(1) Background: Glioblastoma is the most frequent and lethal primary tumor of the central nervous system. Through many years, research has brought various advances in glioblastoma treatment. At this time, glioblastoma management is based on maximal safe surgical resection, radiotherapy, and chemotherapy with temozolomide. Recently, bevacizumab has been added to the treatment arsenal for the recurrent scenario. Nevertheless, patients with glioblastoma still have a poor prognosis. Therefore, many efforts are being made in different clinical research areas to find a new alternative to improve overall survival, free-progression survival, and life quality in glioblastoma patients. (2) Methods: Our objective is to recap the actual state-of-the-art in glioblastoma treatment, resume the actual research and future perspectives on immunotherapy, as well as the new synthetic molecules and natural compounds that represent potential future therapies at preclinical stages. (3) Conclusions: Despite the great efforts in therapeutic research, glioblastoma management has suffered minimal changes, and the prognosis remains poor. Combined therapeutic strategies and delivery methods, including immunotherapy, synthetic molecules, natural compounds, and glioblastoma stem cell inhibition, may potentiate the standard of care therapy and represent the next step in glioblastoma management research.

Hemifacial spasm is characterized by unilateral, paroxysmal, and involuntary contractions. It is more common in women on the left side. Its evolution is progressive, and it rarely improves without treatment. Microvascular decompressions (N = 226) were performed in 194 Hispanic patients (May 1992-May 2011). Outcomes were evaluated on a 4-point scale: Excellent (complete remission); good (1-2 spasms/day); bad (>2 spasms/day); and recurrence (relapse after initial excellent/good response). Most patients were female (n = 123); 71 were male. Mean (±SD) age was 49.4 (±11.7) years; age at onset, 43.9 (±11.9) years; time to surgery, 5.7 (±4.7) years. The left side was affected in 114 patients. Typical syndrome occurred in 177 (91.2%); atypical in 17 (8.8%). Findings were primarily vascular compression (n = 185 patients): Anterior inferior cerebellar artery (n = 147), posterior inferior cerebellar artery (n = 12), basilar artery (n = 10), superior cerebellar artery (n = 8), and 2 vessels (n = 8); 9 had no compression. Postsurgical results were primarily excellent (79.9% [n = 155]; good, 4.6% [n = 9]; bad, 15.5% [n = 30]), with recurrence in 21 (10.8%) at mean 51-month (range, 1-133 months) follow-up. Complications included transient hearing loss and facial palsy. The anterior inferior cerebellar artery is involved in most cases of hemifacial spasm. Failure to improve postsurgically after 1 week warrants reoperation. Sex, side, and onset are unrelated to treatment response. Microvascular decompression is the preferred treatment. It is minimally invasive, nondestructive, and achieves the best long-term results, with minor morbidity. To our knowledge, this series is the largest to date on a Hispanic population.

Corticotroph cells give rise to aggressive and rare pituitary neoplasms comprising ACTH-producing adenomas resulting in Cushing disease (CD), clinically silent ACTH adenomas (SCA), Crooke cell adenomas (CCA) and ACTH-producing carcinomas (CA). The molecular pathogenesis of these tumors is still poorly understood. To better understand the genomic landscape of all the lesions of the corticotroph lineage, we sequenced the whole exome of three SCA, one CCA, four ACTH-secreting PA causing CD, one corticotrophinoma occurring in a CD patient who developed Nelson syndrome after adrenalectomy and one patient with an ACTH-producing CA. The ACTH-producing CA was the lesion with the highest number of single nucleotide variants (SNV) in genes such as USP8, TP53, AURKA, EGFR, HSD3B1 and CDKN1A. The USP8 variant was found only in the ACTH-CA and in the corticotrophinoma occurring in a patient with Nelson syndrome. In CCA, SNV in TP53, EGFR, HSD3B1 and CDKN1A SNV were present. HSD3B1 and CDKN1A SNVs were present in all three SCA, whereas in two of these tumors SNV in TP53, AURKA and EGFR were found. None of the analyzed tumors showed SNV in USP48, BRAF, BRG1 or CABLES1. The amplification of 17q12 was found in all tumors, except for the ACTH-producing carcinoma. The four clinically functioning ACTH adenomas and the ACTH-CA shared the amplification of 10q11.22 and showed more copy-number variation (CNV) gains and single-nucleotide variations than the nonfunctioning tumors.

Background: Although the essential components of pain pathways have been identified, a thorough comprehension of the interactions necessary for creating focused treatments is still lacking. Such include more standardised methods for measuring pain in clinical and preclinical studies and more representative study populations. Objective: This review describes the essential neuroanatomy and neurophysiology of pain nociception and its relation with currently available neuroimaging methods focused on health professionals responsible for treating pain. Methods: Conduct a PubMed search of pain pathways using pain-related search terms, selecting the most relevant and updated information. Results: Current reviews of pain highlight the importance of their study in different areas from the cellular level, pain types, neuronal plasticity, ascending, descending, and integration pathways to their clinical evaluation and neuroimaging. Advanced neuroimaging techniques such as fMRI, PET, and MEG are used to better understand the neural mechanisms underlying pain processing and identify potential targets for pain therapy. Conclusions: The study of pain pathways and neuroimaging methods allows physicians to evaluate and facilitate decision-making related to the pathologies that cause chronic pain. Some identifiable issues include a better understanding of the relationship between pain and mental health, developing more effective interventions for chronic pain's psychological and emotional aspects, and better integrating data from different neuroimaging modalities for the clinical efficacy of new pain therapies.

Background: Glioblastoma (GB) represents the most aggressive type of glioma with a poor prognosis despite the therapies used. As of today, data availability for therapeutic and prognosis experiences is limited. The cornerstone for this study is to create a framework overview of Mexico´s experience throughout 17 years of research. Methods: Retrospective analysis from 2000 to 2017 including patients with a histological diagnosis of GB was performed. Data were collected from the ABC Medical Center and the Neurology and Neurosurgery National Institute. Results: One hundred and thirty-seven patients were included with a mean age of 54 years. Histological diagnosis was made in all patients, of which 58.1% had a total resection, 31.6% had a partial resection, and 10.3% of them underwent biopsy. In all cases, patients received treatment under the following conditions: 10 patients were treated exclusively with stereotactic radiotherapy (RT). In 55 patients, a combination of RT and TMZ was used, the other 40 patients received RT plus CBP. Eighteen patients RT added to nitrosourea medication and lastly, 14 patients received a combination of RT/TMZ and Bevacizumab, a monoclonal antibody that inhibits the formation of blood vessels (BVZ). The progression-free survival (PFS) and overall survival (OS) were higher in the RT/TMZ/BVZ group (16.5 to 22.9 months) and the RT/TMZ group (11 to 17 months), the prognostic parameters included: Isocitrate dehydrogenase 1 mutation (IDH1), usage of BVZ and TMZ in the PLS and OS, considering as well, age range (<70 years) as a favorable prognostic factor. Conclusions: GB represents the most frequent intracranial neoplasia. Combined fractionated stereotactic RT added to Temozolomide and Bevacizumab received in our population reports favorable and superior results compared to the ones described in the literature. Further studies are necessary to know the biological behavior of our population.