Neuro-- radiology 9 Springer-Verlag 1991

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Neuroradiology (1991) 33:207-211 Neuro-- radiology 9 Springer-Verlag 1991 Hyperdense middle cerebral artery CT sign Comparison with angiography in the acute phase of ischemic supratentorial

1 Neuroradiology (1991) 33: Neuro-- radiology 9 Springer-Verlag 1991 Hyperdense middle cerebral artery CT sign Comparison with angiography in the acute phase of ischemic supratentorial infarction S. Bastianello, A. Pierailini, C. Colonnese, G. Brughitta, U. Angeloni, M. Antonelli, L. M. Fantozzi, C. Fieschi, and L. Bozzao Department of Neurological Sciences, University of Rome "La Sapienza", Rome, Italy Received: 16 February 1990 Summary. The early CT finding of an hyperdensity of a portion of the middle cerebral artery Hyperdense Middle Cerebral Artery Sign (HMCAS), in patients with supratentorial stroke, is often indicative of an embolic occlusion. Aim of this study was to verify the incidence and reliability of the HMCAS and its possible correlation with early CT findings and with the extent of late brain damage. We studied 36 patients presenting with symptoms of stroke in the MCA territory, by means of CT and angiography performed respectively within 4 and 6 hours. Follow-up CT scans were then obtained after one week and three months from the ischemic event. The HMCAS was present in 50% of our patients and in this group it always correlated positively with the angiographic finding of occlusion. The same group presented a high incidence of early CT hypodensity (88%). Finally the presence of HMCAS might be considered a negative prognostic sign for the development of extensive brain damage. Key words: CT - Cerebral infarction - MCA - Embolism - Angiography Cerebral angiography performed in the very early phase of ischemic stroke reveals a high frequency of intracranial vessel embolic occlusion [1, 2]. Non-invasive techniques, like transcranial Doppler sonography (TCD) [3] and CT scan [4, 5], may also identify an intracranial vessel occlusion shortly after an ischemic stroke. On plain CT performed in the acute phase the presence of an embolus appears as a spot of increased density along the middle cerebral artery (MCA) course [4-12]. This will provide an early diagnosis which may be useful to identify a specific therapy before brain damage has developed [1:3]. We had the opportunity to study, by CT and angiography performed within 6 h, a consecutive series of supratentorial ischemic patients. This allowed us to evaluate the reliability of the hyperdensity MCA sign (HMCAS) in diagnosing vessel occlusion. Its significance in the development of hemorrhagic infarction and of chronic brain damage is also discussed. Materials and methods A consecutive series of 44 patients with focal supratentorial ischemic stroke, was examined by CT and angiography performed respectively within 4 and 6 h from the onset of symptoms. Three patients died during the first few days and five were excluded from the study because they showed a vascular territory involvement different from the MCA. Therefore CT and angiographic data refer to 36 patients. A high resolution CT scanner (Siemens - Somatom CR) was used to obtain axial orbito-meatal sections of 2 mm thickness at 4 mm intervals from the occipital foramen to the sellar region; the remainder of the brain was studied with 8 mm sections at 10 mm intervals each. CT scans were repeated after one week and three months. Early CT scans were particularly searched for the presence of a hyperdense spot along the main trunk of the MCA. HMCAS was classified: proximal when it involved the medial segment of the horizontal part of the MCA; lateral when it involved its lateral segment at the trifurcation or one of the main branches; complete when the whole horizontal part was involved. The presence of precocious parenchymal hypodensity of the basal ganglia and or of the cortex was considered too [14]. Disappearance, persistence and changes in location of HMCASs of different types, were recorded from the one week control CT scan. At the same time the CT was examined for the presence of hemorrhagic infarction (HI) in the cortex, the basal ganglia or both. The follow-up CT after three months allowed us to define the extent of chronic brain damage [15, 16]. Angiography was performed in all 36 patients with digital equipment by direct carotid injection or retrograde brachial catheterization and was generally restricted to the carotid territory responsible for the clinical symptoms.

208 Fig.la-d. Proximal MCA occlusion. A proximal HMCAS (a) is evident in the early CT scan (arrow); this picture is still present in the control CT scan (arrow) after one week (b).

