Melatonin attenuated early brain injury induced by subarachnoid hemorrhage via regulating NLRP3 inflammasome and apoptosis signaling.

Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation associated with the upregulation of apoptotic signaling pathway has been implicated in various inflammatory diseases including hemorrhagic insults. Melatonin is reported to possess substantial anti-inflammatory properties, which is beneficial for early brain injury (EBI) after SAH. However, the molecular mechanisms have not been clearly identified. This study was designed to investigate the protective effects of melatonin against EBI induced by SAH and to elucidate the potential mechanisms. The adult mice were subjected to SAH. Melatonin or vehicle was injected intraperitoneally 2 hr after SAH. Melatonin was neuroprotective, as shown by increased survival rate, as well as elevated neurological score, greater survival of neurons, preserved brain glutathione levels, and reduced brain edema, malondialdehyde concentrations, apoptotic ratio, and blood-brain barrier (BBB) disruption. Melatonin also attenuated the expressions of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), cleaved caspase-1, interleukin-1ß (IL-1ß), and interleukin-6 (IL-6); these changes were also associated with an increase in the anti-apoptotic factor (Bcl2) and reduction in the pro-apoptotic factor (Bim). In summary, our results demonstrate that melatonin treatment attenuates the EBI following SAH by inhibiting NLRP3 inflammasome-associated apoptosis.

CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling.

Promoting hematoma absorption is a novel therapeutic strategy for intracerebral hemorrhage (ICH); however, the mechanism of hematoma absorption is unclear. The present study explored the function and potential mechanism of CD36 in hematoma absorption using in vitro and in vivo ICH models. Hematoma absorption in CD36-deficient ICH patients was examined. Compared with patients with normal CD36 expression, CD36-deficient ICH patients had slower hematoma adsorption and aggravated neurologic deficits. CD36 expression in perihematomal tissues in wild-type mice following ICH was increased, whereas the hematoma absorption in CD36(-/-) mice was decreased. CD36(-/-) mice also showed aggravated neurologic deficits and increased TNF-α and IL-1ß expression levels. The phagocytic capacity of CD36(-/-) microglia for RBCs was also decreased. Additionally, the CD36 expression in the perihematoma area after ICH in TLR4(-/-) and MyD88(-/-) mice was significantly increased, and hematoma absorption was significantly promoted, which was significantly inhibited by an anti-CD36 Ab. In vitro, TNF-α and IL-1ß significantly inhibited the microglia expression of CD36 and reduced the microglia phagocytosis of RBCs. Finally, the TLR4 inhibitor TAK-242 upregulated CD36 expression in microglia, promoted hematoma absorption, increased catalase expression, and decreased the H2O2 content. These results suggested that CD36 mediated hematoma absorption after ICH, and TLR4 signaling inhibited CD36 expression to slow hematoma absorption. TLR4 inhibition could promote hematoma absorption and significantly improve neurologic deficits following ICH.

[CRANIO­CEREBRAL TRAUMA WITH ESTIMATED SEVERITY OF 13­15 POINTS IN ACCORDANCE TO GLASGOW SCALE ­ A LIGHT TRAUMA].

Retrospective analysis of cranio­cerebral trauma (CCT) in 141 injured persons, ageing (38.3 ± 14.3) yrs at average, severity of which in accordance to Glasgow scale was estimated in 13 ­ 15 points, was performed. The injured persons were managed in accordance to actual recommendations of Ministry of Health of Ukraine. In accordance to CT data, the brain commotion was noted in 40 patients, the brain contusion type І ­ in 25, the brain contusion type ІІ with the skull fornix fracture ­ in 30, with linear fracture of the skull bones and traumatic hematomas into the brain­tunics ­ in 30, with fracture of the temporal bone pyramid ­ in 16. In indices 14 points and less (in accordance to Glasgow scale) in terms up to 24 h after CCT and absence of alcohol intoxication in 76.9% injured persons in accordance to CT data the intracranial traumatic affections were revealed. In indices of 15 points in 21% of injured persons false­negative results were determined, witnessing disparity of CCT signs with a CT data.

Traumatic brain injury presenting with bilateral basal ganglia hemorrhage.

