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Carotid and Vertebral Artery Dissection Syndromes B Thanvi, S K Munshi, S L Dawson, T G Robinson

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Carotid and Vertebral Artery Dissection Syndromes B Thanvi, S K Munshi, S L Dawson, T G Robinson 383 REVIEW Postgrad Med J: first published as 10.1136/pgmj.2003.016774 on 3 June 2005. Downloaded from Carotid and vertebral artery dissection syndromes B Thanvi, S K Munshi, S L Dawson, T G Robinson ............................................................................................................................... Postgrad Med J 2005;81:383–388. doi: 10.1136/pgmj.2003.016774 Cervicocerebral arterial dissections (CAD) are an dissections, but with the advent of Doppler ultrasonography, MRI/MRA, and CT angiogra- important cause of strokes in younger patients accounting phy, most dissections can now be diagnosed for nearly 20% of strokes in patients under the age of 45 non-invasively. The treatment of symptomatic years. Extracranial internal carotid artery dissections CAD is essentially medical and neurosurgical interventions are rarely required. As thromboem- comprise 70%–80% and extracranial vertebral dissections bolism is the most probable mechanism behind account for about 15% of all CAD. Aetiopathogenesis of any neurological deficit, anticoagulants (heparin CAD is incompletely understood, though trauma, and warfarin) and antiplatetelets are commonly used, although there have not been any rando- respiratory infections, and underlying arteriopathy are mised studies to evaluate their effectiveness. The considered important. A typical picture of local pain, prognosis depends on the severity of neurological headache, and ipsilateral Horner’s syndrome followed deficit but is generally good in extracranial after several hours by cerebral or retinal ischaemia is rare. dissections. The recurrence rate of CAD is very low. This review focuses on the pathogenesis, Doppler ultrasound, MRI/MRA, and CT angiography are clinical features, diagnosis, and medical treat- useful non-invasive diagnostic tests. The treatment of ment of these syndromes. extracranial CAD is mainly medical using anticoagulants or antiplatelet agents although controlled studies to show EPIDEMIOLOGY Although reported in all age groups, CADs are their effectiveness are lacking. The prognosis of most common between the ages of 35 and 50 extracranial CAD is generally much better than that of the years, with a peak incidence in the fifth decade.2 intracranial CAD. Recurrences are rare in CAD. They account for up to 20% of strokes in patients under the age of 45 years.3 A community based ........................................................................... study showed an incidence of cervicocerebral dissections of 2.6 per 100 000 per year.4 However, he term dissection implies a tear in the wall cervicocerebral dissections may be asymptomatic of a major artery leading to the intrusion of or may cause only minor symptoms and there- Tblood within the layers of an arterial wall fore, their true incidence is difficult to ascertain. http://pmj.bmj.com/ (intramural haematoma). This causes stenosis of The incidence of CADs is non-significantly the lumen when blood collects between the higher in women. Trauma during forceps deliv- intima and media or an aneurysmal dilatation ery can cause CAD in neonates. of the artery when the haematoma predomi- nantly involves the media and adventitia. Once CLASSIFICATION OF CERVICOCEREBRAL thought to be rare, cervicocerebral arterial dis- DISSECTION SYNDROMES sections (CADs) have been increasingly recog- CADs include ICDs and vertebral artery dissec- on September 27, 2021 by guest. Protected copyright. nised as a cause of stroke, particularly in young tions (VADs). In each arterial system, the people. It was the work of Fisher et al in the late segment of the artery involved can be extra- 1970s that led to the recognition of the clinical cranial (dissection involving the artery in the and radiological features of dissection syndromes neck before it enters the cranium) or intracranial 1 facilitating their antemortem diagnosis. Among (when dissections affect the intracranial part of CADs, internal carotid artery dissections (ICDs) the artery) (box). ICD are at least three times are much more common than vertebral dissec- commoner than VAD. The clinical features in tions. The aetiopathogenesis of CAD is not fully See end of article for these two types are distinct in view of the authors’ affiliations understood. A history of preceding neck trauma different areas of brain supplied by the two ....................... is common although not universal. Heritable arteries. Dissections tend to affect extracranial connective disorders such as Ehlers-Danlos Correspondence to: segments of the arteries much more commonly Dr B Thanvi, Department of syndrome, Marfan’s syndrome, a1 antitrypsin than intracranial