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Cerebral aneurysm

A cerebral or brain aneurysm is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel. A common location of cerebral aneurysms is on the arteries at the base of the brain, known as the Circle of Willis. Aneurysms may result from congenital defects, preexisting conditions such as high blood pressure and atherosclerosis (the buildup of fatty deposits in the arteries), or head trauma. Cerebral aneurysms occur more commonly in adults than in children and are slightly more common in women than in men, but they may occur at any age. more...

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A small, unchanging aneurysm will produce no symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and usually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic, experiencing no symptoms at all. Onset is usually sudden and without warning. Rupture of a cerebral aneurysm is dangerous and usually results in bleeding into the meninges or the brain itself, leading to a subarachnoid hemorrhage or intracranial hematoma, either of which constitutes a stroke. Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm of the blood vessels), or multiple aneurysms may also occur. An unruptured cerebral aneurysm has a 4% chance of rupturing each year.

In outlining symptoms of ruptured cerebral aneurysm, it is useful to make use of the Hunt and Hess scale of subarachnoid hemorrhage severity:

  • Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity. Approximate survival rate 70%.
  • Grade 2: Moderate to severe headache; nuchal rigidity; no neurologic deficit except cranial nerve palsy. 60%.
  • Grade 3: Drowsy; minimal neurologic deficit. 50%.
  • Grade 4: Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances. 20%.
  • Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Surgery is usually performed within the first three days to clip the ruptured aneurysm and reduce the risk of rebleeding. When aneurysms are discovered before rupture occurs, microcoil thrombosis or balloon embolization may be performed on patients for whom surgery is considered too risky. During these procedures, a thin, hollow tube (catheter) is inserted through an artery to travel up to the brain. Once the catheter reaches the aneurysm, tiny balloons or coils are used to block blood flow through the aneurysm. Other treatments may include bedrest, drug therapy, or hypertensive-hypervolemic therapy (which elevates blood pressure, increases blood volume, and thins the blood) to drive blood flow through and around blocked arteries and control vasospasm.

The prognosis for a patient with a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, the person's age, general health, and neurological condition. Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit. However, estimates are, that of the 30,000 people per year in the United States who suffer a ruptured aneurysm, only 20% will be alive and well in one year's time. 20% will be alive but disabled, and 60% will have died.

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Spontaneous disappearance and reappearance of a ruptured cerebral aneurysm: One case found in a group of 33 consecutive patients with subarachnoid hemorrhage
From Neurological Research, 9/1/00 by Nakajima, Yoshikazu

The spontaneous disappearance and reappearance of a ruptured cerebral aneurysm is generally assumed to be a rare phenomenon although the actual incidence is unknown. Among 39 consecutive cases of acute subarachnoid hemorrhage (SAN), 33 were studied by three-dimensional computed tomographic angiography (CTA) within 6 h after the onset of SAH, followed by digital subtraction angiography (DSA) within 24 h after the ictus. Of those patients, one, a 58-year-old woman, had a saccular aneurysm at the distal anterior cerebral artery; the aneurysm was clearly demonstrated by CTA 2.5 h after the SAH onset, but was not shown by a subsequent DSA performed 8.5 h after the ictus. A follow-up DSA detected the neck of aneurysm on day 11, and the whole aneurysm was visualized on day 19. The observations in this particular case suggest that the spontaneous disappearance of a ruptured cerebral aneurysm may occur during the ultra-early stage of SAH and that reappearance may follow during the next few weeks. The patient did not suffer complications such as vasospasm or systemic hypotension nor was she treated with antifibrinolytic agents. The aneurysmal shape and the surrounding clot are considered as putative factors possibly related to the intermittent appearance of the aneurysm. [Neurol Res 2000; 22: 583-587]

Keywords: Cerebral aneurysm; angiography, computed tomography; thrombosis; subarachnoid hemorrhage; three-dimensional reconstruction

INTRODUCTION

Although most neurosurgeons agree that the spontaneous disappearance and reappearance of a ruptured cerebral aneurysm does occur, this belief is mostly based on sporadic, incidental findings in uncontrolled clinical settings',z. The incidence and the natural course of such intermittent appearances are largely unknown.

The recently developed, three-dimensional computed tomographic angiography (CTA) is a good tool for studying patients with acute subarachnoid hemorrhage (SAN) because it is non-invasive3-5. In the present series of 33 consecutive cases of ultra-early stage SAH, each patient was first studied with CTA for screening of the ruptured aneurysm and then with digital cerebral angiography (DSA) a few hours later for pre-surgical evaluation. Among those patients, we found one in whom the initial CTA clearly demonstrated an aneurysm but the follow-up DSA failed to show it. The aneurysm gradually re-appeared on follow-up DSAs performed over the next few weeks. We examined the angiographic features and possible mechanisms of this supposedly rare phenomenon, taking into consideration the lack of data concerning its actual incidence.

