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Posterior Circulation Stroke
Dr.RAVI TEJA
EMERGENCY MEDICINE
Posterior circulation stroke accounts for 20-25% of ischaemic strokes
● Posterior circulation ischaemic stroke is a clinical syndrome associated with
ischaemia related to stenosis, in situ thrombosis, or embolic occlusion of the
posterior circulation arteries
● the vertebral arteries in the neck
● the intracranial vertebral
● Basilar
● posterior cerebral arteries and their branches
INTRODUCTION
● It can be difficult to determine the vascular territory of an acute ischaemic clinical
syndrome on purely clinical grounds, but this knowledge may be needed to determine
the most appropriate acute treatment and prevention strategy
● Although in the past posterior circulation ischaemia was considered to have a lower
recurrence risk than anterior circulation ischaemia, current data suggest that the risk is
at least as high, if not higher
RISK FACTORS
● Hypertension
● Diabetes mellitus
● Obesity
● Cardiac diseases
● Smoking
● Alcohol
● Dyslipidemia
● Renal dysfunction
● Behavioral: sedentary lifestyle, unhealthy diet
● Nonmodifiable: family history/genetics
PATHOGENESIS
70 % of strokes occur in those aged > 70 yrs, but they can occur at any age Cerebral
infarction (80 % )
Results from:
● Thrombosis secondary to atherosclerosis, hypertension and rarely arteritis.
● Cerebral embolism from AF, valve disease/replacement, post-MI, ventricular
aneurysm, myxoma, endocarditis or cardiomyopathy.
● An episode of hypoperfusion (shock)
● Cerebral haemorrhage (20 % )
Associated with:
● Hypertension (rupture of small arteries in the brain)
● Subarachnoid haemorrhage
● Bleeding disorders (including anticoagulants) and intracranial tumours.
ETIOLOGY
● most common causes of posterior circulation stroke are occlusion or embolism from
large artery vertebrobasilar atherosclerosis or dissection, and embolism from the heart
● Dissection of the extracranial vertebral artery is also an important cause of stroke,
especially in young patients
CLINICAL FEATURES
Posterior circulation stroke 5D’s:
D
D
DYSARTHRIA
DYSPHASIA
DIPLOPIA
DIZZINESS
DETERIORATION OF
CONSCIOUSNESS AND ATAXIA
VERTIGO 58.5%
MOTOR WEAKNESS 51.2%
SLURRED SPEECH 43.9%
HEADACHE 43.9%
VOMITING 39%
DYSARTHRIA 34.1%
ALTERED
SENSORIUM
31.1%
SEIZURES 12.2%
MUMBNESS 4.9%
POSTERIOR CEREBRALARTERY INFARCTION
Clinical features:
● Ataxia
● Nystagmus
● AMS
● Vertigo
● Neurological deficits may indicates a brainstem
lesion
Symptoms:
● U/L limb weakness
● Dizziness
● Blurring of vision
● Dysarthria
● supply the posteromedial surface of the temporal lobe and the occipital lobe
Most common presentations signs:
● Visual field loss, classically as contralateral homonymous hemianopia and U/L
cortical blindness is specific for distal posterior circulation stroke
● U/L limb ataxia
● Lethargy
● Sensory deficits
● Alexia
● Inability to name the colours
● Recent memory loss
● U/L 3rd nerve palsy and hemiballismus
BASILAR ARTERY OCCLUSION
Branches of basilar artery
● Anterior inferior cerebellar artery
(AICA) supplies inferior surface of the
cerebellum
● Labyrinthine artery supplies the
membranous labyrinth of the internal ear
● Pontine arteries supply pons and
pontine tegmentum
● Superior cerebellar artery supplies
pons, superior cerebellar peduncle, and
inferior colliculus, etc.
Presents with:
● U/L limb weakness
● Dizziness
● Dysarthria
● Diplopia
● Headache
Most common:
● U/L limb weakness dysarthria
● Babinski sign
● Ocular motor signs
● Dysphagia, nausea or vomiting, dizziness, and Horner’s syndrome are positively
correlated with basilar artery occlusion
Basilar artery occlusion can also rarely cause locked-in syndrome
● which occurs with bilateral pyramidal tract lesions in the ventral pons and is
characterized by complete muscle paralysis except for upward gaze and blinking.
