[Progress in application of adult endogenous neurogenesis in brain injury repair].

Persistent neurogenesis exists in the subventricular zone (SVZ) of the ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus in the adult mammalian brain. Adult endogenous neurogenesis not only plays an important role in the normal brain function, but also has important significance in the repair and treatment of brain injury or brain diseases. This article reviews the process of adult endogenous neurogenesis and its application in the repair of traumatic brain injury (TBI) or ischemic stroke, and discusses the strategies of activating adult endogenous neurogenesis to repair brain injury and its practical significance in promoting functional recovery after brain injury.

Ability of Fibrin Monomers to Predict Progressive Hemorrhagic Injury in Patients with Severe Traumatic Brain Injury.

BACKGROUND: Progressive hemorrhagic injury (PHI) is common in patients with severe traumatic brain injury (TBI) and is associated with poor outcomes. TBI-associated coagulopathy is frequent and has been described as risk factor for PHI. This coagulopathy is a dynamic process involving hypercoagulable and hypocoagulable states either one after the other either concomitant. Fibrin monomers (FMs) are a direct marker of thrombin action and thus reflect coagulation activation. This study sought to determine the ability of FM to predict PHI after severe TBI. METHODS: We conducted a prospective, observational study including all severe TBI patients admitted in the trauma center. Between September 2011 and September 2016, we enrolled patients with severe TBI into the derivation cohort. Between October 2016 and December 2018, we recruited the validation cohort on the same basis. Study protocol included FM measurements and standard coagulation test at admission and two computed tomography (CT) scans (upon arrival and at least 6 h thereafter). A PHI was defined by an increment in size of initial lesion (25% or more) or the development of a new hemorrhage in the follow-up CT scan. Multivariate logistic regression analysis was applied to identify predictors of PHI. RESULTS: Overall, 106 patients were included in the derivation cohort. Fifty-four (50.9%) experienced PHI. FM values were higher in these patients (151 [136.8-151] vs. 120.5 [53.3-151], p < 0.0001). The ROC curve demonstrated that FM had a fair accuracy to predict the occurrence of PHI with an area under curve of 0.7 (95% CI [0.6-0.79]). The best threshold was determined at 131.7 µg/ml. In the validation cohort of 54 patients, this threshold had a negative predictive value of 94% (95% CI [71-100]) and a positive predictive value of 49% (95% CI [32-66]). The multivariate logistic regression analysis identified 2 parameters associated with PHI: FM ≥ 131.7 (OR 6.8; 95% CI [2.8-18.1]) and Marshall category (OR 1.7; 95% CI [1.3-2.2]). Coagulopathy was not associated with PHI (OR 1.3; 95% CI [0.5-3.0]). The proportion of patients with an unfavorable functional neurologic outcome at 6-months follow-up was higher in patients with positive FM: 59 (62.1%) versus 16 (29.1%), p < 0.0001. CONCLUSIONS: FM levels at admission had a fair accuracy to predict PHI in patients with severe TBI. FM values ≥ 131.7 µg/ml are independently associated with the occurrence of PHI.

Using components of the Glasgow coma scale and Rotterdam CT scores for mortality risk stratification in adult patients with traumatic brain injury: A preliminary study.

OBJECTIVE: The Glasgow Coma Scale (GCS) and Rotterdam Computed Tomography Score (RCTS) are widely used to predict outcomes after traumatic brain injury (TBI). The objective of this study was to determine whether the GCS and RCTS components can be used to predict outcomes in patients with traumatic intracranial hemorrhage (IH) after TBI. PATIENTS AND METHODS: Between May 2009 and July 2017, 773 patients with IH after TBI were retrospectively reviewed. Data on initial GCS, RCTS according to initial brain CT, and status at hospital discharge and last follow-up were collected. Logistic regression analysis was performed to evaluate the relationship between GCS and RCTS components with outcomes after TBI. RESULTS: Among the 773 patients, the overall in-hospital mortality rate was 14.0%. Variables independently associated with outcomes were the verbal (V-GCS) and motor components of GCS (M-GCS), epidural mass lesion (E-RCTS) and intraventricular or subarachnoid hemorrhage components of RCTS (H-RCTS) (p < 0.0001). The new TBI score was obtained with the following calculation: [V-GCS + M-GCS] - [E-RCTS + H-RCTS]. CONCLUSION: The new TBI score includes both clinical status and radiologic findings from patients with IH after TBI. The new TBI score is a useful tool for assessing TBI patients with IH in that it combines the GCS and RCTS components that increases area under the curve for predicting in-hospital mortality and unfavorable outcomes and eliminates the paradoxical relationship with outcomes which was observed in GCS score. It allows a practical method to stratify the risk of outcomes after TBI.

