stroke?

A

The 4Ps

  • Pipes- exploration of blood vessels, usually via CT and sometimes MR angiography
  • Parenchyma- exploration of tissue compromise in terms of cell death, usually via non contrast CT or MRI
  • Perfusion and penumbra- continue the theme of tissue compromise but go beyond cell death by clarifying ‘tissue at risk’
39
Q

How to manage an intracerebral haemorrhage?

A
  • Required special anticipation to address raised ICP due to haematoma expansion
    • Blood pressure control- offer rapid BP lowering who present within 6 hrs of symptom onset, have systolic between 150-220
      • Aim for systolic target 130-140 within 1hr starting treatment & maintain this bp for at least 7 days
    • Correcting clotting derangements
    • Maintaining good glycaemic control
    • Coughing, constipation- straining increases abdo pressure, urinary retention causing increase in BP- all these things can contribute to increasing haematoma expansion so pay attention to addressing those
  • Pts with any of the following rarely require surgical intervention and should receive initial medical treatment: small deep haemorrhages, lobar haemorrhage w/o either hydrocephalus or rapid neurological deterioration, large haemorrhage and significant comorbidities before stroke, GCS <8 unless because of hydrocephalus
  • Decompressive hemicraniectomy for clinical deficits suggesting MCA, decreased level of consciousness
40
Q

How is a decision whether to involve neurosurgeons made when someone has haemorrhagic stroke?

A
  • Neurosurgery as a strategy for managing raised ICP is a balance between the following:
    • Surgical accessibility- is it superficial and accessible to surgical evacuation or aspiration
    • Neurological stability- GCS, previously frail?, are they likely to survive anaesthesia or improve neurologically after surgery because raised ICP has already caused irreversible harm
      • If hydrocephalus develops, insert ventricular drain
41
Q

When is a decompressive hemicraniectomy (DHC) indicated?

A
  • For management of malignant oedema in <60years old, but otherwise biologically fit stroke pts above this cut off
    • Malignant oedema means a large MCA infarction
    • Acute brain swelling
  • Referrals should be made within 24 hrs & surgery completed within 48 hrs
42
Q

What are some common post stroke complications?

A
  • Recurrent stroke- due to unaddressed aetiological factors before cause of stroke is clarified and secondary prevention efforts optimised
  • Extension of stroke- due to loss of ischaemic penumbra resulting from suboptimal physiology
  • Raised ICP- due to haematoma expansion, malignant oedema, haemorrhagic transformation or hydrocephalus
  • Infections- aspiration pneumonia, UTI due to incomplete bladder emptying either from constipation or bed bound posture
  • Complications of immobility- VTE, constipation, bed sores
  • Mood & cognitive dysfunction- can affect motivation and compliance with rehabilitation
  • Post stroke pain – due to spasticity, joint dislocation, central/ neuropathic pain
  • Fatigue- due to poor sleep, medications, inherent result of brain cell damage
  • Spasticity, contractures, secondary epilepsy
43
Q

What is haemorrhagic transformation?

A
  • A common complication of acute ischaemic stroke
  • Occurs when peripheral blood extravasates across a disrupted BBB into the brain following ischaemic stroke
  • Usually occurs following cardioembolic strokes and is more likely with larger infarct size
44
Q

What is hydrocephalus?

What are the symptoms and how can stroke cause it?

How to manage?

A
  • Excessive volume of CSF within ventricular system of brain
  • Symptoms of raised ICP- headache worse in morning, lying down, and during Valsalva; N&V; papilloedema; coma
  • Haemorrhage within brain can cause obstructive hydrocephalus due to blocking outflow of CSF
  • Ix- CT head is first line
  • Mx- external ventricular drain (EVD) is used in acute severe hydrocephalus, inserted into right lateral ventricle & drains into a bag bedside
45
Q

What are some complications of intracranial haemorrhage?

