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The ventriculoperitoneal (VP) shunt is one of the most common surgical procedures in neurosurgery, frequently resulting in malfunctions. Shunt malfunctions, which can include mechanical failure, obstruction, infection, or disconnection, occur in a significant percentage of patients, often necessitating multiple revisions. These revisions can lead to increased healthcare costs due to additional surgeries or treatments. Therefore, addressing the economic impacts of these revisions is crucial. Our report presents a cost-effective approach to shunt revisions, demonstrated through a case study of an 82-year-old woman with hydrocephalus. Although initially treated with a VP shunt, she required a revision after six years due to shunt malfunction. Through comprehensive preoperative and intraoperative evaluations, including a shuntogram with iodine contrast and meticulous examination, we identified the cause of malfunction as a connective tissue sac blocking the peritoneal catheter. The surgery involved flushing the catheter lumen with saline to confirm the obstruction and careful removal of the obstructive tissue. This accurate diagnosis facilitated a minimally invasive revision, enabling the reuse of existing shunt components and avoiding the need for new devices, thus reducing costs and surgical invasiveness. Our study serves as a call to action for healthcare providers and surgeons to consider more cost-effective and patient-friendly approaches in managing VP shunt malfunctions, ultimately benefiting both the healthcare system and the patients it serves.
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The majority of low-grade isocitrate dehydrogenase-mutant (IDHmt) gliomas undergo malignant progression (MP), but their underlying mechanism remains unclear. IDHmt gliomas exhibit global DNA methylation, and our previous report suggested that MP could be partly attributed to passive demethylation caused by accelerated cell cycles. However, during MP, there is also active demethylation mediated by ten-eleven translocation, such as DNA hydroxymethylation. Hydroxymethylation is reported to potentially contribute to gene expression regulation, but its role in MP remains under investigation. Therefore, we conducted a comprehensive analysis of hydroxymethylation during MP of IDHmt astrocytoma. Five primary/malignantly progressed IDHmt astrocytoma pairs were analyzed with oxidative bisulfite and the Infinium EPIC methylation array, detecting 5-hydroxymethyl cytosine at over 850,000 locations for region-specific hydroxymethylation assessment. Notably, we observed significant sharing of hydroxymethylated genomic regions during MP across the samples. Hydroxymethylated CpGs were enriched in open sea and intergenic regions (p < 0.001), and genes undergoing hydroxymethylation were significantly associated with cancer-related signaling pathways. RNA sequencing data integration identified 91 genes with significant positive/negative hydroxymethylation-expression correlations. Functional analysis suggested that positively correlated genes are involved in cell-cycle promotion, while negatively correlated ones are associated with antineoplastic functions. Analyses of The Cancer Genome Atlas clinical data on glioma were in line with these findings. Motif-enrichment analysis suggested the potential involvement of the transcription factor KLF4 in hydroxymethylation-based gene regulation. Our findings shed light on the significance of region-specific DNA hydroxymethylation in glioma MP and suggest its potential role in cancer-related gene expression and IDHmt glioma malignancy.
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Neoplasias Encefálicas , Metilação de DNA , Progressão da Doença , Regulação Neoplásica da Expressão Gênica , Glioma , Isocitrato Desidrogenase , Fator 4 Semelhante a Kruppel , Mutação , Humanos , Isocitrato Desidrogenase/genética , Glioma/genética , Glioma/patologia , Glioma/metabolismo , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Ilhas de CpG/genética , Feminino , Masculino , Astrocitoma/genética , Astrocitoma/patologia , Astrocitoma/metabolismo , Pessoa de Meia-Idade , 5-Metilcitosina/análogos & derivados , 5-Metilcitosina/metabolismo , AdultoRESUMO
Ependymomas encompass multiple clinically relevant tumor types based on localization and molecular profiles. Tumors of the methylation class "spinal ependymoma" (SP-EPN) represent the most common intramedullary neoplasms in children and adults. However, their developmental origin is ill-defined, molecular data are scarce, and the potential heterogeneity within SP-EPN remains unexplored. The only known recurrent genetic events in SP-EPN are loss of chromosome 22q and NF2 mutations, but neither types and frequency of these alterations nor their clinical relevance have been described in a large, epigenetically defined series. Transcriptomic (n = 72), epigenetic (n = 225), genetic (n = 134), and clinical data (n = 112) were integrated for a detailed molecular overview on SP-EPN. Additionally, we mapped SP-EPN transcriptomes to developmental atlases of the developing and adult spinal cord to uncover potential developmental origins of these tumors. The integration of transcriptomic ependymoma data with single-cell atlases of the spinal cord revealed that SP-EPN display the highest similarities to mature adult ependymal cells. Unsupervised hierarchical clustering of transcriptomic data together with integrated analysis of methylation profiles identified two molecular SP-EPN subtypes. Subtype A tumors primarily carried previously known germline or sporadic NF2 mutations together with 22q loss (bi-allelic NF2 loss), resulting in decreased NF2 expression. Furthermore, they more often presented as multilocular disease and demonstrated a significantly reduced progression-free survival as compared to SP-EP subtype B. In contrast, subtype B predominantly contained samples without NF2 mutation detected in sequencing together with 22q loss (monoallelic NF2 loss). These tumors showed regular NF2 expression but more extensive global copy number alterations. Based on integrated molecular profiling of a large multi-center cohort, we identified two distinct SP-EPN subtypes with important implications for genetic counseling, patient surveillance, and drug development priorities.
