• posterior circulation strokes account for 20-25% (range 17-40%) of ischemic strokes
  • posterior (vertebrobasilar) circulation includes the vertebral (extra- and intracranial), basilar, and posterior cerebral arteries, as well as their branches
  • it supplies the posterior regions of the brain (brainstem, thalamus, cerebellum, and the occipital and temporal lobes)
  • in general, the term vertebrobasilar insufficiency (VBI) describes inadequate blood flow through the posterior circulation
    • it can be either transient (transient ischemic attack (TIA), drop attack, Bow Hunter’s syndrome) or permanent (infarct)
    • several mechanisms leading to hypoperfusion may be involved and even combined (embolism, atherothrombosis, external mechanical compression, steal syndrome)
    • the term has been overused (often referring to various nonvascular vertiginous conditions in the geriatric population), and its use is currently discouraged
  • certain occlusions cause characteristic clinical patterns and syndromes
  • however, vertebrobasilar stroke shares features with other conditions (stroke mimics); differential diagnosis in the acute setting can be challenging
  • the outcome depends on the location and extent of the stenosis/occlusion, the quality of the collateral circulation, and adequate and timely therapy
    • if extensive basilar artery occlusion (BAO) is left untreated, the mortality rate is over 90%
  • strokes in the posterior territory have a higher risk of recurrence compared to those in the carotid territory  (Werring, 2014)

Anatomic notes

arterie - kmen 1-2

vertebral artery

anterior spinal artery (ASA)

posterior spinal artery

arterie - kmen 2-2

posterior spinal artery

anterior spinal artery (ASA)

vertebral artery

arterie - kmen 3-2

anterior spinal artery (ASA)

vertebral artery

vertebral artery
(V4 segment)

posterior inferior cerebellar artery (PICA)

arterie - kmen 4-2

vertebral artery + caudal BA perforators

posterior inferior cerebellar artery (PICA)

arterie - kmen 5-2

long circumferential branches from BA + AICA

short circumferential branches from BA

paramedian perforators from BA

arterie - kmen 6-2

short circumferential branches from BA

long circumferential branches from BA + SCA

paramedian perforators from BA

basilar artery

arterie - kmen 7-2

PCA

basilar artery

branches from P1 segment + SCA

short nad long branches from P1 + posteromedial choroid artery

anteromedial branches from BA and P1 segment

arterie - kmen 8-2

thalamogeniculate artery

short nad long branches from P1 + posteromedial choroid artery

branches from P1 segment + SCA

anteromedial branches from BA and P1 segment

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Clinical presentation

  • the symptoms of a vertebrobasilar stroke can differ significantly among patients, depending on the type of occluded artery, the extent of occlusion, and the quality of the collateral circulation
  • a combination of symptoms is common → see Topical diagnosis of stroke
  • while traditional brainstem syndromes have been described, some symptoms may not be specific (DDx of vertigo)
  • vestibular syndrome (vertigo, nystagmus, tonic deviations)
    • isolated vertigo is usually of nonvascular origin
    • nonspecific balance disorders must be distinguished (see below)
    • vertigo due to stroke is usually associated with other brainstem and cerebellar symptoms.
  • nausea and vomiting
  • eye movement disorder (nuclear/supranuclear) +/- diplopia
  • visual field disturbances
  • signs of sympathetic lesions
    • Horner’s syndrome (ptosis and miosis, sometimes anhidrosis on the affected side)  Horner syndrom
    • Harlequin sign  Harlequin sign
  • ataxia and/or dysmetria
  • dysarthria/dysphonia
  • dysphagia
  • paresthesia/hypesthesia in the face and/or extremities and trunk
  • combination of paresis or sensory deficit in the extremities
    • hemiparesis or quadriparesis
  • isolated hearing loss is typically not caused by stroke (except for occlusion of the labyrinthine artery)
  • alternating syndromes are typical for localized brainstem lesions with an ipsilateral nuclear lesion of a cranial nerve, Horner’s syndrome or cerebellar syndrome, and contralateral fascicular disorder (hemiparesis or hemihypesthesia)
  • larger occlusions lead to impaired consciousness (coma may be the initial manifestation) → Examination of the patient with impaired consciousness
  • transient circulatory disturbances may also cause drop attacks

Etiopathogenesis

Identifying the underlying mechanism and risk factors is crucial for stroke prevention as it affects the choice of optimum preventive measures

