Cerebral infarction is responsible for an estimated 6.7 million deaths per year representing a major cause of disability worldwide.
Posterior circulation ischaemic stroke is responsible for 20% of cerebral infarctions and carries a mortality rate of above 85% if untreated.
Although recent clinical trials have shifted the paradigm of acute ischaemic stroke (AIS) management towards endovascular treatment (EVT) in the anterior circulation (AC),
posterior circulation AIS remains a challenge due to its complex clinical picture,
with often non-specific symptoms,
leading to delays in diagnosis and treatment.
A posterior circulation (PC) acute ischaemic stroke occurs in the brain territory supplied by the vertebrobasilar system.
ANATOMY
The vertebral arteries (VA) are paired arteries that arise as the first branches of the subclavian arteries,
having an ascending course through the transverse foramina of the cervical vertebrae and the foramen magnum into the posterior fossa,
converging at the pontomedullary junction to form the basilar artery trunk (BA).
They are divided into 4 segments (Fig.
1):
- V1 - preforaminal
- V2 - foraminal
- V3 - extraspinal
- V4 - intradural/ intracranial.
The BA is an unpaired artery with a cephalad course,
ventral to the medulla and pons up to the pontomesencephalic junction,
where it bifurcates into the posterior cerebral arteries (PCAs).
The intracranial vertebrobasilar system has been topographically divided into proximal,
middle and distal territories (Table 1).
CEREBRAL ISCHAEMIA
Etiologically,
arterial occlusion leading to cerebral ischaemia is divided into the following subtypes:
- Thrombotic - occurring in the context of arterial wall disease,
such as atherosclerosis,
dissection or fibromuscular dysplasia
- Embolic - debris from an extra cranial origin,
most commonly cardiac
- Systemic hypoperfusion - in the context of low cardiac output,
due to cardiac dysfunctions
PC STROKE MECHANISMS
Large vessel atherosclerosis is responsible for roughly 35% of PC strokes,
other aetiologies include penetrating artery occlusions,
embolism from cardiac source or cervical artery dissections (CADs).
It has been shown that often the occlusive process is in the neck segments and not in the head (Fig.
2),
posterior circulation transient ischaemic attacks (TIAs),
aka “vertebrobasilar insufficiency”,
often forewarning fatal brainstem infarction.
Vertebrobasilar insufficiency (VBI) is defined as posterior circulation ischaemia symptoms due to haemodynamic failure.
VBI can precede a PC stroke in around 25% of cases.
DEFINING TANDEM LESIONS
Tandem lesions are defined by concomitant intracranial and extracranial vascular pathology,
typically:
- Proximal VA steno-occlusive disease and
- Distal BA,
PICA or SCA occlusion.
VERTEBROBASILAR STROKE SYMPTOMS
Multiple posterior circulation stroke syndromes have been described,
their corresponding vascular territories and clinical symptoms are given below.
(Table 2 and 3).
A few featuring characteristics distinguishing a vertebrobasilar stroke from a carotid system stroke are the following:
- Cranial nerve signs are ipsilateral,
whereas motor deficits involve the contralateral hemibody (“alternating syndromes”)
- Cerebellar signs are usually present (ataxia,
dysmetria)
- Vertigo,
nausea,
vomiting and nystagmus show involvement of the vestibular system
- Horner syndrome/ oculosympathetic paresis (palpebral ptosis,
miosis,
enophtalmos and hemifacial anhidrosis) present in brainstem lesions
- Dysphagia,
dysarthria usually present
- Visual field deficits as the occipital lobes are involved
- Dissociated sensory loss
- Absence of cortical deficits such as aphasia,
cognitive decline.
NIHSS
The National Institutes of Health Stroke Scale (NIHSS) is a systematic clinical assessment tool that provides a quantitative measure of stroke-related neurologic deficit. It has been found to be a good predictor of patient outcome,
a NIHSS over 16 indicating a strong possibility of death.
NIHSS was not designed for the posterior circulation,
specific elements for exploring signs/ symptoms of PC stroke are currently assessed for the application of an expanded NIHSS (e-NIHSS).
NEUROIMAGING STUDIES
The initial study performed in a stroke is a NECT,
that is highly sensitive for detecting/ excluding intra or extra axial haemorrhage and can detect a hyperdense basilar artery.
Posterior fossa streak artefacts can make evaluation of neural structures difficult.
Evaluation of the cerebral vasculature is achieved with CT angiography or contrast-enhanced MRI,
CTA being more frequently used due to its wider availability and shorter scanning time.
Evaluation of the supraaortic vessels and their origin should be performed in every acute ischaemic stroke case that is eligible for endovascular treatment (EVT),
allowing a better understanding and approach planning in this time sensitive setting (Fig.
3 and 4).
Cerebral catheter angiography remains the gold standard for brain vasculature imaging.
EVT OF STROKE
Patients with partial/ complete early recanalization perform better that those with delayed/ no recanalization.
There are two endovascular techniques available for thrombus removal in AIS.
- The ADAPT technique consists of thrombus aspiration using negative pressure as a first approach.
- Stent-retriever thrombectomy is based on mechanical thrombus extraction using a stent-like self-expanding device (stent retriever) which works by capturing the thrombus.
- The two can be combined.
ANGIOPLASTY
Angioplasty of the extracranial vascular lesion can be performed with or without stent placement.
Technical success is defined by full lesion coverage with complete wall apposition of the stent - if used,
minimal (<30%) or no residual stenosis and good antegrade flow on digital subtraction angiography (DSA) (Fig.
5).
TANDEM LESIONS
The treatment of concomitant intra and extra cranial lesions can employ an antegrade or a retrograde technique.
- Antegrade technique: angioplasty with or without stenting of the extracranial VA lesion is performed before intracranial thrombus removal
- Retrograde technique: intracranial thrombus removal is performed first,
followed by PTA of the extracranial VA lesion.
Navigation to the intracranial occlusion site can be performed via the steno-occlusive VA (“dirty-road”) or via the contralateral patent one (“clean-road”).