Neurol Med Chir (Tokyo) 41, 271¿278, 2001 Dissecting Aneurysms at the A1 Segment of the Anterior Cerebral Artery —Two Case Reports— Jun HIRAO, Hisayo OKAMOTO, Takashi WATANABE, Shuichiro ASANO*, and Akira TERAOKA* Department of Neurosurgery, Institute of Neurological Sciences, Tottori University School of Medicine, Yonago, Tottori; *Department of Neurosurgery, Teraoka Memorial Hospital, Hiroshima Abstract Two rare cases of dissections which involve the anterior cerebral artery (ACA) are reported. A 58-yearold woman presented with a ruptured dissecting aneurysm manifesting as sudden onset of severe headache and consciousness disturbance followed by aphasia, right hemiparesis, paresis of the left lower extremity, and choreoathetotic movements of the upper arms and face. Computed tomography and angiography revealed subarachnoid hemorrhage due to a dissecting aneurysm at the left A1 segment. The dissecting aneurysm was trapped surgically on the day of onset. Her neurological deficits disappeared within a month. A 39-year-old woman experienced continuous dull headache from the day before onset, and then suffered right hemiparesis. Magnetic resonance (MR) imaging revealed cerebral infarction at the left globus pallidus. Angiography and MR imaging revealed a dissecting aneurysm at the left A1 segment and occlusion of the left Heubner's artery. She received conservative treatment and her neurological findings were improved. Dissections or dissecting aneurysms involving the ACA can be classified into three types: Extension of a dissection to the ACA from the internal carotid artery, dissection at the A1 segment, and dissection at the A2–A4 segments. These types of dissection have distinct uniform clinical features. Key words: dissection, dissecting aneurysm, A1 segment, anterior cerebral artery Introduction Case Reports Dissections or dissecting aneurysms of intracranial arteries are rather rare35) and most frequently occur in the territories of the middle cerebral artery (MCA) or vertebrobasilar system.17,24) Dissections which involve the anterior cerebral artery (ACA) are extremely rare, with only five reported cases of dissections at the A1 segment.6,10,19,23,31) Four dissections were identified by postmortem examination and one by angiography. We report two cases of dissecting aneurysms at the A1 segment of the ACA which were identified by angiography and magnetic resonance (MR) imaging. Case 1: A 58-year-old previously healthy woman was admitted to the Tottori University Hospital on January 23, 1995. She suffered sudden onset of severe headache and lost consciousness. She was found by her family members, and was transported to our hospital by ambulance. On admission, she was confused and unable to speak due to motor aphasia, but responded to simple verbal orders. Choreoathetotic involuntary movements involving her bilateral upper extremities and face were apparent. Complete paraplegia of the lower extremities as well as slight weakness of the right arm was observed. Laboratory findings were negative. Computed tomography (CT) revealed diffuse subarachnoid hemorrhage (SAH), especially in the anterior part of the interhemispheric fissure which was classified as Fisher's group 3 (Fig. 1). Left carotid angiography disclosed the so-called string Received 2001 October 10, 2000; Accepted March 7, 271 272 Fig. 1 Fig. 2 J. Hirao et al. Case 1. Computed tomography scan on admission showing diffuse subarachnoid hemorrhage, especially in the anterior part of interhemispheric fissure which suggests a ruptured anterior communicating artery aneurysm. Case 1. Left carotid angiogram (oblique view) on admission showing the so-called string and pearl sign, and double contour appearance in the aneurysmal dilatation at the A1 segment of the anterior cerebral artery. Fig. 3 Case 1. Right carotid angiogram (oblique view) with digital compression of the left common carotid artery on admission showing a dissecting aneurysm at the left A1 segment via collateral flow through the anterior communicating artery. and pearl sign at the A1 segment of the ACA. The aneurysmal dilatation had a double contour appearance, which