Accuracy of unenhanced CT in the diagnosis of cerebral venous sinus thrombosis.

OBJECTIVES: To evaluate the diagnostic performance of unenhanced brain CT (NECT) in identifying patients with cerebral venous sinus thrombosis (CVT). METHODS: Forty-eight consecutive patients with CVT and 48 healthy controls were included in our retrospective study. All patients underwent NECT and CT/MR angiography within 24 h. Two radiologists independently evaluated NECT images for the presence of sinus hyperdensity; discrepancies were solved by consensus. Sinus attenuation was measured in seven sites. The obtained data were compared with the presence of CVT at CT/MR angiography and with patients' hematocrit. RESULTS: Interobserver agreement in sinus hyperdensity detection was good (k = 0.64). The presence of sinus hyperdensity at NECT enabled to detect patients with CVT with 81% sensitivity, 77% specificity, 78% PPV, and 80% NPV. Mean attenuation was significantly higher in sinus segments involved by CVT than in patent ones (62.4 ± 10 versus 55.6 ± 6 HU, p < 0.0001). ROC analysis showed that a cutoff value of 63 HU enables to detect patients with CVT with 52% sensitivity and 88% specificity. Hematocrit values were significantly correlated with patent sinus segments attenuation (r = 0.19). CONCLUSIONS: The presence of sinus hyperdensity at NECT enables to detect patients with CVT with 81% sensitivity and 77% specificity. A sinus attenuation cutoff value of 63 HU can be used in order to increase specificity, but lowering sensitivity.

Treatment of inflammatory and paraproteinemic neuropathies.

Acquired demyelinating and inflammatory neuropathies encompass a number of acute and chronic autoimmune conditions characterized by variable degrees of clinical involvement. These disorders, including Guillain-Barre syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy (MMN), and paraprotein-associated neuropathy, have an overall annual incidence of 2-4/100,000 worldwide and are potentially treatable. Over the last few years, several investigations have helped clarify the pathogenesis of immune neuropathies and the definition of molecular targets involved in these diseases, thus providing firmer grounds for treatment with classical immunosuppressive drugs and new biological agents. In GBS and related variants, which are characterized by cellular inflammation and alterations of the blood-nerve barrier, randomized clinical trials show that plasma exchange (PE) and intravenous immunoglobulin (IVIg) are equally effective as disease-modifying treatments, although IVIg has been adopted as the favourite treatment in most centres. In CIDP, controlled clinical trials have established the efficacy of oral prednisone, PE and IVIg, with intermittent IVIg treatment or corticosteroids being usually preferred. Adding azathioprine can help keep lower the required dose of prednisone, while other immunosuppressive agents, such as cyclophosphamide and cyclosporin A may have side effects, limiting their use to selected cases. Currently, the efficacy of interferon beta and alfa is under evaluation. Controlled trials support the view that IVIg is the treatment of choice in MMN. Patients resistant to IVIg administration may benefit of treatments which deplete B cells, such as cyclophosphamide and rituximab. Demyelinating neuropathies associated with circulating paraproteins are clinically heterogeneous, depending on the reactivity and type of the monoclonal (M) protein. In many cases, neuropathies associated with IgM M proteins are not treated because of their slow progression. In patients with a disabling or rapid progression, small trials have shown short-term benefits from IVIg or PE. Recently, fludarabine and rituximab have been reported as beneficial in selected cases.