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Ependimoma , Neoplasias da Medula Espinal , Adulto , Criança , Humanos , Transcriptoma , Perfilação da Expressão Gênica , Mutação , Epigênese GenéticaRESUMO
Severe sepsis is a dreaded disease with high mortality, especially in the case of delayed detection. Early diagnosis and treatment initiation is critical for patient survival. However, the septic conditions might be masked by other clinical conditions such as stroke, which may result in a serious delay in diagnosis and treatment. We report a case of iliopsoas abscess that initially presented with cerebellar infarction and subarachnoid hemorrhage. Although severe neurological symptoms were prominent, some signs indicating systemic infection, such as "psoas position", prompted us to investigate the existence of systemic infection. Consequently, severe sepsis with multiple infectious foci, such as iliopsoas abscess, purulent spondylitis, mitral valve valvulitis, and brain abscess, was revealed and was detected as the cause of stroke. The timely and accurate diagnosis of sepsis minimized the delay of the initiation of antibiotic treatment. Approximately five months of intensive care, including two heart valve surgeries, cured the patient, and she was discharged with no neurological deficit. This case demonstrates the importance of careful assessment of the insidious systemic infection as a covert cause of stroke.
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PURPOSE: Five-aminolevulinic acid (5-ALA) is widely used as an intraoperative fluorescent probe for radical resection of high-grade glioma, and thus aids in extending progression-free survival of patients. However, there exist some cases where 5-ALA fails to fluoresce. In some other cases, it may undergo fluorescence quenching but cannot be orally readministered during surgery. This study aimed to develop a novel hydroxymethyl rhodamine green (HMRG)-based fluorescence labeling system that can be repeatedly administered as a topical spray during surgery for the detection of glioblastoma. EXPERIMENTAL DESIGN: We performed a three-stage probe screening using tumor lysates and fresh tumor tissues with our probe library consisting of a variety of HMRG probes with different dipeptides. We then performed proteome and transcript expression analyses to detect candidate enzymes responsible for cleaving the probe. Moreover, in vitro and ex vivo studies using U87 glioblastoma cell line were conducted to validate the findings. RESULTS: The probe screening identified proline-arginine-HMRG (PR-HMRG) as the optimal probe that distinguished tumors from peritumoral tissues. Proteome analysis identified calpain-1 (CAPN1) to be responsible for cleaving the probe. CAPN1 was highly expressed in tumor tissues which reacted to the PR-HMRG probe. Knockdown of this enzyme suppressed fluorescence intensity in U87 glioblastoma cells. In situ assay using a mouse U87 xenograft model demonstrated marked contrast of fluorescence with the probe between the tumor and peritumoral tissues. CONCLUSIONS: The novel fluorescent probe PR-HMRG is effective in detecting glioblastoma when applied topically. Further investigations are warranted to assess the efficacy and safety of its clinical use.
