Orbital and facial fractures.

This article reviews the importance of particular radiologic findings related to facial trauma and their implications for clinical and surgical management. An emphasis is placed on critical imaging signs that warrant immediate surgical attention.

Natural history and prognostic value of corticospinal tract Wallerian degeneration in intracerebral hemorrhage.

BACKGROUND: The purpose of this study was to define the incidence, imaging characteristics, natural history, and prognostic implication of corticospinal tract Wallerian degeneration (CST-WD) in spontaneous intracerebral hemorrhage (ICH) using serial MR imaging. METHODS AND RESULTS: Consecutive ICH patients with supratentorial ICH prospectively underwent serial MRIs at 2, 7, 14, and 21 days. MRIs were analyzed by independent raters for the presence and topographical distribution of CST-WD on diffusion-weighted imaging (DWI). Baseline demographics, hematoma characteristics, ICH score, and admission National Institute of Health Stroke Score (NIHSS) were systematically recorded. Functional outcome at 3 months was assessed by the modified Rankin Scale (mRS) and the motor-NIHSS. Twenty-seven patients underwent 93 MRIs; 88 of these were serially obtained in the first month. In 13 patients (48%), all with deep ICH, CST-WD changes were observed after a median of 7 days (interquartile range, 7 to 8) as reduced diffusion on DWI and progressed rostrocaudally along the CST. CST-WD changes evolved into T2-hyperintense areas after a median of 11 days (interquartile range, 6 to 14) and became atrophic on MRIs obtained after 3 months. In univariate analyses, the presence of CST-WD was associated with poor functional outcome (ie, mRS 4 to 6; P=0.046) and worse motor-NIHSS (5 versus 1, P=0.001) at 3 months. CONCLUSIONS: Wallerian degeneration along the CST is common in spontaneous supratentorial ICH, particularly in deep ICH. It can be detected 1 week after ICH on DWI and progresses rostrocaudally along the CST over time. The presence of CST-WD is associated with poor motor and functional recovery after ICH.

Delayed acute spinal cord injury following intracranial gunshot trauma: case report.

The authors report the case of a patient who presented with a hoarse voice and left hemiparesis following a gunshot injury with trajectory entering the left scapula, traversing the suboccipital bone, and coming to rest in the right lateral medullary cistern. Following recovery from the hemiparesis, abrupt quadriparesis occurred coincident with fall of the bullet into the anterior spinal canal. The bullet was retrieved following a C-2 and C-3 laminectomy, and postoperative MR imaging confirmed signal change in the cord at the level where the bullet had lodged. The patient then made a good neurological recovery. Bullets can fall from the posterior fossa with sufficient momentum to cause an acute spinal cord injury. Consideration for craniotomy and bullet retrieval should be given to large bullets lying in the CSF spaces of the posterior fossa as they pose risk for acute spinal cord injury.

Temporizing treatment of hyperacute subdural hemorrhage by subdural evacuation port system placement.

An acute subdural hematoma (SDH) requiring surgical intervention is treated with craniotomy or craniectomy, in part because it is generally accepted that coagulated blood present in the acute phase cannot be adequately evacuated by less-invasive means such as bur hole drainage. However, a hyperacute SDH in the first few hours after trauma can have mixed-density components on CT scans that are thought to represent subdural blood that is not yet fully coagulated. The authors report a case in which a hyperacute SDH in a patient receiving antiplatelet therapy was treated with the novel technique of temporizing subdural evacuation port system (SEPS) placement. Placement of an SEPS in the intensive care unit allowed for rapid surgical treatment of the patient's elevated intracranial pressure (ICP) by drainage of 70 ml of fresh subdural blood. After initial SEPS-induced stabilization, the patient underwent operative treatment of the SDH by craniotomy. The combined approach of emergency SEPS placement followed by craniotomy resulted in a dramatic recovery, with improvement from coma and extensor posturing to a normal status on neurological evaluation 5 weeks later. In appropriately selected cases, patients with a hyperacute SDH may benefit from SEPS placement to quickly treat elevated ICP, as a bridge to definitive surgical treatment by craniotomy.

Mechanisms of primary blast-induced traumatic brain injury: insights from shock-wave research.

