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(Stroke. 1999;30:1291.)
© 1999 American Heart Association, Inc.

Letters to the Editor

Surgery for Cerebral Amyloid Angiopathy–Related Hemorrhage

Mark O. McCarron, MRCP James A.R. Nicoll, MD, FRCPath

University of Glasgow, Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, United Kingdom

To the Editor:

The report by Izumihara et al¹ adds to an existing body of evidence^{2 3} that neurosurgery does not have a significant adverse influence on outcome from cerebral amyloid angiopathy–related hemorrhage (CAAH). Although surgery for CAAH appears to be relatively safe, its effectiveness as in intracerebral hemorrhage in general⁴ remains controversial.

The authors identified 3 clinical factors (patients aged over 75 years, a parietal hematoma, and intraventricular hemorrhage) that had an adverse effect on postoperative outcome. However, Glasgow Coma Scale score, which has been shown to be one of the most powerful determinants of outcome in intracerebral hemorrhage,^{5 6} was unfortunately not included in this analysis. This is an important clinical factor, which in our experience with a smaller group of CAAH patients results in a poorer outcome.⁷ Because the report by Izumihara et al¹ examines one of the largest cohorts of patients with pathologically diagnosed CAAH, it would have been clinically useful to confirm this finding for the homogeneous population in their multiple logistic regression analysis of risk factors. Nearly one third of the patients (n=12) had their operation >3 days after hemorrhage onset, suggesting that the good outcome may well have reflected good preoperative Glasgow Coma Scale scores.

Finally, possession of the apolipoprotein E (APOE) 4 allele has recently been recognized as an adverse prognostic factor in intracerebral hemorrhage.^{8 9} It will be interesting to examine whether this genetic determinant of outcome applies to all types of intracerebral hemorrhage (eg, hypertensive deep intracerebral hemorrhage, CAAH, and thrombolytic-related intracerebral hemorrhage). In addition, we can as yet only speculate whether surgical intervention will have less benefit or more benefit for an 4 carrier compared with a noncarrier.

References

1. Izumihara A, Ishihara T, Iwamoto N, Yamashita K, Ito H. Postoperative outcome of 37 patients with lobar intracerebral hemorrhage related to cerebral amyloid angiopathy. Stroke.. 1999;30:29–33.[Abstract/Free Full Text]
2. Greene GM, Godersky JC, Biller J, Hart MN, Adams HP Jr. Surgical experience with cerebral amyloid angiopathy. Stroke.. 1990;21:1545–1549.[Abstract/Free Full Text]
3. Matkovic Z, Davis S, Gonzales M, Kalnins R, Masters CL. Surgical risk of hemorrhage in cerebral amyloid angiopathy. Stroke.. 1991;22:456–461.[Abstract/Free Full Text]
4. Hankey GJ, Hon C. Surgery for primary intracerebral hemorrhage: is it safe and effective? A systematic review of case series and randomized trials. Stroke.. 1997;28:2126–2132.[Abstract/Free Full Text]
5. Portenoy RK, Lipton RB, Berger AR, Lesser ML, Lantos G. Intracerebral haemorrhage: a model for the prediction of outcome. J Neurol Neurosurg Psychiatry.. 1987;50:976–979.[Abstract]
6. Radberg JA, Olsson JE, Radberg CT. Prognostic parameters in spontaneous intracerebral hematomas with special reference to anticoagulant treatment. Stroke.. 1991;22:571–576.[Abstract/Free Full Text]
7. McCarron MO, Nicoll JAR, Love S, Ironside JW. Surgical intervention, biopsy and APOE genotype in cerebral amyloid angiopathy-related haemorrhage. Br J Neurosurg. In press.
8. Alberts MJ, Graffagnino C, McClenny C, DeLong D, Strittmatter WJ, Saunders AM, Roses AD. ApoE genotype and survival from intracerebral haemorrhage. Lancet.. 1995;346:575. Letter.[Medline] [Order article via Infotrieve]
9. McCarron MO, Muir KW, Weir CJ, AG Dyker, I Bone, JAR Nicoll, KR Lees. The apolipoprotein E 4 allele and outcome in cerebrovascular disease. Stroke.. 1998;29:1882–1887.[Abstract/Free Full Text]

Response

Akifumi Izumihara, MD; Naoki Iwamoto, MD; Katsuhiro Yamashita, MD Haruhide Ito, MD

Department of Neurosurgery

Tokuhiro Ishihara, MD

First Department of Pathology, Yamaguchi University School of Medicine, Yamaguchi, Japan

Key Words: amyloid • intracerebral hemorrhage • outcome

We appreciate the comments of Drs McCarron and Nicoll regarding our recent article. They point out that the preoperative neurological condition in patients with intracerebral hemorrhage has been one of the most powerful determinants of the postoperative outcome in several previous studies and that the apoE 4 allele has recently been reported to be an adverse prognostic factor. In our retrospective study, the preoperative neurological condition was assessed not with the Glasgow Coma Scale, but instead with the Japan Coma Scale in some patients, and depended on other clinical data (demographics, medical history, and radiographic characteristics, especially hematoma size). Accordingly, we excluded it from the multiple logistic regression model. We also have a great interest in the apoE 4 allele as a risk factor for cerebral amyloid angiopathy with hemorrhage and an adverse prognostic factor in patients with cerebral amyloid angiopathy–related hemorrhage. On the other hand, the apoE 2 allele has recently been reported to be a risk factor for cerebral amyloid angiopathy with hemorrhage.¹ Further genetic studies might elucidate the relationship between cerebral amyloid angiopathy and hemorrhage and a different prognostic factor in patients with cerebral amyloid angiopathy–related hemorrhage.

We indicated that neurosurgery could be performed relatively safely and did not deteriorate the outcome in patients with cerebral amyloid angiopathy–related hemorrhage. Moreover, we elucidated 3 risk factors for an adverse postoperative outcome (parietal hematomas, age 75 years, and intraventricular hemorrhages). Certainly, our study does not demonstrate that neurosurgery is effective in improving the outcome. In our series, however, 4 patients with a large hematoma had a good outcome. At present, the diagnosis of cerebral amyloid angiopathy involves histological examination of surgical or autopsy specimens. Accordingly, nonsurgical treatments have been investigated mainly in autopsy cases.² Therefore, we consider it difficult to compare surgical and nonsurgical treatments for patients with cerebral amyloid angiopathy–related hemorrhage.

References

1. Nicoll JAR, Burnett C, Love S, Graham DI, Dewar D, Ironside JW, Stewart J, Vinters HV. High frequency of apolipoprotein E 2 allele in hemorrhage due to cerebral amyloid angiopathy. Ann Neurol.. 1997;41:716–721.[Medline] [Order article via Infotrieve]
2. Matkovic Z, Davis S, Gonzales M, Kalnins R, Masters CL. Surgical risk of hemorrhage in cerebral amyloid angiopathy. Stroke.. 1991;22:456–461.

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