ABSTRACT
Hemorrhagic progression of contusion (HPC) often occurs early in cerebral contusions (CC) patients, significantly impacting their prognosis. It is vital to promptly assess HPC and predict outcomes for effective tailored interventions, thereby enhancing prognosis in CC patients. We utilized the Attention-3DUNet neural network to semi-automatically segment hematomas from computed tomography (CT) images of 452 CC patients, incorporating 695 hematomas. Subsequently, 1502 radiomic features were extracted from 358 hematomas in 261 patients. After a selection process, these features were used to calculate the radiomic signature (Radscore). The Radscore, along with clinical features such as medical history, physical examinations, laboratory results, and radiological findings, was employed to develop predictive models. For prognosis (discharge Glasgow Outcome Scale score), radiomic features of each hematoma were augmented and fused for correlation. We employed various machine learning methodologies to create both a combined model, integrating radiomics and clinical features, and a clinical-only model. Nomograms based on logistic regression were constructed to visually represent the predictive procedure, and external validation was performed on 170 patients from three additional centers. The results showed that for HPC, the combined model, incorporating hemoglobin levels, Rotterdam CT score of 3, multi-hematoma fuzzy sign, concurrent subdural hemorrhage, international normalized ratio, and Radscore, achieved area under the receiver operating characteristic curve (AUC) values of 0.848 and 0.836 in the test and external validation cohorts, respectively. The clinical model predicting prognosis, utilizing age, Abbreviated Injury Scale for the head, Glasgow Coma Scale Motor component, Glasgow Coma Scale Verbal component, albumin, and Radscore, attained AUC values of 0.846 and 0.803 in the test and external validation cohorts, respectively. Selected radiomic features indicated that irregularly shaped and highly heterogeneous hematomas increased the likelihood of HPC, while larger weighted axial lengths and lower densities of hematomas were associated with a higher risk of poor prognosis. Predictive models that combine radiomic and clinical features exhibit robust performance in forecasting HPC and the risk of poor prognosis in CC patients. Radiomic features complement clinical features in predicting HPC, although their ability to enhance the predictive accuracy of the clinical model for adverse prognosis is limited.
Subject(s)
Brain Contusion , Hematoma , Tomography, X-Ray Computed , Humans , Prognosis , Male , Female , Hematoma/diagnostic imaging , Middle Aged , Tomography, X-Ray Computed/methods , Adult , Brain Contusion/diagnostic imaging , Aged , Disease Progression , Young Adult , Adolescent , Machine Learning , Retrospective Studies , RadiomicsABSTRACT
RATIONALE: It is rare for a traumatic intracranial hematoma to self-absorb rapidly after conservative treatment. To the best of our knowledge, there has been no report in the relevant literature of rapid absorption of hematoma formation following cerebral contusion and laceration. PATIENT CONCERNS: A 54-year-old male was admitted to our hospital with head trauma at 3 hours prior to admission. He was alert and oriented, glasgow coma scale score of 15. Head computed tomography (CT) showed left frontal brain contusion with hematoma, however, a reexamination of CT about 29 hours following the trauma revealed that the hematoma had been absorbed. DIAGNOSES: A diagnosis of contusion and laceration of left frontal lobe with hematoma formation was made based on the CT images. INTERVENTIONS: The patient underwent conservative treatment. OUTCOMES: After treatment, dizziness and headache subsided for the patient, and no special discomfort was reported. LESSONS: It is likely that the reason for rapid absorption in this case is that the hematoma is prone to liquefaction because of abnormal platelet values and coagulation dysfunction. As the liquefaction hematoma breaks into the lateral ventricle, it is redistributed and absorbed in the lateral ventricle and subarachnoid space. Further evidence is required to support this hypothesis.