● Basilar artery occlusions have a high risk of death and poor outcomes
VERTEBROBASILAR INFARCTION
Presents with:
● Dizziness
● nausea/vomiting
● Headache
● Dysphasia
● U/L limb weakness
● Horner's syndrome
CEREBELLAR INFARCTION
● Presents with:
● Non specific symptoms
● Dizziness
● Nausea/vomitings
● Gait instability
● Headache
● Dysmetria
● Nystagmus
● Hearing loss
● Intractable hiccups
● AMS/COMA
LACUNAR INFARCTION
● Pure motor/Sensory deficits caused by infarction of smell penetrating arteries and are
commonly associated with chronic HTN and increased age
● Prognosis is generally considered more favorable than for other stroke syndrome
● The lacunar artery is a branch of a
large cerebral artery
CAROTID & VERTEBRALARTERY DISSECTION
● It is also referred as cervical artery dissection
● Major common in young adults and middle
age
● Major cause of stroke
● Carotid dissection can progress to cause
cerebral ischemia or rarely retinal infarction
Risk factors:
● H/O trauma to neck in days to week
● HTN
● large-vessel arteriopathies
● H/O Migraine
Presented with:
● dizziness/vertigo
● Headache (occipital)mimics SAH (i.e.,”THUNDERCLAP HEADACHE”),Temporal
arteritis or migraine
● Neck pain it may be U/L or B/L
Symptoms & Signs:
● U/L facial paresthesia
● Dizziness
● Vertigo
● nausea/vomiting
● diplopia
● New onset of headache neck pain of unclear etiology in an important symptoms that
imaging of neck vessel is commended
● Median time b/w an initial presentation of neck pain and development of other
neurological symptoms is 14 days
● But if headache is 1st symptoms follow within a median time of 15 hours
● Other disturbance ataxia, limb weakness,numbness,dysarthria and hearing loss
● Untreated vertebral artery dissection may result in infarction in region of brain
supplied by posterior circulation
ROSIER SCORE
● The Recognition of Stroke in the Emergency Room (ROSIER) scale is a tool used by
emergency room staff to assess a patient's history and physical examination to
determine if they are likely to be experiencing a stroke.
NIHSS SCORE
● The National Institutes of Health (NIH) Stroke Scale (NIHSS) score is a number
between 0 and 42 that indicates the severity of a stroke. A higher score means a more
severe stroke.
● The NIHSS is composed of 11 items, each of which scores a specific ability between
a 0 and 4.
● For each item, a score of 0 typically indicates normal function in that specific ability,
while a higher score is indicative of some level of impairment
● The NIHSS is an excellent predictor of patient outcomes, but its accuracy is
intentionally sacrificed for reproducibility.
● 0: No stroke symptoms
● 1–4: Minor stroke
● 5–15: Moderate stroke
● 16–20: Moderate to severe stroke
● 21–42: Severe stroke
INVESTIGATIONS
● Basic biochemical
● Haematological parameters
● 2-Decho
● EXG
● CXR
● Lipid profile
● Blood sugars
● ABG
Neurological imaging
● CT Head
● MRI Brain
● Doppler of neck vessels
CT BRAIN
● In ischemic stroke , CT done in first 6 hours may be normal
● Earliest CT changes in an ischemic stroke are loss of gray matter and white matter
differentiation
● After 48 hours a well demarcated wedge shaped opacity in the affected vascular
territory
MRI BRAIN
● A MRI stroke protocol study comprises 3 images primarily T2 flair,diffusion
weighted imaging and apparent diffusion coefficient
● This help to delineate the infarcted tissue from the potentially salvageable ischemic
penumbra
● An acute infarct is seen as bright sport in DWI and a dark spot ADC
● In early infarction, DWI shows a bright spot and flair does not show any change
● Carotid vertebral doppler the patency ,flow velocities in the carotid and vertebral
arteries should be assessed for intervention purpose
● CT/MR Angiography should be done to identify the affected artery
MANAGEMENT
● Management of unconscious patient
