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54 55 56 1 Common Carotid : A Case Report 57 2 and Review of the Literature 58 3 59 4 60 5 61 6 Victor Zach, MD, Svetlana Zhovtis, MD, Kathryn F. Kirchoff-Torres, MD, 62 7 and Jesse M. Weinberger, MD 63 8 64 9 65 10 66 11 67 12 68 13 dissection (CCAD) is a rare and poorly characterized cause 69 14 of ischemic . We describe a case of multiple cerebral infarcts in a patient with 70 CCAD initially detected by carotid duplex ultrasonography, and review the litera- 15 71 ture on CCAD. A Medline search from 1960 to the present for cases of CCAD yielded 16 72 17 46 cases. We extracted demographic data, anatomical location, symptoms, neuroso- nography, neuroradiology, pathological findings, treatment, and outcomes. The 73 18 mean age of the patients was 48.8 6 15.8 years (range, 19–89 years). Our search 74 19 found 20 cases of spontaneous CCAD, 11 cases of traumatic CCAD, 4 cases of iatro- 75 20 genic CCAD, and 12 cases of CCAD associated with aortic arch dissection. The most 76 21 common presenting neurologic symptoms of CCAD were hemiparesis, decreased 77 22 consciousness, headache/neck pain, aphasia, and monocularPROOF field deficit. The 78 23 most frequently reported neurosonographic findings included a double lumen, mu- 79 24 ral thrombus, intraluminal hyperechoic/isoechoic lesion, and intimal flap. Most 80 25 cases of CCAD were subsequently confirmed with conventional angiography, com- 81 puted tomography angiography, or magnetic resonance angiography. Treatment dif- 26 82 fered based on etiology; anticoagulation was used most commonly for spontaneous 27 83 28 CCAD, and surgical repair was most often done for traumatic and – associated CCAD. Prognosis was generally good; the majority of patients achieved 84 29 complete clinical recovery, but 3 died. Our findings indicate that carotid Doppler is 85 30 a widely accessible, rapid, and noninvasive technique for diagnosing CCAD. Our 86 31 case and literature review further characterizes the diverse etiologies, clinical 87 32 course, and radiographic features of CCAD. Key Words: Common carotid 88 33 Q2 artery—dissection—cerebral infarct—stroke—carotid duplex—angiography. 89 34 Ó 2010 by National Stroke Association 90 35 91 36 92 37 Arterial dissection accounts for up to 20% of ischemic patients in a stroke database were identified as having 93 1 38 . Whereas dissection extracranial ICAD or vertebral artery dissection (VAD); 94 2 39 (ICAD) is typical, common carotid artery dissection no cases of CCAD were described. Because of its associa- 95 3 40 (CCAD) is an very rare cause of ischemic stroke. In tion with aortic dissection, early recognition of CCAD 96 41 a recent review of cervical artery dissections, 177 of 8800 might affect the decision regarding thrombolysis for acute 97 42 ischemic stroke. We present a patient with CCAD and 98 43 review the available literature to characterize the symp- 99 44 From the Department of Neurology, Mount Sinai School Of Medi- toms, imaging, treatments, and prognosis of CCAD. 100 45 cine, New York, New York. 101 Received January 13, 2010; accepted May 5, 2010. 46 102 47 Supported in part by a postdoctoral training award in cerebrovas- Case Report cular disease research to Mount Sinai School of Medicine 103 48 Q1 (1T32NS051147). UNCORRECTEDA 50-year-old female with migraine was transferred to 104 49 Address correspondence to Victor Zach, Department of Neurology, our hospital with complaints of an atypical, rapidly ex- 105 50 Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, panding visual aura that evolved into a right visual field 106 NY 10029. E-mail: [email protected]. 51 defect, left cervicooccipital pain, disequilibrium, right 107 52 1052-3057/$—see front matter Ó 2010 by National Stroke Association hemiparesis, and expressive aphasia. The symptoms 108 53 doi:10.1016/j.jstrokecerebrovasdis.2010.05.001 lasted for 45 minutes. On arrival, the patient had 109