Subject(s)
Brain Contusion , Craniocerebral Trauma , Lacerations , Male , Humans , Middle Aged , Hematoma/etiology , Frontal Lobe/diagnostic imaging , Brain Contusion/complications , Brain Contusion/diagnostic imagingABSTRACT
BACKGROUND: Traumatic brain injury is a common and devastating injury that is the leading cause of neurological disability and death worldwide. Patients with cerebral lobe contusion received conservative treatment because of their mild manifestations, but delayed intracranial hematoma may increase and even become life-threatening. We explored the noninvasive method to predict the prognosis of progression and Glasgow Outcome Scale (GOS) by using a quantitative radiomics approach and statistical analysis. METHODS: Eighty-eight patients who were pathologically diagnosed were retrospectively studied. The radiomics method developed in this work included image segmentation, feature extraction, and feature selection. The nomograms were established based on statistical analysis and a radiomics method. We conducted a comparative study of hematoma progression and GOS between the clinical factor alone and fusion radiomics features. RESULTS: Nineteen clinical factors, 513 radiomics features, and 116 locational features were considered. Among clinical factors, international normalized ratio, prothrombin time, and fibrinogen were enrolled for hematoma progression. As for GOS, treatment strategy, age, Glasgow Coma Scale score, and blood platelet were associated factors. Eight features for GOS and five features for hematoma progression were filtered by using sparse representation and locality preserving projection-combined method. Four nomograms were constructed. After fusion radiomics features, area under the curve of hematoma progression prediction increased from 0.832 to 0.899, whereas GOS prediction went from 0.794 to 0.844. CONCLUSIONS: A radiomic-based model that merges radiomics and clinical features is a noninvasive approach to predict hematoma progression and clinical outcomes of cerebral contusions in traumatic brain injury.
Subject(s)
Brain Contusion , Brain Injuries, Traumatic , Brain Contusion/diagnostic imaging , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/diagnostic imaging , Brain Injuries, Traumatic/therapy , Glasgow Outcome Scale , Hematoma/diagnostic imaging , Hematoma/etiology , Humans , Nomograms , Retrospective StudiesABSTRACT
BACKGROUND AND OBJECTIVE: Cerebral Contusion (CC) is one of the most serious injury types in patients with traumatic brain injury (TBI). Traumatic intraparenchymal hematoma (TICH) expansion severely affects the patient's prognosis. In this study, the baseline data, imaging features, and laboratory examinations of patients with CC were summarized and analyzed to develop and validate a nomogram predictive model assessing the risk factors for TICH expansion. METHODS: Totally 258 patients were included and retrospectively analyzed herein, who met the CC inclusion criteria, from July 2018 to July 2021. TICH expansion was defined as increased hematoma volume ≥ 30% relative to primary volume or an absolute hematoma increase ≥ 5 ml at CT review. RESULTS: Univariate and binary logistic regression analyses were performed to screen out the independent predictors significantly correlated with TICH expansion: Age, subdural hematoma (SDH), contusion site, multihematoma fuzzy sign (MFS), contusion volume, and traumatic coagulation abnormalities (TCA). Based on these, the nomogram model was established. The differences between the contusion volume and glasgow outcome scale (GOS) were analyzed by the nonparametric tests. Larger contusion volume was associated with poor prognosis. CONCLUSION: This study established a Nomogram model to predict TICH expansion in patients with CC. Meanwhile, the study found that the risk of bleeding tended to decrease when the hematoma volume was > 15 ml, but the larger initial hematoma volume would indicate worse prognosis. We advocate the use of predictive models for TICH expansion risk assessment in hospitalized CC patients, which is low-cost and easy-to-apply, especially in acute settings.