Traumatic brain injury caused by explosive or blast events is traditionally divided into four phases: primary, secondary, tertiary, and quaternary blast injury. These phases of blast-induced traumatic brain injury (bTBI) are biomechanically distinct and can be modeled in both in vivo and in vitro systems. The primary bTBI injury phase represents the response of brain tissue to the initial blast wave. Among the four phases of bTBI, there is a remarkable paucity of information about the cause of primary bTBI. On the other hand, 30 years of research on the medical application of shockwaves (SW) has given us insight into the mechanisms of tissue and cellular damage in bTBI, including both air-mediated and underwater SW sources. From a basic physics perspective, the typical blast wave consists of a lead SW followed by supersonic flow. The resultant tissue injury includes several features observed in bTBI, such as hemorrhage, edema, pseudoaneurysm formation, vasoconstriction, and induction of apoptosis. These are well-described pathological findings within the SW literature. Acoustic impedance mismatch, penetration of tissue by shock/bubble interaction, geometry of the skull, shear stress, tensile stress, and subsequent cavitation formation, are all important factors in determining the extent of SW-induced tissue and cellular injury. Herein we describe the requirements for the adequate experimental set-up when investigating blast-induced tissue and cellular injury; review SW physics, research, and the importance of engineering validation (visualization/pressure measurement/numerical simulation); and, based upon our findings of SW-induced injury, discuss the potential underlying mechanisms of primary bTBI.

Imaging for the diagnosis and management of traumatic brain injury.

To understand the role of imaging in traumatic brain injury (TBI), it is important to appreciate that TBI encompasses a heterogeneous group of intracranial injuries and includes both insults at the time of impact and a deleterious secondary cascade of insults that require optimal medical and surgical management. Initial imaging identifies the acute primary insult that is essential to diagnosing TBI, but serial imaging surveillance is also critical to identifying secondary injuries such as cerebral herniation and swelling that guide neurocritical management. Computed tomography (CT) is the mainstay of TBI imaging in the acute setting, but magnetic resonance tomography (MRI) has better diagnostic sensitivity for nonhemorrhagic contusions and shear-strain injuries. Both CT and MRI can be used to prognosticate clinical outcome, and there is particular interest in advanced applications of both techniques that may greatly improve the sensitivity of conventional CT and MRI for both the diagnosis and prognosis of TBI.

Common data elements in radiologic imaging of traumatic brain injury.

Radiologic brain imaging is the most useful means of visualizing and categorizing the location, nature, and degree of damage to the central nervous system sustained by patients with traumatic brain injury (TBI). In addition to determining acute patient management and prognosis, imaging is crucial for the characterization and classification of injuries for natural history studies and clinical trials. This article is the initial result of a workshop convened by multiple national health care agencies in March 2009 to begin to make recommendations for potential data elements dealing with specific radiologic features and definitions needed to characterize injuries, as well as specific techniques and parameters needed to optimize radiologic data acquisition. The neuroimaging work group included professionals with expertise in basic imaging research and physics, clinical neuroradiology, neurosurgery, neurology, physiatry, psychiatry, TBI research, and research database formation. This article outlines the rationale and overview of their specific recommendations. In addition, we review the contributions of various imaging modalities to the understanding of TBI and the general principles needed for database flexibility and evolution over time to accommodate technical advances.

Head trauma.

Worldwide, an estimated 10 million people are affected annually by traumatic brain injury (TBI). More than 5 million Americans currently live with long-term disability as a result of TBI and more than 1.5 million individuals sustain a new TBI each year. It has been predicted that TBI will become the third leading cause of death and disability in the world by the year 2020. This article outlines the classification of TBI, details the types of lesions encountered, and discusses the various imaging modalities available for the evaluation of TBI.

Common data elements in radiologic imaging of traumatic brain injury.

Traumatic brain injury (TBI) has a poorly understood pathology. Patients suffer from a variety of physical and cognitive effects that worsen as the type of trauma worsens. Some noninvasive insights into the pathophysiology of TBI are possible using magnetic resonance imaging (MRI), computed tomography (CT), and many other forms of imaging as well. A recent workshop was convened to evaluate the common data elements (CDEs) that cut across the imaging field and given the charge to review the contributions of the various imaging modalities to TBI and to prepare an overview of the various clinical manifestations of TBI and their interpretation. Technical details regarding state-of-the-art protocols for both MRI and CT are also presented with the hope of guiding current and future research efforts as to what is possible in the field. Stress was also placed on the potential to create a database of CDEs as a means to best record information from a given patient from the reading of the images.

Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma.

PURPOSE: To study the incidence, pathogenesis, imaging characteristics, and clinical importance of a unique subtype of epidural hematoma (EDH) associated with blunt head trauma. MATERIALS AND METHODS: This study was reviewed and approved by the hospital's Institutional Review Board and was compliant with HIPAA. Informed consent was waived. The investigation was a retrospective study of 200 patients with acute supratentorial EDH, defined as a biconvex, high-attenuating, extraaxial hematoma. A subgroup of 21 patients in whom the EDH was located at the anterior aspect of the middle cranial fossa was defined. Computed tomographic images and inpatient medical records of these 21 patients were evaluated for imaging characteristics of the EDH, presence or absence of associated fracture, presence or absence of midline shift and/or mass effect, additional intracranial injury, and hospital clinical course. RESULTS: Twenty-one (10.5%) of 200 traumatic EDHs localized to the anterior middle cranial fossa. All of these 21 anterior temporal EDHs were juxtaposed to the sphenoparietal sinus, and all but one were limited laterally by the sphenotemporal suture and medially by the orbital fissure; none extended above the lesser sphenoid wing. Maximum thickness was less than 1 cm in 13 (62%) of 21 and less than 2 cm in 20 (95%) of 21 patients. Isolated fractures of the greater sphenoid wing and ipsilateral zygomaticomaxillary fractures were present in 12 (57%) of 21 and nine (43%) of 21 patients, respectively. Concomitant intracranial injury was identified in 15 (71%) of 21 patients. Twenty (95%) of 21 lesions were present at the admission study, and all 21 were stable or smaller at follow-up imaging. No patient required neurosurgical intervention of their anterior temporal EDH. CONCLUSION: Acute EDHs isolated to the anterior aspect of the middle cranial fossa constitute a subgroup of traumatic EDHs with a benign natural history. It is postulated that they arise from venous bleeding due to disruption of the sphenoparietal sinus.

Second-impact syndrome and a small subdural hematoma: an uncommon catastrophic result of repetitive head injury with a characteristic imaging appearance.

There have been a handful of previously published cases of athletes who were still symptomatic from a prior head injury, and then suffered a second injury in which a thin, acute subdural hematoma (SDH) with unilateral hemisphere vascular engorgement was demonstrated on CT scan. In those cases, the cause of the brain swelling/dysautoregulation was ascribed to the presence of the acute SDH rather than to the acceleration/deceleration forces that caused the SDH. We believe that the brain swelling is due to "second-impact dysautoregulation," rather than due to the effect of the SDH on the underlying hemisphere. To support our hypothesis, we present 10 additional cases of acute hemispheric swelling in association with small SDHs in athletes who received a second head injury while still symptomatic from a previous head injury. The clinical history and the unique neuroimaging features of this entity on CT are described and illustrated in detail. The CT findings included an engorged cerebral hemisphere with initial preservation of grey-white matter differentiation, and abnormal mass effect and midline shift that appeared disproportionately greater than the size of the SDH. In addition, the imaging similarities between our patients and those with non-accidental head trauma (shaken-baby syndrome) will be discussed.

Hemicraniectomy: a new model for human electrophysiology with high spatio-temporal resolution.

Human electrophysiological research is generally restricted to scalp EEG, magneto-encephalography, and intracranial electrophysiology. Here we examine a unique patient cohort that has undergone decompressive hemicraniectomy, a surgical procedure wherein a portion of the calvaria is removed for several months during which time the scalp overlies the brain without intervening bone. We quantify the differences in signals between electrodes over areas with no underlying skull and scalp EEG electrodes over the intact skull in the same subjects. Signals over the hemicraniectomy have enhanced amplitude and greater task-related power at higher frequencies (60-115 Hz) compared with signals over skull. We also provide evidence of a metric for trial-by-trial EMG/EEG coupling that is effective over the hemicraniectomy but not intact skull at frequencies >60 Hz. Taken together, these results provide evidence that the hemicraniectomy model provides a means for studying neural dynamics in humans with enhanced spatial and temporal resolution.

Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting.