A
  • Mass effect:
    • Effacement/ displacement/ twisting of ventricles
    • Hydrocephalus
    • Midline shift
    • Cerebral herniation- subfalcine, uncal, tenting, coning
    • Raising ICP
46
Q

What things can be done to identify complications of stroke as early as possible?

A
  • Surveillance
    • Daily review of EWS, obs, mood, chest, legs (DVT), bowel, urine function, progress of impairments
  • Timely bloods eg CRP- infection identification and other complications such as LFTs from statins, HB drop from antithrombin therapy
47
Q

Describe some secondary prevention efforts for stroke patients?

A
  • Antithrombotic therapy (antiplatelet vs anticoagulation- 2 weeks of aspirin 300mg followed by clopidogrel 75mg daily)
  • BP control (average <130/80)
  • Lipid control (commence statins 48 hrs after initiation of a stroke, avoid in cerebral haemorrhage)
  • Glycaemic control (HbA1C <7)
  • Carotid endarterectomy (symptomatic ICA >50% lumen reduction & NASCET 50-99%)
  • Lifestyle- stop smoking, weight loss, optimise sleep, exercise
  • Swallow and nutrition assessment
  • Rehabilitation- all members of MDT such as PT, OT, SALT, dietician, social worker, stroke coordinator, neuropsychologist
  • Palliative care- early recognition and referral for those suspected with poor outcome
48
Q

What sort of vascular risk factors can be optimised to reduce risk of stroke?

A
  • Smoking cessation
  • Maintain avg BP < 130/80
  • Glycaemic control to HbA1c<7
  • Total cholesterol <4 and LDL <2
  • Wt loss BMI <25
  • Promotion of exercise
  • OSA
49
Q

What are some secondary prevention efforts for preventing stroke in pts with AF?

A
  • Anticoagulation- IV or subcut heparin, warfarin, DOACs
  • Left atrial appendage closure- option for stroke secondary prevention in pts with AF in whom anticoagulation is contraindicated
50
Q

What is NIHSS?

A
  • National Institutes of Health Stroke Scale
  • 15 item neurologic examination stroke scale used to evaluate the effect of acute cerebral infarction on the levels of consciousness, language, neglect, visual field loss, extraocular movement, motor strength, ataxia, dysarthria, sensory loss
  • A trained observer rates the pt’s ability to answer Qs and perform activities
  • Provides a quantitative measure of the clinical outcome in stroke
  • Scoring system out of 42: score <4 is good, >22 means a significant proportion of the brain is affected, >26 is often a contraindication for thrombolysis
51
Q

What is the Modified Rankin Scale (MRS)?

A
  • Used to measure the degree of disability in pts who have had a stroke
  • Compared over time to check for recovery and degree of continued disability
  • Score of 0 is no disability, 5 is disability requiring constant care for all needs, 6 is death
    • 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 w/o assistance, but unable to carry out all previous activities
    3. Moderate disability, requires some help, can walk unassisted
    4. Moderately severe disability, unable to attend to own bodily needs w/o assistance and unable to walk w/o assistance
    5. Severe disability, requires constant nursing care and attention, bedridden, incontinent
    6. Dead
52
Q

How to estimate how well a stroke patient is likely to do?

A
  • Broad prognostic groups can be initially derived from NIHSS score and OCSP class
  • Functional prognosis- recovery trajectory. Recovery will continue until a pt reaches their functional plateau- 3 groups
    1. Early, high functioning plateau – the extreme version of this is a TIA or minor stroke, signifying excellent functional prognosis.
    2. 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.
    3. Delayed & 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
53
Q

What are some good and poor prognostic factors after a stroke?

A
  • GOOD
    • Absence of coma
    • Early motor recovery
    • Continence
  • POOR
    • Severe communication deficit
    • Old age
    • Incontinence
    • Neglect
    • No leg movement at 2 weeks
    • Severe upper limb weakness at 4 weeks
54
Q

What are the rules of driving and stroke?

A
  • 4 week driving restriction for standard car licenses
  • 1 year for HGV vehicles
  • Residual visual field dysfunction is subjected to separate requirements before license reinstatement
55
Q

What nutritional support can be offered to stroke patients?

