Aneurysm in the Horizontal Segment of the Anterior Cerebral Artery Confirmed by Cerebral Vasospasm —
Totaro
TAKEUCHI,
Neurosurgical
Case
Report—
Haruhiko
OGAWA
Department, The Municipal Higashimatsuyama,
and
Shin
KIMURA
of Higashimatsuyama Saitama
Hospital,
Abstract A rare aneurysm in the horizontal segment (A) of the right anterior cerebral artery was found in a 58 - year-old male presenting with subarachnoid hemorrhage. No obvious bleeding source was observed on the day of onset, but 7 days later, a definite diagnosis was made based on the discovery of cerebral vasospasm by a repeat angiogram. The aneurysm was clipped via the right frontotemporal approach 15 days after onset. He suddenly developed neurological symptoms such as consciousness disturbance , right hemiplegia, and aphasia on the 4th postoperative day, when remission of the cerebral vasospasm was confirmed by transcranial Doppler ultrasound examinations and cerebral angiography. The ischemic symptoms were probably due to cerebral embolus caused by intraluminal thrombi, which had formed during the maximum phase of vasospasm and became detached during the remission phase. Key words:
cerebral
subarachnoid
hemorrhage
aneurysm,
anterior
cerebral
Introduction Few aneurysms in the horizontal segment (A) of the anterior cerebral artery have been report ed.3,a,',9,i°,'3 15,17,19,20) The source of subarachnoid hemorrhage is not always clarified by the first cerebral angiography. In our case, the presence of an aneurysm in the A, seg ment was demonstrated by the repeat angiography as cerebral vasospasm involving the parent artery. This case demonstrated unusual development of neurological symptoms postoperatively during the remission phase of vasospasm. Here, we describe our case in detail and discuss the relationship with previous
cases. Case
Report
A 58-year-old male suffered a sudden onset of oc cipital headache on April 13, 1988. The headache per sisted and was followed by persistent nausea and vomiting. He therefore visited our department on the same day. Received 1990
January
29,
1990;
Accepted
October
4,
artery,
horizontal
segment,
vasospasm,
The neurological status on admission was grade II on the Hunt and Kosnik scale. There was no con sciousness disturbance, and he only suffered from neck stiffness. Computed tomographic (CT) scans revealed grade II signs on Fischer's scale: a diffuse bilateral high density area centered on the chiasmatic cistern, Sylvian cistern, and median longitudinal fissure and also in the septum pellucidum (Fig. 1). Cerebral angiograms on the day of onset revealed vasodila tion at the right A, portion (Fig. 2A). This suggest ed a possible fusiform-type aneurysm but this could not be confirmed. Repeat angiograms on the 7th day after onset demonstrated a severe diffuse-type vasospasm centered on the bilateral A,, A2, and M, portions, clearly indicating a saccular-type aneu rysm at the right A, portion. The location of the aneurysm appeared to be the A, loop portion, and there was no relationship with the A, perforating branch. No vascular anomaly, such as fenestration, was present in the A, portion (Fig. 2B). An operation was performed by the right fron totemporal approach 15 days after onset. A sac cular-type aneurysm of about 5 mm in diameter was found at the anterior limb of the A, loop portion,
Fig. 3
Fig. 1
CT scans on admission, showing a high-density area in the chiasmatic, interhemispheric, and bilateral Sylvian cisterns and also in the septum pellucidum
(arrow).
located on the central side 3 mm from the right A, A, junction. Clipping was therefore performed (Fig. 3). In the early morning of the 4th postoperative right hemiplegia and aphasia suddenly appeared
Fig. 2
day, ac
Operative photograph (left) and schema (right). An aneurysm (arrowheads) is present at the A, loop portion and is unrelated to the perfo rating artery.
companied by consciousness disturbance. Cerebral angiograms I day later revealed considerable remis sion of the cerebral vasospasm. In particular, neither cerebral vasospasm nor obstructive lesions were ob served in the left anterior cerebral artery and middle cerebral artery (MCA) (Fig. 4). On CT scans, a low density area had appeared when the neurological symptoms occurred, at first in the left anterior
Anteroposterior (left) and oblique views (center) of the right carotid angiogram and anteroposte rior view of the left carotid angiogram (right). A: Angiograms on the day of onset, showing a possible aneurysm in the right A, segment (arrowhead), without vasospasm. B: Angiograms on the 7th day after onset, showing a saccular-type aneurysm in the right A, segment (arrow) con firmed by severe diffuse vasospasm.