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110 left CCA velocity (0.70 m/s.) The small circular area of 165 111 distal CCAD decreased to 3.5 mm in diameter, with com- 166 112 plete neurosonographic resolution of the ‘‘floating’’ 167 113 thrombus (Fig 5). Warfarin for 3–6 months, followed by 168 114 an antiplatelet agent and continued follow-up by CD, 169 115 are planned. 170 116 171 117 Literature Search Q3 172 118 173 We searched titles in Medline from 1960 to the present 119 174 using the following index terms: ‘‘common carotid artery 120 175 dissection,’’ ‘‘common carotid artery dissections,’’ ‘‘com- 121 176 mon carotid artery ,’’ ‘‘common carotid artery ste- 122 177 noses,’’ ‘‘common carotid artery injury,’’ ‘‘common carotid 123 178 artery occlusion,’’ ‘‘common carotid artery occlusions,’’ 124 179 ‘‘common carotid artery ,’’ ‘‘common ca- 125 180 rotid dissection,’’ ‘‘common carotid occlusion,’’ and ‘‘com- 126 181 mon carotid pseudoaneurysm.’’ In addition, we searched 127 182 the Journal of Neuroimaging using Medline and the key- 128 183 word ‘‘common carotid.’’ We retrieved data using the 129 184 Mount Sinai School of Medicine’s Levy Library. Our 130 Figure 1. Carotid ultrasound. Axial view of the left CCA (L CCA) show- 185 searches yielded a total of 369 titles. We excluded any 131 ing an intimal flap (arrowheads) with an underlying thrombus measuring 186 5.7 mm (arrow). L IJV, left internal jugular . papers that providedPROOF no clinical, radiographic, or patho- 132 187 logical evidence of CCAD. We did not exclude papers 133 188 based on language. We reviewed relevant references 134 impaired object recall and labile mood with inappropriate 189 and added any additional cases to our data pool. Four 135 laughter and crying episodes. 190 papers (1 Chinese, 2 Russian, and 1 American) were 136 Urgent carotid duplex ultrasonography (CD) with 191 excluded due to their unavailability in print or online. 137 color-flow imaging revealed a circular area of dissection, 192 Each paper was read by 1 of 2 authors, and a third author 138 5.7 mm in diameter, in the mid to distal left common 193 reviewed all of the papers to ensure standardized and 139 carotid artery (CCA), and a mobile thrombus with a dense 194 complete data abstraction. Including our case study pre- 140 circular rim and lucent core ‘‘floating’’ within the lumen 195 sented here, this yielded 47 cases of CCAD.4–42 141 of the CCA on axial view (Fig 1). Peak left CCA velocity 196 Information regarding age, sex, side of the CCAD, 142 was normal, at 0.64 m/s. Magnetic resonance imaging 197 location within the CCA, presenting signs and 143 (MRI) of the revealed multiple foci of restricted dif- 198 symptoms, CD findings, radiographic and pathological 144 fusion in the left anterior, middle, and posterior cerebral 199 findings, treatment, and prognosis were abstracted. Due 145 artery (PCA) distributions, consistent with acute infarc- 200 to the retrospective nature of this data, information 146 tion (Fig 2). The left PCA was of carotid (ie, fetal) origin. 201 regarding each characteristic was not always available. 147 Gadolinium-enhanced magnetic resonance angiography 202 We indicate the number of published cases that 148 (MRA) of the neck confirmed the distal CCAD and prox- 203 included relevant information for each characteristic. 149 imal ICAD. There was no evidence of aortic dissection on 204 150 this study, or on MRA of the thorax and abdomen (Fig 3). 205 151 Catheter cerebral angiography confirmed the distal left Results 206 207 152 CCAD located on the anteromedial wall. Furthermore, The mean age of the 43 patients in the case studies was 208 153 irregularities of the left cervical vertebral artery and the 48.8 6 15.8 years (range, 19–89 years). Classified by etiol- 4–19 209 154 left internal carotid artery (ICA) were suggestive of ogy, there were 20 cases of spontaneous CCAD, 11 20–28 210 155 fibromuscular dysplasia (Fig 4). cases of traumatic CCAD, 4 cases of iatrogenic 29–32 211 156 Transesophageal echocardiography demonstrated CCAD, and 12 cases of CCAD associated with 33–42 212 157 a normal ejection fraction andUNCORRECTED showed no evidence of aortic arch dissection (AAD). 158 intracardiac shunt or a cardiac source of thrombus. A hy- 213 214 159 percoagulation workup revealed heterozygosity for factor Spontaneous CCAD (n 5 20) 160 V Leiden. The patient was treated with intravenous hep- 215 161 arin and discharged on warfarin with an enoxaparin These patients included 14 males and 4 females, with Q4 216 162 bridge to a therapeutic international normalized ratio a mean age of 53.1 6 15.8 years (range, 34–89 years). Six 217 163 (INR) of 2–3. CCADs occurred in the right CCA, and 12 occurred in 218 164 At a 3-month follow-up, the patient remained asymp- the left CCA. Three CCADs occurred in the proximal 219 tomatic. Follow-up CD continued to show normal peak CCA, 3 occurred in the mid-portion, 5 occurred in the 220