How can swallowing function be assessed?

A
  • Unsafe swallow function-
    • Tube assisted enteral feeding is temporary pending safe swallow function
  • Assessing swallowing- video fluoroscopy and flexible endoscopic evaluation of swallowing (FEES)
  • Prolonged use/ commencement of parenteral feeding is best avoided when pts are approaching end of life- no real improvement to QoL or preventing death
  • If patients are unable to swallow adequate food/ fluids orally by 4 weeks from stroke onset- gastrostomy feeding can be considered
56
Q

What rehabilitation therapies are offered to stroke patients?

A
  • Mobility, ADLs, speech and cognitive therapy
  • Managing spasticity- including orthotic prosthesis and botulinum toxin therapy
  • Environmental modifications
57
Q

What are your differentials for a TIA?

A
  • Hypoglycaemia
  • Migraine aura
  • Focal epilepsy (symptoms spread over seconds & often include twitching & jerking)
  • Hyperventilation
  • Retinal bleeds
  • Rare mimics- malignant htn, MS, intracranial tumours, peripheral neuropathy, phaeochromocytoma, somatization
58
Q

Suggest some causes of isolated peripheral neural dysfunction?

A
  • Dysarthria- peripheral vocal apparatus, facial/tongue/ throat muscles
  • Vertigo- vestibular dysfunction (rather than cerebellum)
  • Diplopia- external ocular muscles, peripheral cranial nerve dysfunction (rather than pons)
  • Peripheral motor/ sensory dysfunction- eg in dermatomal distribution- can be sudden, focal, predominantly negative but won’t fit into a cerebral vascular territory
59
Q

70 year old woken up at 4am with dizziness described as the room spinning around, associated vomiting, further episodes on turning left (resulting in staying in bed)- cause of presentation? What diagnostic assessment does he need? Treatment?

A
  • BPPV
  • Positive Dix-Hallpike test will confirm diagnosis
  • Epley manoeuvre is a therapeutic procedure, additional vestibular exercises
60
Q

45 year old presents with sudden onset dizziness, described as room spinning around, associated vomiting, Dix-Hallpike is negative, Head thrust test is positive to the right- cause of presentation?

A
  • Vestibular neuronitis- common presentation of sudden onset vertigo that may bring suspicion of stroke
  • Head thrust test confirms diagnosis
61
Q

Usually well 58 year old referred to TIA clinic with ‘acute confusion’. Pt currently has no recollection of events, wife reports he was asking same Qs repeatedly, otherwise talking appropriately and no other signs of focal symptoms. Able to make cup of tea during the episode, all completely resolved within 2 hours, neurological examination normal. What is the likely cause for his presentation? Describe a bit about why/ how this happens.

A
  • Transient global amnesia – dysfunction of episodic memory which is the memory of event. 3 steps to episodic memory: registration, storage, retrieval
    • When something first happens, brain registers the events = registration
    • The brain stores the memory it has registered = storage
    • If after a week, you can remember certain things eg recognise a voice = retrieval
    • Other types of memory are preserved eg biographic memory (who you are, where you are), procedural memory (eg making cup of tea)
  • During TGA they are unable to register events hence ask the same questions again and again
  • It can last a few hours
62
Q

39 year old female, gradual onset blurring of vision on right side, 20 mins later right sided pins and needles slowly migrating from fingers up arm and later affecting face and evolving to become numbness. Associated difficulty concentrating and expressing himself verbally and dull frontal headache similar in past. Is this a stroke or a stroke mimic? Describe a bit about why/ how these symptoms have occurred

A
  • This is migraine with aura
  • Visual, sensory, cognitive, speech aura all present in this pt
  • The physiological phenomenon underlying migranous aura is cortical spreading depression and the brain location undergoing CSD explains the nature of the aura. The spreading nature explains why migraine aura are gradual in evolution and separate auras tend to evolve sequentially as CSD moves from one brain location to another
63
Q

Migraine with aura: how does it happen and why do aura occur?

