Neurologic Complications of Varicella-Zoster Virus Infection

Varicella-zoster virus (VZV) causes a diverse spectrum of neurologic complications: aseptic meningitis, encephalitis, cerebral infarction associated with granulomatous vasculitis, myelitis, and cranial polyneuropathy. These VZV-associated central nervous system (CNS) diseases usually result from reactivation of latent infection in immunosuppressive conditions, such as old age, diabetes mellitus, cancer, human immunodeficiency virus (HIV) infection, and the use of immunosuppressive drugs. However, they also occur in immunocompetent subjects. Since VZV antigen or DNA is often detected in the cerebrospinal fluid of these patients, it is thought that reactivated VZV reaches the central nervous system by direct spread from latently infected sensory ganglia. Analysis of cerebrospinal fluid by PCR is important for the diagnosis of VZV-associated CNS diseases particularly in the absence of exanthema/herpes zoster. Clinicians should be aware of the neurologic complications of VZV infection, because early acyclovir therapy is necessary for these disorders

Increased Intrathecal Chemokine Receptor CCR2 Expression in Multiple Sclerosis

Expression of CCR2, CXCR3 and CCR4 on CD4+ T or CD8+ T cells in blood and cerebrospinal fluid (CSF) for multiple sclerosis (MS) was measured by 3-color flow cytometry, and compared to blood from healthy controls and CSF from patients with other inflammatory neurological diseases (INDs). CD4+CXCR3+/CD4+CCR4+ ratio (representing Th1/Th2 balance) was higher in both CSF and blood of MS patients than those of IND patients or healthy controls. Percentage of CCR2-positive T cells was significantly higher in CSF from MS patients. Increased CCR2 expression on T cells in CSF and Th1/Th2 imbalance may reflect the pathological processes involved in MS

Visual field defects of optic neuritis in neuromyelitis optica compared with multiple sclerosis

<p>Abstract</p> <p>Background</p> <p>Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and the spinal cord, and is possibly mediated by an immune mechanism distinct from that of multiple sclerosis (MS). Central scotoma is recognized as a characteristic visual field defect pattern of optic neuritis (ON), however, the differing pathogenic mechanisms of NMO and MS may result in different patterns of visual field defects for ON.</p> <p>Methods</p> <p>Medical records of 15 patients with NMO and 20 patients with MS having ON were retrospectively analyzed. A thorough systemic and neurological examination was performed for evaluating ON. The total number of relapses of ON and visual fields was investigated. Visual fields were obtained by Goldmann perimeter with each ON relapse.</p> <p>Results</p> <p>All MS patients experienced central scotoma, with 90% of them showing central scotoma with every ON relapse. However, 53% of NMO patients showed central scotoma with every ON relapse (p = 0.022), and the remaining 47% of patients experienced non-central scotoma (altitudinal, quadrant, three quadrant, hemianopia, and bitemporal hemianopia). Thirteen percent of NMO patients did not experience central scotoma during their disease course. Altitudinal hemianopia was the most frequent non-central scotoma pattern in NMO.</p> <p>Conclusions</p> <p>NMO patients showed higher incidence of non-central scotoma than MS, and altitudinal hemianopia may be characteristic of ON occurring in NMO. As altitudinal hemianopia is highly characteristic of ischemic optic neuropathy, we suggest that an ischemic mechanism mediated by anti-aquaporin-4 antibody may play a role in ON in NMO patients.</p