Prognostic role of D-dimer level upon admission in patients with traumatic brain injury.

BACKGROUND: The aim of this study was to evaluate the prognostic role of D-dimer level upon admission in patients with traumatic brain injury (TBI) through performing a meta-analysis. METHODS: PubMed, Web of Science, Cochrane Library, and EMBASE were searched for potential eligible literature. The study characteristics and relevant data were extracted. Poor functional outcome was defined according to the Glasgow Outcome Scale (GOS ≤3). Odds ratios (ORs) with 95% confidence intervals (CIs) were pooled to estimate the predictive value of D-dimer for progressive hemorrhagic injury (PHI) and poor functional outcome at 3 months (3M GOS ≤3) in patients with TBI. RESULTS: Eleven studies with 2761 patients were included. Eight studies examined the predictive role of higher D-dimer level for the risk of PHI, and the pooled OR was 1.72 (95% CI, 1.23-2.42). Three studies examined the predictive role of higher D-dimer level for the risk of 3M GOS ≤3, and the pooled OR was 2.00 (95% CI, 0.87-4.59). Significant between-study heterogeneities were observed, and sensitivity analyses and subgroup analyses were performed. No significant publication bias was found. CONCLUSIONS: In conclusion, in patients with TBI, higher D-dimer level upon admission was associated with higher risk of PHI, yet no significant relationship was found between D-dimer level and the risk of 3M GOS ≤3. In the future, this readily available marker could help identify patients at risk and tailor management of these patients, thus reducing PHI and improving outcome.

Low Glasgow Coma Score in Traumatic Intracranial Hemorrhage Predicts Development of Cerebral Vasospasm.

BACKGROUND: The exact mechanism, incidence, and risk factors for cerebral vasospasm after traumatic intracranial hemorrhage (ICH) continue to be poorly characterized. The incidence of post-traumatic vasospasm (PTV) varies depending on the detection modality. OBJECTIVE: We aimed to shed light on the predictors, associations, and true incidence of cerebral vasospasm after traumatic ICH using digital subtraction angiography (DSA) as the gold standard. METHODS: We examined a prospectively maintained database of traumatic brain injury (TBI) patients to identify patients with ICH secondary to TBI enrolled between 2002 and 2015 at our trauma center. Patients with TBI-associated ICH and evidence of elevated velocities on transcranial Doppler and computed tomography angiograms, confirmed with DSA were included. The diagnostic cerebral angiograms were evaluated by 2 blinded neurointerventionalists for cerebral vasospasm. Statistical analyses were conducted to determine predictors of PTV. RESULTS: Twenty patients with ICH secondary to TBI and evidence of vasospasm underwent DSAs. Seven patients (7/20; 35%) with traumatic ICH developed cerebral vasospasm and of those, 1 developed delayed cerebral ischemia (1/7; 14%). Of these 7 patients, 6 presented with subarachnoid hemorrhage (6/7; 85%). Vasospasm was substantially more common in patients with a Glasgow Coma Scale <9 (P = 0.017) than in all other groups. CONCLUSIONS: PTV as demonstrated by DCA may be more common than previously reported. Patients who exhibit PTV were more likely to have a Glasgow Coma Scale <9. This subgroup of patients may benefit from more systematic screening for the development of PTV, and earlier monitoring for signs of delayed cerebral ischemia.

[Cerebrovascular resistance in patients with severe combined traumatic brain injury].