suggested the presence of true and false lumina in a dissecting aneurysm (Fig. 2). Right carotid angiography with digital compression of the left common carotid artery demonstrated the same aneurysmal dilatation at the left A1 segment via the collateral flow through the anterior communicating artery (AcomA) (Fig. 3). Angiography detected no other abnormal findings. The diagnosis was SAH caused by ruptured dissecting aneurysm at the A1 segment of the left ACA. After cerebral angiography, her neurological abnormalities such as motor aphasia, involuntary movement, and left leg paresis disappeared but she was still slightly confused. Her preoperative World Federation of Neurosurgical Societies grade was III, based on the Glasgow Coma Scale score of 14 and the presence of right hemiparesis. Trapping of the dissecting aneurysm was performed via the left pterional approach. After the sylvian fissure was opened, the left internal carotid artery (ICA) was identified and the A1 segment of the Neurol Med Chir (Tokyo) 41, May, 2001 Dissection of ACA 273 " Fig. 4 left ACA was exposed from the bifurcation of the ICA to its distal portion. A reddish fusiform dilatation was seen 12 mm distal to the bifurcation (Fig. 4 right). The wall was so thin that the blood flow could be seen. A perforating branch was observed arising from the A1 segment proximal to the dissecting aneurysm. A straight clip with a 7 mm blade was applied to the A1 segment just proximal to the dissection, causing the aneurysmal dilatation to collapse (Fig. 4 left). The distal part of the A1 segment, the AcomA, and the A2 segment of the left ACA were exposed and identified, and a straight clip with a 7 mm blade was applied to the ACA adjacent to the distal end of the dissecting aneurysm. The postoperative course was uneventful. The right hemiparesis improved gradually, and the patient could walk 2 weeks after the surgery. CT demonstrated no low-density areas during the course, but single photon emission CT using technetium-99m hexamethylpropylene amine oxime showed a low perfusion area at the medial and inferior part of the left frontal lobe. Cerebral angiography obtained 3 weeks after the surgery showed the dissecting aneurysm had disappeared (Fig. 5), and the left A2–A4 segments of ACA were visualized via collateral flow through the AcomA. The left A2 segment was narrowed compared to normal, probably due to delayed vasospasm. She was discharged one month after admission without neurological deficit. She has since resumed her normal activities. Case 2: A 39-year-old woman was admitted to Neurol Med Chir (Tokyo) 41, May, 2001 Fig. 5 Case 1. Operating microscope photographs showing a reddish and fusiform dilatation at the A1 segment (right), and the collapsed aneurysmal dilatation after a straight clip was applied to the A1 segment just proximal to the dissecting aneurysm (left). Case 1. Left carotid angiogram (anteroposterior view) 3 weeks after the onset showing the dissecting aneurysm has disappeared, and the left A1 segment terminates with the perforating branch. Teraoka Memorial Hospital on July 28, 1997. She had suffered from dull frontal headache continuous- 274 J. Hirao et al. ly for a day. Subsequently, she had spoken words without meaning. She manifested right hemiparesis one day later and then was transported to the hospital by ambulance. On admission, she was confused slightly, but responded to simple verbal orders. She had neither weakness nor numbness in her limbs except for right facial nerve paresis. Laboratory findings were negative, and lumbar puncture showed clear cerebrospinal fluid. MR imaging revealed a cerebral infarction at the territory of left Heubner's artery (Fig. 6). Left carotid angiography disclosed a fusiform aneurysm at the A1 segment of the ACA (Fig. 7). There was no double contour appearance at the aneurysmal dilatation, nor any other abnormal findings. Axial MR imaging revealed double contour appearance in the aneurysmal dilatation, which suggested the presence of true and false lumina in the fusiform aneurysm (Fig. 8). The diagnosis was cerebral infarction caused by dissection at the A1 