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221 276 222 277 223 278 224 279 225 280 226 281 227 282 228 283 229 284 230 285 231 286 232 287 233 288 234 289 235 290 236 291 237 292 238 293 239 294 240 295 241 Figure 2. Diffusion-weighted MRI 296 242 showing multiple foci of restricted diffu- 297 sion in the distribution of the left ante- PROOF 298 243 rior, middle, and posterior cerebral 244 . 299 245 300 246 301 247 302 248 303 249 304 250 305 251 306 252 307 253 308 254 309 255 310 256 311 257 312 258 313 259 314 260 315 261 316 262 317 263 318 264 319 265 320 266 321 267 distal CCA, and 2 involved the entire CCA (n 5 13). The neck, and the third had CCAD diagnosed by angiogra- 322 268 presenting signs and symptomsUNCORRECTED (n 5 18) are shown in phy. One patient had CCAD and occlusion diagnosed 323 269 Table 1. by angiography alone. Fourteen patients underwent angi- 324 270 Findings on CD (n 5 13) included a double lumen ography, computed tomography angiography (CTA), 325 271 (4 patients), mural hematoma (4 patients), intimal flap MRI, or MRA of the neck or a combination of these tech- 326 272 (3 patients), carotid occlusion (3 patients), change in niques, which supported the diagnosis of CCAD, and 1 327 273 flow/velocity (3 patients), hyperechoic/isoechoic lesion patient was diagnosed by CD alone (n 5 15). Only our 328 274 within the vessel (2 patients), and pseudoaneurysm (1 pa- case demonstrated fibromuscular dysplasia associated 329 275 tient). Two of the patients with an occlusion detected on with CCAD by angiography. Histological examination 330 CD had CCAD diagnosed by MRI and MRA of the of CCA tissue in 1 patient revealed dissection and 331

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332 CCADs occurred in the mid-portion, 2 occurred in the 387 333 distal segment, and 1 involved the entire CCA (n 5 6). 388 334 The presenting signs and symptoms (n 5 10) are summa- 389 335 rized in Table 1. 390 336 Findings on CD (n 5 7) included a hyperechoic/isoe- 391 337 choic lesion within the vessel (4 patients), intimal flap 392 338 (2 patients), change in flow/velocity (2 patients), occlu- 393 339 sion (2 patients), and double-lumen and mural hematoma 394 340 (each in 1 patient). All 11 patients underwent angiogra- 395 341 phy, CTA, MRI, or MRA of the neck, or a combination 396 342 of these examinations, which supported the diagnosis of 397 343 CCAD. Two patients had CCA occlusion demonstrated 398 344 by angiography; in these patients CCAD was presumed 399 345 based on clinical presentation. Three patients underwent 400 346 histological evaluation of CCA tissue, which demon- 401 347 strated disruption of the intima, internal elastic lamina, 402 23 348 and media in 2 patients and medial dissection in 1 403 26 349 patient. The treatments and outcomes of the patients 404 350 with traumatic CCAD (n 5 11) are summarized in Table 2. 405 351 406 407 352 Iatrogenic CCAD (n 5 4) 353 PROOF 408 354 Iatrogenic CCAD was attributed to misplaced internal 409 355 jugular catheter placement in 2 patients, carotid endarter- 410 356 ectomy (CEA) in 1 patient, and rupture of an eroded 411 357 carotid artery during surgery to remove a hypopharyngeal 412 358 cancer in 1 patient. The mean age of the 1 male and 2 413 359 females was 47.3 6 8.5 years (range, 41–57 years). Three 414 360 CCADs occurred in the right CCA. CCAD was described 415 361 once in the mid-portion and once in the distal CCA 416 362 (n 5 2). The presenting signs and symptoms of the patients 417 363 with iatrogenic CCAD (n 5 3) are shown in Table 1. 418 364 Findings on CD (n 5 2) included double lumen 419 365 (2 patients), mural hematoma (1 patient), intimal flap 420 366 (1 patient), and increased blood flow velocity in the CCA 421 367 with early systolic deceleration in the distal CCA, ICA, 422 368 and external carotid artery (ECA), presumably due to 423 369 a retrograde pressure wave from the contralateral side 424 29 370 (1 patient). In this latter patient, angiography revealed 425 371 Figure 3. Gadolinium-enhanced MRA of the neck showing intimal irreg- a false lumen, which was later confirmed intraoperatively. Q5 426 ularity with suggestion of a flap in the left CCA (top. axial view; bottom. re- Histological examination of a CCA specimen from 1 427 372 constructed view). 373 patient demonstrated degeneration of the media with focal 428 374 thrombus without cystic medial degeneration.17 The muscle loss and accumulation of acid mucopolysaccha- 429 3 375 treatments and outcomes of these patients (n 5 18) are rides suggestive of cystic medial degeneration. The treat- 430 376 summarized in Table 2. ments and outcomes of the patients with iatrogenic CCAD 431 377 (n 5 3) are summarized in Table 2. 432 433 378 Traumatic CCAD (n 5 11) 434 379 UNCORRECTEDCCAD Associated with AAD (n 5 12) 380 Eleven patients (5 male and 6 female; mean age, 38.6 6 435 381 15.2 years; range, 19–68 years) had traumatic CCAD. Four Nine male and 3 female patients (mean age, 52 6 5.9 436 382 cases of CCAD were attributed to blunt trauma to the years; range, 43–64 years) had AAD extending to involve 437 383 neck, 3 cases were attributed to a motor vehicle accident, the branches of the aortic arch. Three cases involved the 438 384 2 cases were related to attempted suicide by hanging, and brachiocephalic artery and bilateral CCAs, 4 cases in- 439 385 1 case involved a fall with neck trauma (n 5 10). Six volved the brachiocephalic artery and right CCA, and 1 440 386 CCADs occurred in the right CCA and 4 occurred in the case involved the brachiocephalic artery and left CCA 441 left CCA, and 1 patient had bilateral CCAD. Three (n 5 8). The left CCA was not involved in isolation. The 442

