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Show STATE OF THE ART Cervicocranial Arterial Dissections Louis R. Caplan MD and Valerie Biousse, MD Abstract: Cervicocranial dissections are an increasingly recognized cause of stroke in the young. When the dissections narrow the vascular lumen, they often alter blood flow enough to cause transient ischemic attacks in the brain. Alterations in the endothelium activate the coagulation cascade, leading to the formation of intramural clot that may embolize distally to cause brain infarction. Pain and neuro- ophthalmic symptoms and signs are common manifestations. ( JNeuro- Ophthalmol 2004; 24: 299- 305) PATHOGENESIS OF CERVICOCRANIAL DISSECTIONS Dissections are tears in arteries, almost always involving the medial coat ( 1- 10). They may be traumatic or " spontaneous" in origin. In fact, the majority of dissections probably involve some trauma or mechanical stress, with sudden neck movements and stretching often implicated. Some inciting events may be trivial, such as lunging for a tennis ball or sudden turning of the neck while driving a car. Many such events are forgotten or considered too inconsequential to be mentioned by the patient ( 5). Congenital and acquired abnormalities of the arterial media and elastic tissue can render patients more vulnerable to dissection ( 5,7,11,12). Inherited disorders of connective tissue ( Marfan syndrome, Ehlers- Danlos syndrome, pseudoxanthoma elasticum), cystic medial necrosis, and fibromuscu-lar dysplasia predispose to dissection ( 5,11,12). Ultrastruc-tural connective tissue abnormalities of collagen and extracellular matrix are sometimes found in the skin of patients with extracranial arterial dissections ( 11,12). In addition, indirect evidence of a generalized arteriopathy is suggested by the association of spontaneous dissections with intracranial pseudoaneurysms, a widened aortic root, arterial redundancies, and increased arterial distensibility ( 5,7,12,13). Migraine is more common in patients with dis- Department of Neurology ( LRC), Harvard Medical School, Boston, Massachusetts and Departments of Ophthalmology and Neurology ( VB), Emory University, Atlanta, Georgia. Address correspondence to Louis R. Caplan, MD, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215; E- mail: lcaplan@ caregroup. harvard. edu section ( 14), and a recent history of upper respiratory tract infection has also been shown to be a risk factor for cervicocranial dissections ( 15). Dissections often involve loops and redundant portions of the extracranial arteries ( Fig. 1) ( 16). They probably begin with a tear in the media, which leads to bleeding within the arterial wall. Intramural blood then dissects longitudinally, spreading along the vessel proximally or distally ( Fig. 2). The dissection can tear through the intima, allowing the partially coagulated intramural blood to enter the arterial lumen. The arterial wall, expanded by intramural blood, can also compress the lumen. Some dissections begin at the intimal surface and dissect into the media. Intimal flaps are then often present. At times, the major dissection plane is between the media and the adventitia, causing an aneurysmal outpouching of the arterial wall ( Fig. 1) ( 5,7,9,17- 27). Extracranial dissections cause symptoms primarily by the presence of luminal compromise and luminal clot. Dissections through the adventitia may rupture into the surrounding neck muscles and fascia with formation of a pseu-doaneurysm. They may compromise blood flow. Partially clotted blood in the media may rupture into the lumen. Irritation of the endothelium causes release of endothelins, which activate platelets and the coagulation cascade, contributing to formation of intraluminal thrombus. The luminal clot is usually loosely adherent to the intima and can readily embolize distally. In the weeks after dissection, the intramural blood is absorbed and the lumen usually returns to its normal size. Aneurysmal pouches may remain as a mark of the healed lesion. Acute luminal compromise or occlusion ( Fig. 3) may cause hypoperfusion and brain ischemia, although infarction is more often caused by embolization or propagation of luminal thrombus ( 