Neurosurgical Review最新文献

Brain tumors involving the primary motor cortex can disrupt corticospinal physiology through mass effect, tract involvement, and maladaptive plasticity. Preoperative transcranial magnetic stimulation (TMS) provides a direct measure of cortical excitability and correlates with intraoperative mapping, but the TMS parameters most relevant to postoperative motor outcomes remain uncertain. This study evaluated whether preoperative TMS excitability measures differ from healthy norms and whether they show signals potentially useful for predicting postoperative motor deficits. We conducted a retrospective, single-center observational study of consecutive adults (18-70 years) with glioblastoma adjacent to the precentral gyrus who underwent standardized preoperative TMS motor mapping (N = 67). Key excitability measures included resting motor threshold, motor-evoked potential (MEP) amplitudes, relative paired-pulse responses, and indices of intracortical inhibition and facilitation. Patient data from the tumor-affected hemisphere were compared with a healthy Brazilian reference cohort using robust, age-stratified median tests and categorical classification based on published normative ranges. Associations with postoperative motor deficits were explored using correlation screening followed by multivariable logistic modeling. Postoperative motor deficits occurred in approximately one-third of patients. Compared with healthy controls, the tumor-affected hemisphere demonstrated consistent alterations in paired-pulse responses and intracortical excitability. Using categorical normative ranges, patients were significantly less likely to show low excitability responses for short- and long-interval paired-pulse measures and for intracortical inhibition and facilitation, indicating a shift toward higher or dysregulated excitability. Age-stratified analyses showed the most pronounced deviations in patients younger than 50 years, particularly for MEP amplitudes and paired-pulse indices. Preoperative TMS mapping revealed that brain tumors adjacent to the motor cortex are associated with selective disturbances in intracortical and paired-pulse excitability, while global corticospinal output measures remain largely preserved. The consistent alterations in intracortical inhibition and facilitation indicate that tumor-related motor dysfunction primarily affects intracortical circuitry rather than overall corticospinal integrity. Age-stratified analyses further suggest that these excitability changes are more pronounced in younger patients, underscoring age-dependent differences in motor network vulnerability. Collectively, these findings support quantitative TMS-derived intracortical measures as physiologically informative biomarkers that extend beyond spatial motor mapping and hold promise for refining surgical risk stratification. Prospective studies linking these markers to postoperative motor outcomes are needed to establish their clinical utility.

To compare intraoperative findings and surgical outcomes in temporal lobe resections in patients with mesial temporal sclerosis in the language dominant hemisphere performed under general (GA) versus asleep-awake-asleep (AAA) anesthesia modalities. Single-center retrospective case-control study involving 31 adults who had clinical/imaging/neurophysiology concordant evidence of mesial temporal lobe epilepsy in the language dominant hemisphere submitted to temporal lobe epilepsy surgery. GA was used in 20 patients and AAA in 11 patients. Presurgical characteristics of the patients, intraoperative hemodynamic and physiological findings or complications and postoperative outcomes including ILAE scale scores at least 1 year of follow-up were analyzed using descriptive statistics and independent t-tests, Fisher's exact test, and χ² tests to identify differences between the groups. During the surgery, there were no notable differences between the groups in terms of hemodynamic parameters, arterial blood gas measurements, or bleeding. However, the surgery length was longer in AAA group. Postoperative outcomes, including hospital stay duration, complication rates, and follow-up periods, were also comparable without significant differences. Neurological deficits were minimal in both groups, with no statistically significant differences between them. Most patients achieved positive results based on the ILAE classification in both groups, with most experiencing either no seizures or rare, non-disabling seizures. AAA showed comparable results to general anesthesia, with no intraoperative complications or postoperative negative outcomes. However, due to the limited sample size, further evidence is needed to confirm its benefits in epilepsy surgery involving eloquent areas over GA.

Inflammation and angiogenesis are critical processes contributing to the progression of chronic subdural hematoma (CSDH). Tissue plasminogen activator (tPA), which is highly abundant in CSDH effusion, has been implicated not only in hematoma liquefaction but also in progressive hematoma enlargement. Notably, tPA expression has also been reported in intracranial neoplasms, where it contributes to the development of peritumoral edema, suggesting roles beyond fibrinolysis. We therefore hypothesized that tPA exerts non-fibrinolytic effects in the pathophysiology of CSDH. Twenty CSDH fluid specimens and eight outer membrane samples were analyzed. The concentrations of tPA and matrix metalloproteinase-9 (MMP-9) were markedly higher in CSDH fluid than in cerebrospinal fluid. Immunoblotting confirmed the presence of low-density lipoprotein receptor-related protein-1 (LRP-1), phosphorylated Mek (p-Mek), Mek, phosphorylated Erk (p-Erk), Erk, MMP-9, caspase-3, and cleaved caspase-3 in the outer membrane. Immunohistochemical analyses revealed that LRP-1, p-Erk, Erk, and MMP-9 were predominantly localized to vascular endothelial cells, whereas LRP-1, caspase-3, and cleaved caspase-3 were mainly expressed in fibroblasts within the outer membrane. Moreover, exposure of fibroblasts to CSDH effusion significantly attenuated staurosporine-induced cleaved caspase-3 expression in vitro. Collectively, these findings suggest that elevated tPA in CSDH effusion is associated with activation of LRP-1-dependent Mek-Erk signaling and increased MMP-9 expression, and may also be linked to anti-apoptotic responses in fibroblasts. These pathology-associated signaling features extend beyond the classical fibrinolytic role of tPA and may have therapeutic implications for refractory CSDH, warranting further functional and interventional studies.