CT prediction of contusion evolution after closed head injury: the role of pericontusional edema.

BACKGROUND: Cerebral contusions have a 51% incidence of evolution in the first hours after injury. Evolution is associated with clinical deterioration and is the reason for ICP monitoring or surgical intervention. We sought to define CT features that predict cerebral contusion evolution. METHODS: Patients treated for cerebral contusion who had 2 CT scans within 24 hours after injury were evaluated (n = 21). CT scans were analyzed for area of contusion, hemorrhagic components, and edema. Increase (%) in contusion size was recorded. Contusion evolution was defined as > 5% size increase. Ratios of hemorrhagic components to surrounding edema were calculated. RESULTS: Ten patients (47.6%) showed contusion evolution and 11 (52.4%) did not. Age, sex ratio, or injury severity between the 2 groups did not differ. Eight of 10 patients with evolving contusions had minimal or no perilesional edema on first CT; only 2 of 11 nonevolution patients had perilesional edema (p < 0.005). Mean ratio of area of surrounding edema to area of hemorrhagic products on first CT was 0.770 in evolution group versus 2.22 in non-evolution group (p = 0.055). CONCLUSIONS: A higher proportion of patients without contusion evolution had perilesional edema present on first CT scan. The absence of pericontusional edema on early CT may be a useful marker to predict contusion evolution.

Bolus tracer delivery measured by MRI confirms edema without blood-brain barrier permeability in diffuse traumatic brain injury.

INTRODUCTION: Previous studies have shown that edema formation after diffuse traumatic brain injury (TBI) with secondary insult is cytotoxic and not vasogenic. This assumption is based on observations of reduced apparent diffusion coefficient (ADC) and lack of significant accumulation of intravascular tracer in brain tissue. However, ADC reduction does not exclude vasogenic edema, and intravascular tracer can only accumulate when it reaches the tissue and is not perfusion limited. This study aims to confirm tissue delivery of intravascular tracer and lack of BBB opening during a phase of rapid brain swelling after diffuse TBI. METHODS: Rats were exposed to either TBI using the impact acceleration model combined with 30 minutes of hypoxia and hypotension, or sham injury. At 2 or 4 hours after injury, ADC and tissue water content were assessed using MRI. Gd-DTPA was given followed by a combination of rapid T2 imaging (60 seconds) and T1 imaging (30 minutes). Signal intensity changes were analyzed to determine a bolus effect (dynamic susceptibility contrast) and longer-term tissue accumulation of Gd-DTPA. RESULTS: Mean increase in cortical water content on the left was 0.8% at 2 hours, 2.1% at 4 hours; on the right it was 0.5% at 2 hours and 1.7% at 4 hours (p < 0.05). Mean ADC reduction over 4 hours was 0.04 x 10(-3) mm2/s on the left and 0.06 x 10(-3) mm2/s on the right. Kinetic analysis of signal intensity changes after Gd-DTPA showed no significant difference in inward transfer coefficient (BBB permeability) between sham injury and 2 or 4 hours post-injury. T2 imaging showed consistent tissue delivery of a bolus of Gd-DTPA to the tissue at 2 and 4 hours post-injury, comparable to sham animals. CONCLUSIONS: Progressive cerebral edema formation after diffuse TBI occurred during ADC reduction and without continued BBB permeability. Tissue delivery of Gd-DTPA was confirmed, verifying that lack of tracer accumulation is due to an intact BBB and not to limited perfusion.

Biomechanical modeling of penetrating traumatic head injuries: a finite element approach.

Due to advances in emergency medical care and modern techniques, treatment of gunshot wounds to the brain have improved and saved many lives. These advances were largely achieved using retrospective analysis of patients with recommendations for treatment. Biomechanical quantification of intracranial deformation/stress distribution associated with the type of weapon (e.g., projectile geometry) will advance clinical understanding of the mechanics of penetrating trauma. The present study was designed to delineate the biomechanical behavior of the human head under penetrating impact of two different projectile geometry using a nonlinear, three-dimensional finite element model. The human head model included the skull and brain. The qualitative comparison of the model output with each type of projectile during various time steps indicated that the deformation/stress progressed as the projectile penetrated the tissues. There is also a distinct difference in the patterns of displacement for each type of projectile. This observation matches our previous study using a physical gelatin model of delineate the penetrating wound profiles for different projectile types. The present study is a first step in the study of biomechanical modeling of penetrating traumatic brain injuries.