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Neoplasias Encefálicas/patologia , Corantes Fluorescentes , Glioblastoma/patologia , Rodaminas , Administração Tópica , Animais , Corantes Fluorescentes/administração & dosagem , Humanos , Camundongos , Rodaminas/administração & dosagem , Células Tumorais CultivadasRESUMO
PURPOSE: Despite numerous studies, the etiology of spinal extradural arachnoid cyst (SEDAC), a lesion associated with neurological symptoms, remains unknown. In this genomic twin study, we investigated the genetic etiology of SEDACs. METHODS: The subjects were identical twins who developed notably similar SEDACs at the same vertebral level. Accordingly, we performed whole-exome sequencing analyses of genomic material from the twins and their parents using a next-generation sequencer. Additionally, we determined their detailed family history and analyzed the family pedigree. RESULTS: The pedigree analysis suggested the potential presence of SEDACs in certain family members, indicating a genetic disease. Sequenced data were analyzed and filtered using a purpose-built algorithm, leading to the identification of 155 novel single-nucleotide polymorphisms (SNPs), of which 118 encoded missense or nonsense variants. A functional analysis of the proteins encoded by these SNP alleles revealed strong enrichment for the fibronectin type III (FN3) protein domain (q = 0.00576). Specifically, the data indicated that a missense variant affecting the FN3 protein domain of fibronectin 1 (FN1, p.P969S) can be the causal mutation underlying the SEDACs. CONCLUSION: The data suggest that deleterious mutations in fibronectin-related genes may cause SEDACs. In particular, it was suspected that a variant of FN1 may be the cause of the SEDACs in the twin cases studied herein. Detailed studies with a larger number of cases are needed.
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Cistos Aracnóideos , Exoma , Cistos Aracnóideos/diagnóstico por imagem , Cistos Aracnóideos/genética , Exoma/genética , Fibronectinas/genética , Humanos , Linhagem , Gêmeos Monozigóticos , Sequenciamento do ExomaRESUMO
PURPOSE: A noninvasive diagnostic method to predict the degree of malignancy accurately would be of great help in glioma management. This study aimed to create a highly accurate machine learning model to perform glioma grading. METHODS AND MATERIALS: Preoperative magnetic resonance imaging acquired for cases of glioma operated on at our institution from October 2014 through January 2018 were obtained retrospectively. Six types of magnetic resonance imaging sequences (T2-weighted image, diffusion-weighted image, apparent diffusion coefficient [ADC], fractional anisotropy, and mean kurtosis [MK]) were chosen for analysis; 476 features were extracted semiautomatically for each sequence (2856 features in total). Recursive feature elimination was used to select significant features for a machine learning model that distinguishes glioblastoma from lower-grade glioma (grades 2 and 3). RESULTS: Fifty-five data sets from 54 cases were obtained (14 grade 2 gliomas, 12 grade 3 gliomas, and 29 glioblastomas), of which 44 and 11 data sets were used for machine learning and independent testing, respectively. We detected 504 features with significant differences (false discovery rate <0.05) between glioblastoma and lower-grade glioma. The most accurate machine learning model was created using 6 features extracted from the ADC and MK images. In the logistic regression, the area under the curve was 0.90 ± 0.05, and the accuracy of the test data set was 0.91 (10 out of 11); using a support vector machine, they were 0.93 ± 0.03 and 0.91 (10 out of 11), respectively (kernel, radial basis function; c = 1.0). CONCLUSIONS: Our machine learning model accurately predicted glioma tumor grade. The ADC and MK sequences produced particularly useful features.