Fig. 4
bilateral MCAs to be 40-56 cm/sec and 2.5-3.6, re spectively. However, the CBFV began to increase 3 days after onset, and 4 days later, the CBFV and S/ D ratio in the right MCA were 126 cm/sec and 2.0, and those in the left MCA were 141 cm/sec and 1.7, respectively. The considerable increase in CBFV and decrease in S/D ratio suggested increase in the cerebral vasospasm. On the day of the neurological symptoms appeared, the CBFV and S/D ratio in the right MCA were 76 cm/sec and 3.2, and those in the left MCA were 80 cm/sec and 2.8, respective ly. The decrease in CBFV and increase in S/D ratio suggested the remission of cerebral vasospasm. The c-AVDO2 value was as low as 5.2 ml% at onset and remained stable in the range of 6.0-8.1 ml%. However, about I day before the neurological symptoms appeared, the c-AVDO2 suddenly dropped to 5.1-5.3 ml%. Disturbance of consciousness improved 4 days after the neurological symptoms appeared. He is now able to walk using an appliance, and is receiving speech training to ameliorate his aphasia.
Anteroposterior views of the right (left) and left carotid angiograms (right) 5 days after the operation, showing reduced vasospasm and no other cerebrovascular occlusive disease.
cerebral artery and then in the MCA territories. As shown in Fig. 5, the cerebral blood flow veloc ity (CBFV) in the bilateral MCAs and the systole diastole (S/D) ratio were regularly measured by transcranial Doppler ultrasound (TCD) (TC2-64 Model, EME Co., Ltd., Germany). The cerebral arteriovenous oxygen content difference (c-AVDO,) was calculated from arterial and jugular vein blood samples collected since admission. Initial TCD mea surements indicated the CBFV and S/D ratio in the
Fig. 5
TCD
and c-AVDO-,
reduced
vasospasm
measurements was
confirmed
with
Discussion I.
portion, excluding bifurcation. Its
clinical
by TCD
General features of aneurysms in the A, segment An aneurysm in the A, segment is located at the A,
course.
examination.
Neurological
the A,-A2 junction incidence among
symptoms
occurred
when
and carotid intracranial
the
aneurysms is estimated as low as 0.8-2.1 %,.4.9,14,17.19,20' In Europe and U.S.A., the incidence is 41 of 2672 cases (1.5%),'' while in Japan, 26 of 3430 cases (0.8%)17); 48 cases have previously been report ed. 3,4,7,9,14,17,19,20) There are no sex or side differences. 17)Quite a few cases of such aneurysms also demonstrated vascular anomalies ,4,17' as Suzuki et al. 17' reported five cases with vascular anomalies among 26 cases (19.2%). Fenestration at the A, portion is the most frequently observed vascular anomaly, with an incidence of 53.3-60%. Histological investigation of cerebral arterial anomalies demonstrated medial defects in the A, portion,'-' which were suggested as the cause of the aneurysms. In addition, 7-10% of cases with anomalies included A, hypoplasia with a vascular diameter of less than 1 MM. 13,15, Morphologically, the aneurysms were mostly of the saccular type 4,17"91(80-92%) and usually small. Kassell and Torner7' reported that the average diameter of aneurysms in the A, segment was 3.6 mm, whereas anterior communicating artery aneu rysms averaged 7.4 mm. The most frequently site for aneurysms is the ramified portion of the lenticulostriate artery. Suzuki et al. 17' reported the frequencies of aneurysms at the carina of the A, truncus and lenticulostriate artery, the A, portion itself, and the proximal portion of A, fenestration to be 57.7%, 19.2%, and 11.5%, respec tively. Wakabayashi et al.19' classified the aneurysms into three types according to its location: type I, the carina of the lenticulostriate artery (70%); type II, the proximal end of A, fenestration (20%); and type III, the loop of the A, portion (10%). The aneurysm in the present case was at the loop of the right A, truncus, thus belonging to Wakabayashi's type III. Other aneurysms complicated in 18-44.4% of cases, of which the aneurysm in the A, segment burst first in 50-63.6%.17' II.
