Corpus Callosal Hematoma by a Trivial Trauma Causing Concussion with "Blood at the Center" Radiological Sign.

Hematoma of corpus callosum is a very rare phenomenon and is caused by severe trauma to head. Most common traumatic injury to corpus callosum is seen in diffuse axonal injury in form of small hemorrhagic foci and associated prolonged unconsciousness. Trivial trauma causing well defined corpus callosal hematoma in absence of coagulation defects or neurological deficits in conscious patient has not been reported in the literature. We present such a unique case and the review the corpus callosal hematoma due to trauma.

[Primary injuries of corpus callosum vessels in craniocerebral injuries]. / Pervichnye povrezhdeniya sosudov mozolistogo tela pri cherepno-mozgovoi travme.

The aim of the scientific work is to establish morphological characteristics of hemorrhages in the corpus callosum as a marker of primary vascular injuries in diffuse axonal injury (DAI) in relation to the goals and objectives of forensic examination. Changes in the structures of corpus callosum were analyzed in 45 corpses of persons with traumatic brain injury who died in hospital from DAI diagnosed according to clinical and instrumental data within 24 hours after the trauma. The changes were characterized by rectic hemorrhages (haemorrhagia per rhexin) in combination with successively developing vascular, tissue, and cellular post-traumatic reactions. These changes were not observed in the control group. The following morphological characteristics of hemorrhages were established: small focal, elongated, clearly contoured hemorrhages of different sizes, up to 4 mm long, up to 0.8 mm wide, unidirectional at an angle from the lower to upper surface of the sagittal corpus callosum section, at least three, grouped in limited areas sized up to 1.5 × 1.0 cm without clear borders. The detected hemorrhages and the course of changes give reason to consider them the result of primary traumatic effects, making them a diagnostic marker of DAI.

Comprehensive rehabilitation in a patient with corpus callosum syndrome after traumatic brain injury: Case report.

RATIONALE: Corpus callosum syndrome is a rare consequence of traumatic brain injuries. We provide a case of a patient with typical corpus callosum syndrome following a traumatic brain injury, and demonstrate neural reorganization and significant neural regeneration after comprehensive rehabilitation, using diffusion tensor imaging fiber bundle tracking. PATIENT CONCERNS: We found typical clinical manifestations of damage to the corpus callosum. DIAGNOSES, INTERVENTIONS, AND OUTCOMES: We diagnosed a Traumatic Brain Injury (diffuse axonal injury and rupture of corpus callosum). The patient underwent a comprehensive multifaceted rehabilitation program including drug therapy, integrated physical therapy, occupational therapy, acupuncture, music therapy, computer-aided cognitive rehabilitation training, transcranial magnetic stimulation, and hyperbaric oxygen therapy. This rehabilitation program resulted in greatly improved physical and communication ability. LESSONS: Comprehensive rehabilitation can significantly improve the function of patients with corpus callosum syndrome and may cause neural remodeling, as seen on diffusion tensor imaging.

Early computed tomography for acute post-traumatic diffuse axonal injury: a systematic review.

PURPOSE: Diffuse axonal injury (DAI) is the rupture of multiple axons due to acceleration and deceleration forces during a closed head injury. Most traumatic brain injuries (TBI) have some degree of DAI, especially severe TBI. Computed tomography (CT) remains the first imaging test performed in the acute phase of TBI, but has low sensitivity for detecting DAI, since DAI is a cellular lesion. The aim of this study is to search in the literature for CT signs, in the first 24 h after TBI, that may help to differentiate patients in groups with a better versus worst prognosis. METHODS: We searched for primary scientific articles in the PubMed database, in English, indexed since January 1st, 2000. RESULTS: Five articles were selected for review. In the DAI group, traffic accidents accounted 70% of the cases, 79% were male, and the mean age was 41 years. There was an association between DAI and intraventricular hemorrhage (IVH) and traumatic subarachnoid hemorrhage (tSAH); an association between the IVH grade and number of corpus callosum lesions; and an association between blood in the interpeduncular cisterns (IPC) and brainstem lesions. CONCLUSION: In closed TBI with no tSAH, severe DAI is unlikely. Similarly, in the absence of IVH, any DAI is unlikely. If there is IVH, patients generally are clinically worse; and the more ventricles affected, the worse the prognosis.