● Intubation i/c/o GCS <7
● Control sugars
● Treat fever as it increases metabolic demand brian
● IV Fluids (avoid hypotonic solutions such as 5D/DNS as they increase cerebral
edema)
● Insert ryles tube and foleys catheter
● DVT prophylaxis
● Ulcer prophylaxis
● Treat seizures
BLOOD PRESSURE MANAGEMENT
BP should be brought down gradually in an ischemic stroke ,as fast reduction in BP will
decrease cerebral blood flow and increase penumbra of stroke
BP should be treated only if >220/120 mm Hg
In case of thrombolysis is needed should be decreased to <185/110 mm Hg
Preferred drugs: Amlodipine and beta blockers
TREATMENT FOR CAROTID & VERTEBRALARTERY DISSECTION
Cervical artery dissection can cause ischemic stroke via thromboembolic process
Or
Decreased flow secondary to vascular lesion
Or
From mixed mechanism
● If cervical artery dissection presents symptoms of acute ischemic stroke
● Treat them similarly to any other stroke patient
● Considered the administration of IV thrombolytic therapy in all eligible patients with
stroke from cervical dissection
● In cervical artery dissection patients who are not candidates for thrombolysis or
endovascular therapy
Two medical choice
1. ANTICOAGULATION
2. ANTIPLATELET THERAPY
● Traditionally treated with IV Heparin f/b warfarin
● Administration of either anticoagulants or antiplatelet therapy in ED if the patient is
not a candidate for IV thrombolysis
THROMBOLYSIS
● Alteplase 0.9mg/kg ,10% bolus and remainder as an infusion in 100ml normal saline
over 1 hour
● Timing: upto 3-4.5 hrs after onset of stroke
● In wake up strokes to go by MRI picture of DW positive and flair negative (<6 hours)
Indications for thrombolysis:
● Clinical impression of stroke causing measurable neurologic deficit
● Age >18 years
● Onset of stroke less than 4.5 hrs
● No oedema or haemorrhage of more than 1/3rd of MCA territory
REFERRALS
posterior circulation ischemic/embolic stroke

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posterior circulation ischemic/embolic stroke

  • 1. Posterior Circulation Stroke Dr.RAVI TEJA EMERGENCY MEDICINE
  • 2. Posterior circulation stroke accounts for 20-25% of ischaemic strokes
  • 3. ● Posterior circulation ischaemic stroke is a clinical syndrome associated with ischaemia related to stenosis, in situ thrombosis, or embolic occlusion of the posterior circulation arteries ● the vertebral arteries in the neck ● the intracranial vertebral ● Basilar ● posterior cerebral arteries and their branches INTRODUCTION
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  • 6. ● It can be difficult to determine the vascular territory of an acute ischaemic clinical syndrome on purely clinical grounds, but this knowledge may be needed to determine the most appropriate acute treatment and prevention strategy ● Although in the past posterior circulation ischaemia was considered to have a lower recurrence risk than anterior circulation ischaemia, current data suggest that the risk is at least as high, if not higher
  • 7. RISK FACTORS ● Hypertension ● Diabetes mellitus ● Obesity ● Cardiac diseases ● Smoking ● Alcohol ● Dyslipidemia ● Renal dysfunction ● Behavioral: sedentary lifestyle, unhealthy diet ● Nonmodifiable: family history/genetics
  • 8. PATHOGENESIS 70 % of strokes occur in those aged > 70 yrs, but they can occur at any age Cerebral infarction (80 % ) Results from: ● Thrombosis secondary to atherosclerosis, hypertension and rarely arteritis. ● Cerebral embolism from AF, valve disease/replacement, post-MI, ventricular aneurysm, myxoma, endocarditis or cardiomyopathy. ● An episode of hypoperfusion (shock)
  • 9. ● Cerebral haemorrhage (20 % ) Associated with: ● Hypertension (rupture of small arteries in the brain) ● Subarachnoid haemorrhage ● Bleeding disorders (including anticoagulants) and intracranial tumours.