This clinical policy provides evidence-based recommendations on select issues in the management of adult patients with mild traumatic brain injury (TBI) in the acute setting. It is the result of joint efforts between the American College of Emergency Physicians and the Centers for Disease Control and Prevention and was developed by a multidisciplinary panel. The critical questions addressed in this clinical policy are: (1) Which patients with mild TBI should have a noncontrast head computed tomography (CT) scan in the emergency department (ED)? (2) Is there a role for head magnetic resonance imaging over noncontrast CT in the ED evaluation of a patient with acute mild TBI? (3) In patients with mild TBI, are brain specific serum biomarkers predictive of an acute traumatic intracranial injury? (4) Can a patient with an isolated mild TBI and a normal neurologic evaluation result be safely discharged from the ED if a noncontrast head CT scan shows no evidence of intracranial injury? Inclusion criteria for application of this clinical policy's recommendations are nonpenetrating trauma to the head, presentation to the ED within 24 hours of injury, a Glasgow Coma Scale score of 14 or 15 on initial evaluation in the ED, and aged 16 years or greater. The primary outcome measure for questions 1, 2, and 3 is the presence of an acute intracranial injury on noncontrast head CT scan; the primary outcome measure for question 4 is the occurrence of neurologic deterioration.

Neuroimaging of traumatic brain injury.

In this article, the neuroradiological evaluation of traumatic brain injury is reviewed. Different imaging strategies in the assessment of traumatic brain injury are initially discussed, and this is followed by a review of the imaging characteristics of both primary and secondary brain injuries. Computed tomography remains the modality of choice for the initial assessment of acute head injury because it is fast, widely available, and highly accurate in the detection of skull fractures and acute intracranial hemorrhage. Magnetic resonance imaging is recommended for patients with acute traumatic brain injury when the neurological findings are unexplained by computed tomography. Magnetic resonance imaging is also the modality of choice for the evaluation of subacute or chronic traumatic brain injury. Mild traumatic brain injury continues to be difficult to diagnose with current imaging technology. Advanced magnetic resonance techniques, such as diffusion-weighted imaging, magnetic resonance spectroscopy, and magnetization transfer imaging, can improve the identification of traumatic brain injury, especially in the case of mild traumatic brain injury. Further research is needed for other advanced imaging methods such as magnetic source imaging, single photon emission tomography, and positron emission tomography.

Survival with good outcome after cerebral herniation and Duret hemorrhage caused by traumatic brain injury.

Brainstem hemorrhage can occur as a primary or secondary event in traumatic brain injury (TBI). Secondary brainstem hemorrhage that evolves from raised intracranial pressure and transtentorial herniation is referred to as Duret hemorrhage. Duret hemorrhage following TBI has been considered an irreversible and terminal event. The authors report on the case of a young adult patient with TBI who presented with a low Glasgow Coma Scale score and advanced signs of cerebral herniation. She underwent an urgent decompressive hemicraniectomy for evacuation of an acute epidural hematoma and developed a Duret hemorrhage postoperatively. In accordance with the family's wishes, aggressive TBI monitoring and treatment in the intensive care unit was continued even though the anticipated outcome was poor. After a lengthy hospital course, the patient improved dramatically and was discharged ambulatory, with good cognitive functioning and a Glasgow Outcome Scale score of 4. Duret hemorrhage secondary to raised intracranial pressure is not always a terminal event, and by itself should not trigger a decision to withdraw care. Aggressive intracranial monitoring and treatment of a Duret hemorrhage arising secondary to cerebral herniation may enable a good recovery in selected patients after severe TBI.

Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting.

This clinical policy provides evidence-based recommendations on select issues in the management of adult patients with mild traumatic brain injury (TBI) in the acute setting. It is the result of joint efforts between the American College of Emergency Physicians and the Centers for Disease Control and Prevention and was developed by a multidisciplinary panel. The critical questions addressed in this clinical policy are: (1) Which patients with mild TBI should have a noncontrast head computed tomography (CT) scan in the emergency department (ED)? (2) Is there a role for head magnetic resonance imaging over noncontrast CT in the ED evaluation of a patient with acute mild TBI? (3) In patients with mild TBI, are brain specific serum biomarkers predictive of an acute traumatic intracranial injury? (4) Can a patient with an isolated mild TBI and a normal neurologic evaluation result be safely discharged from the ED if a noncontrast head CT scan shows no evidence of intracranial injury? Inclusion criteria for application of this clinical policy's recommendations are nonpenetrating trauma to the head, presentation to the ED within 24 hours of injury, a Glasgow Coma Scale score of 14 or 15 on initial evaluation in the ED, and aged 16 years or greater. The primary outcome measure for questions 1, 2, and 3 is the presence of an acute intracranial injury on noncontrast head CT scan; the primary outcome measure for question 4 is the occurrence of neurologic deterioration.