segment of the left ACA and obliteration of the left Heubner's artery. Her neurological deficits improved gradually after conservative treatment. Follow-up MR imaging demonstrated regression of the dissection. Repeat cerebral angiography obtained 4 weeks after admission showed reduction of the dissection and no progression to the distal portion (Fig. 9). Subsequently, She was discharged without neurological deficit and has resumed her normal activities. Fig. 6 Case 2. T2-weighted magnetic resonance image the day after onset revealing cerebral infarction in the territory of the left Heubner's artery. Fig. 7 Case 2. Left carotid angiogram (anteroposterior view) disclosing a fusiform aneurysm at the A1 segment of the anterior cerebral artery. There was no double contour appearance in the aneurysmal dilatation. Fig. 8 Case 2. Axial T1-weighted magnetic resonance image 4 days after onset revealing double contour appearance in the aneurysmal dilatation, which suggested the presence of true and false lumina in the fusiform aneurysm. Neurol Med Chir (Tokyo) 41, May, 2001 Dissection of ACA Fig. 9 Case 2. Repeat cerebral angiogram 4 weeks after onset showing reduction of the dissection and no progression to the distal portion. Discussion Only 32 cases of dissections which involve the ACA have been reported (Table 1), including only five cases of dissections at the A1 segment.6,10,19,23,31) Dissections or dissecting aneurysms involving the ACA can be divided into three types based on the affected site, the age of patients, the onset, progression, and outcome of the disease. Type I dissection usually originates at the ICA and extends to the ACA as well as to the MCA. Type II dissection often occurs at the A1 segment of the ACA. Type III dissection mainly involves distal ACA, namely the A2, A3, and A4 segments. Most type I dissections seem to occur in young adults. All 10 patients were between 14–41 years old3,5,7,13,15,18,25,26,30) except for a 75-year-old woman.1) The mean age was 24 years. The etiology of type I was speculated to be trauma in two cases, congenital fragility of the vascular wall in two, atherosclerosis in one, and unknown in five. Nine of the 10 patients had cerebral infarctions and died within 8 days of the onset. However, the 75-year-old woman1) manifested SAH and survived with mild right Neurol Med Chir (Tokyo) 41, May, 2001 275 hemiparesis and aphasia after surgical clamping of the affected ICA. The high mortality associated with type I dissections may be due to the sharp reduction in collateral flow to the territory of the affected ICA via the AcomA in the presence of the dissections of the A1 segment of ACA. Occlusion at the earlier stage may prevent farther extension of dissection and/or possibly preserve more collateral flow through the AcomA, so we suggest that intravascular occlusion of the affected ICA may be the best treatment. The five cases of type II dissections mostly occurred in young females except for one pediatric case.6,10,19,23,31) Type II dissections often caused SAH. A 26-year-old female suffered SAH but misdiagnosis of ruptured AcomA aneurysm was made. After she died on day 12, autopsy showed a ruptured dissecting aneurysm at the A1 segment of the ACA and an unruptured AcomA aneurysm. A 5-year-old boy manifested headache, right hemiparesis, and aphasia 3 days after minor head injury. Left carotid angiography demonstrated no filling of the left ACA. He died after receiving decompressive craniotomy. Postmortem examination revealed dissecting subintimal hematoma of the left ACA (A1, A2) and massive infarction of left frontal lobe. The poor outcome may have been due to the dissection of the A1 segment of the ACA which extended to the A2 segment, as a result of poor collateral flow through the AcomA. A 22-year-old pregnant female died of massive abdominal hemorrhage, and a 16-year-old female died of intracerebral hematoma (ICH) due to moyamoya disease. Autopsy of both cases disclosed unruptured dissections at the A1 segments of ACA. A 48-yearold female experienced repeated bouts of severe headaches. She eventually lost consciousness one month after cerebral