A Hyperdense Artery Sign and Middle Cerebral Artery Dissection

□ CASE REPORT □

Yusuke Yakushiji 1, Yoshinori Haraguchi 2, Shu Soejima 2, Yukinori Takase 3, Akira Uchino 3, Shunzo Koizumi 2 and Yasuo Kuroda 1

Abstract

We describe a rare case of spontaneous middle cerebral artery (MCA) dissection that caused cerebral infarction and subarachnoid hemorrhage (SAH), which also presented with a hyperdense artery sign. A hyperdense artery sign of the MCA in acute cerebral infarction strongly indicates thromboembolic MCA occlusion, which is often treated with thrombolytic therapy. However, thrombolytic therapy for intracranial artery dissections has both risks and benefits, due to the association of artery dissections with SAH. Therefore, it is im- portant to keep in mind that an MCA dissection can also cause cerebral infarction with a hyperdense artery sign, particularly in young patients presenting with headache.

Key words: Hyperdense middle cerebral artery sign, Computed tomography, Intracranial artery dissection, Cerebral infarction

(DOI: 10.2169/internalmedicine.45.1888)

his blood pressure was 162/126 mmHg. Neurological exami- Introduction nation revealed drowsiness (Japan Coma Scale II-10), motor aphasia, and right-sided hemiplegia. National Institutes of A hyperdense artery sign of the middle cerebral artery Health Stroke Scale (NIHSS) was 15. Laboratory examina- (MCA) in acute cerebral infarction strongly indicates throm- tions were normal, including α1-antitrypsin level and hemat- boembolic MCA occlusion (1), which is often treated with ocrit (45.9%). thrombolytic therapy (2). However, dissection of the intra- Brain computed tomography (CT), performed on admis- cranial cerebral arteries can cause a subarachnoid hemor- sion (Day 1), showed a hyperdensity at the M1 segment rhage (SAH), as well as cerebral infarction (3);therefore, through to the posterior trunk of the M2 segment of the left thrombolytic therapy is generally not indicated in such middle cerebral artery (MCA) (Fig. 1a) and hypodensity of cases. We describe a case of spontaneous MCA dissection more than one-third of the left MCA territory. The MCA at- that caused cerebral infarction and SAH, which also pre- tenuation value was 66 Hounsfield units (HU) on the left sented with a hyperdense artery sign. We also discuss the and 39 HU on the right (the attenuation ratio of the affected literature relating to intracranial artery dissection associated vessel to the normal vessel was 1.69). Brain diffusion- with a hyperdense artery sign. weighted imaging (DWI) and time-of-flight magnetic reso- nance angiography (TOF MRA) were performed the same Case Report day and immediately followed by brain CT. DWI showed that the acute infarction was restricted to the left MCA area. A 40-year-old man with hypertension was admitted due to TOF MRA showed slight dilatation at the distal M1 seg- the sudden onset of disturbance of consciousness without ment, but patency of the left MCA (Fig. 1b). No embolic any traumatic injury. His pulse was regular (90/min), and sources were detected by either transesophageal echocar-

１ Division of Neurology, Department of Internal Medicine, Saga University Faculty of Medicine, Saga, ２ Department of General Medicine, Saga University Faculty of Medicine, Saga and ３ Department of Radiology, Saga University Faculty of Medicine, Saga Received for publication May 22, 2006; Accepted for publication August 21, 2006 Correspondence to Dr. Yusuke Yakushiji, the Division of Neurology, Department of Internal Medicine, Saga University Faculty of Medicine, 5- 1-1 Nabeshima, Saga 849-8501

