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Si Zhang, Hexiang Zhao, Hao Li, Chao You, and Xuhui Hui

OBJECTIVE

Decompressive craniectomy (DC) is a life-saving treatment for severe hemorrhagic cerebral venous thrombosis (CVT). However, the correlations between the clinicoradiological features and surgical outcomes of this disease are not well established. Therefore, the authors endeavored to analyze the potential risk factors for this more severe subtype of CVT and to provide more evidence regarding the benefits of DC in patients with hemorrhagic CVT.

METHODS

The clinical features, radiological findings, and surgical outcomes of patients with severe hemorrhagic CVT who had undergone DC treatment in the period from January 2005 to March 2015 were retrospectively analyzed, and the risk factors for this disease were evaluated.

RESULTS

Fifty-eight patients, 39 females (67.2%) and 19 males (32.8%), with a mean age of 39.7 ± 12.5 years, were included in this study. The mean duration from symptom onset to surgery was 3.3 ± 1.9 days, and 21 patients experienced acute courses. On neuroimaging, the mean mass lesion volume was 114.7 ± 17.7 ml. Nine patients had bilateral lesions, and 7 patients had deep CVT. According to their hemorrhagic proportion, cases were divided into hemorrhage-dominated (27 [46.6%]) and edema-dominated (31 [53.4%]) groups. After 6 months of follow-up, 56.9% of patients had achieved a favorable outcome, and 8 patients had died. The hemorrhage-dominated lesions (p = 0.026) and deep cerebral venous involvement (p = 0.026) were significantly associated with a poor outcome.

CONCLUSIONS

In patients suffering from severe hemorrhagic CVT, DC is an effective life-saving treatment that is associated with favorable outcomes. Hemorrhage-dominated lesions and deep cerebral venous involvement have a significant impact on the outcome of this disease.

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Lei Zhao, Chao Cheng, Wei Zuo, Peng Wang, and Weixin Li

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Dong H. Kim, Xiurong Zhao, Christina H. Tu, Patrizia Casaccia-Bonnefil, and Moses V. Chao

Object. Neurotrophins prevent the death of neurons during embryonal development and have potential as therapeutic agents. During development, neuronal death occurs only by apoptosis and not by necrosis. Following injury, however, neurons can die by both processes. Data from prior studies have not clearly indicated whether neurotrophins can decrease apoptosis compared with necrosis. The goal of this study was to determine the effect of neurotrophin treatment on each of these processes following injury and to characterize the receptor(s) required.

Methods. The authors used an in vitro model of injury with the aid of primary cortical neurons obtained from rat embryos. After 9 days in culture and the elimination of glia, homogeneous and mature neurons were available for experimentation. Noxious stimuli were applied, including radiation, hypoxia, and ischemia. Subsequent cell death by apoptosis or necrosis was noted based on morphological and enzymatic assessments (such as lactate dehydrogenase [LDH] release) and assays for DNA fragmentation. The effect of treatment with nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 was determined. Finally, Western blot analyses were performed to note the neurotrophin receptor status in the neurons (tyrosine kinase receptors [Trks] and p75).

The authors studied different stimuli-induced cell death by using different processes. With the application of radiation, cells died primarily by apoptosis, as evidenced by cell shrinkage, the presence of apoptotic bodies, and specific DNA fragmentation. This was a delayed process (> 6 hours) that could be reduced by gene transcription or protein synthesis inhibitors. With ischemia, cells died immediately by necrosis, showing cell enlargement and rupture. Ischemic cell death was not affected by the inhibition of macromolecular synthesis. Hypoxia produced a mixture of the two cell death processes.

Both BDNF and neurotrophin-3 demonstrated protection against apoptotic cell death only. Statistically significant decreases of both LDH release and apoptosis-specific DNA fragmentation were noted following radiation and hypoxia, but not for ischemia. Nerve growth factor, unlike the other neurotrophins, did not affect apoptosis because a functional receptor, Trk A, was not expressed by the cortical neurons. There was expression of both Trk B and Trk C, which bind BDNF and neurotrophin-3.

Conclusions. These findings have significant clinical implications. Neurotrophins may only be effective in disorders in which apoptosis, and not necrosis, is the major process. Furthermore, the Trk signaling cascade must be activated for this response to occur. Because the expression of these receptors diminishes in adulthood, neurotrophin application may be most appropriate in the pediatric population.

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Xijie Zhou, Bin Zhao, Keshav Poonit, Weidong Weng, Chenglun Yao, Chao Sun, and Hede Yan

OBJECTIVE

Traumatic neuromas represent a prevalent source of neuropathic pain. As of yet, there has been no single treatment method that can guarantee permanent relief of symptoms. Although nerve-capping techniques have shown promise, their exact mechanisms remain elusive. The authors’ aim was to examine the role of the RhoA/ROCK signaling pathway in the prevention of neuroma formation after neurectomy utilizing a nerve-capping technique.