Differences in corpus callosum injury between cerebral concussion and diffuse axonal injury.

BACKGROUND: We investigated differences in corpus callosum (CC) injuries between patients with concussion and those with diffuse axonal injury (DAI) by using diffusion tensor tractography (DTT). METHODS: Twenty-nine patients with concussion, 21 patients with DAI, and 25 control subjects were recruited. We reconstructed the whole CC and 5 regions of the CC after applying Hofer classification (I, II, III, IV, and V). The whole CC and each region of the CC were analyzed to measure DTT parameters (fractional anisotropy [FA], apparent diffusion coefficient [ADC], and fiber number [FN]). RESULTS: In the whole CC, significant differences were observed in all DTT parameters between the concussion and control groups and the DAI and control groups (P < .05). Among the 5 regions of the CC, significant differences were observed in FA and ADC between the concussion and control groups and the DAI and control groups (P < .05). Significant differences in FN were observed in CC regions I and II (connected with the prefrontal lobe and secondary motor area) between the concussion and control groups, in CC regions I, II, III, and IV (connected with the frontoparietal lobes) between the DAI and control groups, and in CC regions III, IV (connected with the motor-sensory cortex) between the concussion and DAI groups (P < .05). CONCLUSION: It was observed that both concussion and DAI patients showed diffuse neural injuries in the whole CC and all 5 regions of the CC. Neural FN results revealed that concussion patients appeared to be specifically injured in the anterior part of the CC connected with the frontal lobe, whereas DAI patients were injured in more diffuse regions connected with whole frontoparietal lobes.

Childhood Transorbital Skull Base Penetrating Injury: Report of 2 Cases and Review of Literature.

BACKGROUND: A foreign object penetrating the brain via orbit is a rare occurrence. Accurate diagnosis and immediate intervention is essential to prevent ophthalmic or neurological deficits and to reduce chances of infection or hemorrhage. CASE DESCRIPTION: We report 2 cases of transorbital orbitocranial penetrating injury of metal objects in children. Computed tomography scan was obtained to assess the extent of the injury and to locate the objects. According to the trajectory, the best craniotomy approach was performed, and the objects were safely removed without any complication. Our cases are unique because of the absence of any neurological deficit on admission, before and after the removal. CONCLUSIONS: The importance of transorbital orbitocranial penetrating injury cannot be neglected because of possible orbital and intracranial damage. Therefore, in this report we aim to heighten awareness of the complexity and severity of transorbital penetrating brain injury.

Traumatic Microbleeds in the Hippocampus and Corpus Callosum Predict Duration of Posttraumatic Amnesia.

OBJECTIVE: Radiologic predictors of posttraumatic amnesia (PTA) duration are lacking. We hypothesized that the number and distribution of traumatic microbleeds (TMBs) detected by gradient recalled echo (GRE) magnetic resonance imaging (MRI) predicts PTA duration. SETTING: Academic, tertiary medical center. PARTICIPANTS: Adults with traumatic brain injury (TBI). DESIGN: We identified 65 TBI patients with acute GRE MRI. PTA duration was determined with the Galveston Orientation and Amnesia Test, Orientation Log, or chart review. TMBs were identified within memory regions (hippocampus, corpus callosum, fornix, thalamus, and temporal lobe) and control regions (internal capsule and global). Regression tree analysis was performed to identify radiologic predictors of PTA duration, controlling for clinical PTA predictors. MAIN MEASURES: TMB distribution, PTA duration. RESULTS: Sixteen patients (25%) had complicated mild, 4 (6%) had moderate, and 45 (69%) had severe TBI. Median PTA duration was 43 days (range, 0-240 days). In univariate analysis, PTA duration correlated with TMBs in the corpus callosum (R = 0.29, P = .02) and admission Glasgow Coma Scale (GCS) score (R = -0.34, P = .01). In multivariate regression analysis, admission GCS score was the only significant contributor to PTA duration. However, in regression tree analysis, hippocampal TMBs, callosal TMBs, age, and admission GCS score explained 26% of PTA duration variance and distinguished a subgroup with prolonged PTA. CONCLUSIONS: Hippocampal and callosal TMBs are potential radiologic predictors of PTA duration.