Specific features of the present case No obvious source of the subarachnoid hemor rhage was observed in the present case on the day of onset. The incidence of subarachnoid hemorrhage without a clear source is less than 10% of all sub arachnoid hemorrhages.") The radiological condi tions are among the factors related to unknown bleeding. Other possibilities are the presence of an arteriovenous malformation or a periventricular tumor lesion. In addition, the angiography might not achieve clear contrast even though an aneurysm is present, possibly due to intraluminal thrombosis, the reduction or disappearance of the aneurysm, a small aneurysm, etc. An important factor is the unfavor
able contrast and morphological changes caused by cerebral vasospasm, emphasizing the need for repeat angiography.8' In the present case, a repeat angio gram demonstrated the aneurysm in the right A, segment, emphasized by the diffuse-type vasospasm affecting the surrounding vessels.
III. Cause of the neurological symptoms Ohta12) classified cases of vasospasm
mor
phologically on the basis of angiographic findings. Among these, the diffuse-type vasospasm especially is usually accompanied by a considerable decrease in cerebral blood flow and frequently causes delayed ischemic attack. Terada et al.'8' classified the course of vasospasm into four categories: initial phase, 6 ± 3 days after onset; progressive phase, 11 ± 5 days after onset; maximum phase, 14 ± 3 days after onset; and remission phase, 26 ± 6 days after onset. They concluded that the clinical symptoms mostly develop during initial and progressive phases. In the present case, the clinical symptoms ap peared on the 19th day after onset, i.e., 4 days after the operation. At that time, great increase in blood flow or marked decrease in S/D ratio, which are re garded as characteristic changes of cerebral vaso spasm,'"5•"' were not noted. Based on TCD measure ments, the CBFV and S/D ratio in the right MCA were 76 cm/sec and 3.2, and in the left MCA were 80 cm/sec and 2.8, respectively. An angiogram per formed the day after the appearance of clinical symp toms (20 days after onset, 5 days after the operation) clearly revealed remission of the cerebral vasospasm. However, the c-AVDO2 had decreased considerably 1 day before the symptoms occurred, suggesting an ischemic change. Thus, the clinical symptoms oc curred during the remission phase of cerebral vasospasm, suggesting the ischemia as the probable cause of the symptoms, although this must represent an extremely rare case. Another possible cause of the symptoms is a vascular lesion (thrombosis or em bolus) unrelated to the cerebral vasospasm. However, this can be excluded in the present case, as no more embolus lesions were found by angiography when the symptoms occurred, and the systemic condi tions such as cardiopulmonary function were un changed. Sakaki et al.") classified the changes of cerebral vasospasm into five phases and reported that in phase II, corresponding to Terada's progressive phase, increased necrosis of the medial smooth muscle and acid mucopolysaccharide levels were ob served, and in phase III, corresponding to Terada's maximum phase, intimal fibrosis and medial atro phy occurred
as well as organization
of thrombi
at
7) 8)
9)
10) Fig. 6
Schematic representation of the possible mor bidity underlying the neurological symptoms in the present case. Intraluminal thrombi may have formed during the maximum phase of vasospasm (B) and became detached during the remission phase (C). A: before vasospasm.
tached to the the ischemic bral embolus on the vessel and became (Fig. 6).
vessel inner wall. In the present case, symptoms were probably due to cere caused by thrombi, which had formed inner wall during the maximum phase detached during the remission phase
Acknowledgment A summary of this report was presented at the 32nd Meeting of the Japan Neurosurgical Society, Kanto District in December, 1988, Tokyo, Japan.