segments. However, intracra- Integrated Medicine, deficiency, etc, may predispose to CAD. nial dissections are usually more severe and carry Leicester General Hospital, Typical clinical features of CAD include uni- a poorer prognosis than extracranial dissections. Gwendolen Road, lateral neck pain, headache, ipsilateral Horner’s University Hospitals of The increased incidence of extracranial involve- Leicester NHS Trust, syndrome followed by manifestations of the ment has been explained by the fact that this Leicester LE5 4PW, UK; cerebral or ocular ischaemia and cranial nerve segment of the artery is more mobile and is also [email protected] palsies. The CAD can cause neurological deficits either because of haemodynamic failure (caused Submitted Abbreviations: CAD, cervicocerbral arterial dissection; 6 November 2003 by luminal stenosis) or by an artery to artery ICD, internal carotid dissection; VAD, vertebral artery Accepted 31 August 2004 thromboembolism. Catheter angiography had dissection; EICD, extracranial internal carotid artery ....................... been the method of choice to diagnose arterial dissection www.postgradmedj.com 384 Thanvi,Munshi,Dawson,etal prone to damage by bony structures such as the vertebrae trauma can cause dissection of the arteries and in many cases Postgrad Med J: first published as 10.1136/pgmj.2003.016774 on 3 June 2005. Downloaded from and styloid processes.5 there is no clear history of antecedent trauma in some cases. The site predilection for CAD is quite different from that of atherosclerosis affecting the cervical arteries. Dissection Genetic factors involves the pharyngeal and distal parts of the internal Several inherited disorders of connective tissue are known to carotid artery, whereas atherosclerosis usually affects the be associated with CAD although in practice they are rarely origin and the carotid bulb. Similarly, dissections affect distal found. Most typical of these is vascular Ehler-Danlos parts of the extracranial vertebral artery, whereas athero- syndrome (EDS), an autosomal dominant disorder. Patients sclerosis tends to involve the proximal segments with this disorder often carry mutations in the gene that encodes pro-a1 (III) collagen.8 Brandt et al showed ultra- AETIOPATHOGENESIS OF CAD structural abnormalities of dermal connective tissue compo- The pathogenesis of CAD is not fully understood. The nents in two thirds of patients with spontaneous dissection of following discussion outlines the current views on this the carotid or vertebral artery but with no other stigmata of a subject. known connective tissue disorder.9 CADs have also been reported in association with fibromuscular dysplasia, a non- Where does the dissection start in the artery? inflammatory disease of medium sized arteries mainly 10 An arterial wall consists of three layers—intima (the inner- affecting the carotid and renal arteries. Patients with ICD most layer), media (the middle muscular layer), and are more likely to have fibromuscular dysplasia than patients 11 adventitia (the outermost layer). It is generally agreed that with VAD. 12 a tear in the wall of an artery leads to a collection of blood a1 Antitrypsin deficiency and abnormalities of neural 13 14 between the layers of the artery, leading to formation of an crest cells, such as angiolipomatosis and lentigenosis have intramural haematoma. However, there is no universal also been associated with an increased risk of CAD. In about agreement as to which wall is the primary site of dissection. 5% of patients with CAD, there is a family history of 15 Some authorities consider a rupture within the connective spontaneous arterial dissections. To date no mutations in tissue and vasa vasorum of the media as the most probable the gene for type III procollagen (COL3A1) have been 16 initial event in dissection.6 The intramural haematoma may identified. The CAD has also been reported in patients with 17 then later penetrate the intima and reconnect with the true osteogenesis imperfecta. arterial lumen. Others think that an intimal tear occurs,7 Interestingly, hyperhomocysteinaemia has recently been 18 which allows blood under arterial pressure to enter the wall reported to be an in association with CAD ; Pezzini et al of the artery. report higher levels of fasting total plasma homocysteine Intimal tears are not always easy to diagnose on (tHcy) in patients with spontaneous CAD (13.2 mmol/l; pathological specimens. Even in the carefully selected range, 7 to 32.8 mmol/l) compared with control subjects 19 patients it is not always possible to show a communication (8.9 mmol/l; range, 5 to 17.3 mmol/l). The authors also noted between the intramural haematoma (the so called false a significant association between the MTHFRT (methylene- lumen) and the true lumen, suggesting that some dissections tetrahydrofolate reductase) genotype and spontaneous CAD. of
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