  • 10. ETIOLOGY ● most common causes of posterior circulation stroke are occlusion or embolism from large artery vertebrobasilar atherosclerosis or dissection, and embolism from the heart ● Dissection of the extracranial vertebral artery is also an important cause of stroke, especially in young patients
  • 11. CLINICAL FEATURES Posterior circulation stroke 5D’s: D D DYSARTHRIA DYSPHASIA DIPLOPIA DIZZINESS DETERIORATION OF CONSCIOUSNESS AND ATAXIA
  • 12. VERTIGO 58.5% MOTOR WEAKNESS 51.2% SLURRED SPEECH 43.9% HEADACHE 43.9% VOMITING 39% DYSARTHRIA 34.1% ALTERED SENSORIUM 31.1% SEIZURES 12.2% MUMBNESS 4.9%
  • 13. POSTERIOR CEREBRALARTERY INFARCTION Clinical features: ● Ataxia ● Nystagmus ● AMS ● Vertigo ● Neurological deficits may indicates a brainstem lesion Symptoms: ● U/L limb weakness ● Dizziness ● Blurring of vision ● Dysarthria ● supply the posteromedial surface of the temporal lobe and the occipital lobe
  • 14. Most common presentations signs: ● Visual field loss, classically as contralateral homonymous hemianopia and U/L cortical blindness is specific for distal posterior circulation stroke ● U/L limb ataxia ● Lethargy ● Sensory deficits ● Alexia ● Inability to name the colours ● Recent memory loss ● U/L 3rd nerve palsy and hemiballismus
  • 15. BASILAR ARTERY OCCLUSION Branches of basilar artery ● Anterior inferior cerebellar artery (AICA) supplies inferior surface of the cerebellum ● Labyrinthine artery supplies the membranous labyrinth of the internal ear ● Pontine arteries supply pons and pontine tegmentum ● Superior cerebellar artery supplies pons, superior cerebellar peduncle, and inferior colliculus, etc.
  • 16. Presents with: ● U/L limb weakness ● Dizziness ● Dysarthria ● Diplopia ● Headache Most common: ● U/L limb weakness dysarthria ● Babinski sign ● Ocular motor signs ● Dysphagia, nausea or vomiting, dizziness, and Horner’s syndrome are positively correlated with basilar artery occlusion
  • 17. Basilar artery occlusion can also rarely cause locked-in syndrome ● which occurs with bilateral pyramidal tract lesions in the ventral pons and is characterized by complete muscle paralysis except for upward gaze and blinking. ● Basilar artery occlusions have a high risk of death and poor outcomes
  • 18. VERTEBROBASILAR INFARCTION Presents with: ● Dizziness ● nausea/vomiting ● Headache ● Dysphasia ● U/L limb weakness ● Horner's syndrome
  • 19. CEREBELLAR INFARCTION ● Presents with: ● Non specific symptoms ● Dizziness ● Nausea/vomitings ● Gait instability ● Headache ● Dysmetria ● Nystagmus ● Hearing loss ● Intractable hiccups ● AMS/COMA
  • 20. LACUNAR INFARCTION ● Pure motor/Sensory deficits caused by infarction of smell penetrating arteries and are commonly associated with chronic HTN and increased age ● Prognosis is generally considered more favorable than for other stroke syndrome ● The lacunar artery is a branch of a large cerebral artery
  • 21. CAROTID & VERTEBRALARTERY DISSECTION ● It is also referred as cervical artery dissection ● Major common in young adults and middle age ● Major cause of stroke ● Carotid dissection can progress to cause cerebral ischemia or rarely retinal infarction Risk factors: ● H/O trauma to neck in days to week ● HTN ● large-vessel arteriopathies ● H/O Migraine
  • 22. Presented with: ● dizziness/vertigo ● Headache (occipital)mimics SAH (i.e.,”THUNDERCLAP HEADACHE”),Temporal arteritis or migraine ● Neck pain it may be U/L or B/L Symptoms & Signs: ● U/L facial paresthesia ● Dizziness ● Vertigo ● nausea/vomiting ● diplopia
  • 23. ● New onset of headache neck pain of unclear etiology in an important symptoms that imaging of neck vessel is commended ● Median time b/w an initial presentation of neck pain and development of other neurological symptoms is 14 days ● But if headache is 1st symptoms follow within a median time of 15 hours
  • 24. ● Other disturbance ataxia, limb weakness,numbness,dysarthria and hearing loss ● Untreated vertebral artery dissection may result in infarction in region of brain supplied by posterior circulation
  • 25. ROSIER SCORE ● The Recognition of Stroke in the Emergency Room (ROSIER) scale is a tool used by emergency room staff to assess a patient's history and physical examination to determine if they are likely to be experiencing a stroke.
