Objective: Asleep deep brain stimulation (DBS) for Parkinson’s disease (PD) is being performed more frequently; however, motor outcomes and safety of asleep DBS have never been assessed in a prospective randomized trial. Methods: We conducted a prospective, randomized, noncomparative trial to assess the motor outcomes of asleep DBS. Leads were implanted in the subthalamic nucleus (STN) according to probabilistic stereotactic coordinates with a surgical robot under O-arm^© imaging guidance under either general anesthesia without microelectrode recordings (MER) (20 patients, asleep group) or local anesthesia with MER and clinical testing (9 patients, awake group). Results: The mean motor improvement rates on the Unified Parkinson’s Disease Rating Scale Part III (UPDRS-3) between OFF and ON stimulation without medication were 52.3% (95% CI: 45.4–59.2%) in the asleep group and 47.0% (95% CI: 23.8–70.2%) in the awake group, 6 months after surgery. Except for a subcutaneous hematoma, we did not observe any complications related to the surgery. Three patients (33%) in the awake group and 8 in the asleep group (40%) had at least one side effect potentially linked with neurostimulation. Conclusions: Owing to its randomized design, our study supports the hypothesis that motor outcomes after asleep STN-DBS in PD may be noninferior to the standard awake procedure.

Background: The control of the anatomic position of the active contacts is essential to understand the effects and adapt the settings of the neurostimulation. The localization is commonly assessed by a registration between the preoperative MRI and the postoperative CT scan. However, its accuracy depends on the quality of the registration algorithm and many software programs are available. Objective: To compare the localization of implanted deep brain stimulation (DBS) leads in the subthalamic nucleus (STN) between four registration devices. Methods: The preoperative stereotactic MRI was co-registered and fused with the 3-month postoperative CT scan in 27 patients implanted in the STN for Parkinson’s disease (53 leads). Localizations of the active contacts were calculated in the stereotactic frame space and compared between software programs. Results: The coordinates of the active contacts were different between software programs in the 3 axes (p < 0.001) with a mean vectorial error between the deepest contact locations of 1.17 mm (95% CI 1.09–1.25). Conclusion: We found a small but significant difference in the coordinates calculated on four different devices. These results have to be considered when performing studies comparing active contact locations or when following patients with an implanted DBS lead.

The incidence of newly diagnosed meningiomas, particularly those diagnosed incidentally, is continually increasing. The indication for treatment is empirical because, despite numerous studies, the natural history of these tumours remains difficult to describe and predict. This retrospective single-centre study included 294 consecutive patients with 333 meningiomas who underwent three or more brain imaging scans. Linear, exponential, power, and Gompertz models were constructed to derive volume–time curves, by using a mixed-effect approach. The most accurate model was used to analyse tumour growth and predictors of rapid growth. The Gompertz model provided the best results. Hierarchical clustering at the time of diagnosis and at the end of follow-up revealed at least three distinct groups, which can be described as pseudoexponential, linear, and slowing growth with respect to their parameters. Younger patients and smaller tumours were more frequent in the pseudo-exponential clusters. We found that the more “aggressive” the cluster, the higher the proportion of patients with grade II meningiomas and who have had a cranial radiotherapy. Over a mean observation period of 56.5 months, 21% of the tumours moved to a cluster with a lower growth rate, consistent with the Gompertz’s law. Meningiomas exhibit multiple growth phases, as described by the Gompertz model. The management of meningiomas should be discussed according to the growth phase, comorbidities, tumour location, size, and growth rate. Further research is needed to evaluate the associations between radiomics features and the growth phases of meningiomas. No funding.

Purpose: Multiple endocrine neoplasia type 1 (MEN1) is thought to increase the risk of meningioma and ependymoma. Thus, we aimed to describe the frequency, incidence, and specific clinical and histological features of central nervous system (CNS) tumors in the MEN1 population (except pituitary tumors). Experimental Design: The study population included patients harboring CNS tumors diagnosed with MEN1 syndrome after 1990 and followed up in the French MEN1 national cohort. The standardized incidence ratio (SIR) was calculated based on the French Gironde CNS Tumor Registry. Genomic analyses were performed on somatic DNA from seven CNS tumors, including meningiomas and ependymomas from patients with MEN1, and then on 50 sporadic meningiomas and ependymomas. Results: A total of 29 CNS tumors were found among the 1,498 symptomatic patients (2%; incidence = 47.4/100,000 person-years; SIR = 4.5), including 12 meningiomas (0.8%; incidence = 16.2/100,000; SIR = 2.5), 8 ependymomas (0.5%; incidence = 10.8/100,000; SIR = 17.6), 5 astrocytomas (0.3%; incidence = 6.7/100,000; SIR = 5.8), and 4 schwannomas (0.3%; incidence = 5.4/100,000; SIR = 12.7). Meningiomas in patients with MEN1 were benign, mostly meningothelial, with 11 years earlier onset compared with the sporadic population and an F/M ratio of 1/1. Spinal and cranial ependymomas were mostly classified as World Health Organization grade 2. A biallelic MEN1 inactivation was observed in 4/5 ependymomas and 1/2 meningiomas from patients with MEN1, whereas MEN1 deletion in one allele was present in 3/41 and 0/9 sporadic meningiomas and ependymomas, respectively. Conclusions: The incidence of each CNS tumor was higher in the MEN1 population than in the French general population. Meningiomas and ependymomas should be considered part of the MEN1 syndrome, but somatic molecular data are missing to conclude for astrocytomas and schwannomas.