Rinsho Shinkeigaku (Clinical Neurology)

Case Report

Cerebral infarction and intracranial aneurysm related to the reactivation of varicella zoster virus in a Japanese acquired immunodeficiency syndrome (AIDS) patient

Chiharu Yasuda, M.D.1), Kazumasa Okada, M.D.1), Norihiro Ohnari, M.D.2), Naoki Akamatsu, M.D.1) and Sadatoshi Tsuji, M.D.1)

1)Department of Neurology, School of Medicine, University of Occupational Environmental Health
2)Department of Radiology, School of Medicine, University of Occupational Environmental Health

A 35-years-old right-handed man admitted to our hospital with a worsening of dysarthria, left facial palsy and left hemiparesis for 2 days. Acquired immunodeficiency syndrome (AIDS) was diagnosed when he was 28 years old. At that time, he also was treated for syphilis. After highly active antiretroviral treatment (HAART) was introduced at the age of 35 years old, serum level of human immunodeficiency virus (HIV) was not detected, but the number of CD4+ T cells was still less than 200/μl. He had no risk factors of atherosclerosis including hypertension, diabetes and hyperlipidemia. He had neither coagulation abnormality nor autoimmune disease. Magnetic resonance imaging (MRI) showed acute ischemic infarction spreading from the right corona radiate to the right internal capsule without contrast enhancement. Stenosis and occlusion of intracranial arteries were not detected by MR angiography. Although argatroban and edaravone were administered, his neurological deficits were worsened to be difficult to walk independently. Cerebrospinal fluid (CSF) examination showed a mild mononuclear pleocytosis (16/μl). Oligoclonal band was positive. The titer of antivaricella zoster virus (VZV) IgG antibodies was increased, that indicated VZV reactivation in the central nervous system (CNS), although VZV DNA PCR was not detected. Therefore, acyclovir (750 mg/day for 2 weeks) and valaciclovir (3,000mg/day for 1 month) were administered in addition to stroke therapy. He recovered to be able to walk independently 2 month after the admission. Angiography uncovered a saccular aneurysm of 3 mm at the end of branch artery of right anterior cerebral artery, Heubner artery, 28 days after the admission. We speculated that VZV vasculopathy caused by VZV reactivation in CNS was involved in the pathomechanism of cerebral infarction rather than HIV vasculopathy in the case.
Full Text of this Article in Japanese PDF (2527K)

(CLINICA NEUROL, 53: 701|705, 2013)
key words: acquired immunodeficiency syndrome, cerebral infarction, intracranial aneurysm, varicella zoster virus

(Received: 31-Oct-12)