MRS and DTI evidence of progressive posterior cingulate cortex and corpus callosum injury in the hyper-acute phase after Traumatic Brain Injury.

The posterior cingulate cortex (PCC) and corpus callosum (CC) are susceptible to trauma, but injury often evades detection. PCC Metabolic disruption may predict CC white matter tract injury and the secondary cascade responsible for progression. While the time frame for the secondary cascade remains unclear in humans, the first 24 h (hyper-acute phase) are crucial for life-saving interventions. Objectives: To test whether Magnetic Resonance Imaging (MRI) markers are detectable in the hyper-acute phase and progress after traumatic brain injury (TBI) and whether alterations in these parameters reflect injury severity. Methods: Spectroscopic and diffusion-weighted MRI data were collected in 18 patients with TBI (within 24 h and repeated 7-15 days following injury) and 18 healthy controls (scanned once). Results: Within 24 h of TBI N-acetylaspartate was reduced (F = 11.43, p = 0.002) and choline increased (F = 10.67, p = 0.003), the latter driven by moderate-severe injury (F = 5.54, p = 0.03). Alterations in fractional anisotropy (FA) and axial diffusivity (AD) progressed between the two time-points in the splenium of the CC (p = 0.029 and p = 0.013). Gradual reductions in FA correlated with progressive increases in choline (p = 0.029). Conclusions: Metabolic disruption and structural injury can be detected within hours of trauma. Metabolic and diffusion parameters allow identification of severity and provide evidence of injury progression.

Cortical compression rapidly trimmed transcallosal projections and altered axonal anterograde transport machinery.

Trauma and tumor compressing the brain distort underlying cortical neurons. Compressed cortical neurons remodel their dendrites instantly. The effects on axons however remain unclear. Using a rat epidural bead implantation model, we studied the effects of unilateral somatosensory cortical compression on its transcallosal projection and the reversibility of the changes following decompression. Compression reduced the density, branching profuseness and boutons of the projection axons in the contralateral homotopic cortex 1week and 1month post-compression. Projection fiber density was higher 1-month than 1-week post-compression, suggesting adaptive temporal changes. Compression reduced contralateral cortical synaptophysin, vesicular glutamate transporter 1 (VGLUT1) and postsynaptic density protein-95 (PSD95) expressions in a week and the first two marker proteins further by 1month. ßIII-tubulin and kinesin light chain (KLC) expressions in the corpus callosum (CC) where transcallosal axons traveled were also decreased. Kinesin heavy chain (KHC) level in CC was temporarily increased 1week after compression. Decompression increased transcallosal axon density and branching profuseness to higher than sham while bouton density returned to sham levels. This was accompanied by restoration of synaptophysin, VGLUT1 and PSD95 expressions in the contralateral cortex of the 1-week, but not the 1-month, compression rats. Decompression restored ßIII-tubulin, but not KLC and KHC expressions in CC. However, KLC and KHC expressions in the cell bodies of the layer II/III pyramidal neurons partially recovered. Our results show cerebral compression compromised cortical axonal outputs and reduced transcallosal projection. Some of these changes did not recover in long-term decompression.

Systemic LPS resulted in a transient hippocampus malfunction but a prolonged corpus callosum injury.

