Neuro-radiology
Neuroradiology(1991) 33:207-211
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 NeurologicalSciences,Universityof 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). 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. M C A 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 H M C A S on plain CT scan performed within 4 hours from the onset of symptoms. The H M C A S 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 M C A (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 M C A segment in 9 (Fig. 1 c, 3 c), at the syphon in two and of the ICA in one.
In patients with lateral H M C A S 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 H M C A S had in the meantime disappeared on CT (Fig. 3), and still showed the presence of an occlusion in the other cases in whom the H M C A S 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 H M C A S 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 H M C A S 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 H M C A S at the follow-up CT after one week. Hemorrhagic infarction was present in 7 (Table 1). The remaining six patients showed persistence of H M C A S in the same place and an H I 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. 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 t h e 18 p a t i e n t s with no e v i d e n c e of H M C A S , angiog r a p h y r e v e a l e d an I C A o c c l u s i o n in 1 case, a t y p e 1 M C A o c c l u s i o n in 2, a t y p e 2 in 2, a t y p e 3 in 4 a n d a t y p e 4 in 3; no a r t e r i a l occlusions w e r e d o c u m e n t e d in 6 cases. T h e s e findings are s u m m a r i z e d in T a b l e 2.
Discussion T h e o c c u r r e n c e of a C T H M C A S , i n d i c a t i n g a t h r o m b o t i c o r e m b o l i c v a s c u l a r occlusion, has b e e n d o c u m e n t e d in a few p r e v i o u s r e p o r t s , b a s e d on r e t r o s p e c t i v e analysis, in
210 Table 1. Angiographic and CT characteristics of the patients presenting an HMCAS on CT after stroke No.
Angiographic occlusion type
CBS
HMCAS 1st CT
HMCAS 2nd CT
HMCAS 3rd CT
1
1
-
Proximal
Proximal
No
2
Syphon
-
Proximal
No
3 4
2 1
+ -
Proximal Proximal
No No
5
1
-
Proximal
Proximal
6 7 8
1 Internal car. art. 1
+ + -
Complete Complete Complete
No No Complete
9 10
1 1
+ -
Complete Complete
No No
11 12 13 14
Syphon 1 3 3
+ +
Complete Complete Lateral Lateral
No Complete No No
Hemorrhagic infarction
Basal ganglia + cortex Not available Basal ganglia + cortex No Basal ganglia No Basal ganglia + cortex No Basal ganglia + cortex No Basal ganglia No No No Basal ganglia + cortex No Basal ganglia No Basal ganglia + cortex No No No No No No No No
Early CT hypodensity
Chronic damage 3rd CT
Basal ganglia + cortex Basal ganglia + cortex Basal ganglia Basal ganglia + cortex Basal ganglia
Complete MCA
Basal ganglia Basal ganglia Basal ganglia + cortex Basal ganglia Basal ganglia
Not available Internal border zone Complete MCA Complete MCA Partial MCA Lacunar infarction Complete MCA Partial MCA Partial MCA
Deep MCA Complete MCA Internal border zone Internal border zone + deep MCA 15 4 + Lateral Lateral No No No Internal border zone 16 4 + Lateral No No Cortex Cortex Superficial MCA 17 3 Lateral Lateral No Cortex Cortex Superficial MCA 18 3 + 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)
18
16
11
Patients without HMCAS (18)
12
2
2
w h i c h the first C T e x a m i n a t i o n was g e n e r a l l y p e r f o r m e d on the d a y of o n s e t of n e u r o l o g i c a l s y m p t o m s [4-12]. T h e t h r o m b o - e m b o l i c origin of t h e a r t e r i a l occlusion was doc u m e n t e d in only s o m e o f t h e s e cases b y a n g i o g r a p h y while in the o t h e r s o f t e n o n l y clinical criteria w e r e considered. W e o b s e r v e d a h i g h e r i n c i d e n c e of H M C A S ( 5 0 % ) t h a n o b s e r v e d b y o t h e r a u t h o r s [8, 10]. This m a y b e d u e to the slice thickness used a n d to p a r t i a l v o l u m e factors. A l l p a t i e n t s with an H M C A S s h o w e d an a r t e r i a l occlusion d o c u m e n t e d b y t h e a n g i o g r a p h y p e r f o r m e d within 6 h. O n t h e o t h e r h a n d 12 p a t i e n t s with p o s i t i v e angio g r a p h y did n o t show H M C A S at e a r l y C T scan e v e n w h e n the occlusion was in t h e M C A s t e m trunk. F o r this r e a s o n t h e a b s e n c e o f focal a r t e r i a l densities on C T is n o t significant in excluding e m b o l i .