References 1)
2)
3)
4)
5)
6)
Aaslid R, Huber P, Nornes H: Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 60: 37-41, 1984 Crompton MR: The pathology of ruptured middle cerebral aneurysms with special reference to the differences between sexes. Lancet 2: 421-425, 1962 Hacker RJ, Krall JM, Fox JL: Data I, in Fox JL (ed): Intracranial Aneurysms, vol I. New York, Springer, 1983, pp 19-62 Handa J, Nakasu Y, Matsuda M, Kyoshima K: Aneurysms of the proximal anterior cerebral artery. Surg Neurol 22: 486-490, 1984 Harders AG, Gilsbach JM: Time course of blood ve locity changes related to vasospasm in the circle of Willis measured by transcranial Doppler ultrasound. J Neurosurg 66: 718-728, 1987 Ishii R, Kuroki M, Tanaka R, Watanabe M, Toyama M, Arai H: Subarachnoid hemorrhage of unknown
11)
12)
13)
14)
15) 16)
17)
18)
19)
20)
cause. Clinical study. Neurol Med Chir (Tokyo) 23: 262-266, 1983 (in Japanese) Kassell NF, Torner JC: Size of intracranial aneurysms. Neurosurgery 12: 291-297, 1983 Kyoshima K, Okada T, Nakasu S, Matsuda M, Handa J: Clinical evaluation of subarachnoid hem orrhage of unknown etiology. No Shinkei Geka 16: 468-474, 1988 (in Japanese) Locksley HB: Natural history of subarachnoid hem orrhage, intracranial aneurysms and arteriovenous malformations: Based on 6368 cases in the coopera tive study. Part I, in Sahs AL, Perret GE, Locksley HB, Nishioka H (eds): Intracranial Aneurysms and Subarachnoid Hemorrhage: A Cooperative Study. Philadelphia, JB Lippincott, 1969, pp 37-57 McCormick WF, Schmalstieg EJ: The relationship of arterial hypertension to intracranial aneurysms. Arch Neurol 34: 285-287, 1977 Moritake K, Yonekawa Y, Nagasawa S, Kaneko T, Handa H: The prospect of usefulness of transcranial Doppler sonography in cerebrovascular surgery. No Shinkei Geka 15: 709-715, 1987 (in Japanese) Ohta T: Formal classification of cerebral vasospasm: Prognosis and correlation. No To Shinkei 21: 1019 -1027, 1969 (in Japanese) Perlmutter D, Rhoton AL Jr: Microsurgical anatomy of the anterior cerebral-anterior communicating recurrent artery complex. J Neurosurg 45: 259-272, 1976 Pia HW: Aneurysm of the anterior cerebral artery, in Pia HW, Langmaid C, Zierski J (eds): Cerebral Aneurysms: Advances in Diagnosis and Therapy. Berlin, Springer, 1979, pp 109-115 Riggs HE, Rupp C: Variations in form of the circle of Willis. Arch Neurol (Chicago) 8: 8-14, 1963 Sakaki T, Tanigake T, Kyoi K, Utsumi S, Murata Y, Hiasa Y, Kikuchi H: Pathological study of late arterial spasm. Neurol Med Chir (Tokyo) 19: 1085 -1093, 1979 (in Japanese) Suzuki M, Onuma T, Sakurai Y, Suzuki J: Twenty -six cases of proximal anterior cerebral artery. No Shinkei Geka 16: 701-705, 1988 (in Japanese) Terada T, Kikuchi H, Karasawa J, Kuriyama Y: Se quential changes in the autoregulation of cerebral blood flow in patients with vasospasm. Neurol Med Chir (Tokyo) 25: 89-94, 1985 (in Japanese) Wakabayashi T, Tamaki N, Yamashita H, Saya H, Suyama T, Matsumoto S: Angiographic classification of aneurysms of the horizontal segment of the anterior cerebral artery. Surg Neurol 24: 31-34, 1985 Yasargil MG, Smith RD: Management of aneurysms of anterior circulation by intracranial procedures, in Youman JR (ed): Neurological Surgery, vol 3. Philadelphia, WB Saunders, 1982, pp 1663-1696
Address
reprint
requests
Neurosurgical Higashimatsuyama Higashimatsuyama,
to:
Department, Hospital, Saitama
T.
Takeuchi, The
M.D.,
Municipal
2392 355, Japan.