1319 DOI: 10.2169/internalmedicine.45.1888

Figure 1. a. An unenhanced brain CT scan, performed on Day 1, shows increased attenuation at the M1 segment of the left middle cerebral artery (arrow). The MCA attenuation value is 66 Hounsfield units (HU) on the left and 39 HU on the right. b. Time-of-flight MR angiography (Advantage 1.5 T system, TR 57 ms, TE 4.5 ms, Flip angle 30°, section thick- Figure 3. Images of selective left internal carotid angiogra- ness 0.9 mm), performed on Day 1 and immediately followed phy done with a rotational three-dimensional digital subtrac- by brain CT, shows patency of the left MCA. tion angiography system. a. Initial examination performed on Day 11 shows an aneurysmal dilatation at the distal M1 segment (arrow) and a “pearl-and-string sign” at the M1 segment through to the posterior trunk of the M2 segment (arrowheads). b. Follow-up examination performed on Day 25 shows reduction of the aneurysmal dilatation (arrow) and improvement of the “pearl-and-string sign” (arrowheads). A narrowing of the M1 segment of the MCA is also seen.

gradually worsened without a fever developing. On the same day, brain CT showed that the hyperdensity of the left MCA was still present (the MCA attenuation value was 63 HU on the left and 40 HU on the right, while the attenuation ratio was 1.58). Meanwhile, TOF MRA, which was performed immediately after brain CT, demonstrated patency and aneurysmal dilatation at the posterior trunk of the left MCA. On Day 7, xanthochromia was found on examination of the cerebrospinal fluid. Selective left internal carotid angiography using a rotational three-dimensional digital subtraction angiography system (3-D DSA) was conducted on Day 11 Figure 2. A brain CT, performed on Day 2, demonstrates and showed an aneurysmal dilatation at the distal M1 seg- SAH (arrowheads) and hypodensity with edema in the left ment and a “pearl-and-string sign” at the M1 segment MCA area. through to the posterior trunk of the M2 segment (Fig. 3a). On follow-up CT on Day 14, the hyperdensity of the left MCA was no longer seen, and the MCA attenuation value diography or conventional carotid ultrasonography. was 41 HU on the left and 40 HU on the right (the attenu- On Day 2, brain CT demonstrated SAH and hypodensity ation ratio was 1.03). On Day 20, 3-dimensional spoiled with edema in the left MCA area (Fig. 2). On Day 4, the gradient-recalled acquisition (SPGR) identified a narrowing patient’s disturbance of consciousness gradually improved, of the proximal region of the M1 segment of the left MCA but he began to complain of a left-sided headache, which (Fig. 4a). The distal M1 segment of the left MCA was more

1320 DOI: 10.2169/internalmedicine.45.1888

which suggested that a gentle flow was present in the false lumen (Fig. 4d). Follow-up selective left internal carotid angiography using rotational 3-D DSA was performed on Day 25 and showed reduction of the aneurysmal dilatation at the distal M1 segment, improvement of the “pearl-and-string sign” at the M1 segment through to the posterior trunk of the M2 segment, and narrowing of the M1 segment of the MCA (Fig. 3b). Based on these findings, a diagnosis of cerebral infarction and SAH due to spontaneous MCA dissection was made. With conservative therapy the patient’s hospital course was uneventful. He was able to walk with a cane, and was dis- charged from hospital on an antihypertensive agent. At dis- charge, NIHSS was 7, Barthel index was 85 and modified Rankin Scale score was 3. At 10 months of follow-up, the patient has had no recurrent strokes.