Basal ganglia Basal ganglia No Basal ganglia
Six p a t i e n t s d i d n o t show a n g i o g r a p h i c e v i d e n c e of art e r i a l occlusions n o r d i d h e y p r e s e n t a h y p e r d e n s e s p o t along the MCA. A l l H M C A S w e r e l o c a t e d in t h e h o r i z o n t a l s e g m e n t o r t r i f u r c a t i o n of the M C A n e a r t h e s p h e n o i d wing as des c r i b e d b y o t h e r a u t h o r s [4, 5]. T h e g r o u p of p a t i e n t s w h o h a d an h y p e r d e n s e spot in t h e p r o x i m a l p a r t o r involving t h e w h o l e M C A h o r i z o n t a l s e g m e n t , c o m m o n l y p r e s e n t e d a t r u n k s t e m M C A occlusion at a n g i o g r a p h y ( F i g s . l , 3); t h o s e in w h o m t h e H M C A S was visible l a t e r a l l y always h a d a t y p e I I I o r I V M C A occlusion (Fig. 2), I n o u r series, m o s t p a t i e n t s ( 6 6 % ) d i d n o t s h o w t h e H M C A S a f t e r o n e w e e k , c o m f i r m i n g the m o b i l e n a t u r e of the clot. O n t h e o t h e r h a n d t h e p e r s i s t e n c e of t h e H M C A S b e y o n d o n e w e e k can still b e i n t e r p r e t e d as a M C A t h r o m b u s in spite of t h e p o s s i b i l i t y t h a t it c o u l d b e a n a t h e r o sclerotic a r t e r i a l calcification [4]. L i k e w i s e , in the p a t i e n t s w h o u n d e r w e n t r e p e a t e d angiography, t h e d i s a p p e a r a n c e of the H M C A S was associa t e d with r e c a n a l i z a t i o n p r o v e d b y a n g i o g r a p h y (Fig. 3) in o n e case, while t h e p e r s i s t e n c e of t h e H M C A S in t h e o t h e r was c o u p l e d with an a n g i o g r a p h i c a l l y d o c u m e n t e d occlusion (Fig. 1). A t the t h r e e m o n t h s f o l l o w - u p C T n o H M C A S was o b served, c o n f i r m i n g the t h r o m b o e m b o l i c n a t u r e o f t h e h y p e r d e n s e spot.
211 O u r 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 M C A for H I of basal ganglia, while the hemorrhagic transformation of the cortex seems to be due to the late development of CBS [18]. O t h e r authors [8] have previously reported the presence of initial signs of parenchymal damage in patients with H M C A S . In our series almost all patients (88%) with H M C A S presented an early hypodensity. The hypodensity of the basal ganglia associated with proximal and complete H M C A S 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 H M C A S developed a larger area of parenchymal damage than the patients with lateral H M C A S , and these findings depend on m o r e proximal M C A occlusion and development of cerebral blood supply, as documented in our previous reports [14, 15].
Conclusion
The finding of H M C A S in the early CT is always indicative of an arterial occlusion, possibly of its angiographic location and it m a y prove important in predicting the severity of ischemia; yet the absence of this sign is not to be interpreted as absence of M C A occlusion. T h e r e is a close relation between the presence of H M C A S and early CT hypodensity and both signs are early indicators of brain injury, predicting the development of H I 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 16:459-466 2. 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 Neuro1236:340-342
3. Mattle H, Grolimund R Huber R Sturzenegger M, Zurbrugg H (1988) Transcranial doppler sonographic findings in middle cerebral artery disease. Arch Neuro145:289-295 4. Yock DH jr (1981) CT demonstration of cerebral emboli. J Cornput Assist Tomogr 5:190-196 5. Gacs G, Fox AJ, Barnett HJM, Vinuela F (1983) CT visualization of intracranial arterial thromboembolism. Stroke 14:756-762 6. Granstrom P (1986) CT visualization of thrombus in cerebral artery. Comput Assist Tomogr 10:541-548 7. 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: 11 14 8. Pressman BD, Tourj e EJ, Thompson JR (1987) An early CT sign of ischemic infarction: increased density in a cerebral artery. AJNR 8:645-648 9. Schuierer G, Huk W (1988) The unilateral hyperdense middle cerebral artery: an early CT-sign of embolism or thrombosis. Neuroradiology 30:120-122 10. 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: 312-315 11. 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 10:873 12. Lutman M (1989) Diagnosi precoce dell'infarto eerebrale. L'iperdensita' dell'arteria cerebrale media come primo segno TC di lesione ischemica. Radiol Med 77:171-173 13. Zeumer H, Hacke W, Ringelstein EB (1983) Local intraarterial thrombolysis in vertebro-basilar thromboembolic disease. AJNR 4:401~404 14. 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: 1215-1222 15. 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 20:735-740 16. Damasio H (1983) A computed tomography guide to the identification of cerebral vascular territories. Arch Neuro140:138-142 17. 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: 863-868 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 17-23 June 1990. Springer, Berlin Heidelberg New York, pp 42-44 S. B astianello, M. D., Ph. D. Cattedza di Neuroradiologia Dipartimento Scienze Neurologiche Universitfi Studi Roma "La Sapienza" Viale dell'Universit~ 30 1-00185 Roma Italia
Neuroradiology(1991) 33:207-211
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 NeurologicalSciences,Universityof 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). 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. M C A 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 H M C A S on plain CT scan performed within 4 hours from the onset of symptoms. The H M C A S 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 M C A (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 M C A segment in 9 (Fig. 1 c, 3 c), at the syphon in two and of the ICA in one.
