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Ther Adv Neurol Disord. 2010 September; 3(5): 323–325.
PMCID: PMC3002662

Acute stroke and cytomegalovirus encephalitis: a coincidence?

Michael Harzheim
Department of Neurology, Kamillus-Klinik, Hospitalstrasse 6, D-53567 Asbach, Germany
Bernd Sommer
Radiologische Gemeinschaftspraxis, Bad Honnef, Germany


Cytomegalovirus infection is usually asymptomatic in healthy and immunocompetent patients, but is associated with the pathological process of artherosclerosis [Yi et al. 2008] and with vasculitic processes [Lidar et al. 2009b; Tranos et al. 2008], i.e. giant cell arteritis [Wirtz et al. 2008] and Wegener’s granulomatosis [Lidar et al. 2009a], which may affect brain arteries and result in ischemic strokes.

Case report

We here report the case of a 41-year-old female patient presenting with a right-sided hemiparesis accompanied by global aphasia and dysphagia for at least 1 hour. In medical history she suffered from an ischemic stroke in the middle cerebral artery territorium on the right side and bibulosity with one epileptic seizure during alcohol deprivation. Cranial magnetic resonance imaging (MRI) showed a hyperintense signal in diffusion-weighted images and in the fluid-attenuated inversion recovery (FLAIR) sequence in the left parietal lobe (Figure 1A and C). T1-weighted images did not show any gadolinium enhancement (Figure 1E). The time-of-flight (TOF) magnetic resonance (MR) angiography showed a significant stenosis of the right middle cerebral artery as the only pathologic finding. Extracranial and transcranial duplexsonography revealed atherosclerosis of the carotids. Cerebrospinal fluid (CSF) yielded a mild lymphomonocytic pleocytosis of 102 cells/µl, a massive elevated protein content (3.955 g/l), oligoclonal bands by isoelectric focusing, an elevated IgG content (114.09 mg/dl), Cytomegalovirus IgG antibodies (5695 U, in the serum 30,441 U) and an elevated specific antibody quotient in the CSF (2.4) as well as positive detection of Borrelia burgdorferi-IgG and -IgM antibodies in the CSF and serum by enzyme-linked immunosorbent assay (ELISA) and Western blot, but CSF–serum antibody quotient was normal. Further microbiological investigations yielded negative polymerase chain reaction (PCR) for Listeria, herpes simplex virus (HSV) type I and II and IgG antibodies against rubella and measles in serum and CSF (CSF–serum quotient was normal). Electroencephalography showed a focal deceleration frontoparietal on the left side and laboratory investigations revealed a homozygote MTHFR mutation as a risk factor of stroke in the young. In addition to the prevention of a further stroke by the administration of acetylsalicylic acid we initiated an intravenous antiviral therapy using ganciclovir. Cranial MRI 2 weeks later revealed a small hyperintense area in diffusion-weighted images (Figure 1B) but surprisingly gadolinium-positive signal alteration in the left parietal lobe in T1-weighted images (Figure 1F) and cortical signal alteration in the FLAIR sequence (Figure 1D). To that time CSF showed cytomegalovirus IgG antibodies (7106 U, in the serum 35,398 U) and an increased specific antibody quotient in the CSF (4.2). In the clinical course the patient improved slowly.

Figure 1.
(A) Axial cranial magnetic resonance imaging (MRI), diffusion-weighted (day 3). (B) Axial cranial MRI, diffusion-weighted (day 17). (C) Coronar cranial MRI, fluid-attenuated inversion recovery (FLAIR) sequence (day 3). (D) Coronar cranial MRI, FLAIR sequence ...

In this case, both entities, acute ischemic stroke as well as focal encephalitis, occurred concomitantly. At first the clinical and MRI diagnosis of acute ischemic stroke was made and, in the course of the disease, CSF findings with increasing cytomegalovirus antibody titer and specific antibody quotient supported the MRI aspect of a focal encephalitis.


Cytomegalovirus is well known to cause cortical dysplasia and atrophy in congenital infections, but may also cause MRI signal abnormalities in the optic nerves, chiasm, and tracts [Pershing et al. 2009], may occur in a leukodystrophic aspect [Tati et al. 2005], and is reported to cause diffuse white matter hyperintensity [Miller et al. 1997]. Moreover nonherpetic encephalitis may present with unilateral temporal cortical lesions in cranial MRI [Suzuki et al. 1999].

This case raises the question of whether the juvenile stroke occurred independent of the cytomegalovirus encephalitis, which is explainable as an opportunistic infection in an immunoincompetent alcoholic, or was caused by cytomegalovirus vasculitis of the brain arteries. Whereas cytomegalovirus antibodies in immune complexes are reported as an independent strong stroke risk factor, other investigations failed to show any significant predictive value for stroke in patients with cytomegalovirus infection [Oliveras et al. 2003; Tarnacka et al. 2002]. In conclusion, in strokes in the young, CSF examination should always be performed and in the case of inflammatory findings cranial MRI should be repeated within a few weeks. Whether homozygote MTHFR mutation is an independent risk factor of stroke is not clear in general and especially in strokes in the young without any other cardiovascular risk factors.


This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of interest statement

The authors declare that there is no conflict of interest.


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Articles from Therapeutic Advances in Neurological Disorders are provided here courtesy of SAGE Publications