Cerebrovascular Disease Flashcards
What kind of ages do strokes occur
25% of all strokes occur before 65;
Death rate 20-25%
What is stroke?
Syndrome of rapid onset Cerebral Deficit (Usually Focal) lasting >24hr or leading to
head, with a vascular cause
What is a TIA?
Brief episode of Neurological Dysfunction due to
temporary Focal Cerebral/Retinal Ischaemia without Infarction; Seconds to minutes for
complete recovery; May precede Stroke
Types of Ischaemic stroke
Thrombotic Large Artery Stenosis Small vessel disease Cardioembolic Hypoperfusion Might be lacunae
Types of Haemorrhagic stroke
Intracerebral
Subarachnoid
Other causes of stroke
Arterial dissection
Venous sinus thrombosis
Vasculitis
Pathophysiology of Ischaemic Strokes: Thromboembolism
Peripheral Vascular Disease (Including Atherosclerosis) related; Bifurcations (e.g. Arch of Aorta) are particularly affected; Caucasians tend to have more extracranial disease while the
opposite is true for other populations
Thrombosis at site of plaque rupture leads to Embolism or Vessel Occlusion; Large Artery Stenosis typically leads to Embolism
Pathophysiology of Ischaemic Strokes: Small Vessel Disease
Lacunae infarction of Small Penetrating Arteries that supply the Brain Parenchyma; Pathology is due to Hypertension leading to Occlusive Vasculopathy
(Lipohyalinosis) rather than Thromboembolic disease
o Accumulation of diffuse Ischaemic changes in deep White Matter
Pathophysiology of Ischaemic Strokes: Cardioembolic Stroke
Atrial Fibrillation and
other Arrhythmias, Valvular disease including
Infective Endocarditis, Wall Motion Abnormalities, DVT if PFO is present; Rarer
causes include Fat Emboli secondary to fracture, Atrial Myxomas, Air Embolism
o Simultaneous Infarction in different vascular territories are very suggestive of proximal source of
Emboli (e.g. Heart, Aorta)
Pathophysiology of Ischaemic Strokes: Hypoperfusion
Hypoperfusion e.g. In Cardiogenic Shock can
lead to Watershed Infarction (Balint’s Syndrome) in the Parieto-Occipital Area
between MCA and PCA territories
Carotid and Vertebral Artery Dissection: Aetiology
Accounts for 20% of Strokes under 40yrs; Sequelae of trivial Neck Trauma or Hyperextension
(e.g. Whiplash injury); Thought to be predisposed by occult Collagen disorders e.g. Partial Marfan’s Syndrome
Carotid and Vertebral Artery Dissection: Pathophysiology
Most dissections occur in Large Extracranial vessels; Blood penetrates Subintimal Vessel wall forming a false lumen; Thrombosis within true lumen due to Thromboplastin release leads to Thrombosis at the site, as well as Thromboembolic stroke
Carotid and Vertebral Artery Dissection: Presentation
Pain in Neck/Face; Horner’s Syndrome or Lower Cranial Nerve Palsies
Venous Stroke
1% of Stokes; Thrombosis within Intracranial Venous Sinuses E.g. Superior Sagittal Sinus, Cortical Veins especially in Hypercoagulable states (Pregnancy, Dehydration/Alcohol,
Malignancy), Thrombotic disorders
• Cortical Infarction, Seizures and raised ICP can occur
TIA: Aetiology
Usually due to Microemboli; Different mechanisms than Embolic Stroke; TIAs may be caused by fall in Cerebral Perfusion (Dysrhythmia, Postural Hypotension, Atheroma); Infarction
averted by Autoregulation
o Emboli typically from Cardiac Thrombus or Atheromatous plaque
o Infective Endocarditis and Polycythaemia can cause TIAs
• Tumours and Subdural Haematomas might present similarly to TIA
TIA: Management
All patients given Aspirin 300mg and referred to TIA clinic and seen within 24hrs