Discussion

Although a hyperdense artery sign can be seen in patients with a high hematocrit level or with calcification of the intracranial arteries (4), it is usually seen in patients with thromboembolic arterial occlusion, which results in an increased vessel attenuation value (1). Under such conditions, the MCA, which presents with a hyperdense artery sign, has a higher attenuation value than the contralateral MCA (5), which disappears within a couple of weeks (6). Both of Figure 4. MR examinations done to evaluate the intracra- these findings were demonstrated in our patient. Koo et al nial artery on Day 20 (GE Signa Horizon, 1.5 T system). a. 3- reported that a hyperdense artery sign associated with acute dimensional spoiled gradient-recalled acquisition (SPGR: TR ischemic stroke can be distinguished from normal vessels 35 ms, TE 4.4 ms, Flip angle 30°, section thickness 0.7 mm) and false positives by measuring the absolute attenuation shows narrowing of the proximal region of the M1 segment and the ratios of the affected and the normal vessels; an ab- of the left MCA (arrow). b. SPGR shows the distal M1 segment of the left MCA is more distended than that of the right solute density of >43 HU and an MCA ratio of >1.2 define MCA. A laminar low intensity signal along the rostral left hyperdensity (7). In the present patient, the absolute densi- MCA is seen, suggesting the presence of a false lumen ties of the affected MCA and the MCA ratios, which were (arrowheads). c. A non-contrast T1-weighted image (spin- obtained from brain CTs on Day 1 and Day 4, also met echo sequences, TR 500 ms, TE 9.0 ms, Flip angle 30°, section these requirements. Thus, there was a high degree of cer- thickness 6 mm) shows a high intensity signal along the arte- tainty regarding the presence of a hyperdense artery sign of rial wall at the M1 segment through to the posterior trunk of the left MCA in our patient. the M2 segment of the left MCA (arrowheads), thus suggest- Some patients with major hemispheric stroke syndrome ing an intramural hematoma. d. T1-weighted images with show a rapid recovery, also known as the “spectacular contrast show enhancement of the posterior trunk of the M2 shrinking deficit” (SSD), due to migration of an embolus segment of the left MCA (arrow), suggesting slight flow in (8). The present patient had contradictory findings in that the false lumen. we could repeatedly demonstrate a hyperdense artery sign of the MCA on brain CTs and patency of the affected MCA on TOF MRAs (both done on Day 1 and Day 4). A previous distended than that of the right MCA, and a laminar low in- report demonstrated that a hyperdense artery sign disap- tensity signal was seen along the rostral left MCA. These peared after the recanalization of the affected artery (6). SPGR findings suggested the presence of a false lumen The findings in the present patient could possibly be ex- (Fig. 4b). T1-weighted images demonstrated a high intensity plained by the repeated occurrence of thromboembolic MCA signal along the arterial wall at the M1 segment through to occlusions and the migration of emboli. However, the pa- the posterior trunk of the M2 segment of the left MCA, tient’s uneventful clinical course from Day 1 to Day 4 con- which suggested an intramural hematoma (Fig. 4c). The T1- flicts with both repeated thromboembolic MCA occlusions weighted images with contrast material showed enhancement and SSDs. Our case had some clinical features suggestive of of the posterior trunk of the M2 segment of the left MCA, an intracranial artery dissection (9), including:sudden onset

1321 DOI: 10.2169/internalmedicine.45.1888 cerebral infarction in a young person; a severe headache lo- current case, 2 cases of intracranial arterial dissection have calized ipsilateral to the affected MCA; and demonstrated demonstrated hyperdense artery signs without arterial occlu- SAH. In addition to the clinical findings, the antemortem di- sion. So how should the hyperdense artery sign be inter- agnosis of an intracranial artery dissection is based on the preted without arterial occlusion? It is known that plain CT presence of certain radiological features. The pearl-and- in acute aortic dissection shows an intramural hematoma string sign is known to be a reliable angiographic finding of with crescentic high-attenuation areas along the aortic wall an arterial dissection (9). An intramural hematoma on T1- (14). Therefore, we considered that the hyperdense artery weighted images and a double lumen on SPGR are MR sign seen in the present patient might have been due to an findings that are suggestive of an arterial dissection (10). intramural hematoma in the false lumen of the dissected Furthermore, our patient showed serial spontaneous changes MCA. of affected vessel form on angiography, which is rare with Nontraumatic dissection of the intracranial carotid circula- atherosclerotic disease (9). Thus, both the clinical and ra- tion usually occurs in young persons and can cause cerebral diological features in our case are consistent with an intrac- infarction and SAH (3). There is no established standard ranial artery dissection. medical treatment for dissections causing cerebral infarction. Previously, five cases of intracranial artery dissection with An acute ischemic stroke with HMCAS and without hy- a hyperdense artery sign on CT have been reported (11-13). podensities of more than one-third of the MCA territory on Of these, one had an MCA dissection associated with a trau- baseline CT is considered to be an indication for intravascu- matic injury (11), one had an internal carotid artery-MCA lar t-PA administration (2). However, thrombolytic therapy dissection of unknown etiology (12), and three had verte- for intracranial artery dissections has both risks and benefits, bral artery dissections (in two patients these were related to due to their association with SAH (15). Therefore, it is im- exercise, in the other, etiology was unknown) (12, 13). An- portant to keep in mind that an MCA dissection can also giographic evaluations, which were performed in 4 patients, cause cerebral infarction with a hyperdense artery sign, par- revealed 3 patients with distal arterial occlusion (12, 13) ticularly in young patients presenting with headache. and one with irregular stenosis (12). Thus, including the

