Basilar Artery Thrombosis

Article Author:
Nathaniel Reinemeyer
Article Author (Archived):
Prasanna Tadi
Article Editor:
Forshing Lui
Updated:
6/4/2019 4:32:30 PM
PubMed Link:
Basilar Artery Thrombosis

Introduction

The basilar artery is a vital vessel contributing to the posterior cerebral circulation. It is formed at the junction of the pons and medulla by the convergence of the dual vertebral arteries. The vertebral arteries join the basilar artery to form the vertebrobasilar system, which supplies blood to the posterior portion of the circle of Willis. Its crucial purpose is to serve the cerebellum, brainstem, thalamus, occipital and medial temporal lobes of the brain with oxygen-rich blood. With an average diameter of 3 to 4 millimeters, it furnishes 20 paramedian and circumflex perforating arteries thus providing a robust collateral network to the pons and midbrain. Throughout its course, the basilar artery distributes the median, paramedian, short, and long circumferential branches. It is located on the ventral surface of the neuronal "bridge" also known as the pons (Latin for "bridge") that connects the forebrain to the cerebellum.[1][2] Overall, the basilar artery is one of the most important arteries of the human body. 

Etiology

The cause can occur from thromboembolism, atherosclerotic disease, or vascular dissection. The mechanism differs depending on the affected segment. The atherosclerotic disease more commonly affects the mid-portion of the basilar artery, followed by the vertebrobasilar junction. Lodging of an embolic source is much more frequent in the distal third of the basilar artery especially at the top of the basilar artery and the vertebrobasilar junction. Arterial dissection is more common in the extracranial vertebral artery and has been associated with neck injuries and cervical chiropractic adjustments. Intracranial dissections are exceedingly rare.[1]

Epidemiology

Risk factors are similar to the known general risk factors for stroke. The most common is hypertension which is found in as many as 70% of cases. Other risk factors include diabetes mellitus, coronary artery disease, peripheral vascular disease, cigarette smoking, and hyperlipidemia.

The frequency, incidence, and prevalence are not well known in the medical literature. 20% of cerebral blood flow goes through the posterior circulation (vertebrobasilar system), it is logical to understand why posterior circulation occlusions accounts for 1/5 of all strokes. Fortunately, basilar artery occlusions are believed to account for approximately only 1% of all strokes. Basilar artery occlusion has been reported in 2 out of 1000 post-mortem cases. Basilar artery thrombosis may explain as many as 27% of ischemic strokes occurring in the posterior circulation. An increased prevalence exists in males, with a 2:1 ratio. Occlusion due to atherosclerotic disease is most prevalent in patients of advanced age, usually in the sixth and seventh decades of life. Distal basilar artery occlusion is usually secondary to embolism and is most prevalent in the fourth decade of life.[3][4][5]

History and Physical

Most commonly, patients experiencing basilar artery occlusion exhibit acute neurologic signs including motor deficits, hemiparesis or quadriparesis, and facial palsies, dizziness, headache, and speech abnormalities–especially dysarthria and difficulty articulating words. Patients may also complain of nausea, vomiting, and changes in vision. An altered level of consciousness is commonly present.

 Basilar artery thrombosis may present in three general constellations:

  1. Rapid onset of advanced motor and bulbar symptoms with a decreased level of consciousness.
  2. Insidious or stuttering symptoms over a few days as a combination of the above that end with disabling motor and bulbar symptoms, a decreased level of consciousness, or both.
  3. Prodromal symptoms that may include headache, neck pain, loss of vision, binocular diplopia, dysarthria, dizziness, hemiparesis, paresthesias, ataxia, and tonic-clonic type movements. “Herald hemiparesis” is the phrase to describe the momentary, unilateral weakness that may precede later permanent symptoms.

An abnormal level of consciousness and focal motor weakness are the hallmark symptoms manifested in the majority of patients. Pupillary abnormalities, oculomotor signs, and pseudobulbar manifestations (facial palsy, dysphonia, dysarthria, dysphagia) are seen in more than 40% of patients.[1][6][7][8]. Variable degrees of hemiparesis or quadriparesis are part of the clinical picture. As basilar artery thrombosis presents in various ways it is very important to have high clinical suspicion to detect basilar artery thrombosis. 

Evaluation

The primary goals of the evaluation are to establish the location of the vascular lesion and determine whether acute intervention is indicated to achieve recanalization in a time sensitive manner.

Laboratory studies have limited utility but may include a complete blood count (CBC), electrolytes, blood urea nitrogen (BUN) and creatinine, international normalized ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (aPTT). Younger patients or patients without evidence of atherosclerosis should be investigated for the presence of procoagulant conditions. These include protein C, protein S, and antithrombin III deficiencies, lupus anticoagulant and anticardiolipin antibodies, and homocysteine levels. An electrocardiogram helps to screen for arrhythmias which may be suggestive of a thrombotic etiology.