1,2,19). SITES OF CERVICOCRANIAL DISSECTIONS Dissections usually involve mobile portions of arteries. They do not occur at the fixed origins of the carotid and vertebral arteries from the common carotid and subclavian arteries, respectively. The extracranial internal carotid artery ( ICA), the most commonly affected artery, is fixed at its origin and at its dural penetration, making the cervical portion the most mobile and vulnerable to dissections ( Fig. J Neuro- Ophthalmol, Vol. 24, No. 4, 2004 299 JNeuro- Ophthalmol, Vol. 24, No. 4, 2004 Caplan and Biousse FIG. 1. Conventional angiogram showing a spontaneous internal carotid artery ( ICA) dissection involving a complete loop ( coil) in the distal portion of the ICA. The dissected artery is irregular below the loop. There is a pseudoaneu-rysm within the loop ( arrow). 2) ( 1,3,4,7,17- 25). The upper cervical segment is an unusual site for atherosclerosis, which almost invariably affects the ICA origin or the carotid siphon. Emboli arising from nuchal ICA dissections most often go into middle cerebral artery ( MCA) branches. The extracranial vertebral arteries ( ECVAs) are relatively fixed at their origins from the subclavian arteries, in their intraosseous portion ( V2), and by the dura at the point of intracranial penetration. The short, moveable portions between these segments are vulnerable to tearing, stretching, and dissection. Therefore, dissections tend to involve the proximal ( Vx) portion of the ECVA well above its origin from the subclavian artery or the distal ( V3) segment. In some cases, all segments of the vessel are dissected ( Fig. 4). Vj dissections are almost always unilateral. The distal extracranial portion ( V3) is the most common location for dissection within the posterior circulation ( 2,19,22,27). Distal ( V3) ECVA dissections often extend into the intracranial vertebral artery ( ICVA) and occasionally caudally into the intraosseous ( V2) segment. Distal ECVA dissections are often bilateral, even though pain and other symptoms may be unilateral. Emboli from ECVA dissections most often go to the ICVAs, causing posterior inferior cerebellar artery territory cerebellar or lateral medullary ischemia and infarction. Less often emboli reach the distal basilar, superior cerebellar, or posterior cerebral arteries ( 2,7,19). Intracranial vascular dissections are less common than extracranial dissections. They can cause infarction, FIG. 2. Conventional angiogram showing a spontaneous extracranial ICA dissection with long, irregular stenosis beginning well above the ICA origin ( arrow). FIG. 3. Magnetic resonance angiography of the circle of Willis in a patient with a dissection of the right internal carotid artery. The ipsilateral middle cerebral artery is poorly seen ( arrow) compared with the contralateral middle cerebral artery, suggesting distal hypoperfusion secondary to the dissection. 300 © 2004 Lippincott Williams & Wilkins Cervicocranial Arterial Dissections JNeuro- Ophthalmol, Vol. 24, No. 4, 2004 FIG. 4. Conventional angiogram showing a spontaneous extracranial vertebral artery dissection producing irregular contour of all segments of the vessel. subarachnoid bleeding, or mass effects ( 2,19,26,27). When arteries dissect between the media and the intima, luminal narrowing and local hypoperfusion usually occur and lead to infarction in the regions of supply. In the anterior circulation, the supraclinoid ICA and mainstem MCA are most often involved. In the posterior circulation, the ICVAs and the basilar artery are most often affected ( Fig. 5). When dissections extend between the media and the adventitia, pseudoaneurysms and tears through the adventitia may lead to subarachnoid hemorrhage, which can be recurrent. At times, dissections lead to prominent aneurysmal masses, which can present as space- taking lesions that compress adjacent cranial nerves or brain parenchyma ( Fig. 5). CLINICAL MANIFESTATIONS OF CERVICOCRANIAL DISSECTIONS Internal Carotid Artery Dissections In patients with ICA neck dissections, pain is often the most impressive feature ( Table 1) ( 1,3,4,7,17- 31). Ipsi-lateral throbbing headache and sharp pain in the neck, jaw, pharynx, or face separate dissection