2 208 Fig.la-d. Proximal MCA occlusion. A proximal HMCAS (a) is evident in the early CT scan (arrow); this picture is still present in the control CT scan (arrow) after one week (b). The angiography performed within 6 h showed an occlusion of the MCA at its origin (c), which was still present after one week (d) In 2 cases the angiography was repeated after one week for clinical purposes. MCA occlusions were divided into four types according to the site of occlusion [14, 15]. The efficacy of the collateral blood supply (CBS) through cortical anastomoses or via the anterior communicating artery or the external carotid artery, was evaluated [17]. Results Eighteen out of 36 patients (50%) showed a HMCAS on plain CT scan performed within 4 hours from the onset of symptoms. The HMCAS lay in the proximal segment of MCA in 5 cases (Fig. 1. a), in the lateral in 6 (Fig. 2 a) and in 7 it involved the whole of the horizontal part of the MCA (Fig.3a). An arterial occlusion documented by angiography was present in all these patients (Table 1). In those cases in which there was a proximal or complete HMCAS, angiography showed an arterial occlusion of the proximal portion of the horizontal MCA segment in 9 (Fig. 1 c, 3 c), at the syphon in two and of the ICA in one. In patients with lateral HMCAS a distal occlusion was always present at angiography (Fig. 2 b, Table 1). In the 2 patients in whom the angiography had been repeated one week after the stroke, the study showed recanalization in one in whom the HMCAS had in the meantime disappeared on CT (Fig. 3), and still showed the presence of an occlusion in the other cases in whom the HMCAS remained for a period of one week (Fig. 1). Sixteen of these 18 patients showed an early CT hypodensity. All cases with proximal or complete HMCAS always presented an early hypodensity of the basal ganglia and, in the 4 with no CBS, the cortex was involved too. Four of the 6 patients with lateral HMCAS presented early hypodensity in the cortex in 2 and in the basal ganglia in 2. Twelve out of the 18 cases showed no evidence of HMCAS at the follow-up CT after one week. Hemorrhagic infarction was present in 7 (Table 1). The remaining six patients showed persistence of HMCAS in the same place and an HI of the cortex was evident in 4. The chronic brain damage at the three months CT scan is reported in Table 1.

209 Fig.2a-b. Lateral MCA occlusion. An HMCAS is evident in the early CT scan (arrow) (a) and a distal MCA occlusion was confirmed by the early angiography (arrow) (b) Fig.3a--d.

The angiography performed in the acute phase shows a stem MCA occlusion (arrow) (c), with a complete recanalization in the angiography performed after one week (arrow) (D) In the 18 patients with no

3 209 Fig.2a-b. Lateral MCA occlusion. An HMCAS is evident in the early CT scan (arrow) (a) and a distal MCA occlusion was confirmed by the early angiography (arrow) (b) Fig.3a--d. Complete occlusion of the MCA. An HMCAS involving the whole horizontal tract is evident in the early CT scan (arrow) (a), and not any more in the control scan (b). The angiography performed in the acute phase shows a stem MCA occlusion (arrow) (c), with a complete recanalization in the angiography performed after one week (arrow) (D) In the 18 patients with no evidence of HMCAS, angiography revealed an ICA occlusion in 1 case, atype 1 MCA occlusion in 2, a type 2 in 2, a type 3 in 4 and a type 4 in 3; no arterial occlusions were documented in 6 cases. These findings are summarized in Table 2. Discussion The occurrence of a CT HMCAS, indicating a thrombotic or embolic vascular occlusion, has been documented in a few previous reports, based on retrospective analysis, in