Subject(s)
Brain Contusion/diagnosis , Intracranial Hemorrhage, Traumatic/diagnosis , Models, Neurological , Nomograms , Adult , Aged , Brain Contusion/diagnostic imaging , Female , Humans , Intracranial Hemorrhage, Traumatic/diagnostic imaging , Male , Middle Aged , Practice Guidelines as Topic , Prognosis , Retrospective Studies , Young AdultABSTRACT
The National Institutes of Health/National Institute of Neurological Disorders and Stroke (NIH-NINDS) Traumatic Brain Injury (TBI) Imaging Common Data Elements (CDEs) are standardized definitions for pathological intracranial lesions based on their appearance on neuroimaging studies. The NIH-NINDS TBI Imaging CDEs were designed to be as consistent as possible with the U.S. Food and Drug Administration (FDA) definition of biomarkers as "an indicator of normal biological processes, pathogenic processes, or biological responses to an exposure or intervention." However, the FDA qualification process for biomarkers requires proof of reliable biomarker test measurements. We determined the interrater reliability of TBI Imaging CDEs on subacute brain magnetic resonance imaging (MRI) performed on 517 mild TBI patients presenting to 11 U.S. level 1 trauma centers. Three U.S. board-certified neuroradiologists independently evaluated brain MRI performed 2 weeks post-injury for the following CDEs: traumatic axonal injury (TAI), diffuse axonal injury (DAI), and brain contusion. We found very high interrater agreement for brain contusion, with prevalence- and bias-adjusted kappa (PABAK) values for pairs of readers from 0.92 [95% confidence interval, 0.88-0.95] to 0.94 [0.90-0.96]. We found intermediate agreement for TAI and DAI, with PABAK values of 0.74-0.78 [0.70-0.82]. The near-perfect agreement for subacute brain contusion is likely attributable to the high conspicuity and distinctive appearance of these lesions on T1-weighted images. Interrater agreement for TAI and DAI was lower, because signal void in small vascular structures, and artifactual foci of signal void, can be difficult to distinguish from the punctate round or linear areas of slight hemorrhage that are a common hallmark of TAI/DAI on MRI.
Subject(s)
Brain Concussion/diagnostic imaging , Brain Injuries, Traumatic/diagnostic imaging , Magnetic Resonance Imaging/methods , Adolescent , Adult , Aged , Artifacts , Biomarkers , Brain Contusion/diagnostic imaging , Common Data Elements , Diffuse Axonal Injury/diagnostic imaging , Female , Humans , Male , Middle Aged , Observer Variation , Reproducibility of Results , United States , Young AdultABSTRACT
Abusive head trauma (AHT) is the leading cause of child physical abuse fatalities, and survivors frequently face life-long consequences. Victims of AHT are typically infants, and many are subjected to repeat AHT if not accurately identified and protected. Identifying the timing of AHT is often a medical-forensic process, and investigative personnel use the determination of timing of AHT to guide safety decisions for the child victim. If the medical-forensic timing of AHT is incorrect, a child could be inappropriately placed and/or an innocent caregiver could be subject to prosecution. Victims of AHT who suffer severe/permanent injury are felt to demonstrate symptoms immediately after the trauma, and AHT victims with milder injury are thought to generally have persistent or recurrent clinical signs shortly after the trauma. Periods of normal neurologic appearance, in which a victim of AHT is completely asymptomatic for an extended time after the trauma, are felt to be rare and have not been well characterized in the literature. This case involves a 2-month-old infant victim of AHT who presented to medical care with mild neurologic symptoms that resolved without intervention from medical personnel. While hospitalized, the infant had an asymptomatic period of approximately 38 hours prior to more severe neurologic decompensation, then later returned to neurologic baseline. This case highlights the challenges in accurately timing AHT in very young victims who return to neurologic baseline by characterizing a verifiable prolonged period of normal neurologic appearance and function after AHT.
Subject(s)
Child Abuse/diagnosis , Craniocerebral Trauma/etiology , Physical Abuse , Brain Contusion/diagnostic imaging , Hematoma, Subdural, Acute/diagnostic imaging , Humans , Infant , Magnetic Resonance Imaging , Male , Neurologic Examination , Seizures/etiology , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Traumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epilepsy. We prospectively assessed structural imaging biomarkers differentiating patients who develop seizures secondary to TBI from patients who do not. DESIGN: Multicentre prospective cohort study starting in 2018. Imaging data are acquired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (up to 90 days post-TBI). RESULTS: From a sample of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficits in subcortical areas (analysable sample: 57 patients; 35 no seizure, 14 early, 8 late) and cortical ribbon thinning (analysable sample: 46 patients; 29 no seizure, 10 early, 7 late). Right hippocampal volume deficit and inferior temporal cortex thinning demonstrated a significant effect across groups. Additionally, the degree of left frontal and temporal pole thinning, and clinical score at the time of the MRI, could differentiate patients experiencing early seizures from patients not experiencing them with 89% accuracy. CONCLUSIONS AND RELEVANCE: Although this is an initial report, these data show that specific areas of localised volume deficit, as visible on routine imaging data, are associated with the emergence of seizures after TBI.