from the ordinarily painless atherosclerotic occlusion. After being present for several days, pain may disappear, only to recur days or even weeks later, and may be accompanied by ischemic attacks or strokes. The sympathetic nerve fibers traveling along the wall of the ICA are usually disturbed, leading to an ipsilat-eral partial Horner syndrome, characterized by ptosis and miosis. Facial sweat function is preserved because the sympathetic innervation of the sweat glands travels along the external carotid artery. In internal carotid artery dissection, transient ischemic attacks are common and may involve the ipsilateral eye and brain. The spells often come more frequently than in atherosclerotic carotid stenosis, which led C. Miller Fisher, MD, to coin the term " carotid allegro" ( 3,4). Some patients with ICA dissection have visual scintillations and bright sparkles resembling migraine, even though many have had FIG. 5. Intracranial basilar artery dissection in a patient with polycystic kidney disease. The magnetic resonance imaging of the brain ( A) shows a pontine infarction on the T2- weighted image ( left) and an abnormally high signal within the basilar artery on the T1- weighted image ( right). The angiogram ( B) shows a tight stenosis ( arrow, left) of the distal basilar artery associated with a large pseu-doaneurysm ( arrow, right). 301 JNeuro- Ophthalmol, Vol. 24, No. 4, 2004 Caplan and Biousse TABLE 1. Clinical features in 635 patients with extracranial carotid artery dissections** Gender Male Female Laterality Unilateral Bilateral Major presenting event* Brain infarction Transient ischemic attack Neck or head pain Pulsatile tinnitus only Associated features at diagnosis Head or neck pain Tinnitus or bruit Horner syndrome Lingual paresis Clinical outcome No neurologic sequelae Mild deficit Moderate to severe deficit Death 53% 47% 86% 14% 46% 30% 21% 2% 67% 3% 32% 6% 50% 21% 25% 4% * Major presenting complaint leading to evaluation, not necessarily the initial symptom. ** Adapted from Saver JL, Easton JD. Dissections and trauma of cer-vicocerebral arteries. In Barnett HJM, Mohr JP, Stein BM, Yatsu FM, Eds. Stroke, pathology, diagnosis and management. 3rd Ed. Churchill Livingston 1998. pp 769- 786. Mean presenting age = 44.4 years, range 4- 74 years. no personal or family history of migraine ( 32). Some patients hear a pulsatile noise in the head or ear. Transient ischemic attacks are probably caused by luminal compromise, with distal hypoperfusion, but most patients with severe strokes have evidence of embolization of clot to the MCA from thrombus at the site of the dissection ( 7,19). When the ICA dissection extends to the carotid siphon, ischemic optic neuropathy can develop as a result of decreased perfusion of arteries supplying the optic nerve ( 33,34). Stroke may occur soon after the ICA dissection or days to weeks later ( 7,17- 23,3 5- 3 7). Very late stroke is rare ( 35). At times, clinical manifestations of dissection may occur in steps as an initial tear extends and more intramural bleeding develops. Both carotid arteries and even the ECVAs may become dissected at the same time. If pseudoaneurysm formation results from ICA dissection, dysfunction of the lower cranial nerves at the skull base may develop in the patient. Dysgeusia, weakness, and atrophy of the tongue are the most common cranial nerve signs. The lingual weakness and atrophy are caused by compression of the hypoglossal ( XII) nerve as it lies adjacent to the carotid sheath. At times, cranial nerves IX, X, XI, and XII are involved together. Intracranial ICA dissections are characterized by headache, together with signs of hemispheral MCA territory infarction ( 7,19). Vertebral Artery Dissections Extracranial vertebral artery dissections were first recognized in patients who had sustained neck trauma or had undergone chiropractic manipulation ( 2,19,3 8- 45), but ECVA injuries have also been reported in patients who manipulate their own necks ( 39,40), who have maintained their necks in a fixed position for some time ( 41- 45), or who make sudden abrupt neck movements ( Table 2) ( 2,42,44). ECVA dissections also occur after surgery and resuscitation ( 45), presumably because of