ABSTRACT
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.
Subject(s)
Diffuse Axonal Injury/diagnostic imaging , Diffuse Axonal Injury/etiology , Tomography, X-Ray Computed , Accidents, Traffic , Brain Stem/injuries , Cerebral Hemorrhage, Traumatic/diagnostic imaging , Cerebral Hemorrhage, Traumatic/etiology , Cerebral Intraventricular Hemorrhage/diagnostic imaging , Cerebral Intraventricular Hemorrhage/etiology , Corpus Callosum/injuries , Humans , Prognosis , Subarachnoid Hemorrhage/diagnostic imaging , Subarachnoid Hemorrhage/etiologyABSTRACT
Diffuse axonal injury (DAI) is a hallmark of traumatic brain injury (TBI) pathology. Recently, the Closed Head Injury Model of Engineered Rotational Acceleration (CHIMERA) was developed to generate an experimental model of DAI in a mouse. The characterization of DAI using diffusion tensor magnetic resonance imaging (MRI; diffusion tensor imaging, DTI) may provide a useful set of outcome measures for preclinical and clinical studies. The objective of this study was to identify the complex neurobiological underpinnings of DTI features following DAI using a comprehensive and quantitative evaluation of DTI and histopathology in the CHIMERA mouse model. A consistent neuroanatomical pattern of pathology in specific white matter tracts was identified across ex vivo DTI maps and photomicrographs of histology. These observations were confirmed by voxelwise and regional analysis of DTI maps, demonstrating reduced fractional anisotropy (FA) in distinct regions such as the optic tract. Similar regions were identified by quantitative histology and exhibited axonal damage as well as robust gliosis. Additional analysis using a machine-learning algorithm was performed to identify regions and metrics important for injury classification in a manner free from potential user bias. This analysis found that diffusion metrics were able to identify injured brains almost with the same degree of accuracy as the histology metrics. Good agreement between regions detected as abnormal by histology and MRI was also found. The findings of this work elucidate the complexity of cellular changes that give rise to imaging abnormalities and provide a comprehensive and quantitative evaluation of the relative importance of DTI and histological measures to detect brain injury.
Subject(s)
Diffuse Axonal Injury/diagnostic imaging , Diffuse Axonal Injury/etiology , Diffusion Magnetic Resonance Imaging , Head Injuries, Closed/complications , Acceleration/adverse effects , Amyloid beta-Protein Precursor/metabolism , Animals , Anisotropy , Calcium-Binding Proteins/metabolism , Diffuse Axonal Injury/pathology , Disease Models, Animal , Glial Fibrillary Acidic Protein/metabolism , Head Injuries, Closed/etiology , Image Processing, Computer-Assisted , Male , Mice , Mice, Inbred C57BL , Microfilament Proteins/metabolism , Optic Tract/pathologyABSTRACT
A 9 year-old male sustained multiple maxillofacial fractures after falling from a two-store building. Frontal sinuses suffered a bilateral non-displaced linear fractures extending into the anterior and posterior walls. Magnetic resonance imaging (MRI) at this time showed a small encephalocele extending into the right frontal sinus. Operative repair was performed using an Endoscopic-Assisted Trephination approach.
Subject(s)
Encephalocele/surgery , Endoscopy/methods , Frontal Sinus/injuries , Skull Fractures/surgery , Trephining/methods , Accidental Falls , Bioprosthesis , Cerebrospinal Fluid Leak/etiology , Cerebrospinal Fluid Leak/surgery , Child , Deafness/etiology , Diffuse Axonal Injury/etiology , Encephalocele/etiology , Fibrin Tissue Adhesive/therapeutic use , Frontal Sinus/surgery , Hearing Loss, Sensorineural/etiology , Humans , Male , Meningitis/etiology , Skull Fractures/complications , Surgical Mesh , TitaniumABSTRACT
Traumatic brain injury (TBI) is a worldwide health problem that is especially prevalent in young adults. It is characterized by one or more primary injury foci, with secondary spread to initially not compromised areas via cascades of inflammatory response, excitotoxicity, energy failure conditions, and amplification of the original tissue injury by glia. In theory, such progression of injury should be amenable to management. However, all neuroprotective drug trials have failed, and specific treatments remain lacking. These negative results can be explained by a neuron centered approach, excluding the participation of other cell types and pathogenic mechanisms. To change this situation, it is necessary to secure a better understanding of the biological mechanisms determining damage progression or spread. We discuss the biological mechanisms involved in the progression of post-trauma tissue damage, including the general physiopathology of TBI and cellular mechanisms of secondary damage such as inflammation, apoptosis, cell tumefaction, excitotoxicity, and the role of glia in damage propagation. We highlight the role of glia in each cellular mechanism discussed. Therapeutic approaches related to the described mechanisms have been included. The discussion is completed with a working model showing the convergence of the main topics.