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Neoplasias Encefálicas/diagnóstico por imagem , Imagem de Difusão por Ressonância Magnética/métodos , Glioma/diagnóstico por imagem , Aprendizado de Máquina , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Anisotropia , Astrocitoma/diagnóstico por imagem , Astrocitoma/patologia , Neoplasias Encefálicas/patologia , Conjuntos de Dados como Assunto , Diagnóstico Diferencial , Imagem de Tensor de Difusão/métodos , Feminino , Glioblastoma/diagnóstico por imagem , Glioblastoma/patologia , Glioma/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Gradação de Tumores/métodos , Oligodendroglioma/diagnóstico por imagem , Oligodendroglioma/patologia , Estudos Retrospectivos , Adulto JovemRESUMO
Immune-based therapies have shown limited efficacy in glioma thus far. This might be at least in part due to insufficient numbers of neoantigens, thought to be targets of immune attack. In addition, we hypothesized that dynamic genetic and epigenetic tumor evolution in gliomas might also affect the mutation/neoantigen landscape and contribute to treatment resistance through immune evasion. Here, we investigated changes in the neoantigen landscape and immunologic features during glioma progression using exome and RNA-seq of paired primary and recurrent tumor samples obtained from 25 WHO grade II-IV glioma patients (glioblastoma, IDH-wild-type, n = 8; grade II-III astrocytoma, IDH-mutant, n = 9; and grade II-III oligodendroglioma, IDH-mutant, 1p/19q-codeleted, n = 8). The number of missense mutations, predicted neoantigens, or expressed neoantigens was not significantly different between primary and recurrent tumors. However, we found that in individual patients the ratio of expressed neoantigens to predicted neoantigens, designated the "neoantigen expression ratio," decreased significantly at recurrence (P = 0.003). This phenomenon was particularly pronounced for "high-affinity," "clonal," and "passenger gene-derived" neoantigens. Gene expression and IHC analyses suggested that the decreased neoantigen expression ratio was associated with intact antigen presentation machinery, increased tumor-infiltrating immune cells, and ongoing immune responses. Our findings imply that decreased expression of highly immunogenic neoantigens, possibly due to persistent immune selection pressure, might be one of the immune evasion mechanisms along with tumor clonal evolution in some gliomas.
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Antígenos de Neoplasias/imunologia , Biomarcadores Tumorais/imunologia , Neoplasias Encefálicas/imunologia , Glioma/imunologia , Evasão da Resposta Imune/imunologia , Linfócitos do Interstício Tumoral/imunologia , Recidiva Local de Neoplasia/imunologia , Adulto , Idoso , Antígenos de Neoplasias/genética , Biomarcadores Tumorais/genética , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/cirurgia , Exoma , Feminino , Seguimentos , Regulação Neoplásica da Expressão Gênica , Glioma/genética , Glioma/patologia , Glioma/cirurgia , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Mutação , Recidiva Local de Neoplasia/genética , Recidiva Local de Neoplasia/patologia , Recidiva Local de Neoplasia/cirurgia , Prognóstico , Estudos Retrospectivos , Taxa de Sobrevida , Adulto JovemRESUMO
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
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In conducting medical research, a system which can objectively predict the future trends of the given research field is awaited. This study aims to establish a novel and versatile algorithm that predicts the latest trends in neuro-oncology. Seventy-nine neuro-oncological research fields were selected with computational sorting methods such as text-mining analyses. Thirty journals that represent the recent trends in neuro-oncology were also selected. As a novel concept, the annual impact (AI) of each year was calculated for each journal and field (number of articles published in the journal × impact factor of the journal). The AI index (AII) for the year was defined as the sum of the AIs of the 30 journals. The AII trends of the 79 fields from 2008 to 2017 were subjected to machine learning predicting analyses. The accuracy of the predictions was validated using actual past data. With this algorithm, the latest trends in neuro-oncology were predicted. As a result, the linear prediction model achieved relatively good accuracy. The predicted hottest fields in recent neuro-oncology included some interesting emerging fields such as microenvironment and anti-mitosis. This algorithm may be an effective and versatile tool for prediction of future trends in a particular medical field.
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To elucidate the mechanisms of malignant progression of lower-grade glioma, molecular profiling using methylation array, whole-exome sequencing, and RNA sequencing was performed for 122, 36 and 31 gliomas, respectively. This cohort included 24 matched pairs of initial lower-grade gliomas and recurrent tumors, most of which showed malignant progression. Nearly half of IDH-mutant glioblastomas that had progressed from lower-grade gliomas exhibited characteristic partial DNA demethylation in previously methylated genomic regions of their corresponding initial tumors, which had the glioma CpG island methylator phenotype (G-CIMP). In these glioblastomas, cell cycle-related genes, RB and PI3K-AKT pathway genes were frequently altered. Notably, late-replicating domain was significantly enriched in the demethylated regions that were mostly located in non-regulatory regions, suggesting that the loss of DNA methylation during malignant transformation may involve mainly passive demethylation due to a delay in maintenance of methylation during accelerated cell division. Nonetheless, a limited number of genes including IGF2BP3, which potentially drives cell proliferation, were presumed to be upregulated due to demethylation of their promoter. Our data indicated that demethylation of the G-CIMP profile found in a subset of recurrent gliomas reflects accelerated cell divisions accompanied by malignant transformation. Oncogenic genes activated by such epigenetic change represent potential therapeutic targets.