Subject(s)
Brain Contusion/diagnostic imaging , Brain Hemorrhage, Traumatic/diagnostic imaging , Cerebral Cortical Thinning/diagnostic imaging , Epilepsy, Post-Traumatic/diagnostic imaging , Frontal Lobe/diagnostic imaging , Hippocampus/diagnostic imaging , Temporal Lobe/diagnostic imaging , Adult , Brain Contusion/complications , Brain Hemorrhage, Traumatic/complications , Brain Injuries, Traumatic/diagnostic imaging , Clinical Decision Rules , Computational Biology , Electroencephalography , Epilepsy, Post-Traumatic/epidemiology , Epilepsy, Post-Traumatic/etiology , Female , Frontal Lobe/pathology , Glasgow Coma Scale , Hippocampus/pathology , Humans , Image Processing, Computer-Assisted , Logistic Models , Magnetic Resonance Imaging , Male , Middle Aged , Organ Size , Prospective Studies , Temporal Lobe/pathology , Time Factors , Young AdultABSTRACT
Several studies have reported a strong association between semantic system impairment and LARC error production. However, our patient with a left temporal lobe contusion, including the fusiform gyrus, showed LARC errors even in two-Kanji compound words, the meanings of which the patient understood. Also, the poor results of lexical decision and picture naming suggested problems in orthographic and phonological retrieval. From these results, we concluded that at least some LARC errors are independent of semantic impairment, and other explanations are needed for this type of error.
Subject(s)
Aphasia/etiology , Brain Contusion/complications , Dyslexia/etiology , Temporal Lobe/injuries , Aged , Aphasia/physiopathology , Brain Contusion/diagnostic imaging , Dyslexia/physiopathology , Female , Humans , Japan , Pattern Recognition, Visual/physiology , Temporal Lobe/diagnostic imagingABSTRACT
BACKGROUND: Guillain-Barre syndrome (GBS) is a rare but serious disorder involving peripheral nerve inflammatory demyelination characterized by acute onset tetraparesis and areflexia. Generally, GBS is preceded by a bacterial or viral infection, and post-traumatic or postsurgical GBS is rarely seen. CASE DESCRIPTION: A 41-year-old man with severe craniocerebral gunshot injury and open depressed occipital bone fracture was operated urgently. Two weeks postoperatively, he suffered from sudden quadriparesis. He had flaccid paralysis of his bilateral muscle lower extremities (0/5), along with bilateral upper extremity weakness (2/5). CONCLUSIONS: We report the first case, to our knowledge, with post-traumatic GBS after craniocerebral gunshot injury. We want to indicate the possibility of post-traumatic GBS in cases of unexplained quadriparesis or quadriplegia after trauma or surgery.
Subject(s)
Fractures, Open/surgery , Guillain-Barre Syndrome/diagnosis , Head Injuries, Penetrating/surgery , Postoperative Complications/diagnosis , Quadriplegia/physiopathology , Respiratory Insufficiency/physiopathology , Skull Fractures/surgery , Wounds, Gunshot/surgery , Adult , Brain Contusion/diagnostic imaging , Electrodiagnosis , Fractures, Open/diagnostic imaging , Guillain-Barre Syndrome/physiopathology , Guillain-Barre Syndrome/therapy , Head Injuries, Penetrating/diagnostic imaging , Hematoma, Subdural, Intracranial/diagnostic imaging , Hematoma, Subdural, Intracranial/surgery , Humans , Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Male , Neural Conduction , Neurosurgical Procedures , Occipital Bone/diagnostic imaging , Occipital Bone/injuries , Occipital Bone/surgery , Postoperative Complications/physiopathology , Postoperative Complications/therapy , Quadriplegia/therapy , Respiratory Insufficiency/therapy , Skull Fractures/diagnostic imaging , Wounds, Gunshot/diagnostic imagingABSTRACT
INTRODUCTION: Temporal contusions are common in patients with head injuries and require close monitoring due to the propensity of these patients to deteriorate rapidly and fatally. This study attempts to introduce a radiological grading system for temporal lobe contusions and analyse its prognostic value so as to better identify patients at risk of deterioration. METHODS: The study was conducted as a cross-sectional observational study from April 2011-March 2017 on 42 patients with temporal lobe contusion. Each patients was graded according to the proposed system from a minimum of four to a maximum of 13 and then further grouped in three grades - grade 1 (score = 4), grade 2 (score 5-7) and grade 3 (score > 7) - and their clinical course was closely observed. RESULTS: The minimum and maximum scores observed were four and 11 respectively. The proposed grading system has statistically significant correlation to the Glasgow Coma Scale (p-value < 0.05). All patients in grade 1 (17) could be managed conservatively, while all those in grade 3 (five) needed immediate surgical intervention. Of 20 patients in grade 2, 11 had a score of 5-6 and did not require surgery, whereas nine patients had a score of seven and of these eight required delayed surgical intervention. This correlation was statistically significant (p-value < 0.05). CONCLUSION: The proposed temporal lobe contusion grading system is a good radiological tool to predict the clinical course of patients and thereby identify patients at higher risk of delayed deterioration.
