EBERVAL GADELHA FIGUEIREDO

(Fonte: Lattes)
Índice h a partir de 2011
19
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Neurologia, Faculdade de Medicina - Docente
LIM/62 - Laboratório de Fisiopatologia Cirúrgica, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 6 de 6
  • article 0 Citação(ões) na Scopus
    Decompressive craniectomy Response
    (2012) BOR-SENG-SHU, Edson; FIGUEIREDO, Eberval G.; TEIXEIRA, Manoel Jacobsen; PANERAI, Ronney B.
  • article 54 Citação(ões) na Scopus
    Decompressive craniectomy and head injury: brain morphometry, ICP, cerebral hemodynamics, cerebral microvascular reactivity, and neurochemistry
    (2013) BOR-SENG-SHU, Edson; FIGUEIREDO, Eberval G.; FONOFF, Erich Talamoni; FUJIMOTO, Yasunori; PANERAI, Ronney B.; TEIXEIRA, Manoel Jacobsen
    There has been renewed interest in decompressive craniectomy as a surgical treatment for elevated intracranial pressure (ICP), although evidence-based clinical data are still lacking and some experimental results are conflicting. Ongoing clinical trials on the use of this operation after traumatic brain injury (TBI) may clarify the clinical application of this technique, however, some pathophysiological issues, such as the timing of this operation, its effect on brain edema formation, and its role for secondary brain damage, are still controversial. This review addresses recent clinical data on the influence of decompressive craniectomy on the brain pathophysiology in TBI. Decompressive craniectomy with dural augmentation enlarges intracranial space so that the swollen cerebral hemisphere could expand out of normal cranial limits, avoiding progression of brain herniation. The gain in intracranial volume results in both the improvement of cerebral compliance and a decrease in ICP; the latter favors a rise in both cerebral blood flow and cerebral microvascular perfusion, which can be accompanied by elevation in brain tissue oxygen tension (PbtO(2)) as well as the return of abnormal metabolic parameters to normal values in cases of cerebral ischemia. Enhancement of edema formation, impairment of cerebrovascular pressure reactivity, and non-restoration of brain aerobic metabolism due to metabolic crisis may occur after craniectomy and require further investigations. This review suggests that decompressive craniectomy as the sole treatment is likely to be insufficient; efforts must be made to maintain adequate brain hemodynamics, preferably coupled with brain metabolism, in addition to treating brain metabolic abnormalities, during postoperative stages.
  • article 68 Citação(ões) na Scopus
    Cerebral hemodynamics: concepts of clinical importance
    (2012) BOR-SENG-SHU, Edson; KITA, William S.; FIGUEIREDO, Eberval G.; PAIVA, Wellingson S.; FONOFF, Erich T.; TEIXEIRA, Manoel J.; PANERAI, Ronney B.
    Cerebral hemodynamics and metabolism are frequently impaired in a wide range of neurological diseases, including traumatic brain injury and stroke, with several pathophysiological mechanisms of injury. The resultant uncoupling of cerebral blood flow and metabolism can trigger secondary brain lesions, particularly in early phases, consequently worsening the patient's outcome. Cerebral blood flow regulation is influenced by blood gas content, blood viscosity, body temperature, cardiac output, altitude, cerebrovascular autoregulation, and neurovascular coupling, mediated by chemical agents such as nitric oxide (NO), carbon monoxide (CO), eicosanoid products, oxygen-derived free radicals, endothelins, K+, H+, and adenosine. A better understanding of these factors is valuable for the management of neurocritical care patients. The assessment of both cerebral hemodynamics and metabolism in the acute phase of neurocritical care conditions may contribute to a more effective planning of therapeutic strategies for reducing secondary brain lesions. In this review, the authors have discussed concepts of cerebral hemodynamics, considering aspects of clinical importance.
  • article 7 Citação(ões) na Scopus
    Subthalamic low beta bursts differ in Parkinson's disease phenotypes
    (2022) NETO, Arnaldo Fim; LUCCAS, Julia Baldi de; BIANQUETI, Bruno Leonardo; SILVA, Luiz Ricardo da; ALMEIDA, Tiago Paggi; TAKAHATA, Andre Kazuo; TEIXEIRA, Manoel Jacobsen; FIGUEIREDO, Eberval Gadelha; NASUTO, Slawomir J.; ROCHA, Maria Sheila Guimaraes; SORIANO, Diogo Coutinho; GODINHO, Fabio
    lObjective: Parkinson's disease (PD) patients may be categorized into tremor-dominant (TD) and postural-instability and gait disorder (PIGD) motor phenotypes, but the dynamical aspects of subthalamic nucleus local field potentials (STN-LFP) and the neural correlates of this phenotypical classification remain unclear.Methods: 35 STN-LFP (20 PIGD and 15 TD) were investigated through continuous wavelet transform and machine-learning-based methods. The beta oscillation - the main band associated with motor impair-ment in PD - dynamics was characterized through beta burst parameters across phenotypes and burst intervals under specific proposed criteria for optimal burst threshold definition.Results: Low-frequency (13-22 Hz) beta burst probability was the best predictor for PD phenotypes (75% accuracy). PIGD patients presented higher average burst duration (p = 0.018), while TD patients exhibited higher burst probability (p = 0.014). Categorization into shorter and longer than 400 ms bursts led to sig-nificant interaction between burst length categories and the phenotypes (p < 0.050) as revealed by mixed-effects models. Long burst durations and short bursts probability positively correlated, respec-tively, with rigidity-bradykinesia (p = 0.029) and tremor (p = 0.038) scores.Conclusions: Subthalamic low-frequency beta bursts differed between TD and PIGD phenotypes and cor-related with motor symptoms.