Matsuyama,
of
Totaro
TAKEUCHI,
Neurosurgical
Case
Report—
Haruhiko
OGAWA
Department, The Municipal Higashimatsuyama,
and
Shin
KIMURA
of Higashimatsuyama Saitama
Hospital,
Abstract A rare aneurysm in the horizontal segment (A) of the right anterior cerebral artery was found in a 58 - year-old male presenting with subarachnoid hemorrhage. No obvious bleeding source was observed on the day of onset, but 7 days later, a definite diagnosis was made based on the discovery of cerebral vasospasm by a repeat angiogram. The aneurysm was clipped via the right frontotemporal approach 15 days after onset. He suddenly developed neurological symptoms such as consciousness disturbance , right hemiplegia, and aphasia on the 4th postoperative day, when remission of the cerebral vasospasm was confirmed by transcranial Doppler ultrasound examinations and cerebral angiography. The ischemic symptoms were probably due to cerebral embolus caused by intraluminal thrombi, which had formed during the maximum phase of vasospasm and became detached during the remission phase. Key words:
cerebral
subarachnoid
hemorrhage
aneurysm,
anterior
cerebral
Introduction Few aneurysms in the horizontal segment (A) of the anterior cerebral artery have been report ed.3,a,',9,i°,'3 15,17,19,20) The source of subarachnoid hemorrhage is not always clarified by the first cerebral angiography. In our case, the presence of an aneurysm in the A, seg ment was demonstrated by the repeat angiography as cerebral vasospasm involving the parent artery. This case demonstrated unusual development of neurological symptoms postoperatively during the remission phase of vasospasm. Here, we describe our case in detail and discuss the relationship with previous
cases. Case
Report
A 58-year-old male suffered a sudden onset of oc cipital headache on April 13, 1988. The headache per sisted and was followed by persistent nausea and vomiting. He therefore visited our department on the same day. Received 1990
January
29,
1990;
Accepted
October
4,
artery,
horizontal
segment,
vasospasm,
The neurological status on admission was grade II on the Hunt and Kosnik scale. There was no con sciousness disturbance, and he only suffered from neck stiffness. Computed tomographic (CT) scans revealed grade II signs on Fischer's scale: a diffuse bilateral high density area centered on the chiasmatic cistern, Sylvian cistern, and median longitudinal fissure and also in the septum pellucidum (Fig. 1). Cerebral angiograms on the day of onset revealed vasodila tion at the right A, portion (Fig. 2A). This suggest ed a possible fusiform-type aneurysm but this could not be confirmed. Repeat angiograms on the 7th day after onset demonstrated a severe diffuse-type vasospasm centered on the bilateral A,, A2, and M, portions, clearly indicating a saccular-type aneu rysm at the right A, portion. The location of the aneurysm appeared to be the A, loop portion, and there was no relationship with the A, perforating branch. No vascular anomaly, such as fenestration, was present in the A, portion (Fig. 2B). An operation was performed by the right fron totemporal approach 15 days after onset. A sac cular-type aneurysm of about 5 mm in diameter was found at the anterior limb of the A, loop portion,
Fig. 3
Fig. 1
CT scans on admission, showing a high-density area in the chiasmatic, interhemispheric, and bilateral Sylvian cisterns and also in the septum pellucidum
(arrow).
located on the central side 3 mm from the right A, A, junction. Clipping was therefore performed (Fig. 3). In the early morning of the 4th postoperative right hemiplegia and aphasia suddenly appeared
Fig. 2
day, ac
Operative photograph (left) and schema (right). An aneurysm (arrowheads) is present at the A, loop portion and is unrelated to the perfo rating artery.
companied by consciousness disturbance. Cerebral angiograms I day later revealed considerable remis sion of the cerebral vasospasm. In particular, neither cerebral vasospasm nor obstructive lesions were ob served in the left anterior cerebral artery and middle cerebral artery (MCA) (Fig. 4). On CT scans, a low density area had appeared when the neurological symptoms occurred, at first in the left anterior
Anteroposterior (left) and oblique views (center) of the right carotid angiogram and anteroposte rior view of the left carotid angiogram (right). A: Angiograms on the day of onset, showing a possible aneurysm in the right A, segment (arrowhead), without vasospasm. B: Angiograms on the 7th day after onset, showing a saccular-type aneurysm in the right A, segment (arrow) con firmed by severe diffuse vasospasm.