Subject(s)
Brain Contusion/diagnostic imaging , Craniocerebral Trauma/diagnostic imaging , Temporal Lobe/diagnostic imaging , Adolescent , Adult , Aged , Aged, 80 and over , Child , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Prognosis , Severity of Illness Index , Tomography, X-Ray Computed , Young AdultSubject(s)
Blood Flow Velocity , Brain Edema/physiopathology , Brain Injuries, Traumatic/physiopathology , Kidney Failure, Chronic/therapy , Middle Cerebral Artery/diagnostic imaging , Renal Dialysis/adverse effects , Status Epilepticus/physiopathology , Vascular Resistance , Aged , Blood-Brain Barrier/metabolism , Brain Contusion/complications , Brain Contusion/diagnostic imaging , Brain Contusion/metabolism , Brain Contusion/physiopathology , Brain Edema/diagnostic imaging , Brain Edema/etiology , Brain Edema/metabolism , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/diagnostic imaging , Brain Injuries, Traumatic/metabolism , Cerebral Hemorrhage, Traumatic/complications , Cerebral Hemorrhage, Traumatic/diagnostic imaging , Cerebral Hemorrhage, Traumatic/metabolism , Cerebral Hemorrhage, Traumatic/physiopathology , Consciousness Disorders/etiology , Consciousness Disorders/metabolism , Consciousness Disorders/physiopathology , Headache/etiology , Headache/metabolism , Headache/physiopathology , Hematoma, Subdural, Acute/complications , Hematoma, Subdural, Acute/diagnostic imaging , Hematoma, Subdural, Acute/metabolism , Hematoma, Subdural, Acute/physiopathology , Humans , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/metabolism , Male , Middle Cerebral Artery/physiopathology , Monitoring, Physiologic , Nausea/etiology , Nausea/metabolism , Nausea/physiopathology , Pulsatile Flow , Status Epilepticus/etiology , Status Epilepticus/metabolism , Ultrasonography, Doppler, Transcranial , Vomiting/etiology , Vomiting/metabolism , Vomiting/physiopathologyABSTRACT
BACKGROUND: Failure of cerebral autoregulation and progression of intracranial lesion have both been shown to contribute to poor outcome in patients with acute traumatic brain injury (TBI), but the interplay between the two phenomena has not been investigated. Preliminary evidence leads us to hypothesize that brain tissue adjacent to primary injury foci may be more vulnerable to large fluctuations in blood flow in the absence of intact autoregulatory mechanisms. The goal of this study was therefore to assess the influence of cerebrovascular reactivity measures on radiological lesion expansion in a cohort of patients with acute TBI. METHODS: We conducted a retrospective cohort analysis on 50 TBI patients who had undergone high-frequency multimodal intracranial monitoring and for which at least two brain computed tomography (CT) scans had been performed in the acute phase of injury. We first performed univariate analyses on the full cohort to identify non-neurophysiological factors (i.e., initial lesion volume, timing of scan, coagulopathy) associated with traumatic lesion growth in this population. In a subset analysis of 23 patients who had intracranial recording data covering the period between the initial and repeat CT scan, we then correlated changes in serial volumetric lesion measurements with cerebrovascular reactivity metrics derived from the pressure reactivity index (PRx), pulse amplitude index (PAx), and RAC (correlation coefficient between the pulse amplitude of intracranial pressure and cerebral perfusion pressure). Using multivariate methods, these results were subsequently adjusted for the non-neurophysiological confounders identified in the univariate analyses. RESULTS: We observed significant positive linear associations between the degree of cerebrovascular reactivity impairment and progression of pericontusional edema. The strongest correlations were observed between edema progression and the following indices of cerebrovascular reactivity between sequential scans: % time PRx > 0.25 (r = 0.69, p = 0.002) and % time PAx > 0.25 (r = 0.64, p = 0.006). These associations remained significant after adjusting for initial lesion volume and mean cerebral perfusion pressure. In contrast, progression of the hemorrhagic core and extra-axial hemorrhage volume did not appear to be strongly influenced by autoregulatory status. CONCLUSIONS: Our preliminary findings suggest a possible link between autoregulatory failure and traumatic edema progression, which warrants re-evaluation in larger-scale prospective studies.
