P 189. The extent of perifocal edema in function associated motor fibers correlates to the primary motor deficit in patients with M1-adjacent intracerebral tumors. A volumetric analysis of presurgically acquired data based on MRI, FET-PET and navigated TMS on primary motor functions

Question Many patients with brain tumors adjacent to the primary motor (M1) region initially present with transient or permanent motor deficits. Factors like compression by tumor mass, tumor infiltration, as well as the extent of the perifocal edema might contribute to the motor deficit. In order to assess the relevance of these factors, we analyzed the spatial relationship between M1 cortical representation assessed with navigated transcranial magnetic stimulation (nTMS) and the anatomical and metabolic extension of tumors in the M1 region in patients prior to surgery. Methods To date, 21 patients with M1-adjacent tumors (glioblastoma ( n  = 14), anaplastic astrocytoma ( n  = 1), carcinoma metastasis ( n  = 4), anaplastic ependymoma ( n  = 1), lymphoma ( n  = 1)) underwent an anatomical MRI protocol including a T2-weighted sequence, a gadolinium-contrast-enhanced sequence (GCE) and diffused tensor imaging as well as 18F-fluoroethyl-L-tyrosine (FET) PET for presurgical planning. Cortical M1 representations for the hand, foot and tongue were assessed by nTMS within 7 days. “Functional” fiber tracking of the corticospinal tract (CST) consisted of the following processing steps: (1) setting the seed points defined by the coordinate revealing the highest motor evoked potential (MEP) when stimulated by nTMS at 110% of the resting motor threshold and the surrounding 5 mm, according to the registration and E-field calculation mismatch and (2) a seed volume at the midbrain level. Total volumes and intersection volumes of the CST and the anatomically defined areas were expressed in cm 3 ±standard deviation (SD). Results 15 out of the 21 patients had a primary motor deficit recorded in either the upper or lower limb, the facial muscles or initially presented with a hemiparesis, 6 patients had not developed any deficit prior to or at admission to surgery. Neither the GCE ( p  = .96) nor the FET ( p  = .45) tumor volume statistically differed between the group of patients with a motor deficit (GCE: 19.7 ± 17.2 cm 3 ; FET: 9.6 ± 5.3 cm 3 , n  = 15) compared to one without a motor deficit (GCE: 12.1 ± 16.8 cm 3 ; 6.4 ± 6.5 cm 3 , n  = 6). The mean perifocal edema volume based on the T2-weighted MRI data was slightly greater in the motor deficit group (64.2 ± 38.1 cm 3 ) than in the group of patients without any motor deficit (43.4 ± 28.6 cm 3 ) but did again not pass the statistical threshold ( p  = .37). However, the mean relative volume of functional fibers intersected by the T2-weighted edema volume was statistically greater in the primary motor deficit group (16.1 ± 13.1%) than in the one without motor deficits (0.1 ± 0.0%). By contrast, the mean relative volume of cortical M1 representation intersected by the edematous area did not statistically differ between the two groups ( p  = .09). Nor the mean relative volume of functional fibers or functional motor cortex intersected by GCE or PET tumor volumes were statistically different between the two groups. Likewise, neither the mean absolute volume of supratentorial functional fibers nor of the cortical M1 representation volumes differed between the two groups. Conclusion The study implicates that neither direct tumor infiltration of the M1 region or the CST nor the tumor volume nor the extension of perifocal edema in total may be the main causes for the primary motor deficit of brain tumor patients at initial presentation. In contrast, the extent of the perifocal edema affecting CST fibers seems to be responsible for motor deficits prior to surgery.