ISCHEMIC STROKE
Vertebrobasilar stroke
Created 20/06/2023, last revision 20/09/2023
- the vertebrobasilar (posterior) circulation comprises the vertebral, basilar, and posterior cerebral arteries, as well as their branches
- it supplies the posterior regions of the brain (brainstem, thalamus, cerebellum, and areas of the occipital and temporal lobes)
- the term vertebrobasilar insufficiency (VBI) describes inadequate blood flow through the posterior circulation
- it may manifest either as a transient condition (transient ischemic attack (TIA), drop attack, Bow Hunter’s syndrome) or as a permanent condition (infarct)
- several mechanisms leading to hypoperfusion may be involved and may even be 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 discouraged
- vertebrobasilar ischemia shares features with other etiologies; DDx in the acute setting can be challenging
- DDx of vertigo (labyrinthitis, vestibular neuritis, benign paroxysmal positional vertigo, etc.)
- DDx of impaired consciousness (metabolic coma, nonconvulsive seizure, etc.)
- the outcome depends on the location and extent of the stenosis/occlusion, the quality of the collateral circulation, and adequate and timely therapy
- mortality > 90% in untreated extensive basilar artery occlusions (BAO)
- posterior stroke is associated with a higher risk of recurrence compared to strokes in carotid territory
- the risk of recurrence after a previous stroke/TIA with VA/BA stenosis ≥ 50% is approx. 22%/90 days [Marquardt, 2009]
Clinical presentation
- the symptoms of a vertebrobasilar stroke can vary greatly 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
- traditional brainstem syndromes have been described, but some symptoms may be nonspecific (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 a stroke is usually accompanied by other brainstem and cerebellar symptoms
- nausea and vomitus
- eye movement disorder (nuclear/supranuclear) +/- diplopia
- visual field disturbances
- signs of sympathetic lesions
- 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 impairment is usually not caused by a stroke (except for the 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 lead to drop attacks
- 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 the P1 segment of the posterior cerebral artery (PCA)
- occlusion of a perforator results in lacunar stroke
- 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 the P1 segment of the posterior cerebral artery (PCA)
- arterial dissection most commonly affects the V3 segment
- 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 in 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 (mostly 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
- flow stasis increasing the likelihood of thrombus formation
- arterial wall stress predisposing to dissection or even rupture
- 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
Neuroimaging
Brain imaging
- brain CT
- 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
Vascular imaging
- CT angiography / MR angiography
- CTA is a fast and widely available method with high sensitivity (about 94%)
- the accuracy of MRI in the distal posterior circulation is comparable to CTA; problematic is the imaging of the aortic arch and the origin of vertebral arteries
- in the acute stage, exclude occlusion of the V4 segment, vertebral junction, BA, and/or PCA, which could be solved by recanalization therapy
- 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)
- neurosonology
- allows to assess hemodynamics, steal phenomenon
- enables repeated monitoring
- carefully examine the V0 segment
- dynamic tests (during rotation, ante-and retroflexion) can exclude external VA compression (Bow Hunter’s syndrome)
- exclude steal phenomenon
- 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
Radiological predictors of clinical outcome in basilar artery occlusion
Etiology
- the same etiologies apply to both vertebrobasilar and carotid territories → Etiologic classification of ischemic stroke
- Bow-Hunter’s syndrome and subclavian steal phenomenon are specific to the posterior circulation
Differential diagnosis
- ischemia or bleeding in the brain stem and cerebellum does not usually cause diagnostic difficulties due to typical symptoms
- it is necessary to exclude a nonvascular etiology (external brainstem compression, brainstem tumor)
- isolated vertigo and altered consciousness presents considerable challenges due to the broad spectrum of potential etiologies involved
- 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 disorders (weakness, fainting, blurred vision, or unsteady gait)
- to determine whether the dizziness is vestibular, nonvestibular, or caused by another balance disorder, we should obtain and evaluate the following:
- an accurate description of the current condition, incl. associated symptoms (hearing impairment, 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 improving)
- consider the age of the patient
- these possibilities must be distinguished based on the patient’s history:
- true vertigo (usually rotational) caused by vestibular pathway dysfunction (central or peripheral)
- balance disorder without rotatory vertigo
- instability manifesting mainly when walking or standing; symptoms typically alleviate when sitting or lying down
- the absence of rotational vertigo suggests a nonvestibular etiology
- presyncope (fainting) and other nonspecific symptoms
- feeling of impending fainting but without actual loss of consciousness, lightheadedness or general malaise
- e.g., due to hypoglycemia, hyperventilation, anemia, side effects of drugs, etc.