Computed tomography (CT) scanning is usually the first imaging study performed. CT may be effective at identifying larger areas of ischemic insult and can highlight hemorrhagic pathology. A hyperdense basilar artery may be present on CT scan. However, CT scanning has a low sensitivity for early ischemia and is less effective at evaluating the brainstem, cerebellum, and posterior circulation. Ultimately, one needs a high index of suspicion in the correct clinical context to diagnosis an easily missed disease. Additional evaluation with CT angiography may be considered, and a filling defect noted within the basilar artery. Catheter angiography is still a criterion for diagnosis; however, with the availability of noninvasive imaging modalities such as magnetic resonance imaging (MRI) and angiography (MRA), the role of angiography has changed. MRI/MRA is more sensitive than CT scanning for identifying early ischemia and vascular occlusion.[6][9][10][11][12][13]. MRI is the best imaging modality for any posterior fossa lesion including acute ischemic infarction. DWI MRI sequence can show an acute brainstem or cerebellar infarct within seconds of the arterial occlusion. MR angiogram can show the site of vascular occlusion non-invasively. Presence of microhemorrhages in GRE-T2* or SWI imaging can help to indicate underlying hypertensive etiology.

Treatment / Management

Acute occlusion of the basilar artery is potentially life-threatening. All patients should be admitted to a stroke unit when available. Recanalization of the basilar artery is key to the successful treatment of basilar artery thrombosis and to improving prognosis. This can be accomplished by systemic thrombolysis (IVT), intra-arterial thrombolysis, (IAT) or mechanical endovascular thrombectomy. Recanalization occurs in more than half of basilar artery occlusion patients treated with IAT or IVT. Treatment is time sensitive; the earlier the intervention, the better the functional outcomes. There is no good large-scale study to define the treatment window for basilar thrombosis. It is clearly much longer than the accepted window of 6 to 8 hours recommended for large vessel occlusion in anterior circulation infarct. The commonly accepted time window is at least 12 hours and potentially up to 24 hours.  In some situations, if the patient is having symptoms and minimal stroke on MRI brain it is reasonable to consider for mechanical endovascular thrombectomy up to 2-3 days. Subsequent therapy for secondary prevention focuses on treating the underlying causes and modifying risk factors.[14][15][16][17][18][19]

Differential Diagnosis

When considering the diagnosis, it is important to consider other etiologies that may cause similar overlapping symptoms. These include meningitis, basilar migraine, cerebellar hemorrhage with brainstem compression, cerebellar infarct or hemorrhage with edema, space-occupying lesions in the posterior fossa including metastatic disease, and supratentorial mass lesions with mass effect, herniation, and brainstem compression. Consider hypoglycemia, Todd paralysis, and conversion disorder as possible mimics.[20][21]

Prognosis

The patient mortality rate is greater than 85%, although it drops to as low as 40% in patients with recanalization. One can expect good functional outcomes in as few as 24% to 35% of patients treated with intravenous or intra-arterial thrombolysis. For symptomatic patients who survive, the risk of recurrent stroke is 10% to 15%.[15] The most important prognostic factors are the extent and duration of thrombosis. Therefore, a high index of suspicion of the diagnosis followed by expedited recanalization will give the patient the best hope of an improved outcome.

Complications

Overall outcomes can be expected to be poor in patients with basilar artery thrombosis. Advances in pharmacologic and mechanical thrombosis and endovascular therapy may reduce the subsequent mortality and disability rates. Catheter-directed thrombolysis and IV heparin also carry a risk of hemorrhage. Complications can include the following: aspiration, aspiration pneumonia, thromboembolic disease (DVT and PE), myocardial infarction, and recurrent stroke. Patients with advanced functional debility secondary to stroke are increasingly prone to contractures, pressure ulcers, and sepsis. Many patients who survive basilar artery thrombosis require ongoing physical and occupational therapy to regain and maintain functionality.[15][22]

Enhancing Healthcare Team Outcomes

Managing a patient with acute neurologic symptoms requires timely and coordinated efforts by a multidisciplinary team. This team might initially include a physician, nurse, pharmacist, and multiple ancillary personnel such as phlebotomists, radiography technicians, and laboratory personnel. A wide array of physician specialists such as neurologists, radiologists, interventional radiologists, internists, cardiologists, and physical medicine and rehabilitation physicians may be involved in the care of a patient with basilar artery thrombosis. With almost any acute ischemic event, not limited to basilar artery thrombosis, studies have shown that the earlier the intervention is undertaken, the better off the patient's functional outcomes might be. With the mantra "Time is of the Essence" in mind, one can recognize that the presence of an integrated multi-functional team is vitally important in providing the rapid stabilization, evaluation, diagnosis, and intervention of patients suffering from acute neurologic conditions.

The coordination of this type of specialty care has made comprehensive stroke centers (CSCs) an increasingly common part of large tertiary healthcare centers. CSCs are designated to provide more complex services, including around the clock availability of endovascular procedures. Many questions are worth exploring in the near future: Do CSCs offer any appreciable benefit to ischemic stroke patients? and, if so, what types? Do all patients with an acute stroke need to be referred to a CSC? Medicine looks forward to exploring these questions, and many more as the optimal outline for treating patients with ischemic intracranial pathology and basilar artery thrombosis is better defined and advanced.


References

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