UNLABELLED: Cerebrovascular resistance is an important parameter of the microcirculation. The main objective of cerebrovascular resistance is to maintain the constancy of cerebral blood flow and protect downstream vessels when changing perfusion pressure. The purpose of the study was to assess cerebrovascular resistance (CVR) in patients with severe combined traumatic brain injury (CTBI) with and without intracranial hematomas (IHs). MATERIAL AND METHODS: We analyzed treatment outcomes in 70 patients with severe CTBI (42 males and 28 females). The mean age was 35.5 ± 14.8 years (min 15 years; max 73 years). All patients were divided into 2 groups, depending on the presence of intracranial hemorrhage. The first group included 34 patients without IH, and the second group included 36 patients with epidural (6), subdural (26), and multiple (4) hematomas. The GCS score was 10.4 ± 2.6 in the first group and 10.6 ± 2.8 in the second group. The ISS severity injury score was 32 ± 8 in the first group and 31 ± 11 in the second group. All patients were operated on within the first 3 days, with 30 (83.3%) patients being operated on during the first day. Perfusion computed tomography (PCT) of the brain was performed within 1-14 days after TBI in the first group and within 2-8 days after surgical evacuation of hematoma in the second group. After PCT, the mean arterial pressure was measured, and the blood flow rate in the middle cerebral artery was determined using transcranial dopplerography. Cerebrovascular resistance was calculated using the formula modificated by P. Scheinberg. Comparisons between the groups were performed using the Student t-test and χ² criterion. RESULTS: The mean CVR values in each group (both with and without hematomas) were statistically significantly higher than the mean normal value of this parameter. Intergroup comparison of CVR values demonstrated a statistically significant increase in the CVR level in group 2 on the side of removed hematoma compared to group 1 (p=0.037). CVR in the perifocal zone of removed hematoma remained significantly higher compared to the symmetrical zone of the contralateral hemisphere (p=0.0009). CONCLUSION: Cerebrovascular resistance in patients with combined traumatic brain injury is significantly increased compared to the normal value. Cerebrovascular resistance in the perifocal zone after evacuation of hematoma in patients with multiple injury remains significantly increased compared to the symmetrical zone in the contralateral hemisphere.

Extracorporeal membrane oxygenation use in patients with traumatic brain injury.

Venovenous extracorporeal membrane oxygenation (ECMO) is used for patients with severe, potentially reversible, respiratory failure unresponsive to conventional management. It is relatively contraindicated in patients with traumatic brain injury (TBI) due to bleeding complications and use of anticoagulation. We report two cases of TBI patients treated with ECMO.

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury.

BACKGROUND: Blast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves affect the brain is poorly understood. To understand their effects, we analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI. RESULTS: Rats were sacrificed 24 hours or between 4 and 10 months after exposure. Intraventricular hemorrhages were commonly observed after 24 hrs. A screen for neuropathology did not reveal any generalized histopathology. However, focal lesions resembling rips or tears in the tissue were found in many brains. These lesions disrupted cortical organization resulting in some cases in unusual tissue realignments. The lesions frequently appeared to follow the lines of penetrating cortical vessels and microhemorrhages were found within some but not most acute lesions. CONCLUSIONS: These lesions likely represent a type of shear injury that is unique to blast trauma. The observation that lesions often appeared to follow penetrating cortical vessels suggests a vascular mechanism of injury and that blood vessels may represent the fault lines along which the most damaging effect of the blast pressure is transmitted.

Noninvasive estimation of cerebral perfusion pressure with transcranial Doppler ultrasonography in traumatic brain injury.

AIM: In traumatic brain injury (TBI) patients, to overcome the secondary insults, cerebral perfusion pressure (CPP) oriented therapy is recommended. The study is assigned to estimate CPP values with middle cerebral artery (MCA) flow velocities measured noninvasively using transcranial Doppler ultrasonography (TCD). MATERIAL AND METHODS: Forty-seven TBI patients were studied. Intracranial pressure (ICP), mean arterial pressure (MAP) and MCA flow velocities of the patients were monitored. Invasive CPP was calculated as the difference between MAP and ICP. The formula : 'MAP x FVd/FVm +14' was used to estimate CPP noninvasively. Correlation of the noninvasive and invasive values were analysed. RESULTS: The mean values of noninvasive CPP and invasive CPP were 66.10 ± 10.55 mmHg and 65.40 ± 10.03 mmHg respectively. The correlation between noninvasive and invasive CPP measurements was strongly significant (p < 0.001) with a correlation coefficient of r = 0.920. CONCLUSION: With ICP monitoring systems, CPP is calculated and the therapy is guided according to these values. As it is recognized that brain perfusion can be assessed with TCD waveforms, noninvasive CPP estimation with MCA flow velocities may help to observe the trends in CPP values.

Cerebral blood flow velocity changes and the value of the pulsatility index post decompressive craniectomy.

