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A 74-year-old woman was hospitalized due to dysuria, weakness and dysesthesia of the lower extremities. She was in an immunosuppressed state following the administration of methylprednisolone therapy for idiopathic interstitial pneumonia. Cerebrospinal fluid and blood cultures were negative, and no infectious biomarkers were found. A gadolinium (Gd)-enhanced T1-weighted image of magnetic resonance imaging (MRI) revealed disseminated nodular lesions along the spinal cord. We suspected a diagnosis of seronegative deep mycosis and initiated anti-fungal therapy with voriconazole, which subsequently alleviated all of the patient's symptoms and MRI findings. Therefore, the presence of Gd-enhanced disseminated nodules on spinal MRI may be a good marker of deep meningeal mycosis.

Viral encephalitis is still a life-threatening disease occurring at any age. It is critical to make a rapid and correct diagnosis for a better outcome of the disease. Accumulating evidence has suggested that MRI is a powerful tool for the detection of any lesion of the CNS caused by viral infections and helps to initiate the timely treatment. In this review, we summarize the current understanding of MRI findings of viral encephalitis, especially related to HSV, HIV, varicella zoster, Japanese encephalitis, John Cunningham, and influenza viruses. With these considerations, we learnt that the inclusion of diffusion-weighted image sequences on routine MRI examination would have a significant value in detecting the pathologic changes that occur following viral invasion of the CNS.

Background: The data on cerebrospinal fluid (CSF) levels of neurotrophins (NTs) in patients with meningoencephalitis are scarce, especially in adult patients. Methods: We measured CSF levels of NTs such as nerve growth factor (NGF), brain-derived neurotrophic factor, and neurotrophin-3 (NT-3) in adult patients with various meningitis (n = 10) and encephalitis (n = 10) in both acute phase and recovery phase and adult control subjects (n = 21) by the enzyme-linked immunosorbent assay for NTs. Results: Data show that NGF and NT-3 CSF levels were markedly elevated in the patient group in the acute phase compared with non-neurological controls (p < 0.001 and p < 0.05, respectively) and later returned to the levels of controls. Most intriguingly, we only recognized a significant correlation between NGF and NT-3 CSF levels in the patients in the acute phase. Conclusion: Such strong correlation of NGF and NT-3 CSF levels strongly suggests that in adult patients, some common regulatory mechanism(s) might be present among various kinds of NTs to cope with central nervous system infection. Copyright (C) 2011 S. Karger AG, Basel

Previous studies have shown that patients with the axonal form of Guillain-Barre syndrome (CBS) develop autoantibodies against GM1 ganglioside (GM1) Nerve growth factor (NGF) is essential for neuronal survival in vivo and its functional receptor is Trk-tyrosine kinase Here we examined the biological effects of sera from patients with the axonal form of GBS on the morphology and the phosphorylation state of Trk-tyrosine kinase in PC12 cells Furthermore we examined the effect of the sera on the integrity of membrane lipid rafts biochemically The data show that anti GM1 antibodies found in patients sera but not control sera inhibit NGF-induced Trk autophosphorylation Most intriguingly the autoantibodies alter the distribution of Trk in lipid rafts without shifting the distribution of a rafts marker protein These data strongly suggest that anti GM1 antibodies directly influence the integrity of the signaling platform lipid rafts implicating the importance of lipid rafts in the development of this disorder (C) 2010 Elsevier Inc All rights reserved

Clioquinol is considered to be a causative agent of subacute myelo-optico neuropathy (SMON), although the pathogenesis of SMON is yet to be elucidated. To investigate the mechanism of neurotoxicity of clioquinol, we used PC12 cell line and focused on nerve growth factor (NGF) signaling through Trk receptor, which is essential for survival and differentiation of neuronal cells. Clioquinol inhibited NGF-induced Trk autophosphorylation in a dose-dependent manner. This inhibitory activity was further confirmed by the data of the inhibition of NGF-induced mitogen-activated protein kinase (MAPK) phosphorylation, which is located in the down stream of NGF-Trk intracellular signaling pathway. Clioquinol also caused neurite retraction induced by NGF and cell death. NGF-stimulated (differentiated) cells were more vulnerable than naive cells. These results strongly suggest that choquinol may cause the perturbation of the intracellular survival pathway by inhibiting Trk-initiated signaling pathway. (C) 2009 Elsevier B.V. All rights reserved.

Acute autonomic, sensory and motor neuropathy (AASMN) is a rare peripheral nerve disorder characterized by prominent dysautonomia with somatic sensory and motor impairment. Dysautonomia in AASMN is intractable even with corticosteroid therapy or plasmapheresis. Here we report a case of AASMN with severe orthostatic hypotension. Although the effectiveness of corticosteroid was insufficient, high dose intravenous immunoglobulin therapy (IVIg) was effective for not only sensorimotor symptoms but also autonomic symptoms. This is the first case of AASMN showing favorable responses to IVIg treatment, suggesting that IVIg should be considered when corticosteroid therapy or plasmapheresis is ineffective or insufficient.