Extensive subdural mass.

An unusual case of a 62-year-old man with focal seizures, tinnitus, and progressive left hemiparesis due to an extensive subdural plasma cell granuloma is presented. Five-year clinical and radiologic follow-up demonstrating the chronic yet progressive nature of this granuloma is presented. This is the first report of focal calcification seen in an intracranial plasma cell granuloma. The imaging, neuropathologic, and clinical characteristics of this rare lesion are reviewed.

Mechanisms and factors involved in hip injuries during frontal crashes.

This study was conducted to collect data and gain insights relative to the mechanisms and factors involved in hip injuries during frontal crashes and to study the tolerance of hip injuries from this type of loading. Unembalmed human cadavers were seated on a standard automotive seat (reinforced) and subjected to knee impact test to each lower extremity. Varying combinations of flexion and adduction/abduction were used for initial alignment conditions and pre-positioning. Accelerometers were fixed to the iliac wings and twelfth thoracic vertebral spinous process. A 23.4-kg padded pendulum impacted the knee at velocities ranging from 4.3 to 7.6 m/s. The impacting direction was along the anteroposterior axis, i.e., the global X-axis, in the body-fixed coordinate system. A load cell on the front of the pendulum recorded the impact force. Peak impact forces ranged from 2,450 to 10,950 N. The rate of loading ranged from 123 to 7,664 N/msec. The impulse values ranged from 12.4 to 31.9 Nsec. Injuries were not apparent in three tests. Eight tests resulted in trauma. Fractures involving the pelvis including the acetabulum and proximal femur occurred in five out of the eight tests, and distal femoral bone fracture occurred in one test. These results underscore the importance of leg pre-positioning and the orientation of the impacting axis to produce specific types of trauma to the pelvic region of the lower extremity.

Sphenoid sinus mucocele: a rare complication of transsphenoidal hypophysectomy.

Only seven cases of a sphenoid mucocele occurring after transsphenoidal hypophysectomy have been previously reported in the world literature. In this article, we report a new case, which occurred in a 67-year-old man. The sphenoid sinus mucocele developed 12 years following transsphenoidal hypophysectomy and adjunctive radiotherapy. The patient was successfully managed with incision and drainage. Although transsphenoidal hypophysectomy is a common operation, this particular complication appears to be rare or at least under-reported. Sphenoid sinus mucocele deserves consideration in the differential diagnosis of a sphenoidal parasellar mass in a patient who has undergone an earlier transsphenoidal hypophysectomy.

Airbag effectiveness on brain trauma in frontal crashes.

The purpose of this study was to evaluate the effectiveness of frontal restraint systems in reducing the potential for head injuries, specifically brain injuries and skull fractures. The US DOT NASS database files from 1991-1998 were evaluated for drivers and right front seat occupants in frontal crashes. Of the total driver and right front seat occupants in this data set, 3.83% sustained a brain injury without skull fracture, 0.05% sustained a skull fracture without a brain injury, and 0.16% sustained both brain injury and skull fracture. The incidence of head injury was lowest among occupants who were restrained by belt alone (2.76%) and by both airbag and belt systems (3.51%). The unrestrained population had a 10.39% incidence of at least one type of head injury. In general, for maximum AIS > or = 2 head injuries, airbag effectiveness was greatest between 16-45 kph crash delta V. For the more severe maximum AIS > or = 3 head injuries, the airbag restraint had its greatest effect up to 35 kph. It can be concluded that brain injury in frontal crashes is substantially reduced with the presence of a restraint system and the use of both airbag and belt restraint offers the greatest protection across all delta V categories. Restraint system effectiveness for the non-head-injured occupant is variable but, generally, the belted occupant sustained the lowest percentage of injuries. Skull fractures in frontal impact were relatively rare and the incidence appeared to be unaffected by the presence of a restraint system.