sustained neck postures in patients who are anesthetized or unresponsive. These lesions most often involve the distal ECVA ( V3). Spontaneous ECVA dissections closely mimic those related to trauma. Pain in the posterior neck or mastoid region often precedes neurologic symptoms by hours, days, and, rarely, weeks, and may be the only manifestation. Transient ischemic attacks, less common than in ICA dissections, are TABLE 2. Clinical features in 174 patients with extracranial vertebral artery dissections** Gender Male Female Laterality Unilateral Bilateral Major presenting event* Brain infarction At onset After onset " Lateral medullary" symptoms Transient ischemic attack Neck or head pain Clinical outcome No or mild neurologic deficit Mild deficit Moderate or severe deficit Death 43% 57% 69% 31% 75% 17% 83% 33% 25% 75% 83% 21% 11% 6% * Major presenting complaint leading to evaluation, not necessarily the initial symptom. * * Adapted from Saver JL, Easton JD. Dissections and trauma of cer-vicocerebral arteries. In Barnett HJM, Mohr JP, Stein BM, Yatsu FM, Eds. Stroke, pathology, diagnosis and management. 3rd Ed. Churchill Livingston 1998. pp 769- 786. Mean presenting age = 38.9 years, range 3- 67 years. 302 © 2004 Lippincott Williams & Wilkins Cervicocranial Arterial Dissections JNeuro- Ophthalmol, Vol. 24, No. 4, 2004 manifested by dizziness, diplopia, veering, staggering, and dysarthria. Infarcts are explained by embolization of fresh thrombus to the ICVA ( 9,19). Occasionally, dissections extend or begin intracranially. They usually occur in the posterior inferior cerebellar artery domain, affecting the cerebellum and often the dorsolateral medulla. Sometimes emboli reach the superior cerebellar arteries, the main basilar artery, or the posterior cerebral arteries. Aneurysmal dilatation of the ECVA adjacent to nerve roots may cause radicular pain and can lead to radicular motor, sensory, and reflex abnormalities ( 46,47). Occasionally, spinal cord infarction results because of hypoperfusion in the branches of the ECVA that supply the cervical spinal cord ( 48). ICVA dissections usually extend into the basilar artery, causing brainstem infarction ( 2,7,18,19). Subarachnoid hemorrhage is another important presentation of ICVA dissection ( 2,9,10,19,26,27). Occasionally, dissections develop in the basilar artery and rarely in the posterior cerebral arteries. In the past, intracranial dissections were considered neurologically devastating or fatal, but modern technology has led to increased recognition that patients with intracranial dissections may have only minor signs. Neuro- ophthalmic manifestations of carotid and vertebral dissections are common ( Tables 1- 3). In carotid dissections, Horner syndrome is a presenting manifestation in up to 80% of cases evaluated by a neuro- ophthalmologist ( Table 3). The second most common symptom is ipsilateral transient monocular visual loss, estimated to a presenting symptom in 61% of cases ( Table 3). In vertebral dissections, persistent manifestations of lateral medullary dysfunction ( Horner syndrome, nystagmus, skew deviation, ocular lateropulsion, or ipsilateral first division trigeminal sensory loss) are found in more than 50% o of cases ( Table 2). TABLE 3. Neuro- ophthalmic manifestations in 146patients with carotid artery dissections*** Frequency as Overall presenting frequency manifestation Neuro- ophthalmic manifestations 62.5% 52% Painful Horner syndrome 44.5% 80% Transient monocular visual loss 28%>** 61%> Ischemic optic neuropathy 2.5%) 0% Central retinal artery occlusion 0% 0% Ischemic ocular syndrome 0% 0% Ocular motor nerve palsy < 1 % 0% * Isolated in 49%; with TIA or stroke in 51%. ** Associated with pain in 75.5%; with Horner syndrome in 31.5%. *** Adapted from Biousse V, Touboul PJ, D'Anglejan- Chatillon J, Levy C, Schaison M, Bousser MG. Ophthalmic manifestations of internal carotid artery dissection. Am J Ophthalmol 1998; 126: 565- 577. FIG. 6. Color Doppler study showing an internal carotid artery dissection. The dissected artery is enlarged secondary to the hematoma within the arterial wall { white arrow). The lumen is reduced { arrow). INVESTIGATION OF PATIENTS WITH SUSPECTED CERVICOCRANIAL