infarction at the territory of the left ACA. Surgery identified a dissecting aneurysm at the left A1 and A2 portions of the ACA. She recovered after the surgery. Our cases are considered to be type II dissection based on the affected site and the progression of the disease. Case I was the first to be identified angiographically and treated with trapping surgery. Although only seven cases of type II dissection including ours have been reported, some dissections or dissecting aneurysms at A1 segments may be misdiagnosed as such aneurysms. For example, 38 of 4295 aneurysms (0.88%) were aneurysms at the A1 segment of ACA and nine (0.2%) of these were fusiform aneurysms or saccular aneurysms which did not arise from a bifurcation.27) Two of 1000 aneurysms (0.2%) were fusiform aneurysms at the A1 segment.33) All of these cases may harbor type II dissection. Alternatively, type II dissection may be clas- J. Hirao et al. 276 Table 1 Table 1 Classification of dissecting aneurysms involving the anterior cerebral artery Type* Author (Year) Age/ Sex I Dratz and Woodholl (1947)5) Anderson and Schechter (1959)3) 21/F 41/M infarction infarction Wolman (1959)30) 16/M infarction Scott et al. (1960)25) 29/F infarction Nedwich et al. (1963)18) Grosman et al. (1980)7) 30/F 23/M infarction infarction Adams et al. (1982)1) 75/F SAH Steiner et al. (1986)26) 23/F infarction Linden et al. (1987)15) Kitani et al. (1987)13) 23/F 14/M infarction infarction Gherardi and Lee (1967)6) Nelson (1968)19) 26/F 5/M SAH infarction Pilz (1977)23) 22/F incidental Yamashita et al. (1983)31) 16/F incidental Honda et al. (1997)10) 48/F infarction ª SAH Present Case 1 58/F SAH Present Case 2 39/F infarction Nakazawa et al. (1984)17) 43/M infarction Amagasa et al. (1988)2) 44/M infarction Sasaki et al. (1991)24) 57/M infarction Terai and Matsubara (1991)29) 51/M infarction Guridi et al. (1993)8) 72/F SAH ＋ ICH Nomura et al. (1993)20) 37/M infarction Yasukawa et al. (1993)34) 62/M infarction ＋ SAH Kidooka et al. (1993)12) 45/M infarction 45/M infarction Ishikawa et al. (1993)11) 42/M infarction Yano et al. (1995)32) 27/M SAH ＋ ICH Nagata and Sato (1996)16) 43/M infarction Hayashi et al. (1996)9) 36/M ICH II III Manifestation Symptoms and signs Etiology Outcome** rt hemiparesis, semicoma rt hemiparesis, aphasia, rt hemianopia headache, nasal bleeding, lt hemiplegia, aphasia lt hemiparesis, lt facial nerve palsy, aphasia lt hemiparesis dysphagia, rt hemiparesis headache trauma arteriosclerosis dead dead congenital defect of the vessel wall dead trauma (surgical complication) dead unknown unknown dead dead unknown headache, lt hemiparesis, semicoma lt hemiplegia, coma headache, lt hemiplegia headache, coma headache, rt hemiparesis, aphasia congenital weakness of elastic lamina moderately disabled dead headache, rt hemiparesis headache, paraplegia, involuntary movement of face and arms headache, rt hemiparesis headache, vertigo, involuntary movement of legs, convulsion, rt hemiparesis aphasia, rt hemiparesis headache, weakness of lt leg headache, rt hemiparesis headache, neck pain, loss of consciousness, rt hemiparesis headache, weakness of lt leg rt hemiparesis, dysarthria headache, rt hemiparesis headache, involuntary movement of legs, rt hemiparesis headache, weakness of lt leg headache, rt hemiparesis headache, weakness of rt leg loss of consciousness, weakness of lt leg unknown unknown dead dead unknown trauma dead dead Guillain-Barr áe dead syndrome moyamoya disease ＋ dead trauma unknown alive unknown good recovery unknown good recovery good recovery unknown trauma unknown unknown arteriosclerosis trauma unknown unknown unknown unknown unknown unknown unknown good recovery moderately disabled good recovery moderately disabled good recovery good recovery good recovery good recovery good recovery good recovery good recovery good recovery Contd. Neurol Med Chir (Tokyo) 41, May, 2001 Dissection of ACA Table 1, Type* III 277 contd. Author (Year) Age/ Sex Manifestation Araki et al. (1996)4) 52/M infarction Okuno et al. (1996)22) 50/M Koyama et al. (1996)14) 45/M hemorrhagic infarction infarction 44/M infarction Symptoms and