Introduction: Hyperthyroid Graves' disease (GD) is a B-cell-mediated condition caused by TSH receptor antibodies (TRAb), which decline when GD remits. Anti-CD20 monoclonal antibody rituximab (RTX) induces transient B-cell depletion that may potentially modify the active inflammatory phase of thyroid-associated ophthalmopathy (TAO). Methods: Nine patients with GD, (seven with active TAO, two with mild lid signs) were studied. The trial was only approved as an open pilot study; thus we compared the effect of RTX therapy to that of i.v. glucocorticoids (IVGC) in 20 consecutive patients. Patients were treated with RTX (1000 mg i.v. twice at 2-week interval) or with IVGC (500 mg i.v. for 16 weeks). TAO was assessed by the clinical activity score (CAS) and severity was classified using NOSPECS (No signs or symptoms; Only signs (lid); Soft tissue involvement; Proptosis, Extraocular muscle involvement; Corneal involvement; Sight loss). Thyroid function and lymphocyte count were measured by standardized methods. Results: All patients attained peripheral B-cell depletion with the first RTX infusion. Minor side effects were reported in three patients. Thyroid function was not affected by RTX therapy and hyperthyroid patients required therapy with methimazole. After RTX, the changes in the levels of thyroglobulin antibodies, thyroperoxidase antibodies and TRAb were neither significant nor correlated with CD20C depletion (PZNS). CAS values before RTX were 4.7G0.5 and decreased to 1.8G0.8 at the end of follow-up (P!0.0001) and more significantly compared with IVGC (P!0.05). Proptosis decreased significantly after RTX both in patients with active TAO (ANOVA; P!0.0001) and those with lid signs (ANOVA; P!0.003). The degree of inflammation (class 2) decreased significantly in response to RTX (ANOVA; P!0.001). Relapse of active TAO was not observed in patients treated with RTX, but occurred in 10% of those treated with IVGC, who also experienced adverse effects more frequently (45 vs 33% of patients). Conclusions: RTX positively affects the clinical course of TAO, independently of either thyroid function or circulating antithyroid antibodies, including TRAb. If our findings are confirmed in large controlled studies, RTX may represent a useful therapeutic tool in patients with active TAO.
Cerebral magnetic resonance imaging was performed on 63 patients with chronic primary headache (28 with migraine with and without aura, 35 with tension-type headache). Fifty-four headache-free individuals of the same age range were used as controls. The headache sufferers showed an incidence of focal white matter abnormalities on T2-weighted magnetic resonance imaging significantly higher than the age-matched control group (33.3% vs 7.4%). The incidence of white matter abnormalities did not correlate with age (except for patients older than 60 years), sex, headache history, headache status, or ergotamine consumption. Migraine (with and without aura) and tension-type headache patients had similar prevalence of white matter abnormalities (32.1% vs 34.3%). The lesions were predominantly distributed in the frontal region, independent of the side of usual aura or headache. Our findings indicate that both migraine and tension-type headache may be associated with early pathologic changes in the brain and may share, at least in part, common pathogenic pathways.
Objective: To assess the connection between amyloid pathology and white matter (WM) macro-and micro-structural damage in demented patients compared with controls.Methods: Eighty-five participants were recruited: 65 with newly diagnosed Alzheimer's disease (AD), non-AD dementia or mild cognitive impairment (MCI), and 20 age-and sex-matched heatlhy controls. β-amyloid 1-42 (Aβ) levels were determined in cerebrospinal fluid (CSF) samples from all patients and 5 controls. Among patients, 42had pathological CSF Aβ levels (Aβ+), while 23 had normal CSF Aβ levels (Aβ-). All participants underwent neurological examination, neuropsychological testing and brain magnetic resonance imaging (MRI). We used T2-weighted scans to quantify white matter (WM) lesion loads (LL), and diffusion weighted images (DWI) to assess their microstructural substrate. Non-parametric statistical tests were used for between-group comparisons and multiple regression analyses. Results:We found an increased WM-LL in Aβ(+) compared to both, healthy controls (p=0.003) and Aβ(-) patients (p=0.02). Interestingly, CSF Aβ concentration was the best predictor patients' WM-LL (r=-0.30, p<0.05) when using age as a covariate. Lesion apparent diffusion coefficient (ADC) value was higher in all patients than in controls (p=0.0001), and correlated with WM-LL (r=0.41, p=0.001). In Aβ(+), WM-LL correlated with WM microstructural damage in the left peritrigonal WM (p<0.0001).Conclusions: WM damage is crucial in Alzheimer's disease (AD) pathogenesis. The correlation between CSF Aβ levels and WM-LL suggests a direct link between amyloid pathology and WM macro-and microstructural damage.
Sudden sensorineural hearing loss is defined as acute hearing loss of the sensorineural type of at least 30 dB over 3 contiguous frequencies that occurs within a 72-hour period. Although many different causative factors have been proposed, sudden sensorineural hearing loss is still considered "idiopathic" in 71%-85% of cases, and treatments are empiric, not based on etiology. MR imaging implemented with a 3D FLAIR sequence has provided new insights into the etiology of sudden sensorineural hearing loss. Herein, we review the current management trends for patients with sudden sensorineural hearing loss, from the initial clinical diagnosis to therapeutic strategies and diagnostic work-up. We focused primarily on MR imaging assessment and discuss the relevance that MR imaging findings might have for patient management, pointing out different perspectives for future clinical research.
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