4 210 Table 1. Angiographic and CT characteristics of the patients presenting an HMCAS on CT after stroke No. Angiographic CBS HMCAS HMCAS HMCAS Hemorrhagic Early CT hypo- Chronic damage occlusion type 1st CT 2nd CT 3rd CT infarction density 3rd CT Proximal Proximal No Basal ganglia Basal ganglia Complete MCA 2 Syphon - Proximal No Not available Basal ganglia Basal ganglia Not available Proximal No No Basal ganglia Basal ganglia Internal border zone Proximal No No Basal ganglia Basal ganglia Complete MCA Proximal Proximal No Basal ganglia Basal ganglia Complete MCA + cortex Complete No No Basal ganglia Basal ganglia Partial MCA 7 Internal car. art. + Complete No No No Basal ganglia Lacunar infarction Complete Complete No Basal ganglia Basal ganglia Complete MCA Complete No No Basal ganglia Basal ganglia Partial MCA Complete No No Basal ganglia Basal ganglia Partial MCA + cortex 11 Syphon + Complete No No No Basal ganglia Deep MCA Complete Complete No No Basal ganglia Complete MCA Lateral No No No No Internal border zone Lateral No No No Basal ganglia Internal border zone + deep MCA Lateral Lateral No No No Internal border zone Lateral No No Cortex Cortex Superficial MCA Lateral Lateral No Cortex Cortex Superficial MCA Lateral No No No Basal ganglia Internal border zone Angiographic occlusion types: Type I= occlusion of the stem or trunk of the MCA proximal to the internal lenticulo-striate arteries. Type H = occlusion of the stem or trunk of the MCA distal to the internal lenticulo-striate arteries. Type III= occlusion of the MCA at the bifurcation (in our patients the occlusion always involved only the upper branch). Type/V = occlusion of the peripheral branches of the MCA visualized through cortical anastomoses. CBS: Collateral blood supply (" + "= evidenced by early angiography;" - "= not evidenced by early angiography). HMCAS: Hyperdensity of the middle cerebral artery sign. Proximal ~- localized in the proximal segment of the MCA horizontal tract. Complete = involving the whole horizontal tract. Lateral = localized in the distal segment of the horizontal tract of the MCA or in one of its branches. Chronic damage was classified into deep-mca, superficial-mca, complete-mca, internal border zone and lacunar infarcts according to the vascular MCA territory involvement. Table 2. Angiographic and CT characteristics of the 36 patients with supratentorial ischemic stroke Angiographic Early CT Hemorrhagic occlusions hypodensity infarction Patients with HMCAS (18) Patients without HMCAS (18) which the first CT examination was generally performed on the day of onset of neurological symptoms [4-12]. The thrombo-embolic origin of the arterial occlusion was documented in only some of these cases by angiography while in the others often only clinical criteria were considered. We observed a higher incidence of HMCAS (50%) than observed by other authors [8, 10]. This may be due to the slice thickness used and to partial volume factors. All patients with an HMCAS showed an arterial occlusion documented by the angiography performed within 6 h. On the other hand 12 patients with positive angiography did not show HMCAS at early CT scan even when the occlusion was in the MCA stem trunk. For this reason the absence of focal arterial densities on CT is not significant in excluding emboli. Six patients did not show angiographic evidence of arterial occlusions nor did hey present a hyperdense spot along the MCA. All HMCAS were located in the horizontal segment or trifurcation of the MCA near the sphenoid wing as described by other authors [4, 5]. The group of patients who had an hyperdense spot in the proximal part or involving the whole MCA horizontal segment, commonly presented a trunk stem MCA occlusion at angiography (Figs.l, 3); those in whom the HMCAS was visible laterally always had a type III or IV MCA occlusion (Fig. 2), In our series, most patients (66%) did not show the HMCAS after one week, comfirming the mobile nature of the clot. On the other hand the persistence of the HMCAS beyond one week can still be interpreted as a MCA thrombus in spite of the possibility that it could be an atherosclerotic arterial calcification [4]. Likewise, in the patients who underwent repeated angiography, the disappearance of the HMCAS was associated with recanalization proved by angiography (Fig. 3) in one case, while the persistence of the HMCAS in the other was coupled with an angiographically documented occlusion (Fig. 1). At the three months follow-up CT no HMCAS was observed, confirming the thromboembolic nature of the hyperdense spot.

211 Our data confirm that the hemorrhagic transformation of an ischemic area depends on the restoration of the blood flow after an embolic occlusion of the stem of the MCA for HI of basal ganglia,