METHODS

An aligned nanofiber tube was fabricated to cap the sciatic nerve in Sprague Dawley rats. The rats (n = 60) were randomly divided into the aligned SF/P (LLA-CL) capping group (capping group, n = 20), the capping and Y-27632 (ROCK pathway inhibitor) intervention group (intervention group, n = 20), and the no-capping group (control group, n = 20). The authors undertook a comprehensive assessment of the capping group, examining the animals’ behavior, the extent of neuroma development, histology, gene and protein expression, and ultrastructural changes associated with the RhoA/ROCK signaling pathway. These findings were compared with those in the intervention and control groups.

RESULTS

The inciting injury resulted in the expression of the RhoA/ROCK signaling pathway, as well as its further upregulation in peripheral neurons. Axon outgrowth was significantly increased when RhoA/ROCK signaling pathway was suppressed. The average autotomy score in the capping group was observed to be much lower than that of the intervention and control groups. At 30 days postneurectomy, the capping group displayed no obvious neuroma formation, while a bulbous neuroma was found in the nerve stumps of both the control and intervention groups. Quantitative real-time polymerase chain reaction and the Western blot analysis demonstrated that the expression of myelin-associated glycoprotein was substantially upregulated in the capping group; in contrast, the expression of NF-200 was significantly downregulated. The expression of myosin light chain was notably lower in the intervention group, but there was no significant difference when compared with the control group (p > 0.05).

CONCLUSIONS

The RhoA/ROCK signaling pathway has emerged as a critical player in the process of traumatic neuroma formation after neurectomy. It is possible that the nerve-capping technique could generate a “regenerative brake” based on the regulation of the RhoA/ROCK signaling pathway in this event. These findings may provide concrete evidence that could help develop new strategies for the management of painful neuromas.

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Hong-Qi Zhang, Ling-Qiang Chen, Shao-Hua Liu, Di Zhao, and Chao-Feng Guo

Object

The object of this study was to evaluate the efficacy and safety of posterior decompression with kyphosis correction for thoracic myelopathy due to ossification of the ligamentum flavum (OLF) and ossification of the posterior longitudinal ligament (OPLL) at the same level.

Methods

Between January 2003 and December 2005, 11 patients (8 men and 3 women) with thoracic myelopathy due to OLF and OPLL at the same level underwent posterior decompressive laminectomy and excision of OLF. Posterior instrumentation was also performed for stabilization of the spine and reducing the thoracic kyphosis angle by approximately 5–15° (kyphosis correction), and spinal fusion was performed in all cases. The follow-up period ranged from 2 to 4 years (mean 2.8 years). The outcomes were evaluated using a recovery scale based on the Japanese Orthopaedic Association classification. The score of each patient was calculated before surgery, 1 year after surgery, and at the final follow-up visit.

Results

After surgery, the thoracic kyphosis in the stabilization area was reduced from 30.0 ± 4.02° to 20.8 ± 2.14° on average. The mean score on the Japanese Orthopaedic Association scale improved from 3.5 ± 1.69 preoperatively to 8.5 ± 1.63 at the final follow-up, with a recovery rate of 68.0%. The results were good in 9 patients and fair in 2 patients. Postoperative MR imaging showed that the spinal cord was shifted posteriorly and decompressed completely in all cases. Myelopathy was not aggravated in any case after surgery.

Conclusions

A considerable degree of neurological recovery was observed after posterior decompression and kyphosis correction. The procedure is easy to perform with a low risk of postoperative paralysis. The authors therefore suggest that the procedure is useful for patients whose spinal cords are severely impinged by OLF and OPLL at the same level.

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Baotian Zhao, Chao Zhang, Xiu Wang, Yao Wang, Chang Liu, Jiajie Mo, Zhong Zheng, Kai Zhang, Xiao-qiu Shao, Wenhan Hu, and Jianguo Zhang