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443 498 444 499 445 500 446 501 447 502 448 503 449 504 450 505 451 506 452 507 453 508 454 509 455 510 456 511 457 512 458 513 459 514 460 515 461 516 462 517 463 518 464 PROOF 519 465 520 466 521 467 522 468 523 469 524 470 525 471 526 472 527 528 473 Figure 4. Cerebral angiogram demonstrating dissection of the left CCA (L CCA; top, arrow) and vessel wall irregularities (arrowheads) within both the left ICA 529 474 (L ICA) and the left vertebral artery (middle and bottom). 475 530 476 presenting signs and symptoms of the patients with 531 477 CCAD associated with AAD (n 5 12) are summarized 532 478 in Table 1. 533 479 Findings on CD (n 5 5) included a double lumen (5 pa- 534 480 tients), change in flow velocity (5 patients), and intimal 535 481 flap (4 patients). Eleven patients underwent evaluation 536 482 of the aortic arch and branches by angiography, CTA, 537 483 MRI, MRA, or a combination of these examinations, and 538 484 1 patient was diagnosed with CCA by CD alone (n 5 12). 539 485 Two patients underwent histological examination of a re- 540 486 sected aortic arch and CCA tissue. One case reported 541 487 dissecting at the bases of the brachiocephalic 542 488 and left CCA filled with thrombus, with no abnormalities 543 489 in the arrangement of elastic fibers, , or 544 35 490 . In another patient, Marfan’s syndrome was 545 UNCORRECTED 38 491 confirmed by histopathology of the aortic arch. 546 492 547 548 493 Discussion 494 549 43 495 Historically, CCAD has been associated with AAD, 550 reported in as many as 41% of AAD cases.44 Although 551 496 Figure 5. Follow-up performed 1 month after on- 497 set of symptoms showing regression of the thrombus under the intimal flap case reports have been published on the more uncommon 552 (measurement shown in the image, 3.5 mm). L CCA, left CCA; L IJV, left in- causes of CCAD, such as spontaneous, traumatic, and 553 ternal jugular vein.

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554 Table 1. Presenting signs and symptoms of CCAD by etiology 609 555 610 Spontaneous Traumatic Iatrogenic Aortic dissection 556 611 Presenting symptom (n 5 18), n (%) (n 5 10), n (%) (n 5 3), n (%) (n 5 12), n (%) 557 612 558 Hemiparesis/hemiparalysis 11 (61.1) 5 (50) 1 (33.3) 6 (50) 613 559 Decreased consciousness 2 (11.1) 2 (20) - 6 (50) 614 560 Headache/neck pain 7 (38.9) - - - 615 561 Aphasia/dysphasia 5 (27.8) - - 1 (8.3) 616 562 Monocular field deficit 4 (22.2) 1 (10) 1 (33.3) - 617 563 Sensory deficits 1 (5.6) 3 (30) 1 (33.3) 1 (8.3) 618 Vertigo/dizziness 1 (5.6) - - 2 (16.7) 564 619 Visual field deficit 1 (5.6) - 1 (33.3) 1 (8.3) 565 620 Carotid - 2 (20) 1 (33.3) - 621 566 Dysarthria 2 (11.1) - - - 622 567 Oculomotor nerve palsy 1 (5.6) - 1 (33.3) - 623 568 Chest pain 1 (5.6) - - 1 (8.3) 569 Quadriparesis - 1 (10) - - 624 570 Visual disturbance (NOS) - - - 1 (8.3) 625 571 Gaze palsy - - - 1 (8.3) 626 572 Horner’s syndrome - - - 1 (8.3) 627 573 Cognitive changes 1 (5.6) - - - 628 574 Seizure - - - 1 (8.3) 629 Back pain - - - 1 (8.3) 575 630 Asymptomatic - -PROOF 1 (33.3) 1 (8.3) 576 631 632 577 Abbreviation: NOS, not otherwise specified. 578 633 579 634 45 580 iatrogenic CCAD, to the best of our knowledge, no com- CCAD are less likely to be reported in the literature 635 581 prehensive review of this heterogeneous disorder exists. and/or might be underdiagnosed. 636 582 Typically, cervical artery dissection affects the ICA or Cervical trauma resulting in focal neurologic deficits 637 583 the vertebral arteries. The true incidence and prevalence should raise suspicion for CCAD. CCAD can progress 638 8 49 584 of CCAD is unknown. Chen et al reported that 10% of to CCA occlusion, which might be reversible. CCA 639 50 585 patients undergoing angiography at their institution occlusion also may occur in the setting of AAD. It is 640 586 had ICA dissection and 5% had vertebral artery dissec- likely that any subtype of CCAD can result in CCA occlu- 641 21 587 tion, whereas only 0.85% had CCAD. Dittrich et al sion. Emergent diagnosis of CCAD, especially with 642 588 estimated the prevalence of CCAD at ,1% of all cervical subsequent occlusion, is essential, because timely man- 643 589 artery dissections, possibly due to a difference in the agement may improve neurologic outcome. 644 590 architecture of the vessel wall in the CCA. Humans The mechanism through which cervical artery dissec- 645 591 have 2 types of arteries, elastic and muscular. The ICA tion causes cerebral is controversial. Classically, 646 592 is a muscular artery, whereas the CCA is an elastic artery. hypovolemia (especially in patients with poor collateral 647 51 593 The change occurs at the carotid bifurcation. The main vasculature) was invoked as a mechanism for ischemia; 648 594 difference between the 2 is in the tunica media. In elastic however, current theory has expanded to include a vessel- 649 52 595 arteries, the tunica media consists of mostly elastic fibers, to-vessel embolic mechanism. Large intimal tears fre- 650 596 whereas in the muscular arteries it consists mainly of quently result in severe . Acute thrombosis is 651 597 smooth muscle tissue. Muscular arteries have 2 elastic milder with mural contusions, but ischemic stroke can 652 598 layers in the tunica media (the external elastic lamina occur in a delayed manner secondary to progressive 653 23 599 and internal elastic lamina), which may make them stenosis or artery-to-artery . A patient present- 654 46,47 600 more susceptible to dissection. ing with acute ischemic stroke and CCAD should be que- 655 601 ICA dissection presents withUNCORRECTED craniocervical pain, ried for a history of a remote trauma to the neck induced 656 602 Horner’s syndrome, and distal ischemia (central nervous by another person, because they may be a victim of foul 657 48 53 603 system or ocular) and can be traumatic, iatrogenic, or play. 658 604 spontaneous. In the cases that we retrieved, CCAD Unilateral absence of a carotid pulse is a pertinent sign 659 51 49 605 frequently presented with hemiparesis or hemiplegia, in CCA occlusion. Crawford et al noted this finding in 660 606 altered level of consciousness, aphasia, monocular visual all 299 of their CCA occlusion patients. Cervicalgia was 661 607 deficits, and/or headache and neck pain. Publication bias not reported in any of the traumatic CCAD cases in our 662 608 should be considered when interpreting these retrospec- review. The authors of those papers might have presumed 663 tive data. We suspect that asymptomatic patients with that it is obvious that trauma to the neck results in pain 664