TIA: Presentation
Sudden loss of function usually lasting minutes or hours; Hemiparesis (affecting the Motor Cortex) and Aphasia (affecting Wernicke’s/Broca’s/Arcuate Fasciculus) are the commonest
Consciousness is typically preserved during TIA
Amaurosis Fugax
Sudden transient unilateral
loss of sight due to transient loss of Ophthalmic
supply; Might be a sign of Internal Carotid Artery
Stenosis Preceding Hemiparesis
TIA: What else should be investigated for
Carotid Artery Bruit, Atrial Fibrillation, Valvar
Heart Disease or recent MI should be investigated
for;
TIA: Underlying conditions
Atheroma, HTN, Postural Hypotension,Bradycardia/HF, DM
TIA: Rare causes
Arteritis, Polycythaemia,
Neurosyphilis, HIV, Antiphospholipid Syndrome
Cerebral Infarction: Pathophysiology
Following Vessel Occlusion, Brain Ischaemia occurs followed by Infarction; Infarcted area surrounded by swollen area (Ischaemic Penumbra) which is non-functioning but structurally
intact; Can regain function with neurological recovery
• Hypoxia leads to Neuronal damage; Fall in ATP, release of Glutamate; Opening of Calcium Channels and Free Radicals leading to Inflammatory damage, Necrosis and Apoptosis
Cerebral Infarction: Morbidity and Mortality
25% of patients die within 2 years; 10% within first month; Higher early mortality with
Haemorrhagic stroke; Coma, Conjugate Gaze Deficit, Hemiplegia are poor prognostic indicators; Preventable deaths include Aspiration
• Recurrent Strokes are common (10% within first yr); 30 – 40% of Stroke patients alive at 3yrs
Cerebral Infarction: Commonest Sites
Most commonly in Internal Capsule following Thromboembolism of MCA (Takes 80% of Anterior Circulation supply); Similar clinical picture in Internal Carotid Artery Occlusion
Cerebral Infarction: Presentation
o Contralateral Hemiplegia/Hemiparesis with Facial Weakness; Aphasia if Dominant Hemisphere is affected; Weak limbs are at first Flaccid and Areflexic
o Consciousness is usually preserved; Rarely Epileptic seizure occurs at onset; Reflexes return after several days of onset and become hyperreflexia; Extensor Plantar Response appears (Babinski’s)
o Weakness is maximal at first and recovery occurs gradually over the long term
Brainstem Syndromes: Weber’s
Contralateral Hemiparesis, Oculomotor Palsy
Brainstem Syndromes: Ventral Pontine Syndrome
(Millard-Gubler) – Contralateral Hemiparesis, Ipsilateral CNVI Palsy, Ipsilateral CNVII Palsy
Brainstem Syndromes: Bilateral Ventral Pontine Syndrome
Locked in syndrome
Brainstem Syndromes: Reticular Formation
Coma
Brainstem Syndromes: Lateral Medullary Syndrome
(Wallenberg’s) – Acute Vertigo, Cerebellar Signs, Horner’s Syndrome,
Contralateral Spinothalamic loss, Ipsilateral Facial sensory loss
Brainstem Syndromes: Medial Medullary Syndrome
(Dejerine’s) – Contralateral Dorsal Column modalities loss, Ipsilateral Tongue Weakness, Contralateral
Hemiparesis/Hemiplegia
Lacunar Infarction Presentation
Lacunae Infarction – Infarction <1.5cm3
Hypertension is commonly present; Minor strokes (Pure motor, Pure sensory, Sudden
Unilateral Ataxia, Sudden Dysarthria with clumsy hand)
Hypertensive Encephalopathy
Cerebral Oedema causing Severe Headaches, Nausea and Vomiting; Agitation, Confusion, Fits and Coma occurs if HTN not treated
o Papilloedema due to Ischaemic Optic Neuropathy or following multiple acute infarcts; MRI shows Oedematous White Matter in Parieto-Occipital Regions
Vascular Dementia