In patients with lateral H M C A S 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 H M C A S had in the meantime disappeared on CT (Fig. 3), and still showed the presence of an occlusion in the other cases in whom the H M C A S 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 H M C A S 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 H M C A S 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 H M C A S at the follow-up CT after one week. Hemorrhagic infarction was present in 7 (Table 1). The remaining six patients showed persistence of H M C A S in the same place and an H I 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. 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 t h e 18 p a t i e n t s with no e v i d e n c e of H M C A S , angiog r a p h y r e v e a l e d an I C A o c c l u s i o n in 1 case, a t y p e 1 M C A o c c l u s i o n in 2, a t y p e 2 in 2, a t y p e 3 in 4 a n d a t y p e 4 in 3; no a r t e r i a l occlusions w e r e d o c u m e n t e d in 6 cases. T h e s e findings are s u m m a r i z e d in T a b l e 2.
Discussion T h e o c c u r r e n c e of a C T H M C A S , i n d i c a t i n g a t h r o m b o t i c o r e m b o l i c v a s c u l a r occlusion, has b e e n d o c u m e n t e d in a few p r e v i o u s r e p o r t s , b a s e d on r e t r o s p e c t i v e analysis, in
210 Table 1. Angiographic and CT characteristics of the patients presenting an HMCAS on CT after stroke No.
Angiographic occlusion type
CBS
HMCAS 1st CT
HMCAS 2nd CT
HMCAS 3rd CT
1
1
-
Proximal
Proximal
No
2
Syphon
-
Proximal
No
3 4
2 1
+ -
Proximal Proximal
No No
5
1
-
Proximal
Proximal
6 7 8
1 Internal car. art. 1
+ + -
Complete Complete Complete
No No Complete
9 10
1 1
+ -
Complete Complete
No No
11 12 13 14
Syphon 1 3 3
+ +
Complete Complete Lateral Lateral
No Complete No No
Hemorrhagic infarction
Basal ganglia + cortex Not available Basal ganglia + cortex No Basal ganglia No Basal ganglia + cortex No Basal ganglia + cortex No Basal ganglia No No No Basal ganglia + cortex No Basal ganglia No Basal ganglia + cortex No No No No No No No No
Early CT hypodensity
Chronic damage 3rd CT
Basal ganglia + cortex Basal ganglia + cortex Basal ganglia Basal ganglia + cortex Basal ganglia
Complete MCA
Basal ganglia Basal ganglia Basal ganglia + cortex Basal ganglia Basal ganglia
Not available Internal border zone Complete MCA Complete MCA Partial MCA Lacunar infarction Complete MCA Partial MCA Partial MCA
Deep MCA Complete MCA Internal border zone Internal border zone + deep MCA 15 4 + Lateral Lateral No No No Internal border zone 16 4 + Lateral No No Cortex Cortex Superficial MCA 17 3 Lateral Lateral No Cortex Cortex Superficial MCA 18 3 + 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)
18
16
11
Patients without HMCAS (18)
12
2
2
w h i c h the first C T e x a m i n a t i o n was g e n e r a l l y p e r f o r m e d on the d a y of o n s e t of n e u r o l o g i c a l s y m p t o m s [4-12]. T h e t h r o m b o - e m b o l i c origin of t h e a r t e r i a l occlusion was doc u m e n t e d in only s o m e o f t h e s e cases b y a n g i o g r a p h y while in the o t h e r s o f t e n o n l y clinical criteria w e r e considered. W e o b s e r v e d a h i g h e r i n c i d e n c e of H M C A S ( 5 0 % ) t h a n o b s e r v e d b y o t h e r a u t h o r s [8, 10]. This m a y b e d u e to the slice thickness used a n d to p a r t i a l v o l u m e factors. A l l p a t i e n t s with an H M C A S s h o w e d an a r t e r i a l occlusion d o c u m e n t e d b y t h e a n g i o g r a p h y p e r f o r m e d within 6 h. O n t h e o t h e r h a n d 12 p a t i e n t s with p o s i t i v e angio g r a p h y did n o t show H M C A S at e a r l y C T scan e v e n w h e n the occlusion was in t h e M C A s t e m trunk. F o r this r e a s o n t h e a b s e n c e o f focal a r t e r i a l densities on C T is n o t significant in excluding e m b o l i .