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665 720 666 721 667 722 668 723 669 724 670 725 671 726 672 727 673 728 674 729 675 730 676 731 677 732 678 733 679 734 680 735 681 736 682 737 683 738 684 739 685 740 686 PROOF 741 687 742 688 743 689 744 745 690 course, n (%) Death, n (%) Not specified, n (%) Total, n (%) 691 746 Asymptomatic clinical 692 747 693 748 694 749 695 750 696 751

697 CCAD treatment and outcome by etiology 752 698 753 deficit, n (%) 699 754 Persistent neurologic 700 Table 2. 755 701 756 702 757 703 758 704 759 705 760 Complete 761

706 recovery, n (%) 707 762 708 763 709 764 710 765

711 18) 10 (55.5) 6 (33.3) - 1 (5.6) 1 (5.6)766 18 (100) 11) 5 (45.5) 2 (18.2) - 1 (9.1) 3 (27.3) 11 (100) 11) 1 (9.1) 8 (72.7) - 1 (9.1) 1 (9.1) 11 (100) 3) 1 (33.3) 1 (33.3) 1 (33.3) - - 3 (100) 712 5 767 5 antiplatelet 1 (5.6) - - - - 1 (5.6) 5 5

UNCORRECTED anticoagulation 1 (33.3) - - - - 1 (33.3) 713 768 1 43) 17 (39.5) 17 (39.5) 1 (2.3) 3 (7.0) 5 (11.6) 43 (100) 1 A/C - - - - 1 (5.6) 1 (5.6) anticoagulation 1 (9.1) - -769 - - 1 (9.1)

714 5 1 1 715 770 antiplatelet - 1 (5.6) - - - 1 (5.6) 716 urokinase 1 (5.6) - -771 - - 1 (5.6) 1 1 717 772 773 AnticoagulationAntiplateletSurgical repairAntiplatelet 4 (22.2) 2 (11.1) 2 (11.1) 3 (16.7) 1 (5.6) 1 (5.6) ------7 (38.9) 3 (16.7) 3 (16.7) CEA CEA CCA/ICA stent Not specified - - - 1 (5.6) - 1 (5.6) CCA stentNot specifiedAnticoagulationSurgical repairSurgical repair - - - - 1 (9.1) - - 1 (33.3) - 1 (33.3) - - - - 1 (9.1) - - - - - 1 1 (9.1) (9.1) 1 (33.3) 1 (33.3) 718 Surgical repairAnticoagulationAntiplateletAntiplatelet -Surgical - repairAnticoagulationNo treatment -Not specified 4 (36.4) 2 (18.2) 1 (9.1) 2 (18.2) 2 (18.2) 1 (9.1) - - - 2 (18.2) ------1 (9.1) ------5 (45.5) 2 - (18.2) 3 (27.3) 1 (9.1) 1 (9.1) - 7 (63.6) - - 2 (18.2) 1 (9.1) 1 (9.1) Spontaneous CCAD (n Traumatic CCAD (n Iatrogenic CCAD (n AAD with CCAD (n 719 CCAD total (n 774 775

