Lung-protective Ventilation in Patients with Brain Injury: A Multicenter Cross-sectional Study and Questionnaire Survey in China.

BACKGROUND: Over the years, the mechanical ventilation (MV) strategy has changed worldwide. The aim of the present study was to describe the ventilation practices, particularly lung-protective ventilation (LPV), among brain-injured patients in China. METHODS: This study was a multicenter, 1-day, cross-sectional study in 47 Intensive Care Units (ICUs) across China. Mechanically ventilated patients (18 years and older) with brain injury in a participating ICU during the time of the study, including traumatic brain injury, stroke, postoperation with intracranial tumor, hypoxic-ischemic encephalopathy, intracranial infection, and idiopathic epilepsy, were enrolled. Demographic data, primary diagnoses, indications for MV, MV modes and settings, and prognoses on the 60th day were collected. Multivariable logistic analysis was used to assess factors that might affect the use of LPV. RESULTS: A total of 104 patients were enrolled in the present study, 87 (83.7%) of whom were identified with severe brain injury based on a Glasgow Coma Scale ≤8 points. Synchronized intermittent mandatory ventilation (SIMV) was the most frequent ventilator mode, accounting for 46.2% of the entire cohort. The median tidal volume was set to 8.0 ml/kg (interquartile range [IQR], 7.0-8.9 ml/kg) of the predicted body weight; 50 (48.1%) patients received LPV. The median positive end-expiratory pressure (PEEP) was set to 5 cmH2O (IQR, 5-6 cmH2O). No PEEP values were higher than 10 cmH2O. Compared with partially mandatory ventilation, supportive and spontaneous ventilation practices were associated with LPV. There were no significant differences in mortality and MV duration between patients subjected to LPV and those were not. CONCLUSIONS: Among brain-injured patients in China, SIMV was the most frequent ventilation mode. Nearly one-half of the brain-injured patients received LPV. Patients under supportive and spontaneous ventilation were more likely to receive LPV. TRIAL REGISTRATION: ClinicalTrials.org NCT02517073 https://clinicaltrials.gov/ct2/show/NCT02517073.

Transoral penetrating craniocerebral injury by a bamboo chopstick in a child.

We present a 3-year-old girl with a transoral injury by a bamboo chopstick penetrating the middle skull base. The features of imaging are described and the management is discussed. The potential for injury to the cavernous sinus is emphasized, even if no there is no hemorrhage on the initial CT scan. Early intracranial infection in relation to penetrating injuries is a factor in planning treatment by craniotomy.

Two subtypes of meningiomas with different imaging co-existed at sphenoid ridge.

Intracranial multiple meningiomas are not uncommon, but multiple meningiomas consisting of different subtypes are rare. Here, we describe an adult male patient with two meningiomas located at sphenoid ridge, with different features on MRI and CTA. Histological examination revealed that one was fibrous meningioma and the other was psammomatous meningioma.

Large cystic hypoglossal schwannoma with fluid-fluid level: a case report.

Hypoglossal schwannomas are rare skull base tumors. Furthermore, cystic hypoglossal schwannomas are extremely uncommon. We report the first case of a large cystic hypoglossal schwannoma with a fluid-fluid level. A 36-year-old woman presented with increased intracranial pressure and cerebellar signs without hypoglossal nerve palsy. Magnetic resonance imaging showed a predominantly cystic mass with a fluid-fluid level in the foramen magnum region extending into the hypoglossal canal. The intracranial tumor was largely removed via a midline suboccipital subtonsillar approach, leaving only a tiny residue in the hypoglossal canal. Histology confirmed a schwannoma with relative hypervascularity. Twenty months later, the tumor recurred and presented as a multicystic dumbbell-shaped lesion, extending intra- and extracranially through the enlarged hypoglossal canal. A complete resection of the intracranial and intracanalicular parts of the tumor was achieved with a small extracranial remnant treated by radiosurgery. Histology revealed a focal increased K(i)67 proliferative index. In this report, we discuss the possible reasons for the absence of hypoglossal nerve palsy and the potential mechanism of the formation of the fluid-fluid level, and we consider the treatment of this lesion.

[Expression of Aurora-B in human glioma tissue and its significance].