CONTEXT: Traumatic basal ganglia hemorrhage (TBGH) is a rare presentation of traumatic brain injury. Bilateral lesions are even rarer. Only twelve similar cases were previously published. CASE REPORT: We report the case of a patient with bilateral TBGH. He was managed conservatively. Long-term follow-up disclosed a cognitive dysfunctions attributed to associated diffuse axonal injury. Acceleration and deceleration forces may have torn pallidum arterial branches determining hemorrhage. CONCLUSION: Bilateral TBGH is an uncommon presentation of traumatic brain injury. Associated diffuse axonal injury worsens the outcome.

Mouse brain PSA-NCAM levels are altered by graded-controlled cortical impact injury.

Traumatic brain injury (TBI) is a worldwide endemic that results in unacceptably high morbidity and mortality. Secondary injury processes following primary injury are composed of intricate interactions between assorted molecules that ultimately dictate the degree of longer-term neurological deficits. One comparatively unexplored molecule that may contribute to exacerbation of injury or enhancement of recovery is the posttranslationally modified polysialic acid form of neural cell adhesion molecule, PSA-NCAM. This molecule is a critical modulator of central nervous system plasticity and reorganization after injury. In this study, we used controlled cortical impact (CCI) to produce moderate or severe TBI in the mouse. Immunoblotting and immunohistochemical analysis were used to track the early (2, 24, and 48 hour) and late (1 and 3 week) time course and location of changes in the levels of PSA-NCAM after TBI. Variable and heterogeneous short- and long-term increases or decreases in expression were found. In general, alterations in PSA-NCAM levels were seen in the cerebral cortex immediately after injury, and these reductions persisted in brain regions distal to the primary injury site, especially after severe injury. This information provides a starting point to dissect the role of PSA-NCAM in TBI-related pathology and recovery.

Analysis of pituitary lesions in fatal closed head injury.

We analyzed forensic autopsy findings of 66 consecutive patients with fatal closed head injury who survived up to 48 days after trauma to ascertain the causal factors and the time course of development of posttraumatic pituitary lesions. Pituitary lesions were identified in 27 patients. In patients with pituitary lesions, posterior lobe hemorrhage was observed in 21 patients, followed by anterior lobe hemorrhage in 10 patients and anterior lobe infarct in 7 patients. Comparisons between patients with and without pituitary lesions showed that falls and subdural hematoma were significantly frequent in patients with pituitary lesions. Immunohistochemistry of neurophysin showed increased immunoreactivity in the hypothalamus of patients with pituitary lesions and brain edema, providing morphologic evidence of pituitary dysfunction. Hemorrhage in the anterior or posterior lobe was identifiable in patients with short survival periods, whereas infarct in the anterior lobe appeared in patients surviving at least 14 hours. These data further our understanding of the mechanisms of pituitary dysfunctions and help in the estimation of the survival period after head trauma.

[Factors indicative of differentiated approach to the treatment of severe focal lesions of the brain].

The article is devoted the study of complex research 126 patients with a heavy craniocerebral trauma, accompanied vnutrimozgovoy traumatic haematoma and hearth crushing of cerebrum, passing treatment in the clinic of neuro-surgery. The use of modern diagnostic methods of research considerably changed the informative providing of diagnostic and medical process at the different hearth defeats of cerebrum, including traumatic hearth injuries of cerebrum. The long-term looking after intracraneal haematomas allowed to mark that haematomas suffer successive changes which are expressly traced on computer tomography researches in course of time.

White matter and neurocognitive changes in adults with chronic traumatic brain injury.

Diffusion tensor imaging was used to investigate white matter (WM) integrity in adults with traumatic brain injury (TBI) and healthy adults as controls. Adults with TBI had sustained severe vehicular injuries on the average of 7 years earlier. A multivariate analysis of covariance with verbal IQ as the covariate revealed that adults with TBI had lower fractional anisotropy and higher mean diffusivity than controls, specifically in the three regions of interest (ROIs), the centrum semiovale (CS), the superior frontal (SPF), and the inferior frontal (INF). Adults with TBI averaged in the normal range in motor speed and two of three executive functions and were below average in delayed verbal recall and inhibition, whereas controls were above average. Time since injury, but not age, was associated with WM changes in the SPF ROI, whereas age, but not time since injury, was associated with WM changes in the INF ROI, suggesting that the effects of WM on time since injury may interact with age. To understand the utility of WM changes in chronic recovery, larger sample sizes are needed to investigate associations between cognition and WM integrity of severely injured individuals who have substantial cognitive impairment compared to severely injured individuals with little cognitive impairment. (JINS, 2009, 15, 130-136.).