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776 and thus did not report that information. Miosis is a clas- endovascular and stenting, CEA, and bypass 831 23,30 777 sic physical finding in ICA dissection. In addition, CCAD surgery. No evidence-based guidelines exist to guide 832 778 presenting with mydriasis has been reported, suggesting the treatment of CCAD, and prospective, randomized 833 31 779 ischemic injury to the oculomotor nerve. trials are needed to determine optimal treatment. 834 780 There are many options for radiographic diagnosis of In our review, the prognosis was generally good, with 17 835 781 CCAD. CD is readily accessible and safe, and allows for patients achieving complete recovery and 1 patient remain- 836 782 dynamic imaging. When urgent CD is performed for sus- ing asymptomatic, and only 3 deaths among 38 patients. 837 783 pected CCAD, axial views of the vessel should be ac- These data may be subject to publication bias, however; 838 784 quired. In our patient, flow within the vessel was patients with poor outcomes might have been reported 839 785 normal, and the transverse view did not depict the com- less frequently. The prognosis for CCAD after AAD type 840 44 786 plete dissection. Cerebral angiography is the gold stan- I is reportedly good. Awareness of the clinical symptoms 841 787 dard for the diagnosis of CCAD; however, this and risk factors for CCAD is imperative; prompt diagnosis 842 788 technique is invasive and is not readily available in and treatment can result in a favorable clinical outcome. 843 789 many centers. CTA is widely available; however, it re- 844 790 quires infusion of contrast and exposure to radiation. Fi- 845 791 nally, MRA is not as readily available as CTA in many We thank Dr Nils Petersen for his assistance with German 846 792 centers, and it has some drawbacks, including a longer translation and Dr Tamara Zach for her assistance with 847 793 scanning time and higher costs. Gadolinium-enhanced proofreading the manuscript. 848 794 MRA of the neck carries increased risk, especially in pa- 849 795 tients who are pregnant or have renal disease. References 850 796 The standard of care for acute ischemic stroke includes 851 797 thrombolysis with intravenous tissue plasminogen acti- 1. Scott PA, Timmerman CA. Stroke, transient ischemic at- 852 vator (tPA). But thrombolysis is potentially harmful in pa- tack, andPROOF other central focal conditions. In: Tintinalli JE, 853 798 Kelen GD, Stapczynski JS, et al, eds. Tintinalli’s Emer- tients with CCAD associated with AAD,36 and 854 799 gency Medicine: A Comprehensive Study Guide. 6th ed. Q7 800 mechanical clot extraction or intra-arterial thrombolysis 2. Schwartz NE, Vertinsky AT, Hirsch KG, et al. Clinical and 855 801 with a smaller dose of tPA may be more appropriate for radiographic natural history of cervical artery dissec- 856 802 acute ischemic stroke in these patients. Early detection tions. J Stroke Cerebrovasc Dis 2009;18:416-423. 857 of CCAD is imperative in patients with AAD and focal 3. Humphrey PW, Keller MP, Spadone DP, et al. Spontane- 858 803 ous common carotid artery dissection. J Vasc Surg 1993; 859 804 neurologic symptoms. 18:95-99. 805 In cases of CCA occlusion, cerebral angiography has 4. Toelen C, Goverde P, Van Hee R. Dissection of the com- 860 806 been used to detect patency of the ICA, which may then mon carotid artery: A case report. Acta Chir Belg 2009; 861 807 lead to surgical revascularization via bypass graft. After 109:224-227. 862 a CCA occlusion, blood will typically flow from the ECA 5. Kervancioglu S, Sirikci R, Yigiter R, et al. Endovascular 863 808 angioplasty stenting as a definitive treatment for isolated 864 809 to the ICA. Occasionally, reversal may be seen, with the spontaneous common carotid artery dissection: A case re- 54 810 ICA flowing retrograde and into the ECA. Flow in the port. Neuroradiol J 2006;19:348-354. 865 811 ICA can be readily detected by CD. This dynamic informa- 6. Inoue T, Tsutsumi K, Adachi S, et al. Direct and primary 866 812 tion regarding flow within the ICA and ECA distal to the for common carotid artery occlu- 867 CCA occlusion provides complementary information for sion: Report of 2 cases. Surg Neurol 2008;69:620-626. 868 813 7. Neudecker S, Bau V, Behrmann C, et al. Unilateral amau- 869 814 cerebral angiography. In 1 case report, cerebral angiogra- rosis as the only focal symptom caused by dissection of 815 phy showed no flow within the ICA, but CD revealed pat- the common carotid artery. Klin Monatsbl Augenheilkd 870 55 816 ent vasculature. This information was useful for 2004;221:509-512. 871 817 revascularization planning. CD also can spare patients 8. Chen YC, Lee TH, Chen CJ, et al. Spontaneous common 872 from unnecessary surgical procedures based on flow pat- carotid artery dissection: A case report and review of 873 818 the literature. Eur Neurol 2003;50:58-60. 38 874 819 terns identified within the true and false lumen. Purely 9. Lee CC, Kim GW, Crupi RS. A common carotid artery 820 anterograde flow was seen in our patient, with normal dissection. J Emerg Med 2002;23:291-292. 875 821 velocities in all vessels; thus, surgery was not pursued. If 10. Hirth K, Sander S, Ho¨rmann K. Common carotid artery 876 822 surgical or endovascular intervention for CCAD is per- dissection: A rare cause for cervical pain. J Laryngol 877 Otol 2002;116:309-311. Q6 formed, transcranial CD may be used for emboli monitor- 878 823 11. Lubin J, Capparella J, Vecchione M. Acute monocular UNCORRECTED 879 824 ing during the procedure. In the event of an embolism, blindness associated with spontaneous common carotid 825 intra-arterial thrombolysis or mechanical extraction can artery dissection. Ann Emerg Med 2001;38:332-335. 880 30 826 be attempted, with a potentially good outcome. 12. Ramı´rez-Moreno J, Casado-Naranjo I, Go´mez- 881 827 Treatment of CCAD varies based on the etiology. Goals Gutie´rrez M, et al. Cerebral due to spontaneous 882 include prevention of vessel-to-vessel embolism, preven- dissection of the left common carotid artery. Neurologia 883 828 2001;16:276-280. 884 829 tion of thrombus progression, and maintenance of 13. Kawajiri K, Kiyama M, Hayazaki K. Spontaneous dissec- 830 adequate blood flow to ensure distal perfusion. Options tion in the common carotid artery: Case report. Neurol 885 include antiplatelet therapy, anticoagulation therapy, Med Chir 1995;35:373-376. 886