Fig. 4
bilateral MCAs to be 40-56 cm/sec and 2.5-3.6, re spectively. However, the CBFV began to increase 3 days after onset, and 4 days later, the CBFV and S/ D ratio in the right MCA were 126 cm/sec and 2.0, and those in the left MCA were 141 cm/sec and 1.7, respectively. The considerable increase in CBFV and decrease in S/D ratio suggested increase in the cerebral vasospasm. On the day of the neurological symptoms appeared, the CBFV and S/D ratio in the right MCA were 76 cm/sec and 3.2, and those in the left MCA were 80 cm/sec and 2.8, respective ly. The decrease in CBFV and increase in S/D ratio suggested the remission of cerebral vasospasm. The c-AVDO2 value was as low as 5.2 ml% at onset and remained stable in the range of 6.0-8.1 ml%. However, about I day before the neurological symptoms appeared, the c-AVDO2 suddenly dropped to 5.1-5.3 ml%. Disturbance of consciousness improved 4 days after the neurological symptoms appeared. He is now able to walk using an appliance, and is receiving speech training to ameliorate his aphasia.
Anteroposterior views of the right (left) and left carotid angiograms (right) 5 days after the operation, showing reduced vasospasm and no other cerebrovascular occlusive disease.
cerebral artery and then in the MCA territories. As shown in Fig. 5, the cerebral blood flow veloc ity (CBFV) in the bilateral MCAs and the systole diastole (S/D) ratio were regularly measured by transcranial Doppler ultrasound (TCD) (TC2-64 Model, EME Co., Ltd., Germany). The cerebral arteriovenous oxygen content difference (c-AVDO,) was calculated from arterial and jugular vein blood samples collected since admission. Initial TCD mea surements indicated the CBFV and S/D ratio in the
Fig. 5
TCD
and c-AVDO-,
reduced
vasospasm
measurements was
confirmed
with
Discussion I.
portion, excluding bifurcation. Its
clinical
by TCD
General features of aneurysms in the A, segment An aneurysm in the A, segment is located at the A,
course.
examination.
Neurological
the A,-A2 junction incidence among
symptoms
occurred
when
and carotid intracranial
the
aneurysms is estimated as low as 0.8-2.1 %,.4.9,14,17.19,20' In Europe and U.S.A., the incidence is 41 of 2672 cases (1.5%),'' while in Japan, 26 of 3430 cases (0.8%)17); 48 cases have previously been report ed. 3,4,7,9,14,17,19,20) There are no sex or side differences. 17)Quite a few cases of such aneurysms also demonstrated vascular anomalies ,4,17' as Suzuki et al. 17' reported five cases with vascular anomalies among 26 cases (19.2%). Fenestration at the A, portion is the most frequently observed vascular anomaly, with an incidence of 53.3-60%. Histological investigation of cerebral arterial anomalies demonstrated medial defects in the A, portion,'-' which were suggested as the cause of the aneurysms. In addition, 7-10% of cases with anomalies included A, hypoplasia with a vascular diameter of less than 1 MM. 13,15, Morphologically, the aneurysms were mostly of the saccular type 4,17"91(80-92%) and usually small. Kassell and Torner7' reported that the average diameter of aneurysms in the A, segment was 3.6 mm, whereas anterior communicating artery aneu rysms averaged 7.4 mm. The most frequently site for aneurysms is the ramified portion of the lenticulostriate artery. Suzuki et al. 17' reported the frequencies of aneurysms at the carina of the A, truncus and lenticulostriate artery, the A, portion itself, and the proximal portion of A, fenestration to be 57.7%, 19.2%, and 11.5%, respec tively. Wakabayashi et al.19' classified the aneurysms into three types according to its location: type I, the carina of the lenticulostriate artery (70%); type II, the proximal end of A, fenestration (20%); and type III, the loop of the A, portion (10%). The aneurysm in the present case was at the loop of the right A, truncus, thus belonging to Wakabayashi's type III. Other aneurysms complicated in 18-44.4% of cases, of which the aneurysm in the A, segment burst first in 50-63.6%.17' II.