Detrimental effects of aging on outcome from traumatic brain injury: a behavioral, magnetic resonance imaging, and histological study in mice.

Considerable evidence indicates that outcomes from traumatic brain injury (TBI) are worse in the elderly, but there has been little preclinical research to explore potential mechanisms. In this study, we examined the age-related effects on outcome in a mouse model of controlled cortical impact (CCI) injury. We compared the responses of adult (5-6 months old) and aged (21-24 months old) male mice following a moderate lateral CCI injury to the sensorimotor cortex. Sensorimotor function was evaluated with the rotarod, gridwalk and spontaneous forelimb behavioral tests. Acute edema was assessed from hyperintensity on T2-weighted magnetic resonance images. Blood-brain barrier opening was measured using anti-mouse immunoglobulin G (IgG) immunohistochemistry. Neurodegeneration was assessed by amino-cupric silver staining, and lesion cavity volumes were measured from histological images. Indicators of injury were generally worse in the aged than the adult mice. Acute edema, measured at 24 and 48 h post-injury, resolved more slowly in the aged mice (p < 0.01). Rotarod recovery (p < 0.05) and gridwalk deficits (p < 0.01) were significantly worse in aged mice. There was greater (p < 0.01 at 3 days) and more prolonged post-acute opening of the blood-brain barrier in the aged mice. Neurodegeneration was greater in the aged mice (p < 0.01 at 3 days). In contrast, lesion cavity volumes, measured at 3 days post-injury, were not different between injured groups. These results suggest that following moderate controlled cortical impact injury, the aged brain is more vulnerable than the adult brain to neurodegeneration, resulting in greater loss of function. Tissue loss at the impact site does not explain the increased functional deficits seen in the aged animals. Prolonged acute edema, increased opening of the blood-brain barrier and increased neurodegeneration found in the aged animals implicate secondary processes in age-related differences in outcome.

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.

The Role of Forensic Botany in Solving a Case: Scientific Evidence on the Falsification of a Crime Scene.

Forensic botany can provide useful information for pathologists, particularly on crime scene investigation. We report the case of a man who arrived at the hospital and died shortly afterward. The body showed widespread electrical lesions. The statements of his brother and wife about the incident aroused a large amount of suspicion in the investigators. A crime scene investigation was carried out, along with a botanical morphological survey on small vegetations found on the corpse. An autopsy was also performed. Botanical analysis showed some samples of Xanthium spinosum, thus leading to the discovery of the falsification of the crime scene although the location of the true crime scene remained a mystery. The botanical analysis, along with circumstantial data and autopsy findings, led to the discovery of the real crime scene and became crucial as part of the legal evidence regarding the falsity of the statements made to investigators.

Dual-Energy CT in Hemorrhagic Progression of Cerebral Contusion: Overestimation of Hematoma Volumes on Standard 120-kV Images and Rectification with Virtual High-Energy Monochromatic Images after Contrast-Enhanced Whole-Body Imaging.

BACKGROUND AND PURPOSE: In patients with hemorrhagic contusions, hematoma volumes are overestimated on follow-up standard 120-kV images obtained after contrast-enhanced whole-body CT. We aimed to retrospectively determine hemorrhagic progression of contusion rates on 120-kV and 190-keV images derived from dual-energy CT and the magnitude of hematoma volume overestimation. MATERIALS AND METHODS: We retrospectively analyzed admission and follow-up CT studies in 40 patients with hemorrhagic contusions. After annotating the contusions, we measured volumes from admission and follow-up 120-kV and 190-keV images using semiautomated 3D segmentation. Bland-Altman analysis was used for hematoma volume comparison. RESULTS: On 120-kV images, hemorrhagic progression of contusions was detected in 24 of the 40 patients, while only 17 patients had hemorrhagic progression of contusions on 190-keV images (P = .008). Hematoma volumes were systematically overestimated on follow-up 120-kV images (9.68 versus 8 mm3; mean difference, 1.68 mm3; standard error, 0.37; P < .001) compared with 190-keV images. There was no significant difference in volumes between admission 120-kV and 190-keV images. Mean and median percentages of overestimation were 29% (95% CI, 18-39) and 22% (quartile 3 - quartile 1 = 36.8), respectively. CONCLUSIONS: The 120-kV images, which are comparable with single-energy CT images, significantly overestimated the hematoma volumes, hence the rate of hemorrhagic progression of contusions, after contrast-enhanced whole-body CT. Hence, follow-up of hemorrhagic contusions should be performed on dual-energy CT, and 190-keV images should be used for the assessment of hematoma volumes.

Hybrid outcome prediction model for severe traumatic brain injury.

Numerous studies addressing different methods of head injury prognostication have been published. Unfortunately, these studies often incorporate different head injury prognostication models and study populations, thus making direct comparison difficult, if not impossible. Furthermore, newer artificial intelligence tools such as machine learning methods have evolved in the field of data analysis, alongside more traditional methods of analysis. This study targets the development of a set of integrated prognostication model combining different classes of outcome and prognostic factors. Methodologies such as discriminant analysis, logistic regression, decision tree, Bayesian network, and neural network were employed in the study. Several prognostication models were developed using prospectively collected data from 513 severe closed head-injured patients admitted to the Neurocritical Unit at National Neuroscience Institute of Singapore, from April 1999 to February 2003. The correlation between prognostic factors at admission and outcome at 6 months following injury was studied. Overfitting error, which may falsely distinguish different outcomes, was compared graphically. Tenfold cross-validation technique, which reduces overfitting error, was used to validate outcome prediction accuracy. The overall prediction accuracy achieved ranged from 49.79% to 81.49%. Consistently high outcome prediction accuracy was seen with logistic regression and decision tree. Combining both logistic regression and decision tree models, a hybrid prediction model was then developed. This hybrid model would more accurately predict the 6-month post-severe head injury outcome using baseline admission parameters.

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.

Time course of post-traumatic mitochondrial oxidative damage and dysfunction in a mouse model of focal traumatic brain injury: implications for neuroprotective therapy.

In the present study, we investigate the hypothesis that mitochondrial oxidative damage and dysfunction precede the onset of neuronal loss after controlled cortical impact traumatic brain injury (TBI) in mice. Accordingly, we evaluated the time course of post-traumatic mitochondrial dysfunction in the injured cortex and hippocampus at 30 mins, 1, 3, 6, 12, 24, 48, and 72 h after severe TBI. A significant decrease in the coupling of the electron transport system with oxidative phosphorylation was observed as early as 30 mins after injury, followed by a recovery to baseline at 1 h after injury. A statistically significant (P<0.0001) decline in the respiratory control ratio was noted at 3 h, which persisted at all subsequent time-points up to 72 h after injury in both cortical and hippocampal mitochondria. Structural damage seen in purified cortical mitochondria included severely swollen mitochondria, a disruption of the cristae and rupture of outer membranes, indicative of mitochondrial permeability transition. Consistent with this finding, cortical mitochondrial calcium-buffering capacity was severely compromised by 3 h after injury, and accompanied by significant increases in mitochondrial protein oxidation and lipid peroxidation. A possible causative role for reactive nitrogen species was suggested by the rapid increase in cortical mitochondrial 3-nitrotyrosine levels shown as early as 30 mins after injury. These findings indicate that post-traumatic oxidative lipid and protein damage, mediated in part by peroxynitrite, occurs in mitochondria with concomitant ultrastructural damage and impairment of mitochondrial bioenergetics. The data also indicate that compounds which specifically scavenge peroxynitrite (ONOO(-)) or ONOO(-)-derived radicals (e.g. ONOO(-)+H(+) --> ONOOH --> (*)NO(2)+(*)OH) may be particularly effective for the treatment of TBI, although the therapeutic window for this neuroprotective approach might only be 3 h.

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.

A study comparing SPECT and MRI in patients with anosmia after traumatic brain injury.

PURPOSE: The initial or first clinical presentation of altered sensation of smell is directly linked to the degree of impaired sensitivity. We took the opportunity to examine normal and nonspecific MRI findings in 6 patients with known anosmia after traumatic brain injury with perfusion SPECT brain imaging. MATERIAL AND METHODS: Patients included those with primary loss of smell after head injury. All patients underwent standard testing by the Taste & Smell Center. Normal or nonspecific near normal brain MRI studies were subsequently referred for SPECT perfusion neuroimaging. RESULTS: MRI studies were negative in 3 cases. In the remaining studies, one case showed nonspecific white matter change, another low signal in the left frontal gyrus, and the sixth case merely some cortical atrophy. All 6 cases demonstrated lesions on SPECT involving the frontal, temporal, and temporoparietal cortex. CONCLUSION: This study identified altered blood perfusion pattern in otherwise normal anatomic structures on MRI.

Microbleeds may expand acutely after traumatic brain injury.

BACKGROUND AND PURPOSE: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury. MATERIALS AND METHODS: We present here five closed moderate/severe (Glasgow coma scale≤13) TBI patients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points. RESULTS: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time. CONCLUSION: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.

Transient receptor potential channel 1/4 reduces subarachnoid hemorrhage-induced early brain injury in rats via calcineurin-mediated NMDAR and NFAT dephosphorylation.

Transient receptor potential channel 1/4 (TRPC1/4) are considered to be related to subarachnoid hemorrhage (SAH)-induced cerebral vasospasm. In this study, a SAH rat model was employed to study the roles of TRPC1/4 in the early brain injury (EBI) after SAH. Primary cultured hippocampal neurons were exposed to oxyhemoglobin to mimic SAH in vitro. The protein levels of TRPC1/4 increased and peaked at 5 days after SAH in rats. Inhibition of TRPC1/4 by SKF96365 aggravated SAH-induced EBI, such as cortical cell death (by TUNEL staining) and degenerating (by FJB staining). In addition, TRPC1/4 overexpression could increase calcineurin activity, while increased calcineurin activity could promote the dephosphorylation of N-methyl-D-aspartate receptor (NMDAR). Calcineurin antagonist FK506 could weaken the neuroprotection and the dephosphorylation of NMDAR induced by TRPC1/4 overexpression. Contrarily, calcineurin agonist chlorogenic acid inhibited SAH-induced EBI, even when siRNA intervention of TRPC1/4 was performed. Moreover, calcineurin also could lead to the nuclear transfer of nuclear factor of activated T cells (NFAT), which is a transcription factor promoting the expressions of TRPC1/4. TRPC1/4 could inhibit SAH-induced EBI by supressing the phosphorylation of NMDAR via calcineurin. TRPC1/4-induced calcineurin activation also could promote the nuclear transfer of NFAT, suggesting a positive feedback regulation of TRPC1/4 expressions.

Hemosiderin pigmentation of tumour cells in cerebellar pilocytic astrocytoma associated with post-traumatic hemorrhage in adults.

The pilocytic astrocytoma is only rarely associated with gross intratumoral hemorrhage despite rich vasculature and blood vessel changes, accompanied often by perivascular depots of hemosiderin. We report an unusual case of pigmented cerebellar pilocytic astrocytoma presenting with posttraumatic hemorrhage in a 38-year-old man with no history related to the tumor. CT and MRI examination after head injury demonstrated unexpectedly the cystic lesion of 2 cm in diameter in the region of the right cerebellar hemisphere and vermis. The lesion was associated with hematoma and it was surgically removed 3 weeks after trauma. Histopathological examination revealed pilocytic astrocytoma tissue with broad hemorrhagic changes and with an unusual pattern of massive pigmentation of the cytoplasm of pilocytic astrocytes, consistent with hemosiderosis. Positive stains for iron and ferritin and ultrastructural study confirmed deposition of hemosiderin granules in the tumour cells. There was no evidence of melanin or melanosomes. This finding of hemosiderin accumulation in the cytoplasm of neoplastic astroglia seems to be analogous to post-hemorrhagic pigmentation of the normal Bergmann glia and subpial astrocytes. In the literature, the examples of neuroepithelial tumors with hemosiderin pigmentation of tumor cells have been rarely documented. To our knowledge, this is the first reported case of pigmented pilocytic astrocytoma exhibiting extensive intracellular hemosiderin deposition.