Subject(s)
Arterial Pressure/physiology , Brain Edema/physiopathology , Brain Injuries, Traumatic/physiopathology , Cerebrovascular Circulation/physiology , Intracranial Hemorrhage, Traumatic/physiopathology , Intracranial Pressure/physiology , Adult , Brain Contusion/diagnostic imaging , Brain Contusion/physiopathology , Brain Edema/diagnostic imaging , Brain Injuries, Traumatic/diagnostic imaging , Disease Progression , Female , Glasgow Coma Scale , Glasgow Outcome Scale , Homeostasis/physiology , Humans , Intensive Care Units , Intracranial Hemorrhage, Traumatic/diagnostic imaging , Male , Middle Aged , Retrospective Studies , Tomography, X-Ray Computed , Young AdultABSTRACT
Arginine vasopressin (AVP) is a chemical signal in the brain that influences cerebral vascular resistance and brain water permeability. Increases in AVP contribute to the pathophysiology of brain edema following traumatic brain injury (TBI). These effects are mediated through AVP V1a receptors that are expressed in cortical and subcortical brain areas. This exploratory study characterizes the effects of a novel, V1a receptor antagonist, AVN576, on behavioral and magnetic resonance imaging (MRI) measures after severe TBI. Male Sprague Dawley rats were impacted twice producing contusions in the forebrain, putative cerebral edema, and cognitive deficits. Rats were treated with AVN576 after initial impact for 5 days and then tested for changes in cognition. MRI was used to assess brain injury, enlargement of the ventricles, and resting state functional connectivity. Vehicle treated rats had significant deficits in learning and memory, enlarged ventricular volumes, and hypoconnectivity in hippocampal circuitry. AVN576 treatment eliminated the enlargement of the lateral ventricles and deficits in cognitive function while increasing connectivity in hippocampal circuitry. These data corroborate the extensive literature that drugs selectively targeting the AVP V1a receptor could be used to treat TBI in the clinic.
Subject(s)
Antidiuretic Hormone Receptor Antagonists/pharmacology , Brain Contusion/diagnostic imaging , Brain Edema/diagnostic imaging , Brain/drug effects , Cognition/drug effects , Animals , Behavior, Animal/drug effects , Brain/diagnostic imaging , Brain/physiopathology , Brain Contusion/complications , Brain Contusion/drug therapy , Brain Contusion/physiopathology , Brain Edema/etiology , Brain Edema/physiopathology , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/diagnostic imaging , Brain Injuries, Traumatic/drug therapy , Brain Injuries, Traumatic/physiopathology , Functional Neuroimaging , Hippocampus/diagnostic imaging , Hippocampus/physiopathology , Lateral Ventricles/diagnostic imaging , Lateral Ventricles/pathology , Magnetic Resonance Imaging , Maze Learning , Organ Size , Rats , Receptors, VasopressinABSTRACT
Traumatic cerebral contusion and intracerebral hemorrhages (ICH) commonly result from traumatic brain injury and are associated with high morbidity and mortality rates. Current animal models require craniotomy and provide less control over injury severity. This study proposes a highly reproducible and controllable traumatic contusion and ICH model using non-invasive extracorporeal shockwaves (ESWs). Rat heads were exposed to ESWs generated by an off-the-shelf clinical device plus intravenous injection of microbubbles to enhance the cavitation effect for non-invasive induction of injury. Results indicate that injury severity can be effectively adjusted by using different ESW parameters. Moreover, the location or depth of injury can be purposefully determined by changing the focus of the concave ESW probe. Traumatic contusion and ICH were confirmed by H&E staining. Interestingly, the numbers of TUNEL-positive cells (apoptotic cell death) peaked one day after ESW exposure, while Iba1-positive cells (reactive microglia) and GFAP-positive cells (astrogliosis) respectively peaked seven and fourteen days after exposure. Cytokine assay showed significantly increased expressions of IL-1ß, IL-6, and TNF-α. The extent of brain edema was characterized with magnetic resonance imaging. Conclusively, the proposed non-invasive and highly reproducible preclinical model effectively simulates the mechanism of closed head injury and provides focused traumatic contusion and ICH.
