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Posttraumatic cerebral infarction (PTCI) is a serious complication of traumatic brain injury (TBI), and the prevalence and risk factors of PTCI in TBI patients are in dispute. We systematically searched the literature in the PubMed, Embase, and Cochrane library up to October 2021 to identify studies on the prevalence and risk factors of PTCI in patients with TBI. The quality of observational studies was assessed by the Newcastle-Ottawa scale tool. Random-effects model was conducted. The Higgins` I2 statistic was used to measure heterogeneity between trials. Moreover, sensitive analyses were conducted to assess whether the pooled result was credible and robust. Eleven studies (3696 total TBI patients) were included. The pooled prevalence of PTCI in TBI patients was 14% (95% CI, 0.11-0.17; I2 = 83.1%). Sensitive analyses showed that the pooled prevalence of PTCI was 13% (95% CI, 0.10-0.15; I2 = 69.2%) by omitting Su et al. The prevalence of PTCI was associated with a lower Glasgow Coma Scale (GCS) score (OR, 0.33; 95% CI, 0.14-0.77; I2 = 99.2%), pupillary dilation (OR, 4.73; 95% CI, 4.30-5.19; I2 = 85.6%), abnormal PT (OR, 1.16; 95% CI,1.05-2.47; I2 = 99.2%), hematoma location (OR, 1.16; 95% CI,1.05-2.47; I2 = 99.2%) and hematoma volume (OR, 1.16; 95% CI,1.05-2.47; I2 = 99.2%). Whereas hypotensive shock, duraplasty, cerebral herniation, and thrombocytopenia were not statistically associated with PTCI. Lower GCS, pupillary dilation, abnormal PT, hematoma location, and hematoma volume were risk factors for PTCI. Considering some limitations, the conclusion of our study should be interpreted with caution.

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PURPOSE: Posttraumatic cerebral infarction (PTCI) is a common and relatively serious complication of traumatic brain injury (TBI) without a clear etiology. Evaluating risk factors in advance is particularly important to predict and avoid the occurrence of PTCI. PATIENTS AND METHODS: We retrospectively analyzed 297 patients with moderate to severe TBI admitted to the Department of Neurosurgery in our hospital from January 2019 to September 2020 and evaluated the effects of various factors such as age, sex, admission Glasgow Coma Scale (GCS), skull base fracture, subarachnoid hemorrhage (SAH), brain herniation, hypotensive shock, and decompressive craniectomy on the incidence of PTCI. We also performed a multivariate logistics regression analysis on the relevant factors identified and evaluated the diagnostic value of each risk factor in advance by receiver operating characteristic (ROC) analyses. RESULTS: Among the patients, 32 (10.77%) suffered PTCI. The incidence rates of PTCI in those with GCS scores of 3-8 and 9-12 were 15.87% (30/189) and 1.85% (2/108), respectively, while the rates were 18.84% (13/69), 15.03% (29/193), 18.57% (13/70), and 20.59% (14/68) in those with skull base fractures, traumatic SAH, brain herniation, and hypotensive shock, respectively, and 14.38% (23/160) in those who underwent decompressive craniectomy. These differences in PTCI incidence were statistically significant. However, the differences in PTCI incidence caused by patient age and sex were not statistically significant. CONCLUSION: Low GCS score, skull base fractures, traumatic SAH, brain herniation, hypotensive shock, and decompressive craniectomy are risk factors for the occurrence of PTCI, while age and sex are not significantly correlated with the occurrence of PTCI.

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BACKGROUND: Post-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. METHODS: This was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. RESULTS: We enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66-0.82; increased to AUC = 0.79, 95% CI 0.71-0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65-0.81 increased to AUC = 0.80, 95% C.I. 0.69-0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups. CONCLUSIONS: PTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS. TRIAL REGISTRATION: The present study was registered in ClinicalTrial.gov with the ID number NCT02430324.

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BACKGROUND: Subdural effusion with hydrocephalus (SDEH) is a rare complication of traumatic brain injury, especially following decompressive craniectomy (DC) for posttraumatic cerebral infarction. The diagnosis and treatment are still difficult and controversial for neurosurgeons. CASE PRESENTATION: A 45-year-old man developed traumatic cerebral infarction after traumatic brain injury and underwent DC because of the mass effect of cerebral infarction. Unfortunately, the complications of traumatic subdural effusion (SDE) and hydrocephalus occurred in succession following DC. Burr-hole drainage and subdural peritoneal shunt were performed in sequence because of the mass effect of SDE, which only temporarily improved the symptoms of the patient. Cranioplasty and ventriculoperitoneal shunt were performed ultimately, after which SDE disappeared completely. However, the patient remains severely disabled, with a Glasgow Outcome Scale of 3. CONCLUSIONS: It is important for neurosurgeons to consider the presence of accompanying hydrocephalus when treating patients with SDE. Once the diagnosis of SDEH is established and the SDE has no mass effect, timely ventriculoperitoneal shunt may be needed to avoid multiple surgical procedures, which is a safe and effective surgical method to treat SDEH.