  • 26. NIHSS SCORE ● The National Institutes of Health (NIH) Stroke Scale (NIHSS) score is a number between 0 and 42 that indicates the severity of a stroke. A higher score means a more severe stroke. ● The NIHSS is composed of 11 items, each of which scores a specific ability between a 0 and 4. ● For each item, a score of 0 typically indicates normal function in that specific ability, while a higher score is indicative of some level of impairment ● The NIHSS is an excellent predictor of patient outcomes, but its accuracy is intentionally sacrificed for reproducibility.
  • 27. ● 0: No stroke symptoms ● 1–4: Minor stroke ● 5–15: Moderate stroke ● 16–20: Moderate to severe stroke ● 21–42: Severe stroke
  • 28. INVESTIGATIONS ● Basic biochemical ● Haematological parameters ● 2-Decho ● EXG ● CXR ● Lipid profile ● Blood sugars ● ABG Neurological imaging ● CT Head ● MRI Brain ● Doppler of neck vessels
  • 29. CT BRAIN ● In ischemic stroke , CT done in first 6 hours may be normal ● Earliest CT changes in an ischemic stroke are loss of gray matter and white matter differentiation ● After 48 hours a well demarcated wedge shaped opacity in the affected vascular territory
  • 30. MRI BRAIN ● A MRI stroke protocol study comprises 3 images primarily T2 flair,diffusion weighted imaging and apparent diffusion coefficient ● This help to delineate the infarcted tissue from the potentially salvageable ischemic penumbra ● An acute infarct is seen as bright sport in DWI and a dark spot ADC ● In early infarction, DWI shows a bright spot and flair does not show any change
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  • 32. ● Carotid vertebral doppler the patency ,flow velocities in the carotid and vertebral arteries should be assessed for intervention purpose ● CT/MR Angiography should be done to identify the affected artery
  • 33. MANAGEMENT ● Management of unconscious patient ● Intubation i/c/o GCS <7 ● Control sugars ● Treat fever as it increases metabolic demand brian ● IV Fluids (avoid hypotonic solutions such as 5D/DNS as they increase cerebral edema) ● Insert ryles tube and foleys catheter ● DVT prophylaxis ● Ulcer prophylaxis ● Treat seizures
  • 34. BLOOD PRESSURE MANAGEMENT BP should be brought down gradually in an ischemic stroke ,as fast reduction in BP will decrease cerebral blood flow and increase penumbra of stroke BP should be treated only if >220/120 mm Hg In case of thrombolysis is needed should be decreased to <185/110 mm Hg Preferred drugs: Amlodipine and beta blockers
  • 35. TREATMENT FOR CAROTID & VERTEBRALARTERY DISSECTION Cervical artery dissection can cause ischemic stroke via thromboembolic process Or Decreased flow secondary to vascular lesion Or From mixed mechanism
  • 36. ● If cervical artery dissection presents symptoms of acute ischemic stroke ● Treat them similarly to any other stroke patient ● Considered the administration of IV thrombolytic therapy in all eligible patients with stroke from cervical dissection
  • 37. ● In cervical artery dissection patients who are not candidates for thrombolysis or endovascular therapy Two medical choice 1. ANTICOAGULATION 2. ANTIPLATELET THERAPY ● Traditionally treated with IV Heparin f/b warfarin ● Administration of either anticoagulants or antiplatelet therapy in ED if the patient is not a candidate for IV thrombolysis
  • 38. THROMBOLYSIS ● Alteplase 0.9mg/kg ,10% bolus and remainder as an infusion in 100ml normal saline over 1 hour ● Timing: upto 3-4.5 hrs after onset of stroke ● In wake up strokes to go by MRI picture of DW positive and flair negative (<6 hours)
  • 39. Indications for thrombolysis: ● Clinical impression of stroke causing measurable neurologic deficit ● Age >18 years ● Onset of stroke less than 4.5 hrs ● No oedema or haemorrhage of more than 1/3rd of MCA territory