Decompressive craniectomy (DC) is used to relieve intractable intracranial hypertension and/or to prevent or reverse cerebral herniation. Significant controversy exists on selection of candidates, timing of the procedure and neurologic outcomes. Furthermore, the cerebral hemodynamic consequences post-DC have been researched only recently. We report on two consecutive patients who underwent DC in our institution and reviewed the literature on cerebral blood flow changes post-craniectomy. One patient had unilateral DC and the second had a suboccipital decompression (SOC). Cerebral blood flow velocities (FV) and pulsatility indices (PI) were recorded via transcranial Doppler (TCD). To our knowledge, this is the first report on FV/PI monitoring after SOC. TCD is a readily available, non-invasive test. The PI may provide useful information regarding timing and effectiveness of DC.

Fibrillary structure is key for hemostasis: a similar effect of collagen fleece and oxidized cellulose on experimental hemorrhagic brain injury.

BACKGROUND: The choice of the ideal hemostatic agent for intraoperative cerebral bleeding is under continuous debate. Our aim was to assess the influence of such materials on bleeding time in hemorrhagic cerebral contusions. We compared oxidized regenerated cellulose in fibrillar form (ORC) to microfibrillar collagen fleece (CF) in an experimental study. METHODS: N=50 Sprague Dawley rats underwent a bilateral craniectomy. 3 separate standardized superficial cortical impacts were inflicted using a high-speed drill. Immediately after lesion placement, each of the 3 lesions was covered with (a) nothing (control), (b) ORC, or (c) CF. We observed the 3 lesions with a surgical microscope. The bleeding times were recorded for each cerebral lesion and compared using ANOVA test. RESULTS: All traumatic lesions produced significant bleeding. The statistical analysis showed a clear reduction in bleeding time for groups treated with either ORC or CF compared to the control group. Lesions covered with ORC and CF showed no significant difference with regard to bleeding time. CONCLUSIONS: ORC and CF significantly reduce blood loss from hemorrhagic contusions. Our data suggest that they effectively reduce bleeding time. We advocate the use of hemostatic material for limiting bleeding from superficial cortical lesions.

Lateralized cerebellar contributions to word generation: a phonemic and semantic fluency study.

Impairment on verbal fluency tasks has been one of the more consistently reported neuropsychological findings after cerebellar lesions, but it has not been uniformly observed and the possible underlying cognitive basis has not been investigated. We tested twenty-two patients with chronic, unilateral cerebellar lesions (12 Left, 10 Right) and thirty controls on phonemic and semantic fluency tasks. We measured total words produced, words produced in the initial 15 seconds, errors and strategy switches. In the phonemic fluency task, the right cerebellar lesion (RC) group produced significantly fewer words compared to the left cerebellar lesion (LC) group and healthy controls, particularly over the first 15 seconds of the task with no increase in errors and significantly fewer switches over the entire task. In the semantic fluency task there was only a modest decrease in total words in the RC group compared to controls. RC lesions impair fluency with many of the same performance characteristics as left prefrontal lesions. This supports the hypotheses of a prefrontal-lateral cerebellar system for modulation of attention/executive or strategy demanding tasks.

The role of advanced MR imaging findings as biomarkers of traumatic brain injury.

Treatment of traumatic brain injury (TBI) requires proper classification of the pathophysiology. Clinical classifiers and conventional neuroimaging are limited in TBI detection, outcome prediction, and treatment guidance. Advanced magnetic resonance imaging (MRI) techniques such as susceptibility weighted imaging, diffusion tensor imaging, and magnetic resonance spectroscopic imaging are sensitive to microhemorrhages, white matter injury, and abnormal metabolic activities, respectively, in brain injury. In this article, we reviewed these 3 advanced MRI methods and their applications in TBI and report some new findings from our research. These MRI techniques have already demonstrated their potential to improve TBI detection and outcome prediction. As such, they have demonstrated the capacity of serving as a set of biomarkers to reveal the heterogeneous and complex nature of brain injury in a regional and temporal manner. Further longitudinal studies using advanced MRI in a synergistic approach are expected to provide insight in understanding TBI and imaging implications for treatment.

Neuromodulation on cervical spinal cord combined with hyperbaric oxygen in comatose patients--a preliminary report.