OBJECTIVE: To study the expression of Aurora-B in human glioma tissue and its significance. METHODS: The total RNA was extracted from 41 human glioma tissues and 11 normal brain tissues by Trizol reagent. After reverse transcription of the total RNA into cDNAs, Aurora-B mRNA expressions in these samples were detected by quantitative real-time PCR. The protein expression in these samples was detected using immunohistochemical staining. RESULTS: Aurora-B mRNA and protein expressions were significantly increased in glioma tissues as compared with those in normal brain tissues. CONCLUSION: Aurora-B mRNA and protein show markedly higher expressions in glioma tissue, suggesting that Aurora-B may be one of the malignant biomarkers in the pathogenesis and progression of human glioma.

Ischemic preconditioning induces chaperone hsp70 expression and inhibits protein aggregation in the CA1 neurons of rats.

OBJECTIVE: To investigate the effect of ischemic preconditioning on chaperone hsp70 expression and protein aggregation in the CA1 neurons of rats, and to further explore its potential neuroprotective mechanism. METHODS: Two-vesseloccluded transient global ischemia rat model was used. The rats were divided into sublethal 3-min ischemia group, lethal 10-min ischemia group and ischemic preconditioning group. Neuronal death in the CA1 region was observed by hematoxylineosin staining, and number of live neurons was assessed by cell counting under a light microscope. Immunochemistry and laser scanning confocal microscopy were used to observe the distribution of chaperone hsp70 in the CA1 neurons. Differential centrifuge was used to isolate cytosol, nucleus and protein aggregates fractions. Western blot was used to analyze the quantitative alterations of protein aggregates and inducible chaperone hsp70 in cellular fractions and in protein aggregates under different ischemic conditions. RESULTS: Histological examination showed that ischemic preconditioning significantly reduced delayed neuronal death in the hippocampus CA1 region (P < 0.01 vs 10-min ischemia group). Sublethal ischemic preconditioning induced chaperone hsp70 expression in the CA1 neurons after 24 h reperfusion following 10-min ischemia. Induced-hsp70 combined with the abnormal proteins produced during the secondary lethal 10-min ischemia and inhibited the formation of cytotoxic protein aggregates (P < 0.01 vs 10-min ischemia group). CONCLUSION: Ischemic preconditioning induced chaperone hsp70 expression and inhibited protein aggregates formation in the CA1 neurons when suffered secondary lethal ischemia, which may protect neurons from death.

[Study on the activities' alteration of the proteasome in neurons of cortex and its relation with delayed neuron death after reperfusion following ischemia].

OBJECTIVE: To investigate the activities' alteration of the proteasome in neurons of cortex and its relation with delayed neuron death after reperfusion following ischemia. METHODS: 20 minutes transient global ischemia rat model was used. Following different reperfusion period, all the 50 rats were divided into 5 groups, sham-operation group, 0.5 hour recovery group, 4 hours recovery group, 24 hours recovery group and 72 hours recovery group, 10 rats each group. Suc-llvy-amc was used as substrate for measuring proteasome's activities. Delayed neuron death after reperfusion following ischemia was observed under light microscope by HE staining. Proteasome's distribution was observed under laser scanning confocal microscope after immuno-histo-chemical staining. RESULTS: The proteasome activity of sham group was 54 602 +/- 1602, and that of 0.5 h reperfusion following ischemia was 42,036 +/- 1465 (compared with sham group, P < 0.01). Although the proteasome activity temporarily recovered to 47,536 +/- 2532 (P < 0.05) after 4 h reperfusion, it still decreased to 45,450 +/- 649 (P < 0.01) after 24 h reperfusion, and to 43,108 +/- 995 (P < 0.01) after 72 h reperfusion. HE staining showed that parts of neurons in the cortex died after 72 hours reperfusion. Under laser scanning microscope, we could observe that after 24 hours reperfusion, proteasome in both nucleus and cytoplasma significantly decreased; after 72 hours reperfusion, proteasome almost disappeared totally in nucleus and only a small part of proteasome still existed in cytoplasm. CONCLUSIONS: Decreasing of the proteasome's activities is an important factor for delayed neuron death after reperfusion following ischemia.