CONTEXT: After primary infection, varicella zoster virus (VZV) becomes latent in ganglionic neurons. If immunity declines, VZV is reactivated and can spread to the dermatome depending from this ganglion and in some cases to the spinal cord. Myelopathy is rare and may develop in the absence of skin rash making the diagnosis very difficult. FINDINGS: From 1994 to 2014, we collected five observations of clinically and laboratory confirmed zoster myelopathy. The age of our patients ranged from 14 to 78. They did not have any significant past medical history. Four patients had a history of radicular rash. After 3 weeks (4-45 days), patients presented paraparesis, sensory loss, and sphincter dysfunction. Cerebrospinal fluid (CSF) analysis revealed an elevated protein level (5/5cases) and pleocytosis (2/5 cases). Spinal cord magnetic resonance imaging (MRI) demonstrated T2 hyper intense lesions with swelling and contrast enhancement. The diagnosis was supported by laboratory evidence, including the detection of VZV antibodies in the CSF. All patients received intravenous acyclovir and two patients received IV methylprednisolone. A marked improvement was observed in most of the patients within 2 months. CONCLUSION /CLINICAL RELEVANCE: Based on our patients and on previous reports, we highlight the possibility of the occurrence of VZV myelopathy in immunocompetent subjects. The diagnosis must be evoked even in the absence of typical skin lesions. In this case, spinal cord MRI and virological tests are useful tools for the diagnosis. We also emphasize on the importance of accurate diagnosis to enable the specific treatment and ameliorate the outcome.
CONTEXT: After primary infection, varicella zoster virus (VZV) becomes latent in ganglionic neurons. If immunity declines, VZV is reactivated and can spread to the dermatome depending from this ganglion and in some cases to the spinal cord. Myelopathy is rare and may develop in the absence of skin rash making the diagnosis very difficult. FINDINGS: From 1994 to 2014, we collected five observations of clinically and laboratory confirmed zoster myelopathy. The age of our patients ranged from 14 to 78. They did not have any significant past medical history. Four patients had a history of radicular rash. After 3 weeks (4-45 days), patients presented paraparesis, sensory loss, and sphincter dysfunction. Cerebrospinal fluid (CSF) analysis revealed an elevated protein level (5/5cases) and pleocytosis (2/5 cases). Spinal cord magnetic resonance imaging (MRI) demonstrated T2 hyper intense lesions with swelling and contrast enhancement. The diagnosis was supported by laboratory evidence, including the detection of VZV antibodies in the CSF. All patients received intravenous acyclovir and two patients received IV methylprednisolone. A marked improvement was observed in most of the patients within 2 months. CONCLUSION /CLINICAL RELEVANCE: Based on our patients and on previous reports, we highlight the possibility of the occurrence of VZV myelopathy in immunocompetent subjects. The diagnosis must be evoked even in the absence of typical skin lesions. In this case, spinal cord MRI and virological tests are useful tools for the diagnosis. We also emphasize on the importance of accurate diagnosis to enable the specific treatment and ameliorate the outcome.
Entities:
Keywords:
Acyclovir; Immunocompetent; Magnetic resonance imaging; Myelopathy; Varicella zoster virus
Authors: D H Gilden; B R Beinlich; E M Rubinstien; E Stommel; R Swenson; D Rubinstein; R Mahalingam Journal: Neurology Date: 1994-10 Impact factor: 9.910