BACKGROUND: Because both SCS and HBO therapy have shown some promise in treating patients with states of reduced consciousness, we evaluated the combination of therapies in a prospective trial in comatose patients. METHODS: Twelve patients who had received median nerve stimulation for 3 months without improvement in consciousness received cSCS for 1 year combined with simultaneous HBO therapy for the first 3 months. Another group enrolled 12 patients who received median nerve stimulation only were served as control. RESULTS: Six patients emerged from coma at 1 year (after conclusion of treatment). Glasgow Coma Scale score, SPECT imaging, and PVS scores (state and reaction subscores) of the 12 patients were all significantly increased at 1 year compared with enrollment (P < .05). Neither respirator nor tracheostomy was needed to assist respiration in any patient. Only 1 of 12 patients still needed nasogastric tube feeding at 1 year. By contrast, control patients (without cSCS and HBO therapy) showed no apparent improvement. CONCLUSION: Increase of GCS score, cerebral blood perfusion, and PVS scores were observed in comatose patients treated with combined cSCS and HBO therapy.

Key role of sulfonylurea receptor 1 in progressive secondary hemorrhage after brain contusion.

An important but poorly understood feature of traumatic brain injury (TBI) is the clinically serious problem of spatiotemporal progression ("blossoming") of a hemorrhagic contusion, a phenomenon we term progressive secondary hemorrhage (PSH). Molecular mechanisms of PSH are unknown and efforts to reduce it by promoting coagulation have met with equivocal results. We hypothesized that PSH might be due to upregulation and activation of sulfonylurea receptor 1 (SUR1)-regulated NC(Ca-ATP) channels in capillary endothelial cells, predisposing to oncotic death of endothelial cells and catastrophic failure of capillary integrity. Anesthetized adult male rats underwent left parietal craniectomy for induction of a focal cortical contusion. The regulatory subunit of the channel, SUR1, was prominently upregulated in capillaries of penumbral tissues surrounding the contusion. In untreated rats, PSH was characterized by progressive enlargement of the contusion deep into the site of cortical impact, including corpus callosum, hippocampus, and thalamus, by progressive accumulation of extravasated blood, with a doubling of the volume during the first 12 h after injury, and by capillary fragmentation in penumbral tissues. Block of SUR1 using low-dose (non-hypoglycemogenic) glibenclamide largely eliminated PSH and capillary fragmentation, and was associated with a significant reduction in the size of the necrotic lesion and in preservation of neurobehavioral function. Antisense oligodeoxynucleotide against SUR1, administered after injury, reduced both SUR1 expression and PSH, consistent with a requirement for transcriptional upregulation of SUR1. Our findings provide novel insights into molecular mechanisms responsible for PSH associated with hemorrhagic contusions, and point to SUR1 as a potential therapeutic target in TBI.

Progression of traumatic intracerebral hemorrhage: a prospective observational study.

ABSTRACT Preliminary evidence has shown that intracerebral hemorrhages, either spontaneous (sICH) or traumatic (tICH) often expand over time. An association between hemorrhage expansion and clinical outcomes has been described for sICH. The intent of this prospective, observational study was to characterize the temporal profile of hemorrhage progression, as measured by serial computed tomography (CT) scanning, with the aim of better understanding the natural course of hemorrhage progression in tICH. There was also a desire to document the baseline adverse event (AE) profile in this patient group. An important motive for performing this study was to set the stage for subsequent studies that will examine the role of a new systemic hemostatic agent in tICH. Subjects were enrolled if they had tICH lesions of at least 2 mL on a baseline CT scan obtained within 6 h of a head injury. CT scans were repeated at 24 and 72 h. Clinical outcomes and pre-defined AEs were documented. The data showed that 51% of the subjects demonstrated an increase in tICH volume, and that most of the increase occurred early. In addition, larger hematomas exhibited the greatest expansion. Thromboembolic complications were identified in 13% of subjects. This study demonstrates that tICH expansion between the baseline and 24-h CT scans occurred in approximately half of the subjects. The earlier after injury that the initial CT scan is obtained, the greater is the likelihood that the hematoma will expand on subsequent scans. The time frame during which hemorrhagic expansion occurs provides an opportunity for early intervention to limit a process with adverse prognostic implications.

Simvastatin-mediated upregulation of VEGF and BDNF, activation of the PI3K/Akt pathway, and increase of neurogenesis are associated with therapeutic improvement after traumatic brain injury.