BACKGROUND: To investigate the effect of systemic lipopolysaccharide (LPS) on function of hippocampus and corpus callosum (CC) in adult rats. METHODS: Adult rats with mature white matter tract were divided into systemic LPS and saline injection groups. Animal were euthanized following 3 daily injections (day 3) and 3-day after cessation of injections (day 6). At both time points, hippocampal long term potentiation (LTP) and CC compound action potentials (CAP) were recorded, beta amyloid precursor protein (ß-APP) level in CC tissue was measured by Western blot, and microglia activation was examined by immunostaining and proportional area analysis. RESULTS: Systemic LPS significantly decreased amplitude of both post tetanic potentiation (PTP) and LTP at day 3, but PTP and LTP turned to be normal at day 6. CAP was significantly declined at day 3 but was further declined at day 6. The ß-APP levels in CC tissues of LPS injected rats were significantly higher than that of saline group at both time-points. Interestingly, proportional area measurement disclosed that microglial areas in both hippocampus and CC significantly expanded at day3, but at the day 6, microglial area decreased in hippocampus but further increased in CC. CONCLUSION: Systemic LPS resulted in a transient hippocampus malfunction but a prolonged CC injury. Microglia activation may correlate with such LPS induced white matter injury.

Peak linear and rotational acceleration magnitude and duration effects on maximum principal strain in the corpus callosum for sport impacts.

Concussion has been linked to the presence of injurious strains in the brain tissues. Research investigating severe brain injury has reported that strains in the brain may be affected by two parameters: magnitude of the acceleration, and duration of that acceleration. However, little is known how this relationship changes in terms of creating risk for brain injury for magnitudes and durations of acceleration common in sporting environments. This has particular implications for the understanding and prevention of concussive risk of injury in sporting environments. The purpose of this research was to examine the interaction between linear and rotational acceleration and duration on maximum principal strain in the brain tissues for loading conditions incurred in sporting environments. Linear and rotational acceleration loading curves of magnitudes and durations similar to those from impact in sport were used as input to the University College Brain Trauma Model and maximum principal strain (MPS) was measured for the different curves. The results demonstrated that magnitude and duration do have an effect on the strain incurred by the brain tissue. As the duration of the acceleration increases, the magnitude required to achieve strains reflecting a high risk of concussion decreases, with rotational acceleration becoming the dominant contributor. The magnitude required to attain a magnitude of MPS representing risk of brain injury was found to be as low as 2500rad/s2 for impacts of 10-15ms; indicating that interventions to reduce the risk of concussion in sport must consider the duration of the event while reducing the magnitude of acceleration the head incurs.

Callosal injury-induced working memory impairment: a computational network modeling study.

Mild traumatic brain injury (mTBI) often results in working memory (WM) impairment, but the mechanistic relationship between the two remains elusive. We used a computational model of two cortical neuronal networks linked by myelinated callosal axons with distance-dependent conduction delays to simulate callosal dysfunction in mTBI and quantify its impact on WM. WM maintenance and termination in the model network depended on short-term synaptic plasticity. In injured networks, WM duration depended on the extent of callosal injury, consistent with clinical data. The model provides a framework for studying callosal injury-induced neurobehavioral alterations following mTBI, and, to the best of our knowledge, is the first computational model to address mTBI-induced WM impairment.

Application of FTIR spectroscopy for traumatic axonal injury: a possible tool for estimating injury interval.

Traumatic axonal injury (TAI) is a progressive and secondary injury following traumatic brain injury (TBI). Despite extensive investigations in the field of forensic science and neurology, no effective methods are available to estimate TAI interval between injury and death. In the present study, Fourier transform IR (FTIR) spectroscopy with IR microscopy was applied to collect IR spectra in the corpus callosum (CC) of rats subjected to TAI at 12, 24, and 72 h post-injury compared with control animals. The classification amongst different groups was visualized based on the acquired dataset using hierarchical cluster analysis (HCA) and partial least square (PLS). Furthermore, the established PLS models were used to predict injury interval of TAI in the unknown sample dataset. The results showed that samples at different time points post-injury were distinguishable from each other, and biochemical changes in protein, lipid, and carbohydrate contributed to the differences. Then, the established PLS models provided a satisfactory prediction of injury periods between different sample groups in the external validation. The present study demonstrated the great potential of FTIR-based PLS algorithm as an objective tool for estimating injury intervals of TAI in the field of forensic science and neurology.

