Radiological classification of meningiomas with hemorrhagic onset and its clinical significance.

Meningiomas are the most common benign intracranial tumors and frequently present with a gradual onset of neurological deficits; conversely, their acute presentation with hemorrhagic onset appears to be a rare event. Nonetheless, as early surgical evacuation is the foundation of treatment, a timely diagnosis of this rare type of intracranial hemorrhage is necessary. The purpose of the present single-center study was to investigate the radiological characteristics and propose a new bleeding classification for guiding the diagnosis and treatment. A total of 19 patients consecutively diagnosed with hemorrhagic meningioma were enrolled in this retrospective study. Intracranial extra-axial mass, tumor-associated hemorrhage and peritumoral brain edema were the three main radiological features of the hemorrhagic meningiomas. The site of tumor-associated hemorrhage included the peritumoral space, subarachnoid space, subdural space, brain parenchyma and/or intratumor region. Based on the anatomical relationship between meningioma and hematoma, the spontaneous hemorrhage stemming from meningiomas was further summarized into three bleeding patterns involving purely intratumoral hemorrhage (type I), purely extratumoral hemorrhage (type II) and combined intra/extratumoral hemorrhage (type III); furthermore, the type III hemorrhage usually came from type I bleeding that extended into the surrounding regions. The symptoms in type I patients were generally mild and early surgery was performed following adequate preoperative evaluations. The symptoms in type II patients were mild in certain cases and moderate to severe in others, so early or emergency surgery was chosen according to the clinical status of the patient. Almost all type III patients had moderate to severe symptoms and these patients usually required emergency surgery. In addition, patients with different bleeding types may have different pathological mechanisms underlying the tumor bleeding. Apart from being convenient for diagnosis, this concise and practical bleeding classification may aid in the selection of the treatment strategy and facilitate the understanding of the associated mechanisms.

Hemorrhagic abdominal pseudocyst following ventriculoperitoneal shunt: a case report.

BACKGROUND: Abdominal cerebrospinal fluid (CSF) pseudocyst is an uncommon but important complication of ventriculoperitoneal (VP) shunts. While individual articles have reported many cases of abdominal CSF pseudocyst following VP shunts, no case of a hemorrhagic abdominal pseudocyst after VP shunts has been reported so far. CASE PRESENTATION: This article reports a 68-year-old woman with a 4-month history of progressive abdominal pain and distention. She denied any additional symptoms. A VP shunt was performed 15 years earlier to treat idiopathic normal pressure hydrocephalus and no other abdominal surgery was performed. Physical examination revealed an elastic palpable mass in her right lower abdomen, which was dull to percussion. Abdominal computed tomography (CT) scan indicated a large cystic collection of homogenous iso-density fluid in the right lower abdominal region with clear margins. The distal segment of the peritoneal shunt catheter was located within the cystic mass. Abdominal CSF pseudocyst was highly suspected as a diagnosis. Laparoscopic cyst drainage with removal of the whole cystic mass was performed, 15-cm cyst which found with thick walls and organized chronic hematic content. No responsible vessel for the cyst hemorrhage was identified. No further shunt revision was placed. Histological examination showed that the cyst wall consisted of outer fibrous tissue and inner granulation tissue without epithelial lining, and the cystic content was chronic hematoma. The patient had an uneventful postoperative course and remained asymptomatic for 8-mo follow-up. CONCLUSION: To the best of our knowledge, this is the first report of hemorrhagic onset in the abdominal pseudocyst following VP shunt. Such special condition can accelerate the appearance of clinical signs of the abdominal pseudocyst after VP shunts, and its mechanisms may be similar to the evolution of subdural effusion into chronic subdural hematoma (CSDH).

Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury.

The aim of the present study was to assess the neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury (DAI). DAI rats were orally gavaged with berberine at a dose of 200 mg/kg of body weight for 4 weeks. Behavioral tests were used to analyze the neuroprotective effect of berberine against DAI-induced learning and memory deficits. In the present study, treatment with berberine significantly protected against DAI-induced inhibition of learning and memory in rats. Notably, berberine significantly suppressed the levels of tumor necrosis factor, interleukin-1ß and monocyte chemoattractant protein-1, as well as reduced the protein expression levels of nuclear factor-κB, Bcl-2-associated X protein and cytochrome c in DAI rats. In addition, berberine significantly suppressed the protein expression of p38 mitogen-activated protein kinase, activating transcription factor 2 and vascular endothelial growth factor in DAI rats. These results suggested that berberine exhibited a neuroprotective effect against learning and memory deficits in severe DAI through the suppression of inflammation, angiogenesis and apoptosis in a rat model.