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Neoplasias Encefálicas/patologia , Desmetilação do DNA , Glioma/patologia , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/mortalidade , Proteínas de Ciclo Celular/genética , Ilhas de CpG , Progressão da Doença , Glioma/genética , Glioma/mortalidade , Humanos , Isocitrato Desidrogenase/genética , Estimativa de Kaplan-Meier , Mutação , Gradação de Tumores , Proteínas de Fusão Oncogênica/genética , Regiões Promotoras Genéticas , Proteínas de Ligação a RNA/genética , Regulação para CimaRESUMO
Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome often associated with fibroblast growth factor 23 (FGF23)-producing tumors such as phosphaturic mesenchymal tumor, mixed connective tissue variant (PMTMCT) affecting the bone and soft tissue. We experienced a patient with progressive bone and muscle pain due to FGF23-related TIO. Venous sampling had strongly suggested the anterior skull base as a source of FGF23, which led to the discovery of a small tumor in the ethmoid sinus extending intracranially. Radical surgical resection confirmed the histological diagnosis of PMTMCT with FGF23 immunopositivity and achieved durable tumor control with complete resolution of symptoms. We serially measured serum FGF23 level before, during and after surgery and analyzed the data to determine the half-life of FGF23. Serum FGF23 level sharply declined as early as 20 minutes after en bloc tumor resection and completely normalized after surgery. The half-life of FGF23 was calculated to be approximately 18.5 minutes using single phase exponential decay model as well as semilog transformation formula. Serial measurements of serum FGF23 level can potentially declare "complete" resection of a FGF23-producing tumor and total cure of TIO; in this regard, development of its intraoperative measurement would be helpful in the management of this endocrine tumor.
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Fatores de Crescimento de Fibroblastos/sangue , Neoplasias Complexas Mistas/cirurgia , Osteomalacia/prevenção & controle , Neoplasias da Base do Crânio/cirurgia , Adulto , Seio Etmoidal , Feminino , Fator de Crescimento de Fibroblastos 23 , Meia-Vida , Humanos , Neoplasias Complexas Mistas/sangue , Neoplasias Complexas Mistas/fisiopatologia , Osteomalacia/etiologia , Neoplasias da Base do Crânio/sangue , Neoplasias da Base do Crânio/fisiopatologia , Resultado do TratamentoRESUMO
BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is characterized by reversible edematous lesions on radiological examinations as well as symptoms of altered consciousness and seizures. To date, the underlying mechanism remains largely unknown. CASE DESCRIPTIONS: Case 1 is a 72-year-old man with a history of hypertension presented with a subarachnoid hemorrhage. Fourteen days after the successful clipping of a ruptured aneurysm; he experienced inadvertent overdrainage via the intraventricular drain. Nine hours later, he started to have seizures followed by disturbances in consciousness. An emergency magnetic resonance imaging showed multiple high-intensity lesions in the frontal, temporal, parietal, and occipital lobes, basal ganglia, brainstem, and cerebellar hemispheres bilaterally, which are compatible with typical magnetic resonance findings in PRES patients. He was treated conservatively and recovered well. Case 2 is a 68-year-old woman with a mild history of hypertension and a ventriculo-peritoneal shunt for obstructive hydrocephalus, who underwent a cysto-peritoneal shunt placement because of an enlarging symptomatic arachnoid cyst. Immediately following surgery, she experienced disturbances in consciousness and developed status epilepticus. Radiological examinations revealed remarkable shrinkage of the arachnoid cyst and multiple edematous lesions, which led us to strongly suspect PRES. With conservative treatment, her symptoms and the radiological abnormalities disappeared. CONCLUSION: Based on the previous literature and our cases, we believe that the association between rapid reduction of intracranial pressure (ICP) and the development of PRES should be recognized because most neurosurgical procedures such as craniotomy or cerebrospinal fluid diversion present a potential risk of rapid reduction of ICP.
