FDG-PET and MRI in the Evolution of New-Onset Refractory Status Epilepticus.

BACKGROUND AND PURPOSE: New-onset refractory status epilepticus is a clinical condition characterized by acute and prolonged pharmacoresistant seizures without a pre-existing relevant neurologic disorder, prior epilepsy, or clear structural, toxic, or metabolic cause. New-onset refractory status epilepticus is often associated with antineuronal antibodies and may respond to early immunosuppressive therapy, reflecting an inflammatory element of the condition. FDG-PET is a useful diagnostic tool in inflammatory and noninflammatory encephalitis. We report here FDG-PET findings in new-onset refractory status epilepticus and their correlation to disease activity, other imaging findings, and outcomes. MATERIALS AND METHODS: Twelve patients who met the criteria for new-onset refractory status epilepticus and who had FDG-PET and MR imaging scans and electroencephalography at a single academic medical center between 2008 and 2017 were retrospectively identified. Images were independently reviewed by 2 radiologists specialized in nuclear imaging. Clinical characteristics and outcome measures were collected through chart review. RESULTS: Twelve patients underwent 21 FDG-PET scans and 50 MR imaging scans. Nine (75%) patients were positive for autoantibodies. All patients had identifiable abnormalities on the initial FDG-PET in the form of hypermetabolism (83%) and/or hypometabolism (42%). Eight (67%) had medial temporal involvement. All patients (n = 3) with N-methyl-D-aspartic acid receptor antibodies had profound bilateral occipital hypometabolism. Initial MR imaging findings were normal in 6 (50%) patients. Most patients had some degree of persistent hyper- (73%) or hypometabolism (45%) after immunosuppressive therapy. FDG-PET hypometabolism was predictive of poor outcome (mRS 4-6) at hospital discharge (P = .028). CONCLUSIONS: Both FDG-PET hypometabolism and hypermetabolism are seen in the setting of new-onset refractory status epilepticus and may represent markers of disease activity.

Brain metabolic abnormalities associated with developmental venous anomalies.

BACKGROUND AND PURPOSE: Developmental venous anomalies are the most common intracranial vascular malformation and are typically regarded as inconsequential, especially when small. While there are data regarding the prevalence of MR imaging findings associated with developmental venous anomalies, FDG-PET findings have not been well-characterized. MATERIALS AND METHODS: Clinical information systems were used to retrospectively identify patients with developmental venous anomalies depicted on MR imaging examinations who had also undergone FDG-PET. Both the MR imaging and FDG-PET scans were analyzed to characterize the developmental venous anomalies and associated findings on the structural and functional scans. Qualitative and quantitative assessments were performed, including evaluation of the size of the developmental venous anomaly, associated MR imaging findings, and characterization of the FDG uptake in the region of the developmental venous anomaly. RESULTS: Twenty-five developmental venous anomalies in 22 patients were identified that had been characterized with both MR imaging and FDG-PET, of which 76% (19/25) were associated with significant metabolic abnormality in the adjacent brain parenchyma, most commonly hypometabolism. Patients with moderate and severe hypometabolism were significantly older (moderate: mean age, 65 ± 7.4 years, P = .001; severe: mean age, 61 ± 8.9 years, P = .008) than patients with developmental venous aberrancies that did not have abnormal metabolic activity (none: mean age, 29 ± 14 years). CONCLUSIONS: Most (more than three-quarters) developmental venous anomalies in our series of 25 cases were associated with metabolic abnormality in the adjacent brain parenchyma, often in the absence of any other structural abnormality. Consequently, we suggest that developmental venous anomalies may be better regarded as developmental venous aberrancies.

Safety and effectiveness of sacroplasty: a large single-center experience.

BACKGROUND AND PURPOSE: Sacral insufficiency fractures are a common cause of severe low back pain and immobilization in patients with osteoporosis or cancer. Current practice guideline recommendations range from analgesia and physical therapy to resection with surgical fixation. We sought to assess the safety and effectiveness of sacroplasty, an emerging minimally invasive treatment. MATERIALS AND METHODS: We performed a retrospective review of institutional databases for percutaneous sacroplasty performed between January 2004 and September 2013. Demographic and procedural data and pre- and posttreatment Visual Analog Scale, Functional Mobility Scale, and Analgesic Scale scores were reviewed. Overall response was rated by using a 4-point scale (1, complete resolution of pain; 2, improvement of pain; 3, no change; 4, worsened pain) assessed at short-term follow-up. RESULTS: Fifty-three patients were included; most (83%) were female. Fracture etiology was cancer-related (55%), osteoporotic insufficiency (30%), and minor trauma (15%). No major complication or procedure-related morbidity occurred. There were statistically significant decreases in the Visual Analog Scale (P < .001), Functional Mobility Scale (P < .001), and Analgesic Scale scores (P < .01) in 27 patients with recorded data: pretreatment Visual Analog Scale (median [interquartile range], 9.0 [8.0-10.0]); Functional Mobility Scale, 3.0 (2.0-3.0); and Analgesic Scale scores, 3.0 (3.0-4.0) were reduced to 3.0 (0.0-5.8), 1.0 (0.25-2.8), and 3.0 (2.0-3.8) posttreatment. When we used the overall 4-point score at a mean of 27 days, 93% (n = 45) reported complete resolution or improvement in overall pain. CONCLUSIONS: In this single-center cohort, sacroplasty was a safe and effective procedure. There were significant short-term gains in pain relief, increased mobility, and decreased dependence on pain medication.

Crystal structure of two CD46 domains reveals an extended measles virus-binding surface.

Measles virus is a paramyxovirus which, like other members of the family such as respiratory syncytial virus, is a major cause of morbidity and mortality worldwide. The cell surface receptor for measles virus in humans is CD46, a complement cofactor. We report here the crystal structure at 3.1 A resolution of the measles virus-binding fragment of CD46. The structure reveals the architecture and spatial arrangement of two glycosylated short consensus repeats with a pronounced interdomain bend and some flexibility at the domain interface. Amino acids involved in measles virus binding define a large, glycan-free surface that extends from the top of the first to the bottom of the second repeat. The extended virus-binding surface of CD46 differs strikingly from those reported for the human virus receptor proteins CD4 and intercellular cell adhesion molecule-1 (ICAM-1), suggesting that the CD46 structure utilizes a novel mode of virus recognition. A highly hydrophobic and protruding loop at the base of the first repeat bears a critical virus-binding residue, thereby defining an important recognition epitope. Molecules that mimic the conformation of this loop potentially could be effective anti-viral agents by preventing binding of measles virus to CD46.