Basal ganglia Basal ganglia No Basal ganglia
Six p a t i e n t s d i d n o t show a n g i o g r a p h i c e v i d e n c e of art e r i a l occlusions n o r d i d h e y p r e s e n t a h y p e r d e n s e s p o t along the MCA. A l l H M C A S w e r e l o c a t e d in t h e h o r i z o n t a l s e g m e n t o r t r i f u r c a t i o n of the M C A n e a r t h e s p h e n o i d wing as des c r i b e d b y o t h e r a u t h o r s [4, 5]. T h e g r o u p of p a t i e n t s w h o h a d an h y p e r d e n s e spot in t h e p r o x i m a l p a r t o r involving t h e w h o l e M C A h o r i z o n t a l s e g m e n t , c o m m o n l y p r e s e n t e d a t r u n k s t e m M C A occlusion at a n g i o g r a p h y ( F i g s . l , 3); t h o s e in w h o m t h e H M C A S was visible l a t e r a l l y always h a d a t y p e I I I o r I V M C A occlusion (Fig. 2), I n o u r series, m o s t p a t i e n t s ( 6 6 % ) d i d n o t s h o w t h e H M C A S a f t e r o n e w e e k , c o m f i r m i n g the m o b i l e n a t u r e of the clot. O n t h e o t h e r h a n d t h e p e r s i s t e n c e of t h e H M C A S b e y o n d o n e w e e k can still b e i n t e r p r e t e d as a M C A t h r o m b u s in spite of t h e p o s s i b i l i t y t h a t it c o u l d b e a n a t h e r o sclerotic a r t e r i a l calcification [4]. L i k e w i s e , in the p a t i e n t s w h o u n d e r w e n t r e p e a t e d angiography, t h e d i s a p p e a r a n c e of the H M C A S was associa t e d with r e c a n a l i z a t i o n p r o v e d b y a n g i o g r a p h y (Fig. 3) in o n e case, while t h e p e r s i s t e n c e of t h e H M C A S in t h e o t h e r was c o u p l e d with an a n g i o g r a p h i c a l l y d o c u m e n t e d occlusion (Fig. 1). A t the t h r e e m o n t h s f o l l o w - u p C T n o H M C A S was o b served, c o n f i r m i n g the t h r o m b o e m b o l i c n a t u r e o f t h e h y p e r d e n s e spot.
211 O u r 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 M C A for H I of basal ganglia, while the hemorrhagic transformation of the cortex seems to be due to the late development of CBS [18]. O t h e r authors [8] have previously reported the presence of initial signs of parenchymal damage in patients with H M C A S . In our series almost all patients (88%) with H M C A S presented an early hypodensity. The hypodensity of the basal ganglia associated with proximal and complete H M C A S 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 H M C A S developed a larger area of parenchymal damage than the patients with lateral H M C A S , and these findings depend on m o r e proximal M C A occlusion and development of cerebral blood supply, as documented in our previous reports [14, 15].
Conclusion
The finding of H M C A S in the early CT is always indicative of an arterial occlusion, possibly of its angiographic location and it m a y prove important in predicting the severity of ischemia; yet the absence of this sign is not to be interpreted as absence of M C A occlusion. T h e r e is a close relation between the presence of H M C A S and early CT hypodensity and both signs are early indicators of brain injury, predicting the development of H I 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.
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