Subject(s)
Brain Injuries/physiopathology , Animals , Apoptosis , Brain Death , Brain Edema/etiology , Brain Injuries/complications , Brain Injuries/metabolism , Cell Size , Diffuse Axonal Injury/etiology , Diffuse Axonal Injury/pathology , Diffuse Axonal Injury/physiopathology , Glutamic Acid/metabolism , Humans , Hyperglycemia/etiology , Inflammation , Intracranial Hypertension/etiology , Intracranial Hypertension/physiopathology , Ion Transport , Models, Neurological , Neuroglia/physiology , Neurons/pathologyABSTRACT
The term paroxysmal sympathetic storms is used to define episodic alterations in body temperature, blood pressure, heart and respiratory rate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during the episodes of epileptiform activity and without any infectious cause with excellent answer to the treatment with beta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application of unnecessary studies allowing an appropriate treatment.
Subject(s)
Autonomic Nervous System Diseases/diagnosis , Brain Injuries/physiopathology , Diffuse Axonal Injury/physiopathology , Adult , Autonomic Nervous System Diseases/etiology , Autonomic Nervous System Diseases/physiopathology , Brain Injuries/complications , Diagnosis, Differential , Diffuse Axonal Injury/etiology , Fever/physiopathology , Glasgow Outcome Scale , Humans , Hyperhidrosis/physiopathology , Hypertension/physiopathology , Male , Tachycardia, Paroxysmal/physiopathologyABSTRACT
El término tormenta simpática paroxística se utiliza como sinónimo de alteraciones episódicas de la temperatura corporal, la presión arterial, la frecuencia respiratoria y cardíaca, el tamaño pupilary el nivel de conciencia, que coinciden con hiperhidrosis, salivación excesiva y postura extensora. Esto siempreen el contexto de una injuria axonal difusa grave que sigue a un traumatismo encéfalo-craneano (TEC) grave.Presentamos dos pacientes jóvenes con injuria axonal difusa secundaria a TEC grave, que desarrollan en suevolución cuadros de hipertensión arterial, taquicardia y fiebre, sin evidencia durante los episodios de actividad epileptiforme y habiéndose descartado la causa infecciosa, que responden favorablemente al tratamiento con beta-bloqueantes y morfina. Consideramos que el correcto diagnóstico de esta entidad minimiza la solicitud de estudios innecesarios permitiendo iniciar un tratamiento adecuadoc
The term paroxysmal sympatheticstorms is used to define episodic alterations in body temperature, blood pressure, heart and respiratoryrate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during theepisodes of epileptiform activity and without any infectious cause with excellent answer to the treatment withbeta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application ofunnecessary studies allowing an appropriate treatment
Subject(s)
Humans , Male , Adult , Autonomic Nervous System Diseases/diagnosis , Brain Injuries/physiopathology , Diffuse Axonal Injury/physiopathology , Autonomic Nervous System Diseases/etiology , Autonomic Nervous System Diseases/physiopathology , Brain Injuries/complications , Diagnosis, Differential , Diffuse Axonal Injury/etiology , Fever/physiopathology , Glasgow Outcome Scale , Hyperhidrosis/physiopathology , Hypertension/physiopathology , Tachycardia, Paroxysmal/physiopathologyABSTRACT
El término tormenta simpática paroxística se utiliza como sinónimo de alteraciones episódicas de la temperatura corporal, la presión arterial, la frecuencia respiratoria y cardíaca, el tamaño pupilary el nivel de conciencia, que coinciden con hiperhidrosis, salivación excesiva y postura extensora. Esto siempreen el contexto de una injuria axonal difusa grave que sigue a un traumatismo encéfalo-craneano (TEC) grave.Presentamos dos pacientes jóvenes con injuria axonal difusa secundaria a TEC grave, que desarrollan en suevolución cuadros de hipertensión arterial, taquicardia y fiebre, sin evidencia durante los episodios de actividad epileptiforme y habiéndose descartado la causa infecciosa, que responden favorablemente al tratamiento con beta-bloqueantes y morfina. Consideramos que el correcto diagnóstico de esta entidad minimiza la solicitud de estudios innecesarios permitiendo iniciar un tratamiento adecuadoc (AU)