  • article 15 Citação(ões) na Scopus
    Spectral characteristics of subthalamic nucleus local field potentials in Parkinson's disease: Phenotype and movement matter
    (2021) GODINHO, Fabio; FIM NETO, Arnaldo; BIANQUETI, Bruno Leonardo; LUCCAS, Julia Baldi de; VARJAO, Eduardo; TERZIAN FILHO, Paulo Roberto; FIGUEIREDO, Eberval Gadelha; ALMEIDA, Tiago Paggi; YONEYAMA, Takashi; TAKAHATA, Andre Kazuo; ROCHA, Maria Sheila; SORIANO, Diogo Coutinho
    Parkinson's disease (PD) is clinically heterogeneous across patients and may be classified in three motor phenotypes: tremor dominant (TD), postural instability and gait disorder (PIGD), and undetermined. Despite the significant clinical characterization of motor phenotypes, little is known about how electrophysiological data, particularly subthalamic nucleus local field potentials (STN-LFP), differ between TD and PIGD patients. This is relevant since increased STN-LFP bandpower at alpha-beta range (8-35 Hz) is considered a potential PD biomarker and, therefore, a critical setpoint to drive adaptive deep brain stimulation. Acknowledging STN-LFP differences between phenotypes, mainly in rest and movement states, would better fit DBS to clinical and motor demands. We studied this issue through spectral analyses on 35 STN-LFP in TD and PIGD patients during rest and movement. We demonstrated that higher beta(2) activity (22-35 Hz) was observed in PIGD only during rest. Additionally, bandpower differences between rest and movement occurred at the alpha-beta range, but with different patterns as per phenotypes: movement-induced desynchronization concerned lower frequencies in TD (10-20 Hz) and higher frequencies in PIGD patients (21-28 Hz). Finally, when supervised learning algorithms were employed aiming to discriminate PD phenotypes based on STN-LFP bandpower features, movement information had improved the classification accuracy, achieving peak performances when TD and PIGD movement-induced desynchronization ranges were considered. These results suggest that STN-LFP beta-band encodes phenotype-movement dependent information in PD patients.
  • article 153 Citação(ões) na Scopus
    Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury A review
    (2012) BOR-SENG-SHU, Edson; FIGUEIREDO, Eberval G.; AMORIM, Robson L. O.; TEIXEIRA, Manoel Jacobsen; VALBUZA, Juliana Spelta; OLIVEIRA, Marcio Moyses de; PANERAI, Ronney B.
    Object. In recent years, the role of decompressive craniectomy for the treatment of traumatic brain injury (TB!) in patients with refractory intracranial hypertension has been the subject of several studies. The purpose of this review was to evaluate the contribution of decompressive craniectomy in reducing intracranial pressure (ICP) and increasing cerebral perfusion pressure (CPP) in these patients. Methods. Comprehensive literature searches were performed for articles related to the effects of decompressive craniectomy on ICP and CPP in patients with TBI. Inclusion criteria were as follows: 1) published manuscripts, 2) original articles of any study design except case reports, 3) patients with refractory elevated ICP due to traumatic brain swelling, 4) decompressive craniectomy as a type of intervention, and 5) availability of pre- and postoperative ICP and/or CPP data. Primary outcomes were ICP decrease and/or CPP increase for assessing the efficacy of decompressive craniectomy. The secondary outcome was the persistence of reduced ICP 24 and 48 hours after the operation. Results. Postoperative ICP values were significantly lower than preoperative values immediately after decompressive craniectomy (weighted mean difference [WMD] -17.59 mm Hg, 95% CI -23.45 to -11.73, p < 0.00001), 24 hours after (WMD -14.27 mm Hg, 95% Cl -24.13 to -4.41, p < 0.00001), and 48 hours after (WMD -12.69 mm Hg, 95% Cl -22.99 to -2.39, p < 0.0001). Postoperative CPP was significantly higher than preoperative values (WMD 7.37 mm Hg, 95% Cl 2.32 to 12.42, p < 0.0001). Conclusions. Decompressive craniectomy can effectively decrease ICP and increase CPP in patients with TBI and refractory elevated ICP. Further studies are necessary to define the group of patients that can benefit most from this procedure. (http://thejns.org/doi/abs/10.3171/2012.6.JNS101400)