A
  • Physiologically characterised by cortical spreading depression or aura activity
  • Hence gradual onset, migratory and sequential onset of migraine aura symptoms
  • CSD involves altered but continuing brain cell activity- TIA involves cessation of action potentials
  • +/- headache
  • Visual aura (occipital lobe) is the most common but others are possible- tinnitus & dysphasia (temporal lobe), pines and needles/ transient cognitive disturbance (parietal lobe), unsteadiness/ dizziness/ collapse/ hemiparesis (cerebellum, brainstem)
  • Explore triggers
64
Q
  • Explore triggers

What is functional syndrome?

A
  • Functional neurological disorder describes neurological symptoms such as limb weakness, tremor, numbness, blackouts
  • Caused by a problem with the functioning of the nervous system
  • Symptoms-
    • Motor dysfunction- eg functional limb weakness/ paralysis, movement disorders including tremor, spasms (dystonia), myoclonus (jerky movements), gait disorder, dysphonia
    • Sensory dysfunction- eg altered sensation, visual symptoms including loss of vision or diplopia
    • Episodes of altered awareness- eg blackouts, non-epileptic seizures
  • Exact cause is unknown
  • Mx- holistic approach: physiotherapy for motor symptoms, CBT, occupational therapy, speech therapy
65
Q

Suggest some possible stroke chameleons & what do we mean by this?

A
  • Chameleons- when stroke syndrome presentations deviate from the typical presentation
  • Venous infarcts- gradual onset, preponderance for seizure activity
  • Small cortical strokes- peripheral nerve lesions
  • Limb shaking TIA- can appear like a focal seizure- classically due to carotid low flow
  • Occipital strokes- predominant confusion, unexplained delirium- rule out other causes of delirium (should be visual field loss)
  • Stroke amnestic syndromes
  • Stroke mimicking vestibular dysfunction
66
Q

What are the layers of the meninges?

A
  • The meninges cover the brain and the spinal cord- there are three layers
    • Dura mater (outermost)
    • Arachnoid mater
    • Pia mater (innermost- tightly adhered to surface of brain & spinal cord, followed gyri & fissures)
67
Q

Where is the subarachnoid space?

A
  • Underneath the arachnoid mater
  • Contains cerebrospinal fluid- cushion to brain
  • Arachnoid mater projections (arachnoid granulations_ allow CSF to re-enter the circulation via dural venous sinuses
68
Q

What is an extradural haemorrhage, how do they present?

A
  • Acute presentation, young men, 90% have skull fracture
  • Limited by sutures, bi-convex, hyperdense
  • Outer layer (periosteum) lacerates, inner layer (meningeal) is intact
  • Blood collects between naked bone and inner layer of dura mater
69
Q

What are the sources of an extradural bleed?

A
  • Meningeal vessels
  • Dural sinus
70
Q

What is a subdural haemorrhage?

Sources of bleed?

Classic presentation?

A
  • Dissection of subdural space- haematoma spreads around the brain, between arachnoid and dura- arachnoid intact
  • Convex, not crescentic
  • Sources of bleed- torn bridging veins
  • Classic presentation- middle age, severe trauma, bleeding can be rapid, localised, hyperdense
71
Q

How do strokes involving the anterior cerebral artery classically present?

A
  • Contralateral hemiparesis and sensory deficits
  • Lower extremities affected worse than upper
72
Q

How do strokes involving the middle cerebral artery classically present?

A
  • Contralateral hemiparesis and sensory loss
  • Upper extremities affected worse than lower
  • Contralateral homonymous hemianopia may be present
  • Aphasia may be present
73
Q

How do strokes involving the posterior cerebral artery present?

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia
74
Q

What is Weber’s syndrome?

A
  • Branches of the posterior cerebral artery that supply the midbrain become blocked
  • Ipsilateral CN III palsy
  • Contralateral weakness of upper and lower extremity
75
Q

What is lateral medullary syndrome?