Patterns of abdominal injuries in frontal and side impacts.

Public awareness for safety and vehicle improvements has contributed to significant reduction in injuries secondary to motor vehicle crashes. The spectrum of trauma has shifted from one region of the body to another with varying consequences. For example, airbags have minimized head and neck injuries for adults while emphasizing the lower regions of the human body. Studies have concentrated on the changing patterns of these injuries in frontal impacts. However, there is almost a paucity of data with regard to the characterization of abdominal injuries. Consequently, this study was conducted to determine the patterns of abdominal injuries in frontal and side impacts with an emphasis on more recent crashes. In particular, the frequency and severity of trauma were investigated with a focus on the various abdominal organs (e.g., spleen and liver). Results indicate that side crashes contribute to a large percentage of injuries to the abdomen. The liver and spleen organs are most vulnerable; therefore, it may be beneficial to apply concerted efforts to focus on injury biomechanics research and prioritization activities in these areas of the abdomen. These data may be of benefit to develop anthropomorphic dummies with improved biofidelity.

Experimental investigation of cerebral contusion: histopathological and immunohistochemical evaluation of dynamic cortical deformation.

We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n = 6) or high (8 psi, n = 6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p < 0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI-32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.

Suprasellar osteolipoma: case report.

BACKGROUND: Osteolipomas are distinguished from other intracranial lipomas by their arrangement of central adipose and peripheral osseous tissues and by characteristically arising in the suprasellar/interpeduncular region. METHODS: We report computed tomography (CT), magnetic resonance imaging (MRI), and pathology findings from this 34-year-old man who underwent surgical removal of this benign lesion. RESULTS: This case displays the distinctive histopathology that has been reported in 13 of 31 (42%) lipomas in this region. In contrast, ossification of lipomas at other intracranial sites is relatively rare. CONCLUSIONS: Ossification should be expected in many suprasellar/interpeduncular lipomas, and osteolipoma should be included in the radiologic differential diagnosis of fat-intensity masses with calcification in this region.

Magnetic resonance spectroscopy of diffuse brain trauma in the pig.

The acute metabolic events linked to the evolution of selective axonal pathology in the white matter following diffuse brain injury have not previously been evaluated due to the paucity of relevant experimental models. Here, we utilized a new model of inertial brain injury in the pig that selectively damages axons in the white matter, and applied proton and phosphorous magnetic resonance spectroscopy (MRS) to noninvasively monitor the temporal course of metabolic changes following trauma. Evaluating four pigs with MRS prior to injury, within 1 h and 3 and 7 days postinjury, we found that widespread axonal injury was produced in the absence of changes in pH, PCr/Pi, or the concentrations of ATP, and lactate. However, we did observe an acute 60% loss of intracellular Mg2+ levels, which gradually resolved by 7 days postinjury. In addition, we found that the levels of the neuron marker, N-acetylaspartate (NAA), acutely dropped 20% and remained persistently decreased for at least 7 days postinjury. Moreover, the changes in Mg2+ and NAA were found with MRS in the absence of abnormalities with conventional magnetic resonance imaging (MRI). These results show that (1) profound alterations in intracellular metabolism occur acutely following diffuse axonal pathology in the white matter, but in the absence of indicators of ischemia, and (2) axonal pathology may be evaluated with high sensitivity utilizing noninvasive MRS techniques.

Minimally invasive techniques in spinal surgery: current practice.

Minimally invasive spinal surgery under arthroscopic or endoscopic magnification and illumination is emerging as an alternative, reliable method of treatment in a variety of spinal disorders. The operative techniques being used for discectomy and retrieval of herniated disc fragments or stabilization of unstable spinal motion segments are being utilized for visual diagnosis and debridement of infectious discitis and osteomyelitis transpedicular and transforaminal vertebral body biopsy, temporary diagnostic fixation of unstable lumbar motion segments, and transforaminal epidural steroid therapy.