This study was undertaken to evaluate the effect of simvastatin, a cholesterol-lowering agent, on the Akt-mediated signaling pathway and neurogenesis in the dentate gyrus (DG) of the hippocampus in rats after traumatic brain injury (TBI). Adult male Wistar rats were divided into three groups: (1) sham group (n = 8); (2) saline control group (n = 40); and (3) simvastatin-treated group (n = 40). Controlled cortical impact (CCI) injury was performed over the left parietal lobe. Simvastatin was administered orally at a dose of 1 mg/kg starting at day 1 after TBI and then daily for 14 days. Bromodeoxyuridine (BrdU) was injected intraperitoneally into rats. A modified Morris Water Maze (WM) task was performed between 31 and 35 days after treatment to test spatial memory (n = 8/group). Animals were sacrificed at 1, 3, 7, 14, and 35 days after treatment (n = 8/group/time point). Western blot was utilized to investigate the changes in the Akt-mediated signaling pathway. Enzyme-linked immunosorbent assay (ELISA) analyses were employed to measure vascular endothelial growth factor (VEGF) and brain-derived neurotrophin factor (BDNF) expression. Immunohistochemical and fluorescent staining were performed to detect the BrdU- and neuronal nuclei (NeuN)/BrdU-positive cells. Our data show that simvastatin treatment increases phosphorylation of v-akt murine thymoma viral oncogene homolog (Akt), glycogen synthase kinase-3beta (GSK-3beta), and cAMP response element-binding proteins (CREB); elevates the expression of BDNF and VEGF in the DG; increases cell proliferation and differentiation in the DG; and enhances the recovery of spatial learning. These data suggest that the neurorestorative effect of simvastatin may be mediated through activation of the Akt-mediated signaling pathway, subsequently upregulating expression of growth factors and inducing neurogenesis in the DG of the hippocampus, thereby leading to restoration of cognitive function after TBI in rats.

Haematoma of the tentorium cerebelli - new pathology or new prognostic factor in neurotraumatology? A preliminary report.

BACKGROUND AND PURPOSE: The aim of the study was to establish the frequency of haematoma of the tentorium cerebelli, to elucidate the possible pathomechanism related to its formation, and to assess its clinical significance. MATERIAL AND METHODS: 84 patients with haematoma of the tentorium cerebelli were selected out of the 1159 patients treated in our Department from 2003 to 2005 due to craniocerebral trauma. All patients had computed tomography (CT) performed on admission. In selected cases, magnetic resonance imaging (MRI) was performed. Additionally, 4 autopsies were performed using a special technique for better recognition of blood location within the region of the tentorium. RESULTS: The study group comprised 61 men (73%) and 23 women (age range: 18-84 years). Fall on the occiput was the main cause of trauma. The clinical status of patients was rather serious (53% of patients scored below 8 pts on the Glasgow Coma Scale on admission), as was the clinical course (39% of patients eventually died). The following co-existing pathologies were found in CT: traumatic subarachnoid haemorrhage and cerebral contusion (60% of patients), subdural haematoma (45%), intracerebral haematoma (31%), pathology in posterior fossa (12%), and epidural haematoma (8%). MRI revealed subdural collection of blood above or below the tentorium or the subarachnoid haemorrhage beneath the occipital lobes and/or over the cerebellar hemisphere. CONCLUSIONS: The progress in neuroimaging, especially in CT scanning, enables haematoma of the tentorium cerebelli to be discerned as a distinct clinical entity.

Brain abscess following intracerebral haemorrhage.

We report two cases of brain abscess, which developed at the site of an intracerebral haemorrhage (ICH) in a 75-year-old man and a 32-year-old-man. The patients recovered after surgical treatment and systemic antibiotic therapy. The route of infection could not be detected in either case. The literature contains only 13 reported cases of brain abscess as a complication of ICH. Although the interval from initial ICH to abscess formation ranged from 4 to 20 weeks, almost all patients had episodes of high fever, indicating the presence of systemic infection and bacterial seeding, 0-14 days after the onset of their ICH. Therefore, abscess formation appears to be caused by haematogenous seeding of infection in patients with ICH. Abscess formation should be considered when a patient deteriorates clinically with a febrile episode after an ICH.

Cerebellar haemorrhage after non-traumatic evacuation of supratentorial chronic subdural haematoma: report of two cases.

Cerebellar haemorrhage is an unusual complication of supratentorial neurosurgery. Several causative pre-operative factors and medical risk factors may predispose patients to cerebellar haemorrhage, however its etiology remains still unclear. Only two case reports have previously described the occurrence of cerebellar haemorrhage after subdural haematoma evacuation by burr-hole trepanation. We present two patients with this rare postoperative complication of minor supratentorial neurosurgery and possible underlying pathophysiological mechanisms are discussed. Our two cases support the post- rather than per-operative pathogenetic hypothesis. Although the complication is associated with a significant morbidity and mortality, most cases follow a benign course.