An Underlying Pathological Mechanism of Meningiomas with Intratumoral Hemorrhage: Undifferentiated Microvessels.

BACKGROUND: Meningiomas usually present with a gradual onset of symptoms, and their acute presentation with a hemorrhagic event appears to be a rare condition. Although many clinical features of such a condition have been characterized, pathophysiological mechanisms underlying the bleeding remain unclear, and some contradictory results have been reported. The value of tumor vascularity as an index for the bleeding propensity of meningiomas is inconsistent. We sought to identify whether meningiomas have different types of blood vessels, and to explore the association of the different tumor vessels with intratumoral hemorrhage. METHODS: Six patients with meningioma with acute onset due to intratumoral hemorrhage were identified, and 12 nonhemorrhagic meningiomas were matched according to specific clinical data. The characteristics of tumor vessels were examined through immunohistochemical staining of CD31, CD34, and smooth muscle actin (SMA). The number of stained vessels was counted and compared between the 2 groups. RESULTS: Two distinct types of blood vessels were determined in all meningiomas: undifferentiated (CD31+/CD34-) and differentiated (CD31+/CD34+) vessels, and most differentiated vessels were covered by pericytes marked by SMA. However, only the mean number of undifferentiated vessels in hemorrhagic meningiomas was significantly higher than that in controls (15.3 ± 4.9 vs. 6.4 ± 3.6; P < 0.01). Neither the number of differentiated vessels nor the total number of tumor vessels were significantly different between the 2 groups (P > 0.05). CONCLUSIONS: Our results suggest that tumor vasculature in meningiomas is heterogeneous, and that the undifferentiated vessels may play a pivotal role in the spontaneous intratumoral hemorrhage from meningiomas.

Where are we in the modelling of traumatic brain injury? Models complicated by secondary brain insults.

BACKGROUND: Traumatic brain injury (TBI) contributes to a substantial number of deaths and cases of disability. Despite well-established experimental models and years of carefully conducted research, a clinical therapeutic breakthrough in TBI has lagged. This may be due, in part, to the discrepancies between commonly used experimental models and clinical scenarios. METHOD: Secondary insults, such as hypotension and hypoxemia, have been well demonstrated as powerful determinants of outcomes from TBI. Despite the frequency of secondary insults in patients with TBI, they are rarely incorporated into most existing models of TBI. This review focuses on the combined injury models, especially coupled with systemic secondary insults, and aims to provide a new view to guiding future research endeavors in this field. RESULTS: A growing number of experimental models of TBI complicated by certain secondary insult have been gradually introduced and characterized. Correspondingly, the pathophysiological changes following combined injuries and the interactive effects of primary injury with secondary insults can be studied more in-depth. CONCLUSION: A more complete understanding of the interactions between the injured brain and secondary insults represents a potentially fruitful avenue that may increase the likelihood of developing effective therapies. Experimental models of TBI should not only attempt to model the focal or diffuse changes resulting from external forces, but also integrate, when appropriate, secondary insults reminiscent of human situations.

[Effect of gefinitib on airway mucus hypersecretion induced by acrolein in rats].

OBJECTIVE: To test the effect of gefinitib, an EGFR-TKI, on airway mucus hypersecretion induced by acrolein in rats. METHODS: Thirty six rats were randomly divided into six groups, each with six rats. Group A did not get any intervention; group B had airway mucus hypersecretion induced by inhaled acrelein; Gefitinib intervention was given to group C, D, and E, with a dose of 10 mg/kg,20 mg/kg, and 30 mg/kg of gefitnib administered by gavage, respectively, 30 min before exposure to acrolein inhalation; group F served as a control group, with gefitinib (30 mg/kg) administered by gavage 30 min before exposure to saline inhalation. After three weeks, the rats were sacrificed. The lung tissue sections were obtained. The immunohistochemistry and RT-PCR were performed to detect the MUC5AC and its mRNA expression. The EGFR was detected by immunohistochemical staining. The goblet cells were identified with Alician Blue-periodic Acid Schiff (AB-PAS). RESULTS: Overexpression of MUC5AC, EGFR and increased goblet cells in the lungs of the rats were found in the rats exposed to acrolein inhalations. Gefitinib intervention inhibited the expression of MUC5AC and the increase of goblet cells induced by acrolein. Gefitinib also reduced the expression of EGFR in the lungs. CONCLUSION: Acrolein increases the expression of MUC5AC through activating EGFR, which indicates that EGFR-TKI such as gefitinib can be useful in the treatment of mucus hypersecretion by regulating the signal transduction pathways of EGFR.