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Objective To explore the role of continuous pulse output (PICCO) monitoring in treatment of patients with traumatic acute diffuse brain swelling (PADBS). Methods Eighty-six PADBS patients, admitted to our hospital from January 2014 to October 2017, were routinely given brain invasive intracranial pressure (ICP) monitoring after admission. At the same time, the patients were given bone flap decompression and hematoma clearance according to the condition of the diseases. After surgery, according to the wishes of family members, patients were divided into two groups (n=43):patients from treatment group accepted PICCO monitoring on the basis of ICP monitoring, and the treatment plan was adjusted according to the monitoring results; and the treatment plan in patients from control group was adjusted according to traditional central venous pressure (CVP) monitoring results on basis of ICP monitoring. Results One week after operation, the ICP in the treatment group was (14.36±2.82) mmHg when the cerebral perfusion pressure (CPP) was controlled between 50 and 70 mmHg, which was significantly different from the ICP in the control group (18.58±2.25) mmHg (P<0.05). Two weeks after treatment, Glasgow Coma Scale (GCS) scores of the treatment group (10.87±1.72) were significantly higher than those of the control group (8.18±1.16, P<0.05). The incidences of posttraumatic cerebral infarction (PTCI) and neurogenic pulmonary edema (NPE) in the treatment group (11.6％, 18.6％) were significantly lower than those of the control group (25.6％, 34.9％, P<0.05); the recovery rate (76.7％) in the treatment group was significantly higher than that in the control group (60.5％, P<0.05); the mortality rate (9.3％) was significantly lower than that in the control group (18.6％, P<0.05). Conclusion On the basis of intraventricular ICP monitoring, combined PICCO monitoring can effectively control ICP, improve cerebral perfusion, reduce the incidence of PTCI and NPE, improve the prognosis, and reduce the mortality in PADBS patients.

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BACKGROUND: In-hospital major adverse events (IMAEs), mainly including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are associated with poor prognosis after traumatic brain injury (TBI). Thioredoxin, a potent anti-oxidant, has been identified as an oxidative stress marker. This study was designed to explore the association of serum thioredoxin concentrations with IMAEs of patients with severe TBI. METHODS: This prospective, observational study recruited a total of 108 healthy controls and 108 patients with severe TBI. We investigated the possible relation of serum thioredoxin concentrations to IMAEs and trauma severity (reflected by Glasgow coma scale scores) following TBI using a multivariate analysis. RESULTS: Serum thioredoxin concentrations were higher in the patients than in the controls. Serum concentrations of thioredoxin significantly correlated with admission Glasgow coma scale scores. Thioredoxin in serum independently predicted any IMAEs. As compared to admission Glasgow coma scale scores, thioredoxin concentrations had similar areas under receiver operating characteristic curve for any IMAEs. CONCLUSION: Increased serum thioredoxin concentrations are highly associated with trauma severity and IMAEs, indicating thioredoxin might be a potential prognostic biomarker after TBI.

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BACKGROUND: Nesfatin-1 is related to inflammation. Its increased circulating concentrations are associated with the severity and prognosis of subarachnoid hemorrhage. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are correlated with mortality after traumatic brain injury (TBI). The present study was designed to investigate the changes of plasma nesfatin-1 concentrations and further assess its association with inflammation, trauma severity, in-hospital mortality and IMAEs following TBI. METHODS: We measured plasma nesfatin-1 concentrations of 100 severe TBI patients and 100 controls. Progressive hemorrhagic injury and posttraumatic cerebral infarction were diagnosed based on a follow-up computerized tomography scan. Acute traumatic coagulopathy was identified according to a coagulation test. RESULTS: Plasma nesfatin-1 concentrations were significantly higher in patients than in controls and associated highly with Glasgow coma scale (GCS) scores and plasma C-reactive protein concentrations. Nesfatin-1 was indicated as an independent predictor for in-hospital mortality and IMAEs. In accordance with area under receiver operating characteristic curve, its predictive value was similar to GCS scores. CONCLUSION: Increased plasma nesfatin-1 concentrations are associated closely with inflammation, trauma severity and clinical outcomes, indicating that nesfatin-1 might be involved in inflammation and become a good prognostic biomarker following TBI.