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COMMON CAROTID ARTERY DISSECTION 9

887 14. Heilberger P, Kasprzak P, Raithel D. Spontaneous dissec- 35. Higashi S, Yoshida Y, Mitsuoka H. Dissecting aneurysms 942 888 tion of the common carotid artery. Chirurg 1992; at the bases of the brachiocephalic artery and the left com- 943 63:675-678. mon carotid artery due to localized dissection of the aortic 944 889 15. Early TF, Gregory RT, Wheeler JR, et al. Spontaneous ca- arch: Report of a case. Kyobu Geka 2007;60:575-578. 945 890 rotid dissection: Duplex scanning in diagnosis and man- 36. Sojer M, Stockner H, Biedermann B, et al. Images in car- 891 agement. J Vasc Surg 1991;14:391-397. diovascular medicine. Common carotid dissection: A 946 892 16. Tzeng SS, Hu HH, Kao KP, et al. Common carotid artery sign of emergency 2007;115:e181-e185. Q9 947 893 dissection diagnosed by ultrasonic image: Report of 37. Shimazaki Y, Minowa T, Watanabe T, et al. Acute aortic 948 a case. J Formos Med Assoc 1990;89:1093-1095. dissection with new massive : A suc- 949 894 17. Graham JM, Miller T, Stinnett DM. Spontaneous dissec- cessful repair with ligature of the right common carotid 950 895 tion of the common carotid artery: Case report and re- artery. Ann Thorac Cardiovasc Surg 2004;10:64-66. 896 view of the literature. J Vasc Surg 1988;7:811-813. 38. Bonnin P, Giannesini C, Amah G, et al. Doppler sonogr- 951 897 18. Burkland CW. Spontaneous dissecting of the apy with dynamic testing in a case of aortic dissection ex- 952 898 cervical carotid artery. Johns Hopkins Med J 1970; tending to the innominate and right common carotid 953 126:154-159. arteries. Neuroradiology 2003;45:472-475. 954 899 19. O’Dwyer JA, Moscow N, Trevor R, et al. Spontaneous dis- 39. Kubota T, Niwa J, Chiba M, et al. Common carotid artery 955 900 section of the carotid artery. Radiology 1980;137:379-385. dissection propagated from acute aortic dissection: A 901 20. Ueda A, Inatomi Y, Yonehara T, et al. Blunt traumatic dis- case successfully treated by PTA. No Shinkei Geka 956 902 section in common carotid artery with serial morpholog- 2000;28:1015-1021. 957 903 ical changes detected by carotid ultrasonography in the 40. Trattnig S, Rand T, Thurnher M, et al. Colour-coded 958 acute phase. Rinsho Shinkeigaku 2006;46:631-637. Doppler sonography of common carotid artery dissec- 959 904 21. Dittrich R, Draeger B, Nassenstein I, et al. Dissection of tion. Neuroradiology 1995;37:124-126. 960 905 the common and external carotid artery. Cerebrovasc 41. Veyssier-Belot C, Cohen A, Rougemont D, et al. Cerebral 906 Dis 2006;21:208-210. infarction due to painless thoracic aortic and common ca- 961 907 22. Linnau KF, Cohen WA. Radiologic evaluation of attemp- rotid artery dissections. Stroke 1993;24:2111-2113. 962 908 ted suicide by hanging: Cricotracheal separation and 42. Steinke W, Schwartz A, Hennerici M. Doppler color flow 963 common carotid artery dissection. AJR Am J Roentgenol imaging ofPROOF common carotid artery dissection. Neuroradi- 909 964 Q8 2002;178:214. ology 1990;32:502-505. 965 910 23. Okada Y, Shima T, Nishida M, et al. Traumatic dissection 43. Hirst AE, John VJ Jr, Kime SW. Dissecting aneurysm of 911 of the common carotid artery after blunt injury to the the : A review of 505 cases. Medicine 1958; 966 912 neck. Surg Neurol 1999;51:513-520. 37:217-219. 967 913 24. Godfrey DG, Biousse V, Newman NJ. Delayed branch ret- 44. Zurbrugg HR, Leupi F, Schupbach P, et al. Duplex scan- 968 inal artery occlusion following presumed blunt common ner study of carotid artery dissection following surgical 969 914 carotid dissection. Arch Ophthalmol 1998;116:1120-1121. treatment of aortic dissection type A. Stroke 1988; 970 915 25. de Recondo A, Woimant F, Ille O, et al. Posttraumatic 19:970-976. 