signs headache, weakness of lt leg headache, urinary incontinence dizziness, weakness of lt leg rt hemiparesis, dysarthria Etiology unknown unknown unknown unknown Outcome** good recovery good recovery good recovery good recovery *Our classification was assigned as follows: type I, extension of dissection to anterior cerebral artery from internal carotid artery; type II, dissection at A1 segment of anterior cerebral artery; type III, dissection at A2–A4 segments of anterior cerebral artery. **According to Glasgow Outcome Scale. ICH: intracerebral hematoma, SAH: subarachnoid hemorrhage. sified as SAH with unknown etiology, because dissections or dissecting aneurysms are often difficult to identify angiographically. MR imaging may be useful to demonstrate dissection or dissecting aneurysm. The 17 cases of type III dissections were mainly found in middle-aged males, aged between 27–72 years (mean age 47 years).2,4,8,9,11,12,14,16,17,20,22,24,29,32,34) The patients were Japanese except for one.8) The etiology was presumed to be trauma in two cases, arteriosclerosis in one, and unknown in the others. Twelve of the 17 type III dissections caused cerebral infarctions, one SAH and infarction, two SAH and ICH, one hemorrhagic infarction, and one ICH. Fifteen patients had hemiparesis or weakness of the lower extremities. Nine of 12 patients who suffered only ischemic attacks were treated conservatively and two were operated with wrapping surgery of dissecting aneurysms at the chronic stage, whereas one was treated with trapping with A3-A3 anastomosis. Trapping and resection of the dissection was performed in one patient with SAH, trapping with bypass surgery in one, and conservative treatment in one. All 15 patients showed complete improvement of neurological abnormalities with exceptions of moderate hemiparesis in two patients. However, one patient died suddenly of massive and recent gastric bleeding caused by acute erosive gastritis 6 weeks after the onset.8) Headache is a common symptom even in patients with dissections of the ACA causing ischemia without SAH. All 16 patients who showed cerebral ischemia and were able to speak on admission complained of headache at the onset. Our first patient had aphasia, right hemiparesis, paresis of the left lower extremity, and choreoathetotic movements of the upper extremities and face after recovery of consciousness. Thus, hemiparesis and/or paresis of the lower extremities is also a characteristic of type II Neurol Med Chir (Tokyo) 41, May, 2001 dissection of the ACA. Two cases of type III dissection showed transient involuntary movements at the onset.12,17) Involvement of the extra-pyramidal system which is perfused by the ACA might cause such involuntary movements. We selected trapping surgery for the first patient with SAH, because angiography indicated collateral flow through the AcomA, based on reports that trapping surgery is a good treatment for a fusiform aneurysm at the A1 segment,21,33) when collateral flow through the AcomA was sufficient. Treatment for a dissecting aneurysm at the A1 segment is likely to be similar to treatment for fusiform aneurysm.28) Our two cases of dissecting aneurysms at the A1 segment of the ACA were identified by angiography and MR imaging, and one was treated by trapping surgery. We classified dissections or dissecting aneurysms involving the ACA into three types based on the affected site. Type I dissection occurs in relatively younger patients and causes fatal brain infarctions. Type II dissection tends to occur in females and causes SAH or cerebral infarction, although there were only seven cases of this type. The outcome seemed to depend on the sufficiency of collateral flow through the AcomA and the amount of subarachnoid clot in the case of SAH. Type III dissection occurs in middle-aged males and causes transient ischemic attacks and/or rather mild SAH. 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Watanabe, M.D., Department of Neurosurgery, Institute of Neurological Sciences, Tottori University School of Medicine, 36–1 Nishi–cho, Yonago, Tottori 683–8504, Japan. Neurol Med Chir (Tokyo) 41, May, 2001