Focal cortical dysplasia type II (FCD II) is a common histopathological substrate of epilepsy surgery. Here, the authors propose a sulcus-centered resection strategy for this malformation, provide technical details, and assess the efficacy and safety of this technique. The main purpose of the sulcus-centered resection is to remove the folded gray matter surrounding a dysplastic sulcus, particularly that at the bottom of the sulcus. The authors also retrospectively reviewed the records of 88 consecutive patients with FCD II treated with resective surgery between January 2015 and December 2018. The demographics, clinical characteristics, electrophysiological recordings, neuroimaging studies, histopathological findings, surgical outcomes, and complications were collected. After the exclusion of diffusely distributed and gyrus-based lesions, 71 patients (30 females, 41 males) who had undergone sulcus-centered resection were included in this study. The mean (± standard deviation) age of the cohort was 17.78 ± 10.54 years (38 pediatric patients, 33 adults). Thirty-five lesions (49%) were demonstrated on MRI; 42 patients (59%) underwent stereo-EEG monitoring before resective surgery; and 37 (52%) and 34 (48%) lesions were histopathologically proven to be FCD IIa and IIb, respectively. At a mean follow-up of 3.34 ± 1.17 years, 64 patients (90%) remained seizure free, and 7 (10%) had permanent neurological deficits including motor weakness, sensory deficits, and visual field deficits. The study findings showed that in carefully selected FCD II cases, sulcus-centered resection is an effective and safe surgical strategy.

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Baotian Zhao, Chao Zhang, Xiu Wang, Yao Wang, Jiajie Mo, Zhong Zheng, Lin Ai, Kai Zhang, Jianguo Zhang, Xiao-qiu Shao, and Wenhan Hu

OBJECTIVE

The aim of this study was to characterize the clinical and electrophysiological findings of epilepsy originating from the orbitofrontal cortex (OFC) as well as its surgical outcomes.

METHODS

The authors retrospectively reviewed 27 consecutive cases of patients with drug-resistant orbitofrontal epilepsy (OFE) who underwent tailored resective surgery after a detailed presurgical workup. Demographic features, seizure semiology, imaging characteristics, resection site, pathological results, and surgical outcomes were analyzed. Patients were categorized according to semiology. The underlying neural network was further explored through quantitative FDG-PET and ictal stereo-electroencephalography (SEEG) analysis at the group level. FDG-PET studies between the semiology group and the control group were compared using a voxel-based independent t-test. Ictal SEEG was quantified by calculating the energy ratio (ER) of high- and low-frequency bands. An ER comparison between the anterior cingulate cortex (ACC) and the amygdala was performed to differentiate seizure spreading patterns in groups with different semiology.

RESULTS

Scalp electroencephalography (EEG) and MRI were inconclusive to a large extent. Patients were categorized into the following 3 semiology groups: the frontal group (n = 14), which included patients with hyperactive automatisms with agitated movements; the temporal group (n = 11), which included patients with oroalimentary or manual automatisms; and the other group (n = 2), which included patients with none of the abovementioned or indistinguishable manifestations. Patients in the frontal and temporal groups (n = 23) or in the frontal group only (n = 14) demonstrated significant hypometabolism mainly across the ipsilateral OFC, ACC, and anterior insula (AI), while patients in the temporal group (n = 9) had hypometabolism only in the OFC and AI. The ER results (n = 15) suggested distinct propagation pathways that allowed us to differentiate between the frontal and temporal groups. Pathologies included focal cortical dysplasia, dysembryoplastic neuroepithelial tumor, cavernous malformation, glial scar, and nonspecific findings. At a minimum follow-up of 12 months, 19 patients (70.4%) were seizure free, and Engel class II, III, and IV outcomes were observed in 4 patients (14.8%), 3 patients (11.1%), and 1 patient (3.7%), respectively.

CONCLUSIONS

The diagnosis of OFE requires careful presurgical evaluation. Based on their electrophysiological and metabolic evidence, the authors propose that varied semiological patterns could be explained by the extent of involvement of a network that includes at least the OFC, ACC, AI, and temporal lobe. Tailored resections for OFE may lead to a good overall outcome.

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Baotian Zhao, Chao Zhang, Xiu Wang, Yao Wang, Jiajie Mo, Zhong Zheng, Lin Ai, Kai Zhang, Jianguo Zhang, Xiao-qiu Shao, and Wenhan Hu

OBJECTIVE

The aim of this study was to characterize the clinical and electrophysiological findings of epilepsy originating from the orbitofrontal cortex (OFC) as well as its surgical outcomes.

METHODS

The authors retrospectively reviewed 27 consecutive cases of patients with drug-resistant orbitofrontal epilepsy (OFE) who underwent tailored resective surgery after a detailed presurgical workup. Demographic features, seizure semiology, imaging characteristics, resection site, pathological results, and surgical outcomes were analyzed. Patients were categorized according to semiology. The underlying neural network was further explored through quantitative FDG-PET and ictal stereo-electroencephalography (SEEG) analysis at the group level. FDG-PET studies between the semiology group and the control group were compared using a voxel-based independent t-test. Ictal SEEG was quantified by calculating the energy ratio (ER) of high- and low-frequency bands. An ER comparison between the anterior cingulate cortex (ACC) and the amygdala was performed to differentiate seizure spreading patterns in groups with different semiology.

