Acute hydrocephalus secondary to herpes simplex type II meningitis

Acute hydrocephalus secondary to herpes simplex type II meningitis

Case Reports / Journal of Clinical Neuroscience 15 (2008) 1157–1159 1157 Acute hydrocephalus secondary to herpes simplex type II meningitis Peter A...

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Case Reports / Journal of Clinical Neuroscience 15 (2008) 1157–1159

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Acute hydrocephalus secondary to herpes simplex type II meningitis Peter A. Heppner *, Patrick M. Schweder, Stephen J. Monteith, Andrew J.J. Law Department of Neurosurgery, Auckland City Hospital, Grafton Road, Auckland, New Zealand Received 15 May 2007; accepted 1 July 2007

Abstract A 34-year-old woman presented with a rapid onset of meningitic symptoms. Cerebrospinal fluid (CSF) from a lumbar puncture revealed a leucocytosis with a preponderance of monocytes, elevated protein and reduced glucose. Herpes simplex virus (HSV) type II was subsequently confirmed by polymerase chain reaction (PCR) of CSF. The patient’s level of consciousness deteriorated and a CT scan revealed hydrocephalus. The patient required placement of an external ventricular drain for 5 days; however, she made a full recovery without specific antiviral therapy. This is the first reported case of hydrocephalus secondary to isolated HSV type II meningitis. Ó 2007 Elsevier Ltd. All rights reserved. Keywords: External ventricular drain; Herpes simplex type II; Hydrocephalus; Meningitis

1. Introduction Meningitis is a relatively common cause of hydrocephalus with previous infection accounting for 7.6% of cases in one pediatric series.1 However, most of these cases involve bacterial or tuberculous pathogens. We describe the first recorded case of a patient with herpes simplex virus (HSV) type II meningitis causing acute hydrocephalus, and its successful management. 2. Case report A 34-year-old woman presented initially to her regional hospital with headache, neck stiffness and photophobia. She had no significant medical history and on admission her Glasgow Coma Score (CGS) was 15 with no focal neurological deficits. A diagnostic lumbar puncture was performed without the opening pressure being assessed. Analysis of the cerebrospinal fluid (CSF) revealed no organisms, and a white cell count (WCC) of 738  106/L (56% monocytes, 20% lymphocytes, 8% eosinophils and 17% polymorphs). Protein level was 5.48 g/L (normal range 0.15–0.45 g/L) and glucose was 1.0 mmol/L (normal range 2.8–4.4 mmol/L). There was no subsequent growth on bacterial culture. While on the ward, the patient deteriorated to a GCS of 10. An urgent CT scan demonstrated hydrocephalus with relatively large lateral ventricles and a small fourth ventricle (Fig. 1). The patient was intubated and transferred to the regional neurosurgical service.

*

Corresponding author. Tel./fax: +64 9 524 8216. E-mail address: [email protected] (P.A. Heppner).

A right frontal external ventricular drain was placed releasing clear CSF under high pressure. A repeat sample of the CSF confirmed an elevated WCC of 244  106/L of which 48% were lymphocytes and 48% were monocytes. Again there was no growth on bacterial culture. An MRI showed no evidence of encephalitis, parenchymal abnormality or venous sinus thrombosis and the cerebral aqueduct appeared patent (Fig. 2). The patient was then weaned from sedation and extubated the following day before being transferred to the neurosurgical ward. Cerebrospinal fluid taken in both the referring hospital and from the external ventricular drain tested positive for HSV type II DNA via nucleic acid amplification. CSF polymerase chain reaction (PCR) for meningococcus and tuberculosis were negative as was serum serology for HSV. On the advice of the infectious diseases physicians the patient was not treated with antiviral therapy as she was clinically improving and the disease was considered self-limiting. The external ventricular drain was progressively raised and was removed 5 days after insertion. The patient was transferred back to the referring hospital, neurologically intact, the following day. 3. Discussion Herpes simplex viruses predominantly target the peripheral nervous system, displaying an ability to latently infect sensory ganglia and reactivate at an interval to cause recurrent symptoms. Less characteristically, the virus has the ability to infect the central nervous system (CNS) and can result in a number of neurological manifestations, including encephalitis, myelitis, polyradiculopathy and

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Fig. 1. Axial CT scan of the head demonstrating dilatation of the lateral and third ventricles. A relatively small fourth ventricle is seen.

Fig. 2. Midline sagital T1-weighted MRI post-insertion of an external ventricular drain, demonstrating a patent cerebral aqueduct.

meningitis.2 These conditions are usually related to virus reactivation in adults rather than primary infection. Primary encephalitis usually occurs in children.2 In the adult population, patients whose CSF is positive for HSV type I on PCR tend have an encephalitic process (89%), while HSV II is more likely to cause meningitis.3 This meningitis can be sporadic or recurrent. HSV I encephalitis carries a significant risk of mortality and neuropsychiatric morbidity, and is the most common sporadic fatal CNS viral infection in the Western world.2 HSV II meningitis on the other hand tends to be a relatively benign and self-limiting condition. This proved to be the case for our patient once her hydrocephalus was relieved in that she made a rapid and complete recovery without the administration of antiviral therapy.