The term paroxysmal sympatheticstorms is used to define episodic alterations in body temperature, blood pressure, heart and respiratoryrate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during theepisodes of epileptiform activity and without any infectious cause with excellent answer to the treatment withbeta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application ofunnecessary studies allowing an appropriate treatment (AU)
Subject(s)
Humans , Male , Adult , Autonomic Nervous System Diseases/diagnosis , Brain Injuries, Traumatic/physiopathology , Diffuse Axonal Injury/physiopathology , Autonomic Nervous System Diseases/etiology , Brain Injuries, Traumatic/complications , Diagnosis, Differential , Fever/physiopathology , Glasgow Outcome Scale , Hyperhidrosis/physiopathology , Hypertension/physiopathology , Autonomic Nervous System Diseases/physiopathology , Tachycardia, Paroxysmal/physiopathology , Diffuse Axonal Injury/etiologyABSTRACT
El término tormenta simpática paroxística se utiliza como sinónimo de alteraciones episódicas de la temperatura corporal, la presión arterial, la frecuencia respiratoria y cardíaca, el tamaño pupilary el nivel de conciencia, que coinciden con hiperhidrosis, salivación excesiva y postura extensora. Esto siempreen el contexto de una injuria axonal difusa grave que sigue a un traumatismo encéfalo-craneano (TEC) grave.Presentamos dos pacientes jóvenes con injuria axonal difusa secundaria a TEC grave, que desarrollan en suevolución cuadros de hipertensión arterial, taquicardia y fiebre, sin evidencia durante los episodios de actividad epileptiforme y habiéndose descartado la causa infecciosa, que responden favorablemente al tratamiento con beta-bloqueantes y morfina. Consideramos que el correcto diagnóstico de esta entidad minimiza la solicitud de estudios innecesarios permitiendo iniciar un tratamiento adecuadoc (AU)
The term paroxysmal sympatheticstorms is used to define episodic alterations in body temperature, blood pressure, heart and respiratoryrate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during theepisodes of epileptiform activity and without any infectious cause with excellent answer to the treatment withbeta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application ofunnecessary studies allowing an appropriate treatment (AU)
Subject(s)
Humans , Male , Adult , Autonomic Nervous System Diseases/diagnosis , Brain Injuries, Traumatic/physiopathology , Diffuse Axonal Injury/physiopathology , Autonomic Nervous System Diseases/etiology , Brain Injuries, Traumatic/complications , Diagnosis, Differential , Fever/physiopathology , Glasgow Outcome Scale , Hyperhidrosis/physiopathology , Hypertension/physiopathology , Autonomic Nervous System Diseases/physiopathology , Tachycardia, Paroxysmal/physiopathology , Diffuse Axonal Injury/etiologyABSTRACT
BACKGROUND: The cavum of the septum pellucidum (CSP) is a small cavity constantly present in fetuses and newborns, of variable frequency among necropsied adults and with a high frequency in professional boxers. METHOD: A pathologic study was conducted on brains of 626 patients without a history of head trauma (group 1) autopsied consecutively from a general hospital and of 120 random victims of fatal road traffic accidents (group 2). RESULTS: In group 1, 237 (37.9%) cases of CSP were observed, virtually all in a triangular or trapezoidal shape. In group 2, 65 (54.2%) cases of CSP were observed, 50 (76.9%) in triangular or trapezoidal shape and 15 (23.1%) in cleft shape. Cleft CSP was always associated with severe diffuse axonal injury (grades 2 and 3). CONCLUSION: Although described in boxers, the CSP has not been reported in other types of head injury. The largest frequency of CSP found in fatal victims of head trauma, particularly in patients with severe diffuse axonal lesion (grades 2 and 3), when compared with the individuals without a history of head trauma, suggests that the high-intensity angular acceleration of the head causes complementary and independent displacement of the 2 cerebral hemispheres and dislocation of one of the leaves of the septum pellucidum on the other. This could result in separation of the 2 leaves and formation of CSP, usually in cleft shape.