MATERIALS AND METHODS

The subjects of this study were 39 consecutive patients who were admitted to our institution between October 1994 to October 1996 and who had a ruptured saccular aneurysm detected by initial CTA performed within 6 h after the onset of SAH. Nicardipine hydrochloride (Perdipine(R), Yamanouchi Pharmaceutical Co. Ltd., Tokyo, Japan) was administered intravenously to control blood pressure, and buprenorphine hydrochloride (Lepetan(R),, Otsuka Pharmaceutical Co. Ltd., Tokyo, Japan) was used for sedation when necessary. Five patients who were transferred to our institution while in cardiopulmonary arrest (CPA) were studied with CTA after resuscitation. The patients' clinical status and CT findings on admission were evaluated according to the World Federation of Neurological Surgeons grading scaleb and Fisher's grading system7, respectively. After confirmation of SAH by initial conventional CT study, they were examined with CTA to screen for aneurysm. The details of the method are described elsewheres.

Briefly, the volume data were obtained with a Hitachi W-3000 CT scanner (Hitachi Medical Corp., Tokyo, Japan) after injection of 80 ml of iopamidol (lopamiron 300(R), 300 mg ml-1; Nihon-Schering, Tokyo, Japan). Prior to the volume scan, we employed a single slice dynamic CT prescan which optimally visualizes contrast enhancement in arterial phase of the first circulation of contrast material in order to reduce the artifact caused by venous enhancement. The volume data were transferred to the workstation, which generated the angiographic images at a 1-mm reconstruction pitch using a voxel transmission method. When surgical indication was suggested by the patient's condition and CTA, DSA was performed with a Philips Integris V3000 angiographic unit using four-vessel angiography with optional use of the rotational techniques8.

RESULTS

Five patients resuscitated from CPA were studied by CTA but not by DSA because they were not indicated for craniotomy. Another patient was not examined with DSA because of rebleeding during angiography. In the remaining 33 patients, CTA was performed within 60 to 351 min (190 +/- 74 min, mean +/- SD) and DSA within 85 to 1336 min after SAN (555 +/- 392 min). The clinical parameters of 33 patients studied with both CTA and DSA are summarized in Table 1. In 32 patients, DSA confirmed the aneurysms, which were clipped on the same day. In one patient, CTA demonstrated an aneurysm but the subsequent DSA failed to detect it. The details of this particular patient are described below.

Case presentation

A 58-year-old, right-handed woman was admitted to our institution because of sudden onset of severe headache. On admission, she was lethargic and complaining of extremely severe headache. She had been suffering from a hemiweakness of the right side of the body and motor dysphasia for eight years due to the hemorrhagic infarction in the left hemisphere.

A CT scan on admission demonstrated a diffuse SAH and a dense clot around the anterior genu of the corpus callosum (Figure 1). CTA performed 2.5 h after SAH onset, demonstrated a 5-mm saccular aneurysm with a small bleb located at the A2-A3 junction of the right anterior cerebral artery (Figure 2). The neck of the aneurysm appeared to be rather narrow and long. She was treated in the intensive care unit under mild sedation and her blood pressure was controlled with systolic pressure maintained from 100 to 120 mmHg. A

DSA including rotational technique performed 8.5 h after SAH disclosed no aneurysms (Figure 3, left). There was no angiographic evidence of vasospasm. A followup DSA performed on day 11 showed that the neck of the aneurysm had reappeared (Figure 3, center). The entire aneurysm had reappeared by day 19 (Figure 3, right). Craniotomy performed on day 19 disclosed the aneurysmal dome buried in the intracerebral hematoma at the anterior genu of the corpus callosum. The rather narrow, long neck of the aneurysm was readily identified and successfully clipped. She was discharged in good condition after an uneventful post-operative course.