Differences in Callosal and Forniceal Diffusion between Patients with and without Postconcussive Migraine.

BACKGROUND AND PURPOSE: Posttraumatic migraines are common after mild traumatic brain injury. The purpose of this study was to determine if a specific axonal injury pattern underlies posttraumatic migraines after mild traumatic brain injury utilizing Tract-Based Spatial Statistics analysis of diffusion tensor imaging. MATERIALS AND METHODS: DTI was performed in 58 patients with mild traumatic brain injury with posttraumatic migraines. Controls consisted of 17 patients with mild traumatic brain injury without posttraumatic migraines. Fractional anisotropy and diffusivity maps were generated to measure white matter integrity and were evaluated by using Tract-Based Spatial Statistics regression analysis with a general linear model. DTI findings were correlated with symptom severity, neurocognitive test scores, and time to recovery with the Pearson correlation coefficient. RESULTS: Patients with mild traumatic brain injury with posttraumatic migraines were not significantly different from controls in terms of age, sex, type of injury, or neurocognitive test performance. Patients with posttraumatic migraines had higher initial symptom severity (P = .01) than controls. Compared with controls, patients with mild traumatic brain injury with posttraumatic migraines had decreased fractional anisotropy in the corpus callosum (P = .03) and fornix/septohippocampal circuit (P = .045). Injury to the fornix/septohippocampal circuit correlated with decreased visual memory (r = 0.325, P = .01). Injury to corpus callosum trended toward inverse correlation with recovery (r = -0.260, P = .05). CONCLUSIONS: Injuries to the corpus callosum and fornix/septohippocampal circuit were seen in patients with mild traumatic brain injury with posttraumatic migraines, with injuries in the fornix/septohippocampal circuit correlating with decreased performance on neurocognitive testing.

Prognostic value of corpus callosum injuries in severe head trauma.

BACKGROUND: This study was performed to investigate the relationship between corpus callosum (CC) injury and prognosis in traumatic axonal injury (TAI). METHOD: We retrospectively reviewed 264 patients with severe head trauma who underwent a conventional MR imaging in the first 60 days after injury. They were selected from a prospectively collected database of 1048 patients with severe head trauma admitted in our hospital. TAI lesions were defined as areas of increased signal intensity on T2 and FLAIR or areas of decreased signal on gradient-echo T2. We attempted to determine whether any MR imaging findings of TAI lesions at CC could be related to prognosis. Neurological impairment was assessed at 1 year after injury by means of GOS-E (good outcome being GOS-E 4/5 and bad outcome being GOS-E <4). We adjusted the multivariable analysis for the prognostic factors according to the IMPACT studies: the Core model (age, motor score at admission, and pupillary reactivity) and the Extended model (including CT information and second insults). RESULTS: We found 97 patients (37 %) with TAI at CC and 167 patients (63 %) without CC lesions at MR. A total of 62 % of the patients with CC lesions had poor outcome, whereas 38 % showed good prognosis. The presence of TAI lesions at the corpus callosum was associated with poor outcome 1 year after brain trauma (p < 0.001, OR 3.8, 95 % CI: 2.04-7.06). The volume of CC lesions measured on T2 and FLAIR sequences was negatively correlated with the GOS-E after adjustment for independent prognostic factors (p = 0.01, OR 2.23, 95 % CI:1.17-4.26). Also the presence of lesions at splenium was statistically related to worse prognosis (p = 0.002, OR 8.1, 95 % CI: 2.2-29.82). We did not find statistical significance in outcome between hemorrhagic and non-hemorrhagic CC lesions. CONCLUSIONS: The presence of CC is associated with a poor outcome. The total volume of the CC lesion is an independent prognostic factor for poor outcome in severe head trauma.