- exclude vascular etiology, especially in elderly patients with vascular risk factors, and look for subtle lesions on neuroimaging (perform DWI if possible)
- labyrinthine artery arises from 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 therefore 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 older age
- 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
- an inflammatory disorder (viral) affecting the vestibular nerve
- characterized by rotational vertigo, nausea, vomiting, and imbalance, developing over several hours
- typically lacks auditory symptoms such as hearing loss or tinnitus
- and progressive
- occurs more frequently at younger ages and is not accompanied by hearing impairment or brainstem/cerebellar symptoms
→ neuronitis vestibularis
- brief episodes of vertigo provoked by a specific position or during a specific movement → more here
- headaches + aura symptoms originating from the brainstem (dysartria, vertigo, double vision, and ataxia)
- headache often starts on one side of the head and then gradually spreads and gets stronger
- duration:
- typically, the aura symptoms develop gradually over minutes and can last up to 60 minutes
- aura can start 10-45 minutes before the headache occurs
- the headache phase that usually follows, may last for several hours (in some cases up to 72 hours)
- typically, the aura symptoms develop gradually over minutes and can last up to 60 minutes
- at least two attacks that meet 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 headaches are common, and symptoms are typically provoked and worsened by head movement
- 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 of a typical postural nature and are modified by lying down
- presyncope states with a feeling of weakness and uncertainty in space
Management
Acute stroke therapy
- intravenous thrombolysis
- in the case of basilar artery occlusions, thrombolysis or thrombectomy can be performed without a strict time limit due to 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)
- recanalization rate for thrombi > 30 mm is approx. 20%-30% [Strbian, 2014]
- in the case of basilar artery occlusions, thrombolysis or thrombectomy can be performed without a strict time limit due to poor prognosis; imaging methods with the assessment of tissue viability are helpful (see above for prognostic scales) [Strbian, 2013]
- mechanical recanalization
- intra-arterial thrombolysis (IAT)
- consider in patients with inappropriate anatomical conditions for mechanical recanalization
- possible treatment of significant peripheral embolization during thrombectomy
Conservative therapy
- standard acute antiplatelet therapy/anticoagulation in patients ineligible for recanalization therapy
Surgery
- early decompressive craniectomy in patients with expansive ischemia → malignant ischemia
Symptomatic acute stroke therapy
- apply 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 at higher doses
- ondansetron (ONDANSETRON, ZOFRAN)
- diazepam (DIAZEPAM) – 2-10 mg IV for acute vertigo
- increased risk of adverse events in the elderly
- thiethylperazine (TORECAN)
- for chronic conditions, use antivertiginous drugs only for the treatment of a true vertigo
- antivertiginous drugs are not indicated for the treatment of:
- nonspecific balance disorders
- short-term dizziness (lasting seconds to minutes)
- persistent vestibular symptoms
- nonspecific balance disorders
Secondary prevention
- best medical treatment (BMT)
- reconstructive procedures (stenting, endarterectomy, or reconstruction/transposition) should be performed only if the BMT fails
- no evidence suggests that revascularization of vertebral artery stenosis is superior to the BMT (negative VAST trial, etc.)
- no evidence suggests that revascularization of vertebral artery stenosis is superior to the BMT (negative VAST trial, etc.)
Rehabilitation
- speeds up the vestibular compensation process