RESULTS

Scalp electroencephalography (EEG) and MRI were inconclusive to a large extent. Patients were categorized into the following 3 semiology groups: the frontal group (n = 14), which included patients with hyperactive automatisms with agitated movements; the temporal group (n = 11), which included patients with oroalimentary or manual automatisms; and the other group (n = 2), which included patients with none of the abovementioned or indistinguishable manifestations. Patients in the frontal and temporal groups (n = 23) or in the frontal group only (n = 14) demonstrated significant hypometabolism mainly across the ipsilateral OFC, ACC, and anterior insula (AI), while patients in the temporal group (n = 9) had hypometabolism only in the OFC and AI. The ER results (n = 15) suggested distinct propagation pathways that allowed us to differentiate between the frontal and temporal groups. Pathologies included focal cortical dysplasia, dysembryoplastic neuroepithelial tumor, cavernous malformation, glial scar, and nonspecific findings. At a minimum follow-up of 12 months, 19 patients (70.4%) were seizure free, and Engel class II, III, and IV outcomes were observed in 4 patients (14.8%), 3 patients (11.1%), and 1 patient (3.7%), respectively.

CONCLUSIONS

The diagnosis of OFE requires careful presurgical evaluation. Based on their electrophysiological and metabolic evidence, the authors propose that varied semiological patterns could be explained by the extent of involvement of a network that includes at least the OFC, ACC, AI, and temporal lobe. Tailored resections for OFE may lead to a good overall outcome.

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Shih-Shan Lang, Nankee K. Kumar, Chao Zhao, David Y. Zhang, Alexander M. Tucker, Phillip B. Storm, Gregory G. Heuer, Avi A. Gajjar, Chong Tae Kim, Ian Yuan, Susan Sotardi, Todd J. Kilbaugh, and Jimmy W. Huh

OBJECTIVE

Severe traumatic brain injury (TBI) is a leading cause of disability and death in the pediatric population. While intracranial pressure (ICP) monitoring is the gold standard in acute neurocritical care following pediatric severe TBI, brain tissue oxygen tension (PbtO2) monitoring may also help limit secondary brain injury and improve outcomes. The authors hypothesized that pediatric patients with severe TBI and ICP + PbtO2 monitoring and treatment would have better outcomes than those who underwent ICP-only monitoring and treatment.

METHODS

Patients ≤ 18 years of age with severe TBI who received ICP ± PbtO2 monitoring at a quaternary children’s hospital between 1998 and 2021 were retrospectively reviewed. The relationships between conventional measurements of TBI were evaluated, i.e., ICP, cerebral perfusion pressure (CPP), and PbtO2. Differences were analyzed between patients with ICP + PbtO2 versus ICP-only monitoring on hospital and pediatric intensive care unit (PICU) length of stay (LOS), length of intubation, Pediatric Intensity Level of Therapy scale score, and functional outcome using the Glasgow Outcome Score–Extended (GOS-E) scale at 6 months postinjury.

RESULTS

Forty-nine patients, including 19 with ICP + PbtO2 and 30 with ICP only, were analyzed. There was a weak negative association between ICP and PbtO2 (β = −0.04). Conversely, there was a strong positive correlation between CPP ≥ 40 mm Hg and PbtO2 ≥ 15 and ≥ 20 mm Hg (β = 0.30 and β = 0.29, p < 0.001, respectively). An increased number of events of cerebral PbtO2 < 15 mm Hg or < 20 mm Hg were associated with longer hospital (p = 0.01 and p = 0.022, respectively) and PICU (p = 0.015 and p = 0.007, respectively) LOS, increased duration of mechanical ventilation (p = 0.015 when PbtO2 < 15 mm Hg), and an unfavorable 6-month GOS-E score (p = 0.045 and p = 0.022, respectively). An increased number of intracranial hypertension episodes (ICP ≥ 20 mm Hg) were associated with longer hospital (p = 0.007) and PICU (p < 0.001) LOS and longer duration of mechanical ventilation (p < 0.001). Lower minimum hourly and average daily ICP values predicted favorable GOS-E scores (p < 0.001 for both). Patients with ICP + PbtO2 monitoring experienced longer PICU LOS (p = 0.018) compared to patients with ICP-only monitoring, with no significant GOS-E score difference between groups (p = 0.733).

CONCLUSIONS

An increased number of cerebral hypoxic episodes and an increased number of intracranial hypertension episodes resulted in longer hospital LOS and longer duration of mechanical ventilator support. An increased number of cerebral hypoxic episodes also correlated with less favorable functional outcomes. In contrast, lower minimum hourly and average daily ICP values, but not the number of intracranial hypertension episodes, were associated with more favorable functional outcomes. There was a weak correlation between ICP and PbtO2, supporting the importance of multimodal invasive neuromonitoring in pediatric severe TBI.