A
  • AKA Wallenberg syndrome
  • Most commonly due to blockage of the posterior inferior cerebellar artery, causing ischaemia of the lateral part of the medulla oblongata in the brainstem
  • Ipsilateral facial pain and temperature loss
  • Contralateral limb/ torso pain and temperature loss
  • Ataxia and nystagmus
  • Loss of temperature sensation and pain from the involvement of the lateral spinothalamic tract
76
Q

How would a stroke involving the anterior inferior cerebellar artery present?

A
  • = Lateral pontine syndrome
  • Symptoms similar to lateral medullary syndrome- this artery supplies the pons and the cluster of signs is known as the lateral pontine syndrome
  • In addition to the findings of lateral medullary syndrome, ipsilateral facial paralysis and deafness would be expected
77
Q

How does a stroke involving the retinal or ophthalmic artery present?

A
  • Amaurosis fugax
78
Q

Locked in syndrome is a result of stroke in which artery?

A
  • Basilar artery
79
Q

What is Broca’s aphasia?

A
  • Lesion of the inferior frontal gyrus
  • Expressive aphasia where the patient’s speech is non-fluent and halting, repetition is impaired
  • They can comprehend commands as language comprehension remains relatively intact
  • Caused by infarcts to the superior division of the left MCA
  • Broca sounds like ‘broken’ as the patient’s word flow is broken
80
Q

What is conduction aphasia?

A
  • Affecting the arcuate fasciculus, the connection between Wernicke’s and Broca’s area
  • Speech fluent, repetition poor
  • Comprehension relatively intact
81
Q

What is Wernicke’s aphasia?

A
  • Lesion of the superior temporal gyrus
  • Speech fluent, comprehension abnormal, impaired ability to repeat back phrases
  • = Receptive aphasia
  • Commonly secondary to an ischaemic stroke affecting the inferior left MCA
  • Word salad
82
Q

What is global aphasia?

A
  • Both Wernicke’s and Broca’s areas are damaged
  • Impairment of language production, comprehension and repetition
  • Poor stuttering word flow with poor comprehension
  • May be able to communicate w/ facial gestures or movements
83
Q

How do lacunar strokes present?

A
  • Either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
  • Strong association with hypertension
  • Common sites include the basal ganglia, thalamus and internal capsule
84
Q

What is the first line radiological investigation for suspected stroke?

A
  • Non-contrast CT head scan
  • The Question to answer is is this an ischaemic stroke or a haemorrhagic stroke
    • Rarely a third pathology such as a tumour may be detected
  • This allows us to decide whether to thrombolyse the patient
85
Q

What are the CT head findings for ischaemic and haemorrhagic stroke?

A
  • Acute ischaemic stroke
    • May show areas of low density in the grey and white matter of the territory
      • These changes may take time to develop
    • Other signs include the hyperdense artery sign corresponding with the responsible arterial clot
      • This tends to be visible immediately
  • Acute haemorrhagic stroke
    • Typically show areas of hyperdense material (blood) surrounded by low density (oedema)
86
Q

Why do we do a non-contrast CT in suspected stroke?

A
  • To rule out intracerebral haemorrhage
  • Adding contrast is unnecessary and could make any haemorrhages less easy to see
  • A contrast CT scan would therefore NOT be done in the acute investigation of stroke
87
Q

What urgent investigation needs to be performed when a patient initially presents w/ a focal neurological deficit for which you suspect TIA?

A
  • Blood sugar
  • Hypoglycaemia can lead to focal neurological symptoms
  • Especially important in diabetic pts
88
Q

Possible features of TIA?

A
  • Similar to stroke but features resolve within ~1hr
  • Unilateral weakness or sensory loss
  • Aphasia or dysarthria
  • Ataxia, vertigo or loss of balance
  • Visual problems
    • Amaurosis fugax
    • Diplopia
    • Homonymous hemianopia
89
Q

How is TIA defined?

A
  • Tissue-based- a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, w/o acute infarction
  • (Used to be time-based)