  • the most frequent causes of vertebrobasilar stroke are atherosclerosis (AS) and arteriolopathy; cardioembolism is less common
    • AS lesions are most commonly located in the V0 and V4 segments of the vertebral arteries, in the proximal and middle segments of the basilar artery, and in the P1 segment of the posterior cerebral artery (PCA)     Calcified plaques in the V4 segment of the vertebral artery
    • occlusion of a perforator results in lacunar stroke   Pontine lacunar stroke
  • arterial dissection most commonly affects the V3 segment  Dissection of the vertebral artery extending to the basilar artery causing its occlusion
    • typical presentations include neck or occipital pain +/- TIA or infarction
  • stenosis can cause:
    • atherothrombotic occlusion
    • perforator occlusion
    • thromboembolism
    • hypoperfusion in distal segments
    • steal phenomenon
      • occurs with stenosis/occlusion of the proximal segments of the subclavian artery or brachiocephalic trunk
      • usually causes only transient symptoms (dizziness), not stroke
    • Bow-Hunter’s syndrome (also known as rotational vertebral artery syndrome) – transient ischemic symptoms caused by external mechanical compression of the vertebral artery (usually at the C1-2 level) during lateral flexion or rotation of the head, often in combination with contralateral stenosis
  • a less common cause of stroke is dolichoectasia and its complications  Basilar artery dolichoectasia (CTA)
    • flow stasis increases the likelihood of thrombus formation
    • arterial wall stress predisposes to dissection
    • enlarged artery may cause a mass effect on adjacent neural structures

Diagnostic evaluation

  • diagnosis is based on a careful history with a detailed clinical examination and the correct indication and interpretation of imaging studies
  • all cases of suspected stroke require urgent brain imaging to exclude haemorrhage, vessel imaging is essential to identify artery occlusion. It should be performed without delay, as minimizing the time between stroke onset and initiation of thrombolysis is associated with a good outcome

Neuroimaging

Brain imaging

  • brain CT
    • baseline imaging in acute stroke patients (good availability, fast performance, low cost)
    • do not miss BA occlusion (dense sign on NCCT) in patients with brainstem symptoms or altered consciousness!   Dense artery sign in the basilar artery occlusion (NCCT)
  • brain MRI
    • optimal imaging method for posterior circulation stroke
    • higher sensitivity compared to CT; small lesions may not be visible on the initial CT
    • MR DWI confirms ischemia   Infarct in the PICA territory (DWI) Medial medullary syndrome (Dejerine) on DWI

Vascular imaging

  • CT angiography / MR angiography
    • CTA is a fast and widely available method with high sensitivity (~ 94%)
    • the accuracy of MRI in the distal posterior circulation is comparable to CTA, but imaging of the aortic arch and the origin of the vertebral arteries is problematic
    • in the acute stage, exclude occlusion of the V4 segment, vertebral junction, BA, and/or PCA, which could be solved by recanalization therapy  Basilar artery occlusion. Left image shows dense artery sign on NCCT, right image shows absent BA on CTA.  Posterior cerebral artery (PCA) occlusion on CTA
    • it secondary prevention, it is essential to manage potential stenoses properly (mainly in the prevertebral segments of the subclavian artery, the origin of VA, and in the V4 segment and BA) Subclavian artery stenosis on CTA Basilar artery stenosis on CTA  Calcified plaques in the V4 segment of the vertebral artery
  • neurosonology
    • allows to assess hemodynamics, steal phenomenon
    • enables repeated monitoring
    • carefully examine the V0 segment  Stenosis of V0 segment on the ultrasound (PSV 215 cm/s)
    • dynamic tests (during rotation, ante-and retroflexion) can exclude external VA compression (Bow Hunter’s syndrome)
    • exclude steal phenomenon  Subclavian (verterbal) steal ultrasound grades
    • with difficult BA insonation, its patency can be verified by tapping the VA retromastoidally while detecting the undulations in the PCA
  • DSA
    • DSA is reserved for endovascular procedures and is rarely used as a stand-alone diagnostic tool
Basilar artery occlusion on NCCT (dense artery sign)

HDBA sign

Radiological predictors of clinical outcome in basilar artery occlusion

HDBA sign
  • HDBA (HyperDense Basilar Artery) sign on NCCT
  • predictor of BAO – sensitivity 71%, specificity 98% [Goldmakher, 2009]
  • predictor of poor outcome (OR 5.6, mRS > 2 at 6 months)
HDBA sign
FHBA Sign