916 common carotid artery dissection. Stroke 1995; 45. Hart RG, Easton JD. Dissections of cervical and cerebral 971 917 26:705-706. arteries. Neurol Clin 1983;1:155-182. 972 918 26. Noguchi K, Matsuoka Y, Hohda K, et al. A case of com- 46. Hori E, Hayashi N, Hamada H, et al. A development of 973 mon carotid artery stenosis due to hanging. No Shinkei atheromatous plaque is restricted by characteristic arte- 974 919 Geka 1992;20:1185-1188. rial wall structure at the carotid bifurcation. Surg Neurol 975 920 27. Oxorn D, Clark K. Crico-tracheal disruption and com- 2008;69:586-591. 921 mon carotid artery occlusion: A case of blunt trauma. 47. Janzen J, lanzer P, Rothenberger-Janzen K, et al. Variable 976 922 Can J Anaesth 1990;37:913-915. extension of the transitional zone in the medial structure 977 923 28. Gonzalez A. Common carotid artery stenosis due to sub- of carotid artery tripod. Vasa 2001;30:101-106. 978 intimal hematoma following blunt trauma to the neck: 48. Schievink WI. Spontaneous dissection of the carotid and 979 924 Report of a case. J Cardiovasc Surg 1977;18:297-301. vertebral arteries. N Engl J Med 2001;344:898-906. 980 925 29. Aschwanden M, Thalhammer C, Schaub S, et al. Com- 49. Crawford ES, De Bakey ME, Morris GC Jr, et al. Surgical 926 mon carotid dissection after central venous catheteriza- treatment of occlusion of the innominate, common ca- 981 927 tion. Ultraschall Med 2008;29:571-574. rotid, and subclavian arteries: A 10-year experience. Sur- 982 928 30. Furui E, Okamoto Y, Kida S, et al. Images in cardiovascu- gery 1969;65:17-31. 983 lar medicine: Transient occlusion of the middle cerebral 50. Levine SR, Welch KM. Common carotid artery occlusion. 984 929 artery by macroembolism during for Neurology 1989;39:178-186. 985 930 traumatic dissection of the common carotid artery. Circu- 51. Gilbert GJ. Common carotid occlusion. Neurology 1989; 931 lation 2005;112:e33-e34. 39:1406-1407. 986 932 31. Koennecke H, Seyfert S. Mydriatic pupil as the present- 52. Weinberger J, Rudolph S, Lidov M. Evidence for arterial 987 933 ing sign of common carotid artery dissection. Stroke in dissecting aneurysm of the cervical ver- 988 1998;29:2653-2655. tebral artery. J Stroke Cerebrovasc Dis 1991;1:95-97. 989 934 32. Gollub MJ, Friedwald JP, Hartigan M. Iatrogenic dissec- 53. Kelly M. Death Touch: The Science Behind the Legend of UNCORRECTED 990 935 tion of the common carotid artery: Diagnosis by dynamic Dim-Mak: Paladin Press, 2001. 9-16. Q10 936 image and color flow . J Clin Ul- 54. Pretre R, Kalangos A, Bednarkiewicz M, et al. Reversed 991 937 trasound 1991;19:250-253. flow in the internal carotid artery after occlusion of the 992 938 33. Hiraishi T, Motoyama H, Abe H. Case of bilateral com- common carotid artery. Thorac Cardiovasc Surg 1994; 993 mon carotid artery dissections due to localized dissection 42:358-360. 994 939 of the aortic arch. No Shinkei Geka 2009;37:387-391. 55. Bebry AJ, Hines GL. Total occlusion of the common ca- 995 940 34. Zwierzyn´ska E, Bec L, Sklinda K, et al. Common carotid rotid artery with a patent internal carotid artery: Identifi- 941 artery dissection in the course of acute aortic dissection cation by duplex ultrasonography. Report of a case. J Vasc 996 De Bakey type I. Neurol Neurochir Pol 2007;41:472-476. Surg 1989;10:469-470. 997

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