DISSECTION The diagnosis of cervicocranial dissection can be made noninvasively with ultrasound, computed tomography, or magnetic resonance imaging ( MRI)/ magnetic resonance angiography ( MRA) or with catheter angiography. Whereas catheter angiography was formerly considered the gold standard, noninvasive methods are now so accurate that they suffice ( 7,19,49- 53). B- mode ultrasound can show tapering of the ICA lumen, beginning well above the ICA origin, an irregular membrane crossing the lumen, or actual demonstration of true and false lumens ( Fig. 6) ( 49- 51). Doppler can show a typical pattern characterized by a high- amplitude signal with markedly reduced systolic Doppler frequencies and alternating flow directions over the region of luminal narrowing ( 50,51). This Doppler signal probably results from abnormal vessel wall pulsations and some bidirectional movement of the blood column. Duplex scans of the ECVAs can also suggest dissection ( 49,51). Typical findings are increased arterial diameter, decreased pulsatility, intravascular abnormal echoes, and hemodynamic evidence of decreased flow. Color Doppler flow imaging can also show the regions of dissection within the neck. Diminished flow in the high neck at the level of the atlas detected by continuous wave Doppler and decreased flow in the ICVA shown by transcranial Doppler suggest the presence of distal 303 JNeuro- Ophthalmol, Vol. 24, No. 4, 2004 Caplan and Biousse ECVA dissections. In patients with extracranial ICA dissections, transcranial Doppler may show diminished intracranial velocities in the ICA siphon and the MCA. When this occurs in young patients without risk factors for atherosclerosis or embolism who have normal ICA bifurcations in the neck, the diagnosis of dissection is likely. Computed tomography and MRI, taken as axial cross- sections through the area of dissection, have shown the intramural bleeding and mural expansion ( Fig. 7). MRA and computed tomographic angiography can also show dissections ( 52,53). The most common catheter angiographic finding is a string sign, consisting of a long, narrow column of contrast material that begins distal to the carotid bifurcation and often extending to the base of the skull ( Figs. 2 and 3) ( 3,4). There may also be total occlusion of the ICA. This occlusion differs from the typical atherosclerotic occlusion, beginning more than 2 cm distal to the origin of the ICA, sparing the siphon, and having a gradually tapering segment that ends in the occlusion. There may also be localized aneurysmal sacs or outpouchings, both proximal and distal, along a narrowed, a normal, or an unusually dilated portion of the artery. MANAGEMENT OF CERVICOCRANIAL DISSECTIONS Most extracranial dissections heal spontaneously. Their location high in the neck usually makes surgical repair difficult or impossible. When complete occlusion has FIG. 7. T1- weighted magnetic resonance imaging showing a right internal carotid artery dissection as an abnormally high signal within the carotid artery wall. The lumen is very small and is seen as a pinpoint low signal. occurred, the arteries often do not recanalize, and they remain occluded ( 6). Arteries that retain some residual lumen invariably heal and normalize ( 6). Intracranial dissections have been repaired surgically in patients with subarachnoid hemorrhage, but the incidence of spontaneous healing and recurrent bleeding is not known. Although there have been no controlled trials of medical therapy, short- term anticoagulation may be worthwhile ( 54- 56). Prevention of embolization of thrombus at or shortly after the dissection should prevent stroke. Anticoagulants have seemed to prevent an increase in the extent of the dissections, a major theoretical concern. Because of the risk of embolization during the acute period, we recommend initial treatment with intravenous heparin, followed by warfarin. Cerebral blood flow should be maximized during the acute period to augment collateral circulation. This involves maintaining blood volume and pressure. Healing of dissections can be monitored using MRI, MRA, computed tomography angiography, and ultrasound ( 5- 7,54). 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