ABSTRACT
Idiopathic spinal cord herniation (ISCH), where a segment of the spinal cord has herniated through a ventral defect in the dura, is a rarely encountered cause of thoracic myelopathy. The purpose of our study was to increase the clinical awareness of this condition by presenting our experience with seven consecutive cases treated in our department since 2005. All the patients developed pronounced spastic paraparesis or Brown-Séquard syndrome for several years (mean, 4.7 years) prior to diagnosis. MRI was consistent with a transdural spinal cord herniation in the mid-thoracic region in all the cases. The patients underwent surgical reduction of the herniated spinal cord and closure of the dural defect using an artificial dural patch. At follow-up, three patients experienced considerable clinical improvement, one had slight improvement, one had transient improvement, and two were unchanged. Two of the four patients with sphincter dysfunction regained sphincter control. MRI showed realignment of the spinal cord in all the patients. ISCH is probably a more common cause of thoracic myelopathy than previously recognized. The patients usually develop progressive myelopathy for several years before the correct diagnosis is made. Early diagnosis is important in order to treat the patients before the myelopathy has become advanced.
ABSTRACT
OBJECTIVE AND DESIGN: Innate immune pro- and anti-inflammatory responses in patients with chronic subdural hematoma (CSDH) were investigated by measuring and comparing the systemic and subdural fluid levels of cytokines. MATERIALS AND METHOD: Cytokine values were analyzed in samples obtained during surgery of 56 adult patients who were operated on for unilateral CSDHs using a Multiplex antibody bead kit. RESULTS: There were significantly higher levels of the pro-inflammatory IL-2R (p = 0.004), IL-5 (p < 0.001), IL-6 (p < 0.001), and IL-7 (p < 0.001), and anti-inflammatory mediators IL-10 (p < 0.001) and IL-13 (p = 0.002) in CSDH fluid compared with systemic levels. The pro-inflammatory TNF-alpha (p < 0.001), IL-1beta (p < 0.001), IL-2 (p = 0.007) and IL-4 (p < 0.001) were significantly lower in hematoma fluid compared with systemic levels. The ratios between pro- versus anti-inflammatory cytokines were statistically significant higher in CSDH (7.8) compared with systemic levels (1.3). CONCLUSIONS: The innate immune responses occur both locally at the site of CSDH, as well as systematically in patients with CSDH. The local hyper-inflammatory and low anti-inflammatory responses exist simultaneously. The findings suggest poorly coordinated innate immune responses at the site of CSDH that may lead to propagating of local inflammatory process and basically contribute to formation and progression of CSDH.
Subject(s)
Cytokines/immunology , Hematoma, Subdural, Chronic/immunology , Adult , Aged , Aged, 80 and over , Cytokines/blood , Female , Hematoma, Subdural, Chronic/blood , Humans , Male , Middle Aged , Prospective StudiesABSTRACT
OBJECTIVE: The goal of this study was to investigate the chemokines CCL2, CXCL8, CXCL9 and CXCL10 as markers of the inflammatory responses in chronic subdural hematoma (CSDH). METHODS: Samples of peripheral venous blood and CSDH fluid (obtained during surgery) in 76 adult patients were prospectively analyzed. Chemokine values were assessed by a Multiplex antibody bead kit. RESULTS: We found significantly higher levels of chemokines CCL2, CXCL8, CXCL9 and CXCL10 in hematoma fluid compared with serum. CONCLUSIONS: Chemokines are elevated in the hematoma cavity of patients with CSDH. It is likely that these signaling modulators play an important role in promoting local inflammation. Furthermore, biological activity of CCL2 and CXCL8 may promote neovascularization within the outer CSDH membrane, and a compensatory angiostatic activity of CXCL9 and CXCL10 may contribute to repairing this disorder. This phenomenon was restricted to the hematoma site, and the systemic chemokine levels might not reflect local immune responses.