References

1. Petitti N. The hyperdense middle cerebral artery sign. Radiology 8. Minematsu K, Yamaguchi T, Omae T. ’Spectacular shrinking defi- 208: 687-688, 1998. cit’:rapid recovery from a major hemispheric syndrome by migra- 2. Patel SC, Levine SR, Tilley BC, et al. National Institute of Neuro- tion of an embolus. Neurology 42: 157-162, 1992. logical Disorders and Stroke rt-PA Stroke Study Group. Lack of 9. Takis C, Saver J. Cervicocephalic carotid and vertebral artery dis- clinical significance of early ischemic changes on computed to- section:management. In: Cerebrovascular Disease. Batjer HH, Ed. mography in acute stroke. JAMA 286: 2830-2838, 2001. Lippincott-Raven, Philadelphia, 1997: 385-395. 3. Ohkuma H, Suzuki S, Ogane K. Study Group of the Association 10. Hosoya T, Adachi M, Yamaguchi K, Haku T, Kayama T, Kato T. of Cerebrovascular Disease in Tohoku, Japan. Dissecting aneu- Clinical and neuroradiological features of intracranial vertebrobasi- rysms of intracranial carotid circulation. Stroke 33: 941-947, lar artery dissection. Stroke 30: 1083-1090, 1999. 2002. 11. De Caro R, Munari PF, Parenti A. Middle cerebral artery throm- 4. Rauch RA, Bazan C 3rd, Larsson EM, Jinkins JR. Hyperdense bosis following blunt head trauma. Clin Neuropathol 17:1-5, middle cerebral arteries identified on CT as a false sign of vascu- 1998. lar occlusion. AJNR Am J Neuroradiol 14: 669-673, 1993. 12. Pelkonen O, Tikkakoski T, Leinonen S, Pyhtinen J, Sotaniemi K. 5. Moulin T, Cattin F, Crepin-Leblond T, et al. Early CT signs in Intracranial arterial dissection. Neuroradiology 40: 442-447, 1998. acute middle cerebral artery infarction:predictive value for subse- 13. Provenzale JM, Barboriak DP, Taveras JM. Exercise-related dis- quent infarct locations and outcome. Neurology 47: 366-375, section of craniocervical arteries: CT, MR and angiographic find- 1996. ings. J Comput Assist Tomogr 19: 268-276, 1995. 6. Bastianello S, Pierallini A, Colonnese C, et al. Hyperdense middle 14. Yamada T, Tada S, Harada J. Aortic dissection without intimal cerebral artery CT sign. Comparison with angiography in the rupture:diagnosis with MR imaging and CT. Radiology 168: 347- acute phase of ischemic supratentorial infarction. Neuroradiology 352, 1988. 33: 207-211, 1991. 15. Berger MS, Wilson CB. Intracranial dissecting aneurysms of the 7. Koo CK, Teasdale E, Muir KW. What constitutes a true hyper- posterior circulation. Report of six cases and review of the litera- dense middle cerebral artery sign?. Cerebrovasc Dis 10: 419-423, ture. J Neurosurg 61: 882-894, 1984. 2000.

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