Viral etiologies for hydrocephalus have been well described. A recent case report identified 16 cases of hydrocephalus related to mumps, meningitis and meningoencephalitis. Of interest, the hydrocephalus developed anywhere from 1 day to 19 years after the initial infection.4 Similarly, Mazzella et al. reported on a fatal case of congenital varicella zoster infection, which showed evidence of triventricular noncommunicating hydrocephalus on post mortem.5 In both situations, hydrocephalus resulted from obstruction at the level of the aqueduct of Sylvius, and the postulated mechanism was of ependymitis subsequently causing obstruction with a possible role for gliosis. Herpes simplex virus-induced hydrocephalus has been described in the paediatric setting. Tyagi et al.6 reported an infant who developed obstructive hydrocephalus secondary to HSV type I encephalitis contracted perinatally. The CT scan of their patient showed evidence of temporal lobe calcification and suggested stenosis of the cerebral aqueduct. At the time of surgery, vesicles were seen on the floor of the third ventricle.5 What distinguishes our case from this one is the absence of an encephalitic process either clinically or on MRI, the lack of aqueduct obstruction on MRI, the different causative agent (type II vs. type I), and the age of the patient. A large number of viruses have been reported to cause hydrocephalus in animal models. A relevant example utilised intracerebral inoculation of HSV type II in mice that were subsequently treated with the anti-viral agent 2’-fluoro-5-methylarabinosyluracil (FMAU). Evidence of lateral and third ventricular dilatation was found while the cerebral aqueduct remained largely unaffected and the fourth ventricle remained normal. Histological evidence for encephalitis and ependymitis was noted and the degree of parenchymal destruction correlated with the degree of ventricular dilatation, implicating an ‘‘ex-vacuo” pathogenesis.7 Arguing against this pathogenesis for our patient is

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the rapid return to normal size of the ventricles following placement of an external ventricular drain. HSV type I has also demonstrated the ability to cause hydrocephalus in a mouse model.8 An additional theory as to the pathogenesis of hydrocephalus in this case relates to the unusually high protein level in the CSF (5.48 g/L). Hydrocephalus has been noted in other conditions such as Guillian-Barre syndrome associated with an elevated CSF protein.9 Postulated mechanisms of hydrocephalus formation have included increased CSF osmotic pressure and obstruction of CSF absorption. 4. Conclusion We describe the first case of acute hydrocephalus caused by isolated HSV Type II meningitis. A short period of external ventricular drainage without resorting to antiviral therapy appears to provide adequate treatment for this condition as evidenced by the rapid and complete neurological recovery.

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References 1. Amacher AL, Wellington J. Infantile hydrocephalus: Long term results of surgical therapy. Childs Brain 1984;11:217–29. 2. Schmutzhard E. Viral infections of the CNS with special emphasis on herpes simplex infections. J Neurol 2001;248:469–77. 3. O’Sullivan CE, Aksamit AJ, Harrington JR, et al. Clinical spectrum and laboratory characteristics associated with detection of herpes simplex virus DNA in cerebrospinal fluid. Mayo Clin Proc 2003;78:1347–52. 4. Giuseppe C, Spennato P, Ruggiero C, et al. Aqueductal stenosis 9 years after mumps meningoencephalitis: treatment by endoscopic third ventriculostomy. Childs Nerv Syst 2004;20:61–4. 5. Mazzella M, Arioni C, Bellini C, et al. Severe hydrocephalus associated with congenital varicella syndrome. CMAJ 2003;168:561–3. 6. Tyagi A, Chumas P, Ferrie C. Obstructive hydrocephalus following herpes simplex virus type 1 encephalitis treated by repeated third ventriculostomy. Pediatr Neurosurg 2001;34:244–6. 7. Schinazi RF, Yao X. Hydrocephalus induction in mice infected with herpes simplex virus type 2 after antiviral treatment. Antiviral Res 1995;28:291–302. 8. Hayashi K, Iwasaki Y, Yanagi K. Herpes simplex virus type I induced hydrocephalus in mice. J Virol 1986;57:942–51. 9. Liu CH, Kao CD, Chen JT, et al. Hydrocephalus associated with Guillian-Barre syndrome. J Clin Neurosci 2006;13:866–9.

doi:10.1016/j.jocn.2007.07.001

Epidermoid cysts of the velum interpositum Biji Bahuleyan a, Roy T. Daniel a, Geeta Chacko b, Ari G. Chacko a,* a

Section of Neurosurgery, Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu 632004, India b Section of Neuropathology, Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India Received 13 March 2007; accepted 22 June 2007

Abstract The cistern of the velum interpositum is a space located between the corpus callosum dorsally and the roof of the third ventricle ventrally. Lesions located within the velum interpositum are rare and include meningiomas, pilocytic astrocytomas, atypical teratoid/rhabdoid tumors and arachnoid cysts. Epidermoid cysts in this location have not been reported previously. We report the clinical and radiological features of two patients with epidermoid cysts located in the velum interpositum. The patients presented with gait difficulty and features of raised intracranial pressure and magnetic resonance imaging demonstrated large tumors in the velum interpositum with intensities suggestive of epidermoid cysts. There was ventral displacement of the internal cerebral veins and dorsal displacement of the corpus callosum in keeping with a mass in the velum interpositum. Tumors of the third ventricle displace the internal cerebral veins dorsally. A transcallosal approach was used in both patients to effectively excise the tumors. Ó 2007 Elsevier Ltd. All rights reserved. Keywords: Epidermoid cyst; Magnetic resonance imaging; Third ventricle; Velum interpositum

1. Case reports *

Corresponding author. Tel.: +91 416 2222102; fax: +91 416 2232103/ 2232035. E-mail address: [email protected] (A.G. Chacko).

Two men, aged 24 and 29 years, presented with headaches suggestive of raised intracranial pressure and gait ataxia. In the first patient, MRI of the brain with gadolinium