Transverse myelitis caused by varicella. Clin Neurol Neurosurg

Istanbul University, İstanbul, Istanbul, Turkey
Clinical Neurology and Neurosurgery (Impact Factor: 1.25). 01/2002; 103(4):260-1. DOI: 10.1016/S0303-8467(01)00166-4
Source: PubMed
    • "ATM is a condition of sudden weakness of lower extremities with sensory involvement caused due to inflammation of the spinal cord. Viral disease is responsible for 20-40% cases of ATM such as Epstein-Barr, Rubella, mumps, herpes simplex and VZV.[19] The interval between chicken pox and ATM is variable. "
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    ABSTRACT: Varicella zoster infection is known to cause neurological involvement. The infection is usually self-limiting and resolves without sequelae. We present a series of three cases with neurological presentations following chicken pox infection. The first case is a case of meningitis, cerebellitis and polyradiculopathy, the second is a florid case of acute infective demyelinating polyradiculoneuropathy (Guillian-Barré syndrome) in a middle-aged female and the third case is a young man in whom we diagnosed acute transverse myelitis. All these cases presented with distinct neurological diagnoses and the etiology was established on the basis of history and serological tests confirmatory for chicken pox. The cases responded differently to treatment and the patients were left with minimum disability.
    Journal of Neurosciences in Rural Practice 07/2010; 1(2):92-6. DOI:10.4103/0976-3147.71718
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    • "The CSF usually reveals a mild mononuclear pleocytosis with a normal or slightly elevated protein. Steroids are used to treat these patients [75], although some improve spontaneously [76]. "
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    ABSTRACT: Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.
    Neurologic Clinics 08/2008; 26(3):675-97, viii. DOI:10.1016/j.ncl.2008.03.011 · 1.61 Impact Factor
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    ABSTRACT: Acute transverse myelitis is a group of disorders characterized by focal inflammation of the spinal cord and resultant neural injury. Acute transverse myelitis may be an isolated entity or may occur in the context of multifocal or even multisystemic disease. It is clear that the pathological substrate--injury and dysfunction of neural cells within the spinal cord--may be caused by a variety of immunological mechanisms. For example, in acute transverse myelitis associated with systemic disease (i.e. systemic lupus erythematosus or sarcoidosis), a vasculitic or granulomatous process can often be identified. In idiopathic acute transverse myelitis, there is an intraparenchymal or perivascular cellular influx into the spinal cord, resulting in the breakdown of the blood-brain barrier and variable demyelination and neuronal injury. There are several critical questions that must be answered before we truly understand acute transverse myelitis: (1) What are the various triggers for the inflammatory process that induces neural injury in the spinal cord? (2) What are the cellular and humoral factors that induce this neural injury? and (3) Is there a way to modulate the inflammatory response in order to improve patient outcome? Although much remains to be elucidated about the causes of acute transverse myelitis, tantalizing clues as to the potential immunopathogenic mechanisms in acute transverse myelitis and related inflammatory disorders of the spinal cord have recently emerged. It is the purpose of this review to illustrate recent discoveries that shed light on this topic, relying when necessary on data from related diseases such as acute disseminated encephalomyelitis, Guillain-Barré syndrome and neuromyelitis optica. Developing a further understanding of how the immune system induces neural injury will depend upon confirmation and extension of these findings and will require multicenter collaborative efforts.
    Current Opinion in Neurology 07/2002; 15(3):339-47. DOI:10.1097/00019052-200206000-00019 · 5.73 Impact Factor
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