DISCUSSION AND CONCLUSION

So far, the phenomenon involving the disappearance and reappearance of a ruptured cerebral aneurysm has been documented angiographically in only two patients,1,2. One had a small frontopolar artery aneurysm that was visible on admission but disappeared on day 16 of the hospital stay, and then reappeared on day 21^sup 1^. The other patient had a small left anterior cerebral artery aneurysm that was visualized on an angiogram on day 9, but was only partly visible on day 19, when the patient was in systemic hypotension, and had disappeared by day 23. Follow-up angiography demonstrated the complete re-appearance of the aneurysm by Day 37^sup 2^. These two patients were under antifibrinolytic therapy with epsilon-aminocaproic acid. In both cases, the intermittent appearance of aneurysm was presumed to be possibly due to temporary aneurysmal thrombosis related to the antifibrinolytic therapy, or to vasospasm or systemic hypotension1,2. Several factors have been proposed as relevant to the spontaneous thrombosis of intracranial aneurysm: the aneurysmal shape, especially the ratio of the size of the aneurysmal dome to the orifice9; hemodynamic changes due to vasospasm, systemic hypotension compression of the parent artery by the aneurysm2,10,11,thrombosis of the parent artery' , after a high-flow extra-intracranial bypass surgery intramural hemorrhage associated with parent artery dissection14; antifibrinolytic therapy1,2; and the compression by the surrounding brain edema and clot's. In our present case, the size of the aneurysm was not unusual, and there was no evidence of vasospasm, systemic hypotension, or compression or thrombosis of the parent artery. The patient was not treated with antifibrinolytic agents. Although the factors relevant to the intermittent appearance of the aneurysm cannot be specified in the present case, we found the shape of the aneurysm, which had a rather narrow, long neck, and the presence of a dense clot surrounding the aneurysm interesting. Those factors may have contributed to the thrombosis of the aneurysm.

Although repeat angiography had been regarded as beneficial for detecting an aneurysm that was undetectable on initial angiography 16, a recent report claims that even aneurysms not noted on initial angiograms could be seen by careful retrospective examination of those initial angiograms. They stressed the importance of the initial angiography being performed appropriately and evaluated by experienced physicians17. In the present study, we employed rotational DSA because this technique is good for the detection of a small aneurysm or a partially thrombosed aneurysm, especially one located in the anterior communicating artery aneurysm where an aneurysm is highly likely to be overlooked on an initial angiogram 8,18-20. Among 69 patients with nontraumatic SAH who were transferred to our clinic during the same period as this study, the incidence of SAH of unknown origin on the initial DSA was only 5.8% (4 of 69 cases). This incidence is lower than that previously reported in a cooperative study (14.9%)21. We performed every ..DSA in the same setting following a consistent protocol as far as was feasible. In the patient presented in this study, the initial CTA clearly demonstrated the aneurysm, the first DSA detected no aneurysm, the second DSA disclosed a portion of the aneurysm, and the third DSA demonstrated the whole aneurysm. It is very likely that the intermittent appearance of the aneurysm was due to the obliteration of the aneurysmal sac rather than to technical or diagnostic errors.

We conducted this study to evaluate the visualization of cerebral aneurysms in ultra-early phase of SAH using CTA as a less invasive imaging technique. CTA may detect the aneurysm that DSA failed to present because contrast resolution of CTA is much higher than that of DSA. The CT number (Hounsfield Unit) of the aneurysm in our case was 300-450, which is higher than that of the distal ACA (272). The neck and the whole feature of the aneurysm were clearly demonstrated on subsequent DSA. For these reasons, it seems reasonable to suppose that DSA could demonstrate the aneurysm 2.5 h after SAH if it was performed.

For the first time, the present study demonstrated the spontaneous disappearance and re-appearance of a ruptured cerebral aneurysm in a well-controlled series of consecutive patients. The aneurysm was probably thrombosed in the ultra-early stage of SAH, between 2.5 h and 8.5 h after the ictus, and then gradually reappeared during the following few weeks beginning with the neck portion. It was not associated with vasospasm, systemic hypotension, or the administration of an antifibrinolytic agent. The rather narrow, long neck of the aneurysm and the dense clot surrounding the aneurysm are possible factors in the temporary obliteration of this particular aneurysm.

ACKNOWLEDGEMENTS

We wish to thank Kenji Sagara, RT, and Shigeaki Nishiike, RT, for technical support and Hiroshi Hasegawa, MD, Department of Neurosurgery, Osaka Kosei-Nenkin Hospital, for his encouragement to proceed with this study.

REFERENCES

1 Spetzler RF, Winestock D, Newton HT, Boldrey EB. Disappearance and reappearance of cerebral aneurysm in serial arteriograms. Case report. J Neurosurg 1974; 41: 508-510

2 Bohmfalk GL, Story JL. Intermittent appearance of a ruptured cerebral aneurysm on sequential angiograms. Case report. J Neurosurg 1980; 52: 263-265

3 Zouanoui A, Sahel M, Marro B, Clemenceau S, Dargent N, Bitar A, Faillot T, Capelle L, Marsault C. Three-dimensional computed tomographic angiography in detection of cerebral aneurysms in acute subarachnoid hemorrhage. Neurosurgery 1997; 41: 125-130

