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Vertebral artery dissection
Specialty	Cardiology

Vertebral artery dissection (abbreviated VAD, often vertebral dissection) is a dissection (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, narrowing the artery itself and impeding blood flow. The symptoms of vertebral artery dissection include neck pain and intermittent or permanent stroke symptoms such as double vision, impaired coordination and visual loss.

Vertebral dissection may occur after physical trauma to the neck, such as cervical fractures or dislocations, but may also develop spontaneously or after mild trauma (such as rapidly turning the head). Vertebral artery dissection is less common than carotid artery dissection (dissection of the large arteries in the front of the neck). The two conditions combined account for 10–25% of non-hemorrhagic strokes in young and middle-aged people.

Signs and symptoms

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Pain occurs in 50–75% of all cases of vertebral artery dissection. It tends to be located at the back of the head, either on the affected side or in the middle, and develops gradually. It is either dull or pressure-like in character or throbbing. About half of those with VAD consider the headache distinct, while the remainder have had a similar headache before. It is suspected that VAD with headache as the only symptom is fairly common; this comprises 8% of all cases of vertebral and carotid dissection.

The typical features of vertebral artery dissection are neck pain associated with posterior circulation-type stroke symptoms; these include any combination of problems with balance, co-ordination, speech, swallowing and vision.

13–16% of all people with vertebral or carotid dissection have dissection in another cervical artery. It is therefore possible for the symptoms to occur on both sides, or for symptoms of carotid artery dissection to occur at the same time as those of vertebral artery dissection.

Causes

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

Spontaneous

Spontaneous cases are considered to be caused by intrinsic factors that weaken the arterial wall. Only a very small proportion (1–4%) have a clear underlying connective tissue disorder, such as Ehlers–Danlos syndrome type 4 and more rarely Marfan's syndrome. There have also been reports in osteogenesis imperfecta type 1, autosomal dominant polycystic kidney disease and pseudoxanthoma elasticum, α₁ antitrypsin deficiency and hereditary hemochromatosis, but evidence for these associations is weaker. Genetic studies in other connective tissue-related genes have mostly yielded negative results. Other abnormalities to the blood vessels, such as fibromuscular dysplasia, have been reported in a proportion of cases. Atherosclerosis does not appear to increase the risk.

There have been numerous reports of associated risk factors for vertebral artery dissection; many of these reports suffer from methodological weaknesses, such as selection bias. Elevated homocysteine levels, often due to mutations in the MTHFR gene, appear to increase the risk of vertebral artery dissection. Presence of an aneurysm of the aortic root and a history of migraine may predispose to vertebral artery dissection.

Traumatic

Traumatic vertebral dissection may follow blunt trauma to the neck, such as in a traffic collision, direct blow to the neck, or strangulation. 1–2% of those with major trauma may have an injury to the carotid or vertebral arteries. Chiropractic and other forms of neck manipulation have been linked to vertebral artery dissection (16–28% of cases in hospital-based studies). Many of the reports have methodological flaws, and the association is disputed by proponents of these treatment modalities.

In many cases of vertebral dissection, people report recent very mild trauma to the neck or sudden neck movements, e.g. in the context of playing sports. Others report a recent infection, particularly respiratory tract infections associated with coughing. It has been difficult to prove this association statistically. It is likely that many "spontaneous" cases may in fact have been caused by such relatively minor insults in someone predisposed by other structural problems to the vessels.

Mechanism

The vertebral arteries arise from the subclavian artery, and for much of their tract run through the transverse foramen of the lowest five of the six vertebrae of the neck. After exiting at the level of the first cervical vertebra, its course changes from vertical to horizontal, and then enters the skull through the foramen magnum. Inside the skull, the arteries merge to form the basilar artery, which joins the circle of Willis. In total, three quarters of the artery are outside the skull; it has a high mobility in this area due to rotational movement in the neck and is therefore vulnerable to trauma. Most dissections happen at the level of the first and second vertebrae.

Dissection occurs when blood accumulates in the wall of the blood vessel. This is most likely due to a tear in the tunica intima (the inner layer), allowing blood to enter the tunica media, although other lines of evidence have suggested that the blood may instead arise from the vasa vasorum, the small blood vessels that supply the outer layer of larger blood vessels. Various theories exist as to whether people who sustain carotid and vertebral artery dissection, even if not suffering from a connective tissue disorder, have an underlying vulnerability. Biopsy samples of skin and other arteries has indicated that this might be a possibility, but no genetic defect in collagen or elastin genes has been convincingly proven. Other studies have indicated that low-grade inflammation of the blood vessels, as measured by highly sensitive C-reactive protein (hsCRP, a marker of inflammation) in the blood.