Fluorine-18-FDG evaluation of crossed cerebellar diaschisis in head injury.

UNLABELLED: This study investigates the phenomenon of crossed cerebellar diaschisis in head injury patients. METHODS: We visually compared fluorine-18-fluorodeoxyglucose (FDG)-PET images to radiograph computed tomography or magnetic resonance images in 19 patients with head injury. RESULTS: We found that of 68 focal unilateral lesions, 40% were associated with contralateral cerebellar hypometabolism and 19% were associated with ipsilateral cerebellar hypometabolism. Of supratentorial, extraparenchymal lesions (n = 20), 45% were associated with contralateral cerebellar hypometabolism, whereas 15% had ipsilateral cerebellar hypometabolism. Intraparenchymal lesions were associated with contralateral cerebellar hypometabolism in 38% of the patients and with ipsilateral cerebellar hypometabolism in 21% of the patients. Of the cortical lesions that were the patients' most severe injury, 69% were associated with contralateral cerebellar hypometabolism, whereas only 8% were associated with ipsilateral cerebellar hypometabolism. In patients with focal supratentorial lesions alone, 50% of all focal lesions were associated with contralateral cerebellar hypometabolism and 13% had ipsilateral hypometabolism. Of patients with both focal and diffuse brain injuries, 27% of the focal lesions had contralateral cerebellar hypometabolism and 27% had ipsilateral cerebellar hypometabolism to the most severe focal injury. CONCLUSION: Crossed cerebellar diaschisis is seen more often in patients with focal cortical or extraparenchymal injuries and is not seen in patients with multiple or diffuse brain injuries. Furthermore, this predominance is more pronounced with lesions of the greatest severity.

Characterization of diffuse axonal pathology and selective hippocampal damage following inertial brain trauma in the pig.

Dynamic deformation applied to white matter tracts is a common feature of human brain trauma, and may result in diffuse axonal injury (DAI). To produce DAI in an experimental model, we have utilized nonimpact inertial loading to induce brain trauma in miniature swine. This species was chosen due to its large gyrencephalic brain with substantial white matter domains. Twenty anesthetized (2% isoflurane) miniature swine were subjected to pure impulsive centroidal rotation 110 degrees in the coronal plane in 4 to 6 ms; peak accelerations ranged from 0.6 to 1.7 x 10(5) rad/s2. Seven days following injury, the brains were fixed (4% paraformaldehyde). Histopathologic examination was performed on 40 microns sections stained with cresyl violet (Nissl), antibodies targeting neurofilament (axonal damage), GFAP (astrocytes), and pig IgG (protein extravasation). Widespread multifocal axonal injury was observed in combination with gliosis throughout the brain, most commonly in the root of gyri and at the interface of the gray and white matter. Very little vascular disruption was noted in regions of axonal injury. Neuronal damage was primarily found in the CA1 and CA3 subfields of the hippocampus. These results suggest that this model is clinically relevant and useful for evaluating mechanisms of inertial brain trauma.

Is beta-APP a marker of axonal damage in short-surviving head injury?

beta-Amyloid precursor protein (beta-APP), a normal constituent of neurons which is conveyed by fast axonal transport, has been found to be a useful marker for axonal damage in cases of fatal head injury. Immunocytochemistry for beta-APP is a more sensitive technique for identifying axonal injury than conventional silver impregnation. This study was designed to determine how quickly evidence of axonal damage and bulb formation appears. Using this method a variety of brain areas were studied from 55 patients who died within 24 h of a head injury. Immunocytochemical evidence of axonal injury was first detected after 2 h survival, axonal bulbs were first identified after 3 h survival, and the amount of axonal damage and axonal bulb formation increased the longer the survival time.

Decreased follistatin gene expression in gonadotroph adenomas.

What growth factors are involved in the pathogenesis of gonadotroph adenomas is not yet known. Activin is one possible candidate because it stimulates growth and differentiation in many cells, including the gonadotroph cell, and it stimulates FSH secretion, characteristic of gonadotