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NEUROLOGY 2005;64:1238-1244
© 2005 American Academy of Neurology

APOE influences vasospasm and cognition of noncomatose patients with subarachnoid hemorrhage

L. A. Lanterna, MD, M. Rigoldi, MD, G. Tredici, MD, PhD, F. Biroli, MD, C. Cesana, MD, S. M. Gaini, MD, PhD and L. Dalprà, MD, PhD

From the Department of Neurosurgery (Drs. Lanterna and Biroli), Ospedali Riuniti, Bergamo; Department of Neuroscience and Biomedical Technologies (Drs. Lanterna, Tredici, and Gaini), University of Milano-Bicocca; Medical Genetic Laboratory (Drs. Rigoldi, Gaini, and Dalprà) and Department of Neurosurgery (Drs. Cesana, Gaini, and Dalprà), H.S. Gerardo, Monza; and Department of Experimental, Enviromental Medicine and Medical Biotechnology (Dr. Dalprà), University of Milano-Bicocca, Monza, Italy.

Address correspondence and reprint requests to Dr. L.A. Lanterna, Department of Neurosurgery, Ospedali Riuniti, Bergamo, Italy; e-mail: l.lanterna{at}virgilio.it

Objective: To determine the influence of the APOE genotype on functional and cognitive outcome and on the incidence and prognosis of clinical vasospasm (delayed ischemic neurologic deficit [DIND]) in noncomatose patients with aneurysmal subarachnoid hemorrhage (SAH).

Methods: The authors reviewed the data of patients admitted for SAH to the Neurosurgical Departments of the San Gerardo Hospital of Monza (January 1996 to December 2001) and the Ospedali Riuniti of Bergamo (January 2002 to September 2003). The authors considered only noncomatose patients and evaluated outcome by means of the Rankin Disability Index and the Mini-Mental State Examination at least 6 months after the SAH. Statistical analysis: Uni- and multivariate logistic regression.

Results: The authors included 101 patients. They found the {epsilon}4 allele in 26 patients (25.7%). The presence of the {epsilon}4 allele negatively affected the overall outcome (functional morbidity or cognitive morbidity, or both) (p = 0.0087) and, particularly, cognitive morbidity (p = 0.0028). Those with an {epsilon}4 allele had delayed ischemic neurologic deficit DINDs more frequently (p = 0.024) and, in the presence of DIND, they were more likely to show permanent neurologic deficits (p = 0.0051).

Conclusions: ApoE4 negatively affects cognitive morbidity and delayed ischemic neurologic deficit recovery. The presence of an {epsilon}4 allele increases the risk of delayed ischemic neurologic deficit.


Received August 12, 2004. Accepted in final form December 27, 2004.




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