RESUMO
Glioblastoma (GBM) is regarded as an aggressive brain tumor that rarely develops extracranial metastases. Despite well-investigated molecular alterations in GBM, there is a limited understanding of these associated with the metastatic potential. We herein present a case report of a 43-year-old woman with frontal GBM with primitive neuronal component who underwent gross total resection followed by chemoradiation. Five months after surgery, the patient was diagnosed with an intraspinal GBM metastasis. Next-generation sequencing analysis of both the primary and metastatic GBM tissues was performed using the Illumina TruSight Tumor 170 assay. The number of single nucleotide variants observed in the metastatic sample was more than two times higher. Mutations in TP53, PTEN, and RB1 found in the primary and metastatic tissue samples indicated the mesenchymal molecular GBM subtype. Among others, there were two inactivating mutations (Arg1026Ile, Trp1831Ter) detected in the NF1 gene, two novel NOTCH3 variants of unknown significance predicted to be damaging (Pro1505Thr, Cys1099Tyr), one novel ARID1A variant of unknown significance (Arg1046Ser), and one gene fusion of unknown significance, EIF2B5-KIF5B, in the metastatic sample. Based on the literature evidence, the alterations of NF1, NOTCH3, and ARID1A could explain, at least in part, the acquired invasiveness and metastatic potential in this particular GBM case.
RESUMO
High-grade gliomas are primary brain tumors with poor prognosis, despite surgical treatment followed by radiotherapy and concomitant chemotherapy. We present two cases of long-term survival in patients treated for high-grade glioma and concomitant prolonged bacterial wound infection. The first patient treated for glioblastoma IDH-wildtype had been without disease progression for 61 months from the first resected recurrence. Despite incomplete chemotherapy-induced myelosuppression in the second patient with anaplastic astrocytoma IDH-mutant, she died without disease relapse after 14 years from the diagnosis due to other comorbidities. We assume that the documented prolonged survival could be related to the bacterial infection.
RESUMO
Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition associated with the development of early brain injury (EBI) and delayed cerebral ischemia (DCI). Pharmacological treatment of vasospasm following aSAH currently mainly comprises nimodipine administration. In the past few years, many drugs that can potentially benefit cases of subarachnoid hemorrhage have become available. The objective of this review is to critically assess the effects of non-steroidal anti-inflammatory drugs (NSAIDs) following aSAH. A systematic literature review was conducted following PRISMA guidelines. The search was aimed at studies addressing aSAH and NSAIDs during the 2010 to 2019 period, and it yielded 13 articles. Following the application of search criteria, they were divided into two groups, one containing 6 clinical articles and the other containing 7 experimental articles on animal models of aSAH. Inflammatory cerebral changes after aneurysm rupture contribute to the development of EBI, DCI and cerebral vasospasm. It appears that NSAIDs (especially coxibs) are even more effective in reducing vasospasm than nimodipine. Other beneficial effects of NSAIDs include reduction in mortality, improved functional outcome and increased hypoaggregability. However, despite these positive effects, there is only one randomized, double-blind, placebo-controlled trial showing a tendency towards a better outcome with lower incidence of vasospasm or mortality in patients following aSAH.
Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Isquemia Encefálica/tratamento farmacológico , Hemorragia Subaracnóidea/tratamento farmacológico , Vasoespasmo Intracraniano/tratamento farmacológico , Isquemia Encefálica/etiologia , Isquemia Encefálica/fisiopatologia , Método Duplo-Cego , Humanos , Nimodipina/uso terapêutico , Ensaios Clínicos Controlados Aleatórios como Assunto/métodos , Hemorragia Subaracnóidea/complicações , Hemorragia Subaracnóidea/fisiopatologia , Vasoespasmo Intracraniano/etiologia , Vasoespasmo Intracraniano/fisiopatologiaRESUMO
Background/Aims/Objectives: To verify the transfer of evoked potentials through anastomosis of an experimentally created micturition reflex arc and to detect said potentials directly on the detrusor and sphincter of rabbit urinary bladder. METHODS: During 2013-2015, 17 rabbits were operated upon and measurement followed during reoperation 3-16 months later. Suitable ventral spinal roots were electrophysiologically detected following laminectomy, and a somatic-central nervous system-autonomic micturition reflex arc was created. During reoperation, the ventral root was stimulated above and below the anastomosis, the evoked potentials on the bladder detrusor and sphincter were measured, and intravesical pressure was monitored. RESULTS: With stimulation above the anastomosis, 9 animals (53%) displayed a urinary bladder detrusor response and 7 (41%) a sphincter response. Four rabbits (24%) had elevated intravesical pressure. During the control stimulation below the anastomosis, we detected a detrusor response in 7 animals (41%), a sphincter response in 5 (29%), and elevated pressure in 4 (24%). Neither induction of micturition nor decrease in external sphincter activity occurred. CONCLUSIONS: Creation of a somatic-CNS-autonomic reflex arc is technically possible. However reflex activity transferring through the anastomosis is detectable on the detrusor only in some individuals, and is unable to induce a micturition reflex with or without accompanying detrusor-sphincter dyssynergia.