Subject(s)
Brain Contusion/etiology , Cerebral Hemorrhage/etiology , Extracorporeal Shockwave Therapy/adverse effects , Extracorporeal Shockwave Therapy/instrumentation , Animals , Apoptosis , Astrocytes/pathology , Brain Contusion/diagnostic imaging , Brain Contusion/pathology , Brain Edema/etiology , Cell Count , Cerebral Hemorrhage/diagnostic imaging , Cerebral Hemorrhage/pathology , Inflammation , Magnetic Resonance Imaging , Male , Rats , Rats, Sprague-DawleySubject(s)
Brain Contusion/diagnostic imaging , Brain Edema/diagnosis , Brain Hemorrhage, Traumatic/diagnostic imaging , Brain Injuries, Diffuse/diagnostic imaging , Cerebellum/diagnostic imaging , Accidents, Traffic , Adult , Brain Edema/etiology , Cerebellum/physiopathology , Fatal Outcome , Humans , Male , Tomography, X-Ray ComputedABSTRACT
The endoscopic endonasal transsphenoidal (EET) approach for skull base tumors has become increasingly popular. We know that bone defects in the skull base can cause cerebrospinal fluid rhinorrhea, but for patients who need to be intubated through the nose, the tube can enter the brain through a skull base bone defect. Nasogastric tube feeding into the brain is a rare occurrence, and this situation can occur only in the case of a skull base defect. We treated a patient with an unusual complication after the EET approach for pituitary adenoma resection. This particular case suggests that bone defects after EET surgery can not only cause cerebrospinal fluid rhinorrhea but also allow the entry of a nasogastric tube into the brain. For patients with a history of EET surgery, endoscopy-assisted gastric tube implantation can be performed if necessary.
Subject(s)
Adenoma/surgery , Brain Contusion/etiology , Intubation, Gastrointestinal/adverse effects , Pituitary Neoplasms/surgery , Plastic Surgery Procedures/methods , Postoperative Complications/etiology , Skull Base/surgery , Aged , Brain Contusion/diagnostic imaging , Computed Tomography Angiography , Enteral Nutrition , Female , Humans , Nasal Cavity , Neuroendoscopy , Postoperative Complications/diagnostic imaging , Tomography, X-Ray ComputedSubject(s)
Brain Contusion/diagnostic imaging , Brain Edema/diagnostic imaging , Craniotomy , Echoencephalography/methods , Hematoma, Subdural/surgery , Postoperative Complications/diagnostic imaging , Subdural Effusion/diagnostic imaging , Adult , Drainage , Humans , Male , Point-of-Care Systems , Postoperative Complications/surgery , Subdural Effusion/surgery , Tomography, X-Ray Computed , Ultrasonography/methodsABSTRACT
BACKGROUND: Spreading depolarizations (SDs) occur in 50-60% of patients after surgical treatment of severe traumatic brain injury (TBI) and are independently associated with unfavorable outcomes. Here we performed a pilot study to examine the relationship between SDs and various types of intracranial lesions, progression of parenchymal damage, and outcomes. METHODS: In a multicenter study, fifty patients (76% male; median age 40) were monitored for SD by continuous electrocorticography (ECoG; median duration 79 h) following surgical treatment of severe TBI. Volumes of hemorrhage and parenchymal damage were estimated using unbiased stereologic assessment of preoperative, postoperative, and post-ECoG serial computed tomography (CT) studies. Neurologic outcomes were assessed at 6 months by the Glasgow Outcome Scale-Extended. RESULTS: Preoperative volumes of subdural and subarachnoid hemorrhage, but not parenchymal damage, were significantly associated with the occurrence of SDs (P's < 0.05). Parenchymal damage increased significantly (median 34 ml [Interquartile range (IQR) - 2, 74]) over 7 (5, 8) days from preoperative to post-ECoG