Ideomotor Apraxia Due to Injury of the Superior Longitudinal Fasciculus.

We report on a patient who showed ideomotor apraxia due to injury of the superior longitudinal fasciculus following brain tumor and tumor bleeding, which was demonstrated by diffusion tensor tractography (DTT). A 60-yr-old, right-handed male patient underwent removal of brain meningioma and drainage of intraventricular hemorrhage and intracerebral hemorrhage in the left fronto-parietal lobe. At the time of DTT scanning (5 wk after onset), he was able to move the right upper extremity against gravity. The patient exhibited an intact ideational plan for motor performance. In addition, he was able to use actual objects (scissors, eraser) using his right wrist and hand. However, he had difficulty in using his right upper extremity for pantomime of object use, imitating gestures (meaningless or meaningful), and movement of his right upper extremity proximal. Score on the ideomotor apraxia test for the right side was 4 (cut-off score < 32). DTTs for the left superior longitudinal fasciculus to the left premotor cortex and left inferior parietal lobule showed partial injury, compared with the right superior longitudinal fasciculus. These injuries appeared to be the reason for ideomotor apraxia in this patient.

Quantification of structural changes in the corpus callosumin children with profound hypoxic-ischaemic brain injury.

BACKGROUND: Birth-related acute profound hypoxic-ischaemic brain injury has specific patterns of damage including the paracentral lobules. OBJECTIVE: To test the hypothesis that there is anatomically coherent regional volume loss of the corpus callosum as a result of this hemispheric abnormality. MATERIALS AND METHODS: Study subjects included 13 children with proven acute profound hypoxic-ischaemic brain injury and 13 children with developmental delay but no brain abnormalities. A computerised system divided the corpus callosum into 100 segments, measuring each width. Principal component analysis grouped the widths into contiguous anatomical regions. We conducted analysis of variance of corpus callosum widths as well as support vector machine stratification into patient groups. RESULTS: There was statistically significant narrowing of the mid-posterior body and genu of the corpus callosum in children with hypoxic-ischaemic brain injury. Support vector machine analysis yielded over 95% accuracy in patient group stratification using the corpus callosum centile widths. CONCLUSION: Focal volume loss is seen in the corpus callosum of children with hypoxic-ischaemic brain injury secondary to loss of commissural fibres arising in the paracentral lobules. Support vector machine stratification into the hypoxic-ischaemic brain injury group or the control group on the basis of corpus callosum width is highly accurate and points towards rapid clinical translation of this technique as a potential biomarker of hypoxic-ischaemic brain injury.

Granulocyte macrophage colony-stimulating factor treatment results in recovery of motor function after white matter damage in mice.

Clinical stroke usually results from a cerebral ischaemic event, and is frequently a debilitating condition with limited treatment options. A significant proportion of clinical strokes result from specific damage to the subcortical white matter (SWM), but currently there are few animal models available to investigate the pathogenesis and potential therapeutic strategies to promote recovery. Granulocyte macrophage colony-stimulating factor (GM-CSF) is a cytokine that has been previously shown to promote neuroprotective effects after brain damage; however, the mechanisms mediating this effect are not known. Here, it is reported that GM-CSF treatment results in dramatic functional improvement in a white matter model of stroke in mice. SWM stroke was induced in mice by unilateral injections of the vasoconstrictor, endothelin-1 (ET-1). The results reveal that ET-1-induced stroke impairs skilled motor function on the single pellet-reaching task and results in forelimb asymmetry, in adult mice. Treatment with GM-CSF, after stroke, restores motor function and abolishes forelimb asymmetry. The results also indicate that GM-CSF promotes its effects by activating mammalian target of rapamycin signalling mechanisms in the brain following stroke injury. Additionally, a significant increase in GM-CSF receptor expression was found in the ipsilateral hemisphere of the ET-1-injected brain. Taken together, the present study highlights the use of an under-utilized mouse model of stroke (using ET-1) and suggests that GM-CSF treatment can attenuate ET-1-induced functional deficits.