Vertebral artery dissection
Vertebral artery dissection | |
---|---|
Other names | Vertebral dissection |
Anticoagulation, angioplasty, surgery | |
Medication | Aspirin, heparin, warfarin |
Frequency | 1.1 per 100,000 |
Vertebral artery dissection (VAD) is a
Vertebral dissection may occur after
Vertebral artery dissection is less common than carotid artery dissection (dissection of the large arteries in the front of the neck). The two conditions together account for 10–25% of non-hemorrhagic strokes in young and middle-aged people. Over 75% recover completely or with minimal impact on functioning, with the remainder having more severe disability and a very small proportion (about 2%) dying from complications.[1][3] It was first described in the 1970s by the Canadian neurologist C. Miller Fisher.[3]
Classification
Vertebral artery dissection is one of the two types of cervical artery dissection. The other type, carotid artery dissection, involves the carotid arteries. Vertebral artery dissection is further classified as being either traumatic (caused by mechanical trauma to the neck) or spontaneous, and it may also be classified by the part of the artery involved: extracranial (the part outside the skull) and intracranial (the part inside the skull).[1]
Signs and symptoms
Head 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.[1] It is suspected that VAD with headache as the only symptom is fairly common;[2] 8% of all cases of vertebral and carotid dissection are diagnosed on the basis of pain alone.[1]
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 ("
If the dissection of the artery extends to the part of the artery that lies inside the skull,
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.[2] Some give a figure of multiple vessel dissection as high as 30%.[3]
Causes
The causes of vertebral artery dissection can be grouped under two main categories, spontaneous and traumatic.
Spontaneous
Spontaneous cases are considered to be caused by intrinsic factors that weaken the arterial wall.
There have also been reports in other genetic conditions, such as
There have been numerous reports of associated risk factors for vertebral artery dissection; many of these reports suffer from
Traumatic
Traumatic vertebral dissection may follow blunt trauma to the neck, such as in a
Vertebral artery dissection has also been reported in association with some forms of neck manipulation.[12] There is significant controversy about the level of risk of stroke from neck manipulation.[12] It may be that manipulation can cause dissection,[13] or it may be that the dissection is already present in some people who seek manipulative treatment.[14] At this time, conclusive evidence does not exist to support either a strong association between neck manipulation and stroke, or no association.[12] However, the two most authoritative articles on the subject, recent literature reviews and analyses, conclude that although there exists an association between stroke from vertebral artery dissection and chiropractic adjustment, there is insufficient evidence to indicate that the adjustment caused the dissection.[15][16] 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.[16]
Mechanism
The vertebral arteries arise from the
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.[1][2] Various theories exist as to whether people who sustain carotid and vertebral artery dissection, even if they do not have 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 inflammation of the blood vessels, as measured by highly sensitive C-reactive protein (hsCRP, a marker of inflammation) in the blood.[1]
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.[1]
Subarachnoid hemorrhage due to arterial rupture typically occurs if the dissection extends into the V4 section of the artery. This may be explained by the fact that the arterial wall is thinner and lacks a number of structural supports in this section.[1][3][17]
Diagnosis
Various diagnostic modalities exist to demonstrate blood flow or absence thereof in the vertebral arteries. The
More modern methods involve
Treatment
Treatment is focused on reducing stroke episodes and damage from a distending artery.
Anticoagulation and aspirin
From analysis of the existing small treatment trials of cervical artery dissection (carotid and vertebral) it appears that
Professional guidelines in the UK recommend that patients with VA dissection should be enrolled in a clinical trial comparing aspirin and anticoagulation if possible.[23] American guidelines state that the benefit of anticoagulation is not currently established.[24]
Thrombolysis, stenting and surgery
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).[1][2]
Thrombolysis is enzymatic destruction of blood clots. This is achieved by the administration of a drug (such as urokinase or alteplase) that activates plasmin, an enzyme that occurs naturally in the body and digests clots when activated. Thrombolysis is an accepted treatment for heart attacks and stroke unrelated to dissection. In cervical artery dissection, only small case series are available. The thrombolytic drug is administered either intravenously or during cerebral angiography through a catheter directly into the affected artery. The data indicates that thrombolysis is safe, but its place in the treatment of VAD is uncertain.[21]
Stenting involves the catheterization of the affected artery during angiography, and the insertion of a mesh-like tube; this is known as "
Surgery carries a high risk of complications, and is typically only offered in case of inexorable deterioration or contraindications to any of the other treatments. Various arterial repair procedures have been described.[1][17]
Prognosis
Prognosis of spontaneous cervical arterial dissection involves neurological and arterial results. The overall functional prognosis of individuals with stroke due to cervical artery dissection does not appear to vary from that of young people with stroke due to other causes. The rate of survival with good outcome (a modified Rankin score of 0–2) is generally about 75%,[1][3] or possibly slightly better (85.7%) if antiplatelet drugs are used.[1] In studies of anticoagulants and aspirin, the combined mortality with either treatment is 1.8–2.1%.[1][21]
After the initial episode, 2% may experience a further episode within the first month. After this, there is a 1% annual risk of recurrence.[1] Those with high blood pressure and dissections in multiple arteries may have a higher risk of recurrence.[2] Further episodes of cervical artery dissection are more common in those who are younger, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.[2]
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, the incidence increased threefold; this has been attributed to the more widespread use of modern imaging modalities rather than a true increase.[1] 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.[2]
There is controversy as to whether 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%).[1] 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 are usually caused by high blood pressure and other risk factors, and tend to occur in the elderly), they cause 10–25% of strokes in young and middle-aged people.[1][3]
Dissecting aneurysms of the vertebral artery constitute 4% of all
History
Spontaneous vertebral artery dissection was described in the 1970s. Prior to this, there had been isolated case reports about carotid dissection. In 1971,
Notable cases
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.[27]
References
- ^ PMID 19269682.
- ^ S2CID 2209221.
- ^ PMID 19099146.
- PMID 11259724.
- ^ PMID 18328988.
- ^ PMID 19390073.
- ^ PMID 15933263.
- S2CID 3664755.
- S2CID 8487345.
- S2CID 5613911.
- PMID 24300790.
- ^ PMID 22994328.
- S2CID 38571730.
- PMID 19251069.
In persons younger than 45 years, there is an association between chiropractic care and vertebro-basilar artery (VBA) stroke; there is a similar association between family physician care and VBA stroke. This suggests that there is no increased risk of VBA stroke after chiropractic care, and that these associations are likely due to patients with headache and neck pain from vertebral artery dissection seeking care while in the prodromal stage of a VBA stroke. Unfortunately, there is no practical or proven method to screen patients with neck pain and headache for vertebral artery dissection. However, VBA strokes are extremely rare, especially in younger persons.
- S2CID 8179270.
- ^ PMID 27014532.
- ^ S2CID 8755665.
- ^ PMID 19770343.
- PMID 19797189.
- ^ PMID 18492888.
- ^ S2CID 207001321.
- PMID 17656656.
- National Institute for Health and Clinical Excellence. Clinical guideline 68: Stroke. London, 2008.
- PMID 17431204.
- PMID 647502.
- PMID 11692045.
- ^ Coverdale, Brydon (27 November 2014). "Hughes suffered extremely rare, freak injury to neck". ESPN. Retrieved 27 November 2014.
External links
- Cervical Artery Dissections and Ischemic Stroke Patients, international research collaboration into cervical artery dissection