Computer-aided assessment of head computed tomography (CT) studies in patients with suspected traumatic brain injury.

In this study, we sought to determine the accuracy of a computer algorithm that automatically assesses head computed tomography (CT) studies in patients with suspected traumatic brain injury (TBI) for features of intracranial hemorrhage and mass effect, employing a neuroradiologist's interpretation as the gold standard. To this end, we designed a suite of computer algorithms that evaluates in a fully automated fashion the presence of intracranial blood and/or mass effect based on the following CT findings: (1) presence or absence of a subdural or epidural hematoma, (2) presence or absence of subarachnoid hemorrhage, (3) presence or absence of an intraparenchymal hematoma, (4) presence or absence of clinically significant midline shift (>or=5 mm), and (5) normal, partly effaced, or completely effaced basal cisterns. The algorithm displays abnormal findings as color overlays on the original head CT images, and calculates the volume of each type of blood collection, the midline shift, and the volume of the basal cisterns, based on the above-described features. Thresholds and parameters yielding optimal accuracy of the computer algorithm were determined using a development sample of 33 selected, nonconsecutive patients. The software was then applied to a validation sample of 250 consecutive patients evaluated for suspicion of acute TBI at our institution in 2006-2007. Software detection of the presence of at least one noncontrast CT (NCT) feature of acute TBI demonstrated high sensitivity of 98% and high negative predictive value (NPV) of 99%. There was actually only one false negative case, where a very subtle subdural hematoma, extending exclusively along the falx, was diagnosed by the neuroradiologist, while the case was considered as normal by the computer algorithm. The software was excellent at detecting the presence of mass effect and intracranial hemorrhage, but showed some disagreements with the neuroradiologist in quantifying the degree of mass effect and characterizing the type of intracranial hemorrhage. In summary, we have developed a fully automated computer algorithm that demonstrated excellent sensitivity for acute intracranial hemorrhage and clinically significant midline shift, while maintaining intermediate specificity. Further studies are required to evaluate the potential favorable impact of this software on facilitating workflow and improving diagnostic accuracy when used as a screening aid by physicians with different levels of experience.

Focal lesions in acute mild traumatic brain injury and neurocognitive outcome: CT versus 3T MRI.

Mild traumatic brain injury (mTBI) is associated with long-term cognitive deficits. This study compared the detection rate of acute post-traumatic focal lesions on computed tomography (CT) and 3T (Tesla) magnetic resonance (MR) imaging with neurocognitive outcomes. Adults (n = 36; age range, 19-52 years) with a single episode of mTBI (Glasgow Coma Scale 13-15, as well as loss of consciousness and post-traumatic amnesia) were prospectively enrolled and had CT within 24 h of injury and 3T MR within 2 weeks of injury. The CT and MR scans were reviewed by two neuroradiologists who were blinded to clinical information. Twenty-eight of these mTBI subjects and 18 matched healthy volunteers also underwent serial neurocognitive testing. Of the 36 mTBI cases, intraparenchymal lesions were detected in 18 CT and 27 acute MR exams, consisting of hemorrhagic traumatic axonal injury (TAI) (eight CT, 17 MR), non-hemorrhagic TAI (zero CT, four MR), and cerebral contusions (13 CT, 21 MR). Mild TBI patients had significantly worse performance on working memory tasks than matched controls at the acute time point (<2 weeks), and at 1 month and at 1 year post-injury; yet there was no significant correlation of imaging findings with working memory impairment. In conclusion, 3T MR detected parenchymal lesions in 75% of this mTBI cohort with loss of consciousness and post-traumatic amnesia, a much higher rate than CT. However, the CT and 3T MR imaging findings did not account for cognitive impairment, suggesting that newer imaging techniques such as diffusion tensor imaging are needed to provide biomarkers for neurocognitive and functional outcome in mTBI.