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BACKGROUND: Galectin-3 plays a significant role in microglia activation. Its increased circulating concentration has been associated with some inflammatory diseases. In-hospital major adverse events (IMAEs), including acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, have high prevalence and are strong predictors of mortality after severe traumatic brain injury (STBI). The present study was designed to investigate the relationships between plasma galectin-3 concentrations and trauma severity, in-hospital mortality and IMAEs following STBI. METHODS: Plasma galectin-3 concentrations of 100 STBI patients and 100 controls were determined. Diagnosis of progressive hemorrhagic injury and posttraumatic cerebral infarction was made on the follow-up computerized tomography scan. Acute traumatic coagulopathy was defined based on coagulation test. RESULTS: Plasma galectin-3 concentrations were significantly higher in patients as compared to controls and also associated highly with Glasgow Coma Scale scores and plasma C-reactive protein concentrations. Galectin-3 emerged as an independent predictor for in-hospital mortality and IMAEs. Areas under receiver operating characteristic curve of plasma galectin-3 concentrations were similar to those of Glasgow Coma Scale scores for prediction of in-hospital morality and IMAEs. CONCLUSIONS: Plasma galectin-3 concentrations have close relation to inflammation, trauma severity and clinical outcome, suggesting that galectin-3 should have the potential to be a good prognostic biomarker after STBI.

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BACKGROUND: Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of traumatic brain injury (TBI). This study aimed to evaluate the characteristics and risk factors of PTCI after severe TBI (sTBI) and explore possible mechanism. METHODS: This retrospective study included a cohort of 339 patients with sTBI; they were divided into the PTCI and non-PTCI groups. Clinical data and follow-up charts were reviewed for comparison. The logistic regression model was used for multivariate analysis to detect the risk factors of PTCI. The Glasgow Outcome Scale (GOS) and Barthel index (BI) for activities of daily living (ADL) were applied to evaluate their outcome. RESULTS: PTCI led to an increased mortality (43.5 % vs. 10.7 %, P < 0.001) and days of intensive care unit stay (14.3 days vs. 7.1 days, P < 0.001), decreased GOS (3.1 vs. 4.1, P < 0.001) and BI (25.0 vs. 77.9, P < 0.001). Increased infarction volume led to poor outcome assessed by GOS (r = -0.46, P < 0.0001) and BI for ADL (r = -0.36, P = 0.026) for surviving patients. Compared with non-PTCI patients, PTCI patients had a high incidence of midline shift (36.2 % vs. 20.7 %, P = 0.011) and posttraumatic vasospasm (PTV) (42.0 % vs. 27.4 %, P = 0.027). Daily prevalence of PTCI occurred in two peaks: one (73.9 %) was in the first 24 h after injury, while the other (18.8 %) was in the span of 43 to 60 h postinjury. In multivariate analysis, hyperthermia [adjusted odds ratio (OR), 3.11; P = 0.001] in the first 24 h, thrombocytopenia (OR, 27.08; P < 0.001), abnormal prothrombin time (OR, 7.66; P < 0.001) and traumatic subarachnoid hemorrhage (OR, 2.33; P = 0.022) were independent predictors for PTCI. CONCLUSIONS: PTCI deteriorates the outcome of sTBI patients. Mechanical compression and hemocoagulative disturbance serve as potential mechanisms mediating this pathophysiological process. PTV may also contribute to PTCI, but its association with PTCI is weak and needs further exploration. Early recognition and intervention of these factors might be beneficial for preventing PTCI.

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PURPOSE: The purpose was to present a case series of vertical gaze paresis in patients with a history of cranioencephalic trauma (CET). METHODS: The clinical characteristics and management are presented of nine patients with a history of CET secondary to motor vehicle accidents with associated vertical gaze paresis. RESULTS: Neuroimaging studies indicated posttraumatic contusion of the thalamic-mesencephalic region in all nine patients who corresponded to the artery of Percheron region; four patients had signs of hemorrhagic transformation. Vertical gaze paresis was present in all patients, ranging from complete paralysis of the upward and downward gaze to a slight limitation of upward gaze. DISCUSSION: Posttraumatic vertical gaze paresis is a rare phenomenon that can occur in isolation or in association with other neurological deficits and can cause a significant limitation in the quality-of-life. Studies in the literature have postulated that the unique anatomy of the angle of penetration of the thalamoperforating and lenticulostriate arteries makes these vessels more vulnerable to isolated selective damage in certain individuals and can cause-specific patterns of CET.

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Posttraumatic cerebral infarction is a recognized complication of craniocerebral trauma, but, its frequency, cause, and influence on mortality are not well defined. During a two year period, 706 patients with head trauma were examined in our hospital with cranial CT studies. The CT findings which strongly suggested the herniation were seen in 46 patients. The posttraumatic cerebral infarction was diagnosed retrospectively in 18 of these patients. Detailed information, including CT findings were recorded from 1 to 10 days after admission. Posttraumatic cerebral infarctions were seen in the vascular territories of the middle cerebral artery(PCA) in 9 patients, posterior cerebral artery(PCA) in 4 patients, anterior cerebral artery(ACA) in 3 patients, and multiple in 2 patients. Outcomes of these 18 patients were severely disabled in 8 patients, moderate disabled in 6 patients, and death in 3 patients. Only one remaining patient was demonstrated a good recovery. These results suggest that cerebral infarction with severe head trauma might be associated with significantly bad influence on outcome of these patients when compared with those without cerebral infarction.

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