Accuracy of Electrode Insertion Using Frame-Based With Robot Guidance Technique in Stereotactic Electroencephalography: Supine Versus Lateral Position.

BACKGROUND: Placing the patient in lateral position is an option for implantation of stereoelectroencephalography (SEEG) electrodes that have a posterior entry point. Previous studies reported the accuracy of SEEG electrodes but not specifically in relation to position. The aim of this study was to analyze accuracy of SEEG electrodes by position. METHODS: Entry point and target accuracy of electrodes implanted in lateral position were compared with electrodes implanted in supine position using a frame-based with robot guidance technique. Subgroup analysis was performed for insular versus noninsular electrodes. RESULTS: Analysis included 23 consecutive patients (11 in lateral position) with 294 electrodes. The entry point error was similar between lateral (median 1.3 mm [interquartile range 0.8-1.9]) and supine (1.2 mm [0.8-1.7]; P = 0.360) position. Target accuracy was better in lateral (1.8 mm [1.3-2.7]) than supine (2.9 mm [2.0-4.4]; P < 0.001) position. For noninsular electrodes, the median entry point error in lateral and supine position was 1.3 mm (0.8-1.9) and 1.2 mm (0.8-1.7; P = 0.43), respectively. The accuracy was better in lateral position (median 1.7 mm [1.2-2.6]) compared with supine position (2.9 mm [2.0-4.4]; P < 0.001). The accuracy of insular electrodes was similar in both positions for entry point (lateral: median radial error 1.4 mm, [0.7-1.9]; supine: 1.1 mm [0.6-1.8]; P = 0.833) and target (lateral: median three-dimensional error 2.3 mm [1.6-3.2]; supine: 2.9 mm [2.4-4.5]; P = 0.07). CONCLUSIONS: SEEG leads implanted in lateral position exhibit an accuracy and safety profile in accordance with previous studies. In this cohort, target error was smaller in the lateral position, particularly in noninsular electrodes.

Elevated expression of granulocyte-macrophage colony-stimulating factor receptor in multiple sclerosis lesions.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease that disproportionately affects young adults, leading to disability and high costs to society. Infiltration of T cells and monocytes into the central nervous system (CNS) is critical for disease initiation and progression. However, despite a great deal of effort the molecular mechanisms by which immune cells initiate and perpetuate CNS damage in MS have not yet been elucidated. In experimental autoimmune encephalomyelitis (EAE), an animal model of MS, granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by pathogenic Th1 and Th17 cells is critical for the recruitment of monocytes into the CNS during the initial stage of disease. We and others have recently shown that, compared with healthy individuals, MS patients have greater numbers of CD4+ and CD8+ T cells that produce GM-CSF. Here, we describe the expression of GM-CSF and its receptor, GM-CSFR, in normal brain and MS lesions. Our data show that in acute and chronic MS lesions, microglia and astrocytes have upregulated expression of GM-CSFR; in addition, we show that GM-CSF-associated molecules are also upregulated in MS lesions. These findings further strengthen the argument that GM-CSF signaling contributes to MS pathogenesis.