Serum BDNF and cognitive dysfunction in SLE: findings from a cohort of 111 patients.

OBJECTIVE: The association between brain-derived neurotrophic factor (BDNF) and neuropsychiatric systemic lupus erythematosus (NPSLE) is controversial in the literature. Cognitive dysfunction (CD) is a common, underdiagnosed NPSLE manifestation, but its pathophysiology is unknown. Thus, we investigate serum BDNF as a potential biomarker of CD in a cohort of SLE patients. METHODS: We included 63 SLE patients, 48 NPSLE, and 57 age- and gender-matched controls (CON). All participants underwent neuropsychological assessment. Data on cardiovascular comorbidities, SLE disease activity index (SLEDAI), and Systemic Lupus International Collaborating Clinics damage index (SLICC-DI) were compiled. Multiple regression analyses evaluated predictors of serum BDNF levels. RESULTS: Serum BDNF levels were lower in SLE and NPSLE patients than in CON (SLE 800.4 ± 502.7 vs. NPSLE 779.7 ± 426.3 vs. CON 1,345.5 ng/mL ± 438.4; p < 0.001). In addition, hypertension (B: - 192.5, SE: 84.3, 95% CI: - 359.7 to - 25.3, p = 0.024) and SLICC-DI score (B: - 75.9, SE: 27.2, 95% CI: - 129.8 to - 22, p = 0.006) were predictors of serum BDNF levels in SLE. There was no relation between BDNF levels and CD. CONCLUSION: BDNF levels are lower in SLE patients than CON and inversely associated with hypertension and SLICC-DI scores. No association between BDNF levels and CD or NPSLE was observed in this cohort. These findings indicate that BDNF may be associated with overall burden in SLE rather than specific manifestations such as cognition impairment. Key Points • BDNF is associated with an overall burden in SLE rather than specific manifestations such as cognition dysfunction. • BDNF levels are reduced in patients with SLE, and higher SLICC-DI scores and hypertension are independent predictors of lower serum BDNF levels. • The cognitive dysfunction rate is elevated (46%) among Brazilian SLE patients.

Unusual Intracerebral Presentation of a Myxoid Neurofibroma.

BACKGROUND: Neurofibromas are benign nerve sheath tumors that usually affect peripheral nerves and are related to neurofibromatosis type 1; however, they have not been described as a cause of intraparenchymal brain tumor. CASE DESCRIPTION: We report a case of intracranial myxoid neurofibroma in a 19-year-old female patient manifested as an intense and progressive cephalea, followed by nausea, vomiting, photophobia, and phonophobia. Computed tomography and magnetic resonance imaging showed an extant, expansive left frontoparietal parafalcine/parasagittal tumor. Histopathologic examination determined S-100 protein and CD34 positivity, as well as sparse expression of Ki67 protein, and indicated Schwann cells with characteristic wavy nuclei and intraneural fibroblasts in a myxoid background. Together, these observations characterized the tumor as myxoid neurofibroma. The tumor was excised, and the patient recovered without deficits and with no signs of recurrence after 6 years of follow-up. CONCLUSIONS: This is a novel presentation of a myxoid neurofibroma. The tumorigenesis mechanisms are likely complex and possibly involve the differentiation of Schwann cells present in adrenergic autonomic nerves in the subarachnoid arterial branches or in trigeminal nerves present in the meningeal convexity.