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BACKGROUND: Endoscopic ventriculostomy is an attractive surgical alternative to ventriculoperitoneal shunt in the treatment of focal hydrocephalus, including trapped temporal horn (TTH). The major concern of this surgical approach is closure of a stoma, the risk of which may be minimized by placement of a stent after ventriculostomy. CASE DESCRIPTION: The authors report a case of a 60-year-old man with glioblastoma in the corpus callosum and the parietal lobe who developed TTH after partial tumor resection. After the failure of a ventriculoperitoneal shunt, endoscopic ventriculocisternostomy was chosen over the revision of the shunt. A stoma was placed at the medial wall of the dilated temporal horn. Endoscopic inspection confirmed communication with the interpeduncular cistern, but the collapsed lateral ventricle after fenestration suggested the risk of stoma closure. Therefore, a ventricular tube was placed through the stoma as a stent to secure its flow. No further surgical intervention was needed, and the patient was able to complete radiochemotherapy without cessation. CONCLUSIONS: The risk of recurrence of TTH after endoscopic ventriculocisternostomy may be minimized by combining ventriculostomy with stent placement. This surgical procedure would be beneficial, particularly in cases of TTH associated with malignant brain tumors, where the risk of delay or interruption of adjuvant oncologic treatments may negatively impact patient prognosis.
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Neoplasias Encefálicas/cirurgia , Cisterna Magna/cirurgia , Endoscopia/métodos , Glioblastoma/cirurgia , Neuroendoscopia , Procedimentos Neurocirúrgicos/métodos , Stents , Lobo Temporal/cirurgia , Derivação Ventriculoperitoneal/efeitos adversos , Ventriculostomia/métodos , Neoplasias Encefálicas/complicações , Neoplasias Encefálicas/terapia , Quimiorradioterapia , Falha de Equipamento , Glioblastoma/complicações , Glioblastoma/terapia , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
We aimed to determine the sensitivity of CT perfusion (CTP) for the diagnosis of cerebral infarction in the acute stage. We retrospectively reviewed patients with ischemic stroke who underwent brain CTP on arrival and MRI-diffusion weighted image (DWI) after hospitalization between October 2008 and October 2011. Final diagnosis was made from MRI-DWI findings and 87 patients were identified. Fifty-five out of 87 patients (63%) could be diagnosed with cerebral infarction by initial CTP. The sensitivity depends on the area size (s): 29% for S < 3 cm(2), 83% for S ≥ 3 cm(2) - < 6 cm(2), 88% for S ≥ 6 cm(2) - < 9 cm(2), 80% for S ≥ 9 cm(2) - < 12 cm(2), and 96% for S ≥ 12 cm(2) (p < 0.001). Sensitivity depends on the type of infarction: 0% for lacunar, 74% for atherothrombotic, and 92% for cardioembolism (p < 0.001). Sensitivity is not correlated with hours after onset. CT perfusion is an effective imaging modality for the diagnosis and treatment decisions for acute stroke, particularly more serious strokes.
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Infarto Cerebral/diagnóstico , Imagem de Perfusão/métodos , Tomografia Computadorizada por Raios X/métodos , Idoso , Idoso de 80 Anos ou mais , Infarto Cerebral/diagnóstico por imagem , Infarto Cerebral/patologia , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Sensibilidade e EspecificidadeRESUMO
BACKGROUND: We analyzed factors associated with worsened paresis in a large series of patients with brain lesions located within or near the primary motor area (M1) to establish protocols for safe, awake craniotomy of eloquent lesions. METHODS: We studied patients with brain lesions involving M1, the premotor area (PMA) and the primary sensory area (S1), who underwent awake craniotomy (n = 102). In addition to evaluating paresis before, during, and one month after surgery, the following parameters were analyzed: Intraoperative complications; success or failure of awake surgery; tumor type (A or B), tumor location, tumor histology, tumor size, and completeness of resection. RESULTS: Worsened paresis at one month of follow-up was significantly associated with failure of awake surgery, intraoperative complications and worsened paresis immediately after surgery, which in turn was significantly associated with intraoperative worsening of paresis. Intraoperative worsening of paresis was significantly related to preoperative paresis, type A tumor (motor tract running in close proximity to and compressed by the tumor), tumor location within or including M1 and partial removal (PR) of the tumor. CONCLUSIONS: Successful awake surgery and prevention of deterioration of paresis immediately after surgery without intraoperative complications may help prevent worsening of paresis at one month. Factors associated with intraoperative worsening of paresis were preoperative motor deficit, type A and tumor location in M1, possibly leading to PR of the tumor.