CT studies. Patients with and without SDs did not differ in extent of parenchymal damage increase [47 ml (3, 101) vs. 30 ml (- 2, 50), P = 0.27], but those exhibiting the isoelectric subtype of SDs had greater initial parenchymal damage and greater increases than other patients (P's < 0.05). Patients with temporal clusters of SDs (≥ 3 in 2 h; n = 10 patients), which included those with isoelectric SDs, had worse outcomes than those without clusters (P = 0.03), and parenchymal damage expansion also correlated with worse outcomes (P = 0.01). In multivariate regression with imputation, both clusters and lesion expansion were significant outcome predictors. CONCLUSIONS: These results suggest that subarachnoid and subdural blood are important primary injury factors in provoking SDs and that clustered SDs and parenchymal lesion expansion contribute independently to worse patient outcomes. These results warrant future prospective studies using detailed quantification of TBI lesion types to better understand the relationship between anatomic and physiologic measures of secondary injury.
Subject(s)
Brain Contusion/pathology , Brain Contusion/physiopathology , Cortical Spreading Depression/physiology , Hematoma, Subdural, Acute/pathology , Hematoma, Subdural, Acute/physiopathology , Subarachnoid Hemorrhage, Traumatic/pathology , Subarachnoid Hemorrhage, Traumatic/physiopathology , Adult , Brain Contusion/diagnostic imaging , Electrocorticography , Female , Follow-Up Studies , Glasgow Outcome Scale , Hematoma, Subdural, Acute/diagnostic imaging , Humans , Male , Middle Aged , Pilot Projects , Severity of Illness Index , Subarachnoid Hemorrhage, Traumatic/diagnostic imaging , Tomography, X-Ray ComputedABSTRACT
INTRODUCTION: Mild traumatic brain injury (MTBI) can cause persistent functional deficits and healthcare burden. Understanding the association between intracranial contusions and outcome may aid in MTBI treatment and prognosis. METHODS: MTBI patients with Glasgow Coma Scale 13-15 and 6-month outcomes [Glasgow Outcome Scale-Extended (GOSE)], without polytrauma from the prospective TRACK-TBI Pilot study were analyzed. Intracranial contusions on computed tomography (CT) were coded by location. Multivariable regression evaluated associations between intracranial injury type (temporal contusion [TC], frontal contusion, extraaxial [epidural/subdural/subarachnoid], other-intraaxial [intracerebral/intraventricular hemorrhage, axonal injury]) and GOSE. Odds ratios (OR) are reported. RESULTS: Overall, 260 MTBI subjects were aged 44.4 ± 18.1-years; 67.7% were male. Ninety-seven subjects were CT-positive and 46 had contusions (41.3%-frontal, 30.4%-temporal, 21.7%-frontal + temporal, 2.2% each-parietal/occipital/brainstem); 95.7% had concurrent extraaxial hemorrhage. Mortality was 0% at discharge and 2.3% by 6-months. GOSE distribution was 2.3%-death, 1.5%-severe disability, 27.7%-moderate disability, 68.5%-good recovery. Forty-six percent of TC-positive subjects suffered moderate disability or worse (GOSE ≤6) and 41.7% were unable to return to baseline work capacity (RTBWC), compared to 29.1%/20.4% for CT-negative and 26.1%/20.9% for CT-positive subjects without TC. On multivariable regression, TC associated with OR = 3.33 (95% CI [1.16-9.60], p = 0.026) for GOSE ≤6, and OR = 4.48 ([1.49-13.51], p = 0.008) for inability to RTBWC. CONCLUSIONS: Parenchymal contusions in MTBI are often accompanied by extraaxial hemorrhage. TCs may be associated with 6-month functional impairment. Their presence on imaging should alert the clinician to the need for heightened surveillance of sequelae complicating RTBWC, with low threshold for referral to services.