The vertebral artery supplies a number of vital structures in the posterior cranial fossa, such as the brainstem, the cerebellum and the occipital lobes. The brainstem harbors a number of vital functions (such as respiration) and controls the nerves of the face and neck. The cerebellum is part of the diffuse system that coordinates movement. Finally, the occipital lobes participate in the sense of vision. Once dissection has occurred, two mechanisms contribute to the development of stroke symptoms. Firstly, the flow through the blood vessel may be disrupted due to the accumulation of blood under the vessel wall, leading to ischemia (insufficient blood supply). Secondly, irregularities in the vessel wall and turbulence increase the risk of thrombosis (the formation of blood clots) and embolism (migration) of these clots of the brain. From various lines of evidence, it appears that thrombosis and embolism is the predominant problem.

Diagnosis

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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). This is therefore an invasive procedure, and it requires large volumes of radiocontrast that can cause complications such as kidney damage.

More modern methods involve computed tomography (CT angiography) and magnetic resonance imaging (MR angiography). They use smaller amounts of contrast and are not invasive. CT angiography and MR angiography are more or less equivalent when used to diagnose or exclude vertebral artery dissection.

Treatment

This section needs expansion. You can help by adding to it. (November 2010)

The treatment for VA dissection is the administration of anti-coagulation drugs. There is inconclusive evidence as to whether aspirin or heparin followed by warfarin should be the treatment of choice. Professional guidelines therefore recommend that patients with VA dissection should be enrolled in clinical trials if possible.

Epidemiology

The annual incidence is about 1.1 per 100,000 annually in population studies from the United States and France. From 1994 to 2003, incidence increased threefold; this has been attributed to increased use of modern imaging modalities rather than a true increase. Similarly, those living in urban areas are more likely to receive appropriate investigations, accounting for increased rates of diagnosis in those dwelling in cities. It is suspected that a proportion of cases in people with mild symptoms remains undiagnosed.

There is a degree of controversy as to VAD is more common in men or in women; an aggregate of all studies shows that it is slightly higher incidence in men (56% versus 44%). Men are on average 37–44 years old at diagnosis, and women 34–44. While dissection of the carotid and vertebral arteries accounts for only 2% of strokes (which is usually caused by high blood pressure and other risk factors), they cause 10–25% of strokes in young and middle-aged people.

References

1. ^ Kim YK, Schulman S (2009). "Cervical artery dissection: pathology, epidemiology and management". Thromb. Res. 123 (6): 810–21. doi:10.1016/j.thromres.2009.01.013. PMID 19269682. {{cite journal}}: Unknown parameter |month= ignored (help)
2. ^ Debette S, Leys D (2009). "Cervical-artery dissections: predisposing factors, diagnosis, and outcome". Lancet Neurol. 8 (7): 668–78. doi:10.1016/S1474-4422(09)70084-5. PMID 19539238. {{cite journal}}: Unknown parameter |month= ignored (help)
3. ^ Debette S, Markus HS (2009). "The genetics of cervical artery dissection: a systematic review". Stroke. 40 (6): e459–66. doi:10.1161/STROKEAHA.108.534669. PMID 19390073. {{cite journal}}: Unknown parameter |month= ignored (help)
4. ^ Rubinstein SM, Peerdeman SM, van Tulder MW, Riphagen I, Haldeman S (2005). "A systematic review of the risk factors for cervical artery dissection". Stroke. 36 (7): 1575–80. doi:10.1161/01.STR.0000169919.73219.30. PMID 15933263. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
5. Miley ML, Wellik KE, Wingerchuk DM, Demaerschalk BM (2008). "Does cervical manipulative therapy cause vertebral artery dissection and stroke?". Neurologist. 14 (1): 66–73. doi:10.1097/NRL.0b013e318164e53d. PMID 18195663. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
6. Ernst E (2007). "Adverse effects of spinal manipulation: a systematic review". J R Soc Med. 100 (7): 330–8. doi:10.1258/jrsm.100.7.330. PMC 1905885. PMID 17606755. {{cite journal}}: Unknown parameter |month= ignored (help)
7. ^ Provenzale JM, Sarikaya B (2009). "Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature". AJR Am J Roentgenol. 193 (4): 1167–74. doi:10.2214/AJR.08.1688. PMID 19770343. {{cite journal}}: Unknown parameter |month= ignored (help)
8. Kaufmann TJ, Kallmes DF (2008). "Diagnostic cerebral angiography: archaic and complication-prone or here to stay for another 80 years?". AJR Am J Roentgenol. 190 (6): 1435–7. doi:10.2214/AJR.07.3522. PMID 18492888. {{cite journal}}: Unknown parameter |month= ignored (help)
9. National Institute for Health and Clinical Excellence. Clinical guideline 68: Stroke. London, 2008.

External links

• Cervical Artery Dissections and Ischemic Stroke Patients, international research collaboration into cervical artery dissection

• Cardiovascular diseases
• Neurological disorders