4 Anderson GB, Findlay JM, Steinke DE, Ashforth R. Experience with computed tomographic angiography for the detection of intracranial aneurysms in the setting of acute subarachnoid hemorrhage. Neurosurgery 1997; 41: 522-528

5 Nakajima Y, Yoshimine T, Yoshida H, Sakashita K, Okamoto M, Kishikawa M, Yagi K, Yokota ), Hayakawa T. Computed tomography angiography of ruptured cerebral aneurysms: Factors affecting time to maximum contrast concentration. J Neurosurg 1998; 88: 663-669

6 Drake CG. Report on World Federation of Neurological Surgeons Committee on a universal subarachnoid hemorrhage grading scale. / Neurosurg 1988; 68: 985-986 (letter)

7 Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computed tomographic scanning. Neurosurgery 1980; 6: 1-9

8 Tu RK, Cohen WA, Maravilla KR, Bush WH, Patel NH, Eskridge J, Winn HR. Digital subtraction rotational angiography for aneurysms of the intracranial anterior circulation: Injection method and optimization. Am J Neuroradiol 1996; 17: 1127-1136

9 Black SPW, German WJ. Observation on the relationship between the volume and the size of the orifice of experimental aneurysms. / Neurosurg 1960; 17: 984-990

10 Andrews BT, Edwards MSB, Gannon P. Acutely thrombosed aneurysm of the middle cerebral artery presenting as intracerebral hemorrhage in a 3-year-old child. Case report. / Neurosurg 1984; 60: 1303-1307

11 Suzuki J, Onuma T. A giant intracranial aneurysm which disappeared angiographically following pneumoencephalography. Neurol Med Chir (Tokyo) 1976; 16: 105-108

12 Wakui K, Kamijo Y, Seguchi K, Sakai T. Thrombosed aneurysm of the middle cerebral artery with occlusion of the distal parent artery. Case report. Neurol Med Chir (Tokyo) 1992; 32: 842-845

13 Cantor G, Santoro A, Da Pian R. Spontaneous occlusion of supraclinoid aneurysms after the creation of extra-intracranial bypasses using long graft: Report of two cases. Neurosurgery 1999; 44: 216-219

14 Maeda K, Usui M, Tsutsumi K, lijima A. Spontaneous occlusion of a giant basilar tip aneurysm and a basilar artery due to the dissection of both structures: Case report. Surg Neurol 1997; 48: 606-609

15 Matsuzaki T, Takeda R, Wada K, Fukuoka S, Shimada T, Hashimoto I, Toshima M, Satone A, Nakamura J, Suematsu K. Two cases of thrombosis of aneurysm in the acute stage. No Shinkei Geka 1986; 14: 1147-1152 (jpn)

16 Perret G, Nishioka H. Report on the cooperative study of intracranial aneurysms and subarachnoid hemorrhage. Section IV, Cerebral angiography. An analysis of the diagnostic value and complications of carotid and vertebral angiography in 5,484 patients. / Neurosurg 1966; 25: 98-114

17 de Rochemont RdM, Heindel W, Wesselmann C, Kriger K, Laufermann H, Ernestus R-I, Neveling M, Lackner K. Nontraumatic subarachnoid hemorrhage: Value of repeat angiography. Radiology 1997; 202: 798-800

18 Pertuisel B, Haisa T, Bordi L. Abou Ouf S, Eissa M. Detection of a ruptured aneurysmal sac by MRI in a case of negative angiogram. Successful clipping of an anterior communicating artery aneurysm. Case report. Acta Neurochir (Wien) 1989; 100: 84-86

19 )afar JJ, Weiner HL. Surgery for angiographically occult cerebral aneurysms. J Neurosurg 1993; 79: 674-679

20 Iwanaga H, Wakai S, Ochiai C, Narita J, Inoh S, Nagai M. Ruptured cerebral aneurysms missed by initial angiographic study. Neurosurgery 1990; 27: 45-51

21 Kassell NF, Torner JC, Haley EC, Jane JA, Adams HP, Kongable GL. The international cooperative study on the timing of aneurysm surgery. Part I: Overall management results. J Neurosurg 1990; 73: 18-36

Yoshikazu Nakajima, Toshiki Yoshimine*, Hiroshi Mori, Kana Nakamuta, Ichiro Fujimura, Keiji Sakashita, Eiji Kohmura*, Toru Hayakawa* and Junichiro Yokota

Osaka Prefectural Senshu Critical Care Medical Center, *Department of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan

Correspondence and reprint requests to: Yoshikazu Nakajima, MD, PhD, Department of Neurosurgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Accepted for publication March 2000.

Copyright Forefront Publishing Group Sep 2000
Provided by ProQuest Information and Learning Company. All rights Reserved

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