Specific features of the present case No obvious source of the subarachnoid hemor rhage was observed in the present case on the day of onset. The incidence of subarachnoid hemorrhage without a clear source is less than 10% of all sub arachnoid hemorrhages.") The radiological condi tions are among the factors related to unknown bleeding. Other possibilities are the presence of an arteriovenous malformation or a periventricular tumor lesion. In addition, the angiography might not achieve clear contrast even though an aneurysm is present, possibly due to intraluminal thrombosis, the reduction or disappearance of the aneurysm, a small aneurysm, etc. An important factor is the unfavor
able contrast and morphological changes caused by cerebral vasospasm, emphasizing the need for repeat angiography.8' In the present case, a repeat angio gram demonstrated the aneurysm in the right A, segment, emphasized by the diffuse-type vasospasm affecting the surrounding vessels.
III. Cause of the neurological symptoms Ohta12) classified cases of vasospasm
mor
phologically on the basis of angiographic findings. Among these, the diffuse-type vasospasm especially is usually accompanied by a considerable decrease in cerebral blood flow and frequently causes delayed ischemic attack. Terada et al.'8' classified the course of vasospasm into four categories: initial phase, 6 ± 3 days after onset; progressive phase, 11 ± 5 days after onset; maximum phase, 14 ± 3 days after onset; and remission phase, 26 ± 6 days after onset. They concluded that the clinical symptoms mostly develop during initial and progressive phases. In the present case, the clinical symptoms ap peared on the 19th day after onset, i.e., 4 days after the operation. At that time, great increase in blood flow or marked decrease in S/D ratio, which are re garded as characteristic changes of cerebral vaso spasm,'"5•"' were not noted. Based on TCD measure ments, the CBFV and S/D ratio in the right MCA were 76 cm/sec and 3.2, and in the left MCA were 80 cm/sec and 2.8, respectively. An angiogram per formed the day after the appearance of clinical symp toms (20 days after onset, 5 days after the operation) clearly revealed remission of the cerebral vasospasm. However, the c-AVDO2 had decreased considerably 1 day before the symptoms occurred, suggesting an ischemic change. Thus, the clinical symptoms oc curred during the remission phase of cerebral vasospasm, suggesting the ischemia as the probable cause of the symptoms, although this must represent an extremely rare case. Another possible cause of the symptoms is a vascular lesion (thrombosis or em bolus) unrelated to the cerebral vasospasm. However, this can be excluded in the present case, as no more embolus lesions were found by angiography when the symptoms occurred, and the systemic condi tions such as cardiopulmonary function were un changed. Sakaki et al.") classified the changes of cerebral vasospasm into five phases and reported that in phase II, corresponding to Terada's progressive phase, increased necrosis of the medial smooth muscle and acid mucopolysaccharide levels were ob served, and in phase III, corresponding to Terada's maximum phase, intimal fibrosis and medial atro phy occurred
as well as organization
of thrombi
at
7) 8)
9)
10) Fig. 6
Schematic representation of the possible mor bidity underlying the neurological symptoms in the present case. Intraluminal thrombi may have formed during the maximum phase of vasospasm (B) and became detached during the remission phase (C). A: before vasospasm.
tached to the the ischemic bral embolus on the vessel and became (Fig. 6).
vessel inner wall. In the present case, symptoms were probably due to cere caused by thrombi, which had formed inner wall during the maximum phase detached during the remission phase
Acknowledgment A summary of this report was presented at the 32nd Meeting of the Japan Neurosurgical Society, Kanto District in December, 1988, Tokyo, Japan.
References 1)
2)
3)
4)
5)
6)
Aaslid R, Huber P, Nornes H: Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 60: 37-41, 1984 Crompton MR: The pathology of ruptured middle cerebral aneurysms with special reference to the differences between sexes. Lancet 2: 421-425, 1962 Hacker RJ, Krall JM, Fox JL: Data I, in Fox JL (ed): Intracranial Aneurysms, vol I. New York, Springer, 1983, pp 19-62 Handa J, Nakasu Y, Matsuda M, Kyoshima K: Aneurysms of the proximal anterior cerebral artery. Surg Neurol 22: 486-490, 1984 Harders AG, Gilsbach JM: Time course of blood ve locity changes related to vasospasm in the circle of Willis measured by transcranial Doppler ultrasound. J Neurosurg 66: 718-728, 1987 Ishii R, Kuroki M, Tanaka R, Watanabe M, Toyama M, Arai H: Subarachnoid hemorrhage of unknown
11)
12)
13)
14)
15) 16)
17)
18)
19)
20)
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