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|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 327-329
Multifocal cns vasculopathy due to reactivation of latent varicella: A potentially reversible complication following radiofrequency ablation for trigeminal neuralgia
Rajesh S Reddy, Alok Ranjan, Rahul Lath
Department of Neurosurgery, Apollo Institute of Neurosciences, Apollo Health City, Jubilee Hills, Hyderabad, Andhra Pradesh, India
|Date of Submission||17-Feb-2014|
|Date of Decision||24-Feb-2014|
|Date of Acceptance||03-Jun-2014|
|Date of Web Publication||18-Jul-2014|
Rajesh S Reddy
Department of Neurosurgery, Apollo Institute of Neurosciences, Apollo Health City, Jubilee Hills, Hyderabad, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Reddy RS, Ranjan A, Lath R. Multifocal cns vasculopathy due to reactivation of latent varicella: A potentially reversible complication following radiofrequency ablation for trigeminal neuralgia. Neurol India 2014;62:327-9
|How to cite this URL:|
Reddy RS, Ranjan A, Lath R. Multifocal cns vasculopathy due to reactivation of latent varicella: A potentially reversible complication following radiofrequency ablation for trigeminal neuralgia. Neurol India [serial online] 2014 [cited 2021 Jan 16];62:327-9. Available from: https://www.neurologyindia.com/text.asp?2014/62/3/327/137017
Radiofrequency ablation is one of the established treatment modalities for medically refractory trigeminal neuralgia. Although bacterial meningitis, cranial nerve deficits, caroticocavernous fistula, and anesthesia dolorosa are some of the dreaded complications, multifocal central nervous system (CNS) vasculopathy due to reactivation of latent varicella zoster presenting as encephalopathy has never been reported before.  The authors discuss the first case of its kind.
A 53-year-old male was offered radiofrequency (RF) ablation for medically refractory trigeminal neuralgia involving the left maxillary and mandibular divisions. A temperature of 60˚C was used for 60 seconds for each of the two RF lesions. The patient had immediate relief of pain following the ablative procedure. He was brought to the emergency department 10 days later with history of fever with chills, confusion, and speech difficulty of 3-days duration. Upon examination, he was febrile, confused with difficulty in naming, reading, writing, and calculation. No meningeal signs, cranial nerve deficits, or limb weakness was noted. Brain magnetic resonance imaging (MRI) revealed diffuse hypertintensities predominantly in the left middle cerebral artery territory in T2, fluid attenuation inversion recovery (FLAIR), diffusion weighted and apparent diffusion coefficient sequences [Figure 1]a. The lesions were non-enhancing. A history of chicken pox in childhood was elicited. Cerebrospinal fluid (CSF) analysis revealed high leucocyte count with lymphocytic predominance. Varicella zoster virus (VZV) antibody levels in CSF and polymerase chain reaction (PCR) analysis was not performed. A possibility of bacterial/viral meningoencephalitis was considered and patient was started on parenteral cefoperazone-sulbactum and acyclovir; the antibacterial agent was stopped after obtaining negative CSF bacterial cultures. A course of steroids was given for 5 days to prevent the complications of meningoencephalitis. Intravenous acyclovir was given for 21 days. Neurological recovery was noticed during the course of treatment. Diffusion MRI changes had disappeared [Figure 1]b and the patient recovered without residual deficits in 8 months.
|Figure 1: (a) Magnetic resonance imaging (MRI) brain showing hyperintensities on diffusion weighted images (left) as well as on ADC maps (right) in the left parietal and perisylvian areas (arrows) indicating the areas of pathological process, (b) Magnetic resonance imaging (MRI) brain diffusion weighted sequences showing disappearance of intensity changes observed in fi gure 1a following treatment with Acyclovir|
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Primary infection with VZV, a human neurotropic alpha-herpesvirus usually occurs in children and causes varicella (chickenpox). The virus may become latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, VZV can reactivate to cause zoster (shingles) as well as vasculopathy, myelopathy, retinal necrosis, and cerebellitis. Many of these complications can occur without rash. In animal models, and most likely in humans as well, reactivation of various herpesviruses can be induced by local trauma (e.g. in the form of surgery), hyperthermia, systemic stress, decline in cell-mediated immunity to VZV (old age, immunosuppression as in organ-transplant recipients or patients with cancer or acquired immunodeficiency syndrome, AIDS), mental tension, fatigue, and exposure to bright light. 
VZV vasculopathy results from productive virus infection in large or small cerebral arteries, or both. Patients present with headache, fever, mental status changes, transient ischemic attacks, and focal deficits (stroke). CSF examination reveals modest pleocytosis (usually less than 100 cells) with mononuclear cell preponderance. Many patients also have red blood cells in their CSF. Concentrations of CSF protein are commonly increased, whereas those of glucose are normal. OligoclonalIg G, which is antibody directed against VZV, may be present.  MRI findings include unifocal or multifocal lesions involving the gray-white matter junction and white matter more often than gray matter. Most lesions are ischemic, but hemorrhagic lesions also occur. The lesions are hyperintense on T2/FLAIR sequences with some lesions enhancing on contrast administration, indicating breakdown of the blood-brain barrier.  When a clinical diagnosis of VZV vasculopathy is suspected, virologic analysis to detect amplifiable VZV deoxyribonucleic acid (DNA) or anti-VZV IgG antibodies or both in the CSF confirms the diagnosis.  Rapid diagnosis of VZV vasculopathy is important because the mortality without treatment is 25%, whereas treatment with intravenous acyclovir, even after neurologic disease has been present for months, can be curative. 
Our patient also did not have dermatomal rash typical of varicella zoster. Although, we do not have serological evidence of VZV in our patient, previous history of exposure to varicella, MRI features, modest CSF mononuclear pleocytosis, as well as clinical and radiological response to antiviral treatment favor the diagnosis of VZV vasculopathy. The anatomical pathway for the transaxonal spread of virus is provided from studies which have shown that the middle cerebral artery receives its sensory innervation from the ipsilateral trigeminal ganglia.  In our patient, local hyperthermia and breach in the arachnoid of Meckel's cave created during RF lesioning could have favored the reactivation and spread of virus along the middle cerebral vessels.
We emphasize the importance of obtaining a past history of varicella infection in patients undergoing foramen ovale puncture for RF lesioning, glycerol rhizotomy, percutaneous balloon compression, sphenoidal electrode placement for electroencephalography (EEG) and biopsy. Acyclovir prophylaxis during the periprocedural period may prevent reactivation and spread of virus in such patients. However, no recommendations for prophylactic dose and duration of therapy exist in this scenario.
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