5 211 Our data confirm that the hemorrhagic transformation of an ischemic area depends on the restoration of the blood flow after an embolic occlusion of the stem of the MCA for HI of basal ganglia, while the hemorrhagic transformation of the cortex seems to be due to the late development of CBS [18]. Other authors [8] have previously reported the presence of initial signs of parenchymal damage in patients with HMCAS. In our series almost all patients (88%) with HMCAS presented an early hypodensity. The hypodensity of the basal ganglia associated with proximal and complete HMCAS is easily understood on the basis of the absence of perfusion in this area. The hypodensity of the cortex depends on the absence of early CBS. Early hypodensity represents a negative prognostic sign in the development of chronic brain damage, as already reported [14]. We found that after three months the patients with complete or proximal HMCAS developed a larger area of parenchymal damage than the patients with lateral HMCAS, and these findings depend on more proximal MCA occlusion and development of cerebral blood supply, as documented in our previous reports [14, 15]. Conclusion The finding of HMCAS in the early CT is always indicative of an arterial occlusion, possibly of its angiographic location and it may prove important in predicting the severity of ischemia; yet the absence of this sign is not to be interpreted as absence of MCA occlusion. There is a close relation between the presence of HMCAS and early CT hypodensity and both signs are early indicators of brain injury, predicting the development of HI and of late brain damage. Finally, the possibility of diagnosing an arterial occlusion or major intracranial vessels by CT may be of great importance for early initiation of therapeutic procedures. References 1. Olson TS, Skriver EB, Herning M (1985) Cause of cerebral infarction in the carotid territory. Its relation to the size and the location of the infarct and to the underlying vascular lesion. Stroke 16: Bozzao L, Fantozzi LM, Bastianello S, Bozzao A, Argentino C, Lenzi GL, Fieschi C (1989) Isehaemic supratentorial stroke; angiographic findings in patients examined in the very early phase. J Neuro1236: Mattle H, Grolimund R Huber R Sturzenegger M, Zurbrugg H (1988) Transcranial doppler sonographic findings in middle cerebral artery disease. Arch Neuro145: Yock DH jr (1981) CT demonstration of cerebral emboli. J Cornput Assist Tomogr 5: Gacs G, Fox AJ, Barnett HJM, Vinuela F (1983) CT visualization of intracranial arterial thromboembolism. Stroke 14: Granstrom P (1986) CT visualization of thrombus in cerebral artery. Comput Assist Tomogr 10: Matsumara A, Munekata K, Wickboldt J, Hori A (1987) Significance of thrombosed and patent vessels visualized by CT scan. A case report of middle cerebral artery thrombosis. J Med Imag 1: Pressman BD, Tourj e EJ, Thompson JR (1987) An early CT sign of ischemic infarction: increased density in a cerebral artery. AJNR 8: Schuierer G, Huk W (1988) The unilateral hyperdense middle cerebral artery: an early CT-sign of embolism or thrombosis. Neuroradiology 30: Tomsick TA, Brott TC, Olinger CR Barsan W, Spilker J, Eberle R, Adams H (1989) Hyperdense middle cerebral artery: incidence and quantitative significance. Neuroradiology 31: Tomsick TA, Brott TC, Chambers AA, Fox AJ, Gaskil ME Lukin RR, Pleatman CW, Wiot JG, Bourekas E (1989) Hyperdense middle cerebral artery sign: limits of detectability. AJNR 10: Lutman M (1989) Diagnosi precoce dell'infarto eerebrale. L'iperdensita' dell'arteria cerebrale media come primo segno TC di lesione ischemica. Radiol Med 77: Zeumer H, Hacke W, Ringelstein EB (1983) Local intraarterial thrombolysis in vertebro-basilar thromboembolic disease. AJNR 4:401~ Bozzao L, Bastianello S, Fantozzi LM, Angeloni U, Argentino C, Fieschi C (1989) Correlation of angiographic and sequential CT findings in patients with evolving cerebral infarction. AJNR 10: Bozzao L, Fantozzi LM, Bastianello S, Bozzao A, Fieschi C (1989) Early collateral blood supply and late parenchymal brain damage in patients with middle cerebral artery occlusion. Stroke 20: Damasio H (1983) A computed tomography guide to the identification of cerebral vascular territories. Arch Neuro140: Saito I, Segawa H, Shiokawa Y, Taniguchi M, Tsutsumi K (1987) Middle cerebral artery occlusion: correlation of computed tomography and angiography with clinical outcome. Stroke 18: Bozzao L, Angeloni U, Bastianello S, Fantozzi LM, Pierallini A, Fieschi C (1991) The value of early CT hypodensity in predicting MCA hemorrhagic infarction. Proceedings of the XIV Symposium Neuroradiologicum, London June Springer, Berlin Heidelberg New York, pp S. B astianello, M. D., Ph. D. Cattedza di Neuroradiologia Dipartimento Scienze Neurologiche Universitfi Studi Roma "La Sapienza" Viale dell'universit~ Roma Italia

Thrombus Localization with Emergency Cerebral CT

Thrombus Localization with Emergency Cerebral CT Thomas Tomsick, ' Thomas Brott, William Barsan, Joseph Broderick, E. Clarke Haley, and Judith Spilker Purpose: To determine the prevalence of the hyperdense