Multiple Lacunae or larger Infarcts cause Generalised Intellectual loss often seen in advanced Cerebrovascular disease; Late stage presents as Dementia,
Pseudobulbar Palsy, Shuffling gait (Marche à petits pas)
Binswanger’s Disease
Widespread low attenuation in Cerebral White Matter usually with Dementia, TIA, Strokes in HTN patients
Visual Cortex Infarction
– Hemianopia Visual
Loss and Cortical Blindness
Watershed Infarction (Balint’s Syndrome)
Following prolonged periods of low perfusion;Leads to Cortical Visual loss, Memory loss, Intellectual Impairment; Vegetative state or Minimally Conscious state might follow
Immediate Management of Acute Stroke
FAST Recognition – Facial Weakness, Arm
Weakness, Speech (Difficulty, Slurring), Time
• Admission without delay; Imaging, Care and
Investigation; Airway protection post-Stroke
• Routine Bloods (FBC, ESR, INR, Lipids), CXR, ECG, Carotid Doppler, MRA
• Source of embolism to be sought; Carotid Bruit,
Atrial Fibrillation, Valvular Lesion, Endocarditis,
Previous Embolism/TIA; BP assessment
o Brachial BP from both sides; >20mmHg
difference suggests Subclavian Stenosis
• Thrombolysis should be used immediately if
Ischaemic stroke is confirmed
Stroke Imaging: Non contrast Ct
Demonstrate
Haemorrhage immediately; Cerebral Infarction not detected or subtle changes only
Stroke Image: MRI
MRI shows changes early in Infarction; Shows
full extent of damaged area/Penumbra
Stroke Imaging: DW MRI
Detect Cerebral Infarction
immediately but also accurate as CT for
Haemorrhagic stroke
Stroke Imaging: MRA/CTA
MRA or CTA after acute imaging – Confirm surgically accessible Arterial Stenoses
Stroke Imagine: Carotid Doppler and Duplex scanning
Carotid and Vertebral Stenosis and Occlusion
Thrombolysis
Age >18, Measurable Neurological deficit, Imaging and Clinically consistent with Acute Ischaemic Stroke, Timing of onset well-established; up to 4.5hrs after onset
Thrombolysis: History Exclusion Criteria
Stroke/Head Trauma in 3/12, Previous Haemorrhagic Stroke, Major surgery 2/52, GI/GU bleeding 3/52, MI 3/12, LP 1/52,
Thrombolysis: Clinical Exclusion Criteria
Rapidly improving Stroke syndrome, Minor/Isolated signs, Symptoms suggestive of SAH, Acute MI/Dressler’s Syndrome, Severe HTN,
Pregnancy/Lactation, Active Bleeding/Trauma
Thrombolysis: Laboratory Exclusion Criteria
Thrombocytopaenic, Severely Hypo/Hyperglycaemic, INR >1.7 if on Warfarin, Elevated aPTT if on Heparin
Long Term Management of Stroke: Antiplatelet
Dual Antiplatelets (Aspirin and Clopidogrel) for 2 weeks, then continue Clopidogrel lifelong
Long Term Management of Stroke: Antihypertensives
– Primary and Secondary Stroke prevention; Transient HTN following
stroke does not usually need treatment unless DBP >100mmHg; BP should be lowered slowly
to avoid sudden fall in perfusion
Long Term Management of Stroke: Internal Carotid Endarterectomy
For Post- Stroke/TIA, ICA Stenosis >70%; Endarterectomy has 3% mortality but reduces risk of further Stroke/TIA by 75% o Percutaneous Transluminal Angioplasty/Stenting as an alternative
Long Term Management of Stroke: PT
Relieve spasticity and use of walking aids;
Long Term Management of Stroke: SALT+OT
Speech therapy; NG or PEG tube if unsafe swallow; OT – Home adaptations
Long Term Management of Stroke: pharmacotherapy
Pharmacotherapy to relieve spasticity (E.g. Baclofen, Botulinum Toxin)
Stroke Prognosis
One third of patients return to independent mobility, one third have disability requiring
institutional care; If language is intelligible at 3 weeks, good prognosis for speech
