Abstract
Basilar artery occlusion (BAO) represents 1–4% of ischemic strokes and
includes variable symptoms, resulting in delayed diagnosis. Treatment is
not codified and outcome depends on the severity of clinical
presentation and extent of the occlusion. We present a case of two
patients with BAO and we discuss treatment protocols.
Key words : Basilar artery occlusion, Posterior circulation
strokes , treatment
Key Clinical Message : codify therapeutic protocol of Basilar
artery occlusion
Introduction
Posterior circulation strokes account for about 15% to 20% of all
ischemic strokes (1). Basilar artery occlusion (BAO) is a subset of this
category, representing 1% to 4% of all ischemic strokes (8).
Diagnosing a BAO can be difficult and mortality rate can reach
80%–90% if not promptly treated (4). The treatment of patients with
acute BAO is uncertain and prognosis depends on the initial stroke
severity and time to therapy .
Here we present two cases of BAO and we discuss treatment in order to
codify therapeutic protocol.
Observation :
Case 1 :
A 42-year-old man, without pathological medical history, presented to
the emergency with acute left-sided weakness associated with dysarthria
on january 2019. He was admitted in stroke unit of our department. On
initial examination, vital signs were normal. He was drowsy with limited
speech and he had a left hemiplegia. Cranial nerve testing showed
bilateral horizontal gaze palsy with a right peripheral facial palsy and
an inexhaustible nystagmus. His calculated National Institutes of Health
Stroke Scale (NIHSS) was 14 and Modified Rankin Scale (MRS) was 4.
A Stroke Alert was activated. The worsening was rapid, the patient
developed swallowing difficulties and emergent intubation was performed.
Non contrast head computed tomography (CT) showed hyperdensity of the
basilar artery. Brain Magnetic resonance imaging (MRI)
with angiography (MRA) revealed hyperintensities in the pons and left
cerebellar hemisphere as well as a thrombosis in the basilar artery with
extension into the right vertebral artery (Figure 1).
Patient received thrombolysis with i.v. alteplase approximately 17 hours
after symptoms onset.
An exhaustive etiological assessment was carried out including a24-hour
ECG Holter monitoring and a transthoracic echocardiogram which were
normal. Auto immune antibodies were evaluated in serum: anti nuclear
antibody (AAN), C-antineutrophil cytoplasmic antibodies (ANCA), anti
DNA, anti SSA, SSB, anticardiolipin antibodies were negative.The
activities of proteins C and S, antithrombin III, lupus anticoagulants,
mutation for Factor V Leiden , MTHFR mutation and Homocysteine level
were normal.
Treatment with acenocoumarol (Sintrom) was started 24 hours after
thrombolysis. Rehabilitation was initiated. After one year, his clinical
condition gradually improved, he has a mild hemiparesis with dysarthria.
NIHSS was 5 and MRS was 2.
Case 2 :
A 65-year-old man, with a history of type 2 diabetes mellitus,
hyperlipidemia, and hypertension presented to the emergency department
with sudden onset of right arm and leg weakness. The patient had
gradually worsened and he presented a dyarthria and swallowing
difficulty.
On examination, His initial Glasgow Coma Scale score was 13. He was
dysarthric and had a flaccid right hemiplegia. Sensation was preserved.
The remainder of the neurological examination including cranial nerves
was normal. His NIHSS was 10 and MRS was 5.
Brain MRI with angiography revealed a pontine infarction due to an acute
basilar artery occlusion (Figure 2).
Anticoagulant treatment was initiated on the third day of symptoms. We
first introduced low-dose subcutaneous heparin calcium with activated
partial thromboplastin time (aPTT) range between 2 and 3.
Acenocoumarol (Sintrom) was introduced a few days later.
The outcome was favorable and the patient resumed walking after 12
months, though he has residual hemiparesis and dysarthria. NIHSS was 6
and MRS was 3.
Discussion :
BAO presents as a subset of the larger category of posterior circulation
strokes, associated with a poor prognosis and a high mortality rate
carrying > 80% without treatment (1,4).
The severity of presentation can vary from isolated cranial nerve
palsies to tetraplegia, locked-in state, or coma (1).Our patients
presented a severe hemiplegia with dyarthria and swallowing difficulty.
Brain magnetic resonance imaging (MRI) with angiography is the
diagnostic imaging modality of choice which confirm occlusion of the
artery.
Once the diagnosis has been obtained, the next goal is to recanalise the
artery. However There is no consensus for the best management of BAO for
the lack of prospective studies which compare the different therapeutic
strategies and identify the most effective (4).
Emergent arterial recanalization has improved functional outcomes and
reduced mortality (5,6). Median time to treatment with IV tissue-type
plasminogen activator (IV t-PA) was approximately 12 hours (1,5). Some
interventionalists may consider revascularization up to 24 hours after
symptom onset (7). Our patient recived IV t-PA 17 hours after onset of
symptoms. Mechanical thrombectomy is another therapeutic alternative
(8,9), which was not carried out for our patients due to lack of
resources.
In addition to recanalization therapy, anticoagulation is indicated in
these patients to prevent reocclusion of Basilar Artery (10). A study
showed an improved outcome in thrombolysed patients treated with heparin
(10).
Our protocol was to introduce acenocoumarol (Sintrom) from the first 24
hours after thrombolysis and then overlap with the sintrom. Good
functional results were obtained with no increased risk of intracranial
hemorrhage.
To conclude, our objective was to try to codify the treatment of BAO in
order to improve the vital and functional prognosis of these patients.
Our results join those of previous studies on the delay of thrombolysis
which can reach up to 24 hours after the onset of symptoms.
We insist on intensive treatment and we propose to initiate
anticoagulant treatment in hyperacute settings to improve outcomes of
patients.
Conclusion :
BAO has a poor clinical outcomes with high morbidity and mortality.
Arterial recanalization and early introduction of anticoagulant may be
associated with good outcomes. Therapeutic decisions must be
individualized to improve clinical prognosis.Further research should
focus on quicker diagnosis, appropriate imaging, and finding the best
treatment strategy for this patient populatio
The authors declare that there is no conflict of interest