FLAIR-Hyperintense Basilar Artery (FHBA) Sign

  • hyperintense basilar artery (BA) on FLAIR (Fluid-Attenuated Inversion Recovery) imaging – a sign of BA occlusion
  • increased signal is due to dampened flow and signal changes in the thrombus
"The FHBA sign refers to an occluded basilar artery, which is hyperintense on FLAIR images
pc-ASPECTS
  • helps to assess early ischemic changes on non-contrast (NCCT), optionally on CTA-SI (source images)
  • normal brain scores 10, points are subtracted for each affected region:
    • thalami (1 point each)
    • occipital lobes (1 point each)
    • midbrain (2 points – uni- and bilateral)
    • pons (2 points – uni- and bilateral)
    • cerebellar hemispheres (1 point each)
  • pc-ASPECTS < 8 is associated with a poor prognosis   [Puetz, 2009]
  • limitations:
    • recent ischemia superimposed on an older lesion
    • extensive leukoencephalopathy
    • image quality
pc-ASPECTS on NCCT
pc-ASPECT score predicts prognosis [Puetz, 2009]
DWI pc-ASPECTS
  • same scoring principles as with CT
  • DWI pc-ASPECTS ≥ 8 predicts good outcome
  • DWI pc-ASPECTS score < 6 predicts a poor outcome, although even in this group a good outcome can be achieved with successful recanalization [Kim, 2019]
DWI pc-ASPECTS
BATMAN score

Basilar Artery on Computed Tomography Angiography (BATMAN) score

  • the BATMAN score is a 10-point CTA–based grading system that incorporates thrombus burden and the presence of collaterals
  • the posterior circulation is divided into 6 segments
    • vertebral arteries (VA) – considered as 1 segment = 1 point
    • posterior cerebral artery (PCA) – scored separately, 1 point each
    • posterior communicant artery (PComA) – scored separately, 2 points each (or 3 points for fetal PCA)
    • 3 segments of the basilar artery (BA) – 1 point each
  • patients with a lower BATMAN score were more likely to have a poor outcome – the absence of PComA (bilateral or unilateral) was the strongest predictor of poor clinical outcome (OR of 6.8) [Alemseged, 2017]
BATMAN score
Collaterals assessment

Posterior circulation CTA score

  • 0 –  no posterior communicating artery (PComA)
  • 1 –  unilateral PComA
  • 2 –  bilateral PComA
  • the presence of bilateral PComA on CTA was associated with more favorable outcomes in patients with BAO undergoing mechanical thrombectomy [Goyal, 2016]

Posterior Circulation Collateral Score (PC-CS)

  • max. 10 points (normal findings)
  • AICA, PICA, SCA – assign 1 point to each patent artery (assess bilaterally)
  • PComA – assign 1 point if PComA is smaller than the P1 segment, 2 points if larger
  • patients with higher scores have better prognosis  [Goyal, 2016]

Etiology

Differential diagnosis

  • ischemia or hemorrhage in the brain stem and cerebellum does not usually cause diagnostic difficulties due to typical symptoms
  • nonvascular etiologies (external brainstem compression, brainstem tumor) must be excluded
  • isolated vertigo and altered consciousness are challenging because of the wide range of potential etiologies
  • not every vertigo is of vascular origin (especially in the elderly)
  • dizziness should always be specified and accurately described – distinguish vestibular vertigo from various nonvestibular conditions, ataxia, or other balance disorders and psychogenic conditions
    • the term vertigo should be reserved for the dizziness of vestibular origin
    • distinguish other nonspecific conditions (weakness, fainting, blurred vision, or unsteady gait)
  • to determine whether the dizziness is vestibular, nonvestibular, or caused by another balance disorder, the following should be obtained and evaluated:
    • an accurate description of the current condition, including associated symptoms (hearing loss, lesions of other cranial nerves, brainstem, and cerebellar symptoms)
    • onset (sudden x gradual), duration, and provoking factors (e.g.,  head or body movement or position)
    • course (constant x fluctuating, spontaneous worsening x improvement)
  • consider the patient´s age
  • these possibilities must be distinguished based on the patient’s history:
    • true vertigo (usually rotational) is caused by vestibular pathway dysfunction (central or peripheral)
    • impaired balance without rotatory vertigo
      • instability manifesting particularly when walking or standing; symptoms typically alleviate when sitting or in a supine position
      • the absence of rotational vertigo suggests a nonvestibular etiology
    • presyncope (fainting) and other nonspecific symptoms
      • a feeling of impending fainting but without actual loss of consciousness, lightheadedness, or general malaise
      • e.g., due to hypoglycemia, hyperventilation, anemia, side effects of medication, etc.
  • exclude vascular etiology, especially in elderly patients with vascular risk factors, and look for subtle lesions on neuroimaging (perform DWI if possible)
  • the labyrinthine artery arises from the AICA
  • its isolated occlusion (rare) leads to sudden and marked impairment of hearing and vestibular function and may be clinically characterized by a peripheral vestibular syndrome
    • hearing loss is usually permanent
    • vestibular impairment is long-lasting, with some gradual improvement due to central compensation
  • however, there is usually a concomitant occlusion of the AICA or BA, and thus, other brainstem/cerebellar symptoms can be observed
  • labyrinthine infarction may be preceded by transient isolated episodes of vertigo
  • a common cause of nonspecific balance problems in the elderly
  • the maintenance of balance depends on the mutual integration of the visual, vestibular, and somatosensory systems
  • balance problems (other than classic vertigo) can occur when any of these systems are affected in isolation or when several of them are affected simultaneously
  • dizziness can be a side effect of many drugs
  • older people are particularly susceptible
  • aminoglycosides, salicylates (aspirin), and some diuretics (furosemide) may directly affect the vestibular system due to ototoxicity
  • dizziness may also occur with tricyclic antidepressants, beta-blockers, etc.
  • an inflammatory disorder (viral) affecting the vestibular nerve
  • characterized by rotational vertigo, nausea, vomiting, and imbalance that develops over several hours
  • typically lacks auditory symptoms such as hearing loss or tinnitus
  • is progressive
  • occurs more frequently at younger ages and is not accompanied by hearing impairment or brainstem/cerebellar symptoms

