RESUMO
Diabetic peripheral neuropathy (DPN) is a frequent complication of type 2 diabetes mellitus (DM) and may involve small and large peripheral nerve fibers. Recent evidence suggests a role of cytokines in DPN. The paper is aimed at exploring whether the serum concentration of cytokines is associated with small and large nerve fiber function and with neuropathic pain (NP). We recruited a group of 32 type 2 DM patients who underwent serum cytokines (TNF-α, IL-2, IL-4, IL-6, and IL-10) dosage as well as electrodiagnostic and quantitative sensory testing (QST) assessment to explore damage to large and small nerve fibers. Raised serum levels of IL-6 and IL-10 correlated with markers of large nerve fiber sensory and motor axonal damage. Raised IL-10 serum level was associated with signs of motor nerve demyelination. No differences were found in pain characteristics and electrodiagnostic and QST markers of small nerve fiber function in relation to cytokines serum levels. IL-6 and IL-10 serum levels were associated with large nerve fiber damage but not to small fibers function or NP. IL-6 and IL-10 cytokines might play a role in the pathogenesis of nerve fiber damage or represent a compensatory or neuroprotective mechanism.
Assuntos
Citocinas/sangue , Diabetes Mellitus Tipo 2/sangue , Neuropatias Diabéticas/sangue , Nervo Mediano/fisiopatologia , Idoso , Diabetes Mellitus Tipo 2/fisiopatologia , Neuropatias Diabéticas/fisiopatologia , Eletrodiagnóstico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fibras NervosasRESUMO
Association between the site of brain injury and poststroke spasticity is poorly understood. The present study investigated whether lesion analysis could document brain regions associated with the development of severe upper limb poststroke spasticity. A retrospective analysis was conducted on 39 chronic stroke patients. Spasticity was assessed at the affected upper limb with the modified Ashworth scale (shoulder, elbow, wrist, and fingers). Brain lesions were traced from magnetic resonance imaging performed within the first 7 days after stroke and region of interest images were generated. The association between severe upper limb spasticity (modified Ashworth scale ≥ 2) and lesion location was determined with the voxel-based lesion-symptom mapping method implemented in MRIcro software. Colored maps representing the z statistics were generated and overlaid onto the automated anatomical labeling and the Johns Hopkins University white matter templates provided with MRIcron. Thalamic nuclei were identified with the Talairach Daemon software. Injuries to the insula, the thalamus, the basal ganglia, and white matter tracts (internal capsule, corona radiata, external capsule, and superior longitudinal fasciculus) were significantly associated with severe upper limb poststroke spasticity. Further advances in our understanding of the neural correlates of spasticity may lead to early targeted rehabilitation when key regions are damaged.