Vertebral artery dissection

Tear of the inner lining of the vertebral artery

Vertebral artery dissection (VAD) is a flap like tear of the inner lining of the vertebral artery, which is located in the neck and supplies blood to the brain. After the tear, blood enters the arterial wall and forms a blood clot, thickening the artery wall and often impeding blood flow. The symptoms of vertebral artery dissection include head and neck pain and intermittent or permanent stroke symptoms such as difficulty speaking, impaired coordination, and visual loss. It is usually diagnosed with a contrast enhanced CT or MRI scan. Obstruction of blood flow through the affected vessel may lead to dysfunction of part of the brain supplied by the artery. This happens in 77–96% of cases. This may be temporary ("transient ischemic attack") in 10–16% of cases, but many (67–85% of cases) end up with a permanent deficit or a stroke. The vertebral artery supplies the part of the brain that lies in the posterior fossa of the skull, and this type of stroke is therefore called a posterior circulation infarct. Problems may include difficulty speaking or swallowing (lateral medullary syndrome); this occurs in less than a fifth of cases and occurs due to dysfunction of the brainstem. Others may experience unsteadiness or lack of coordination due to involvement of the cerebellum, and still others may develop visual loss (on one side of the visual field) due to involvement of the visual cortex in the occipital lobe. Some give a figure of multiple vessel dissection as high as 30%.

The causes of vertebral artery dissection can be grouped under two main categories, spontaneous and traumatic.

Spontaneous cases are considered to be caused by intrinsic factors that weaken the arterial wall. Ehlers–Danlos syndrome type 4, caused by mutations of the COL3A gene, leads to defective production of the collagen, type III, alpha 1 protein and causes skin fragility as well as weakness of the walls of arteries and internal organs. Marfan syndrome results from mutations in the FBN1 gene, defective production of the protein fibrillin 1, and a number of physical abnormalities including aneurysm of the aortic root. Genetic studies in other connective tissue related genes have mostly yielded negative results. Elevated homocysteine levels, often due to mutations in the MTHFR gene, appear to increase the risk of vertebral artery dissection.

Traumatic vertebral dissection may follow blunt trauma to the neck, such as in a traffic collision, direct blow to the neck, strangulation, 1–2% of those with major trauma may have an injury to the carotid or vertebral arteries. It has been difficult to prove the association of vertebral artery dissection with mild trauma and infections statistically. It may be that manipulation can cause dissection, or it may be that the dissection is already present in some people who seek manipulative treatment. At this time, conclusive evidence does not exist to support either a strong association between neck manipulation and stroke, or no association. A recent meta analysis of the published data on the topic also looked to apply Hill's criteria for assigning causation in biological systems to the relationship between chiropractic adjustment and cervical artery dissection, finding that the relationship did not fulfill the required criteria for causality.

Various diagnostic modalities exist to demonstrate blood flow or absence thereof in the vertebral arteries. The gold standard is cerebral angiography (with or without digital subtraction angiography). This involves puncture of a large artery (usually the femoral artery) and advancing an intravascular catheter through the aorta towards the vertebral arteries. At that point, radiocontrast is injected and its downstream flow captured on fluoroscopy (continuous X ray imaging). Angiography also does not directly demonstrate the blood in the vessel wall, as opposed to more modern modalities. Surgery is only used in exceptional cases. Warfarin is typically continued for 3–6 months, as during this time the flow through the artery usually improves, and most strokes happen within the first 6 months after the development of the dissection. American guidelines state that the benefit of anticoagulation is not currently established.

Thrombolysis, stenting and surgery are not used as widely as anticoagulation or antiplatelet drugs. These treatments are invasive, and are typically reserved for situations where symptoms worsen despite medical treatment, or where medical treatment may be unsafe (e. g. an unacceptable bleeding tendency).

Australian cricketer Phillip Hughes died on 27 November 2014 after developing a vertebral artery dissection as a result of being struck on the side of the neck by a cricket ball, while representing South Australia in a Sheffield Shield match on 25 November 2014 at the S. C. G. The short pitched delivery bowled by N. S. W. player Sean Abbott struck Hughes on the base of the skull, just behind his left ear which caused a vertebral artery dissection complicated by subarachnoid hemorrhage.