→ vestibular neuronitis

  • headaches + brainstem aura symptoms (dysarthria, vertigo, double vision, and ataxia)
  • headache often starts on one side of the head and then gradually spreads and becomes more severe
  • duration:
    • typically, the aura symptoms develop gradually over minutes and can last up to 60 minutes
      • aura can start 10-45 minutes before the onset of the headache
    • the headache that usually follows may last for several hours (in some cases up to 72 hours)
  • at least two attacks meeting the above criteria are required to establish the diagnosis (International Classification of Headache Disorders)
  • cervical vertigo – not a true rotational vertigo with nystagmus, but rather a disturbance of balance, a feeling of instability with vegetative symptoms. Concurrent headache is common, and symptoms are typically provoked and worsened by head movements
  • cardiac insufficiency – leads to impaired cerebral perfusion and may be manifested by dizziness (but never true rotational vertigo) or a tendency to faint. Symptoms are usually postural and improve in supine position
  • presyncope with a feeling of weakness and spatial uncertainty

Management

Acute stroke therapy

  • intravenous thrombolysis
    • in the case of basilar artery occlusion, thrombolysis or thrombectomy can be performed without a strict time limit due to the poor prognosis; imaging methods with the assessment of tissue viability are helpful (see above for prognostic scales)    [Strbian, 2013]
    • recanalization is achieved in 50-70% (depending on etiology and extent of occlusion)
  • mechanical recanalization
    • most commonly, thrombectomy is performed; angioplasty may be considered in selected cases   Successful recanalization of an occluded basilar arteryy
    • thrombectomy is usually preceded by bridging IVT
    • thrombectomy has a high rate of successful recanalization (66-100%)
    • early recanalization significantly increases the chance of a good outcome
  • intra-arterial thrombolysis (IAT)
    • consider in patients with inappropriate anatomical conditions for mechanical recanalization
    • possible treatment of significant peripheral embolization during thrombectomy

Conservative therapy

Surgery

  • early decompressive craniectomy in patients with extensive ischemia → malignant ischemia
  • external ventricular drainage may be lifesaving in large-volume cerebellar infarction with a decreased level of consciousness attributable to acute hydrocephalus

Symptomatic acute stroke therapy

  • adhere to the principles of general acute stroke management
  • vertebrobasilar stroke is usually associated with vertigo, nausea, and vomiting
    • thiethylperazine (TORECAN)
      • available in oral, rectal, and intravenous forms
      • acute extrapyramidal dystonia may occur with higher doses
    • ondansetron (ONDANSETRON, ZOFRAN)
    • diazepam (DIAZEPAM) –  2-10 mg IV for acute vertigo
      • there is a higher risk of adverse events in the elderly
  • for chronic conditions, use antivertiginous drugs only to treat true vertigo
  • antivertiginous drugs are not indicated for the treatment of:
    • nonspecific imbalance
    • short-term dizziness (lasting seconds to minutes)
    • persistent vestibular symptoms

Secondary prevention

  • best medical treatment (BMT)
  • reconstructive procedures (stenting, endarterectomy, or reconstruction/transposition) should only be performed if the BMT fails
    • no evidence suggests that revascularization of vertebral artery stenosis is superior to the BMT (negative VAST trial, etc.)

→  Vertebrobasilar steno-occlusive diasese
→  Prevention of ischemic stroke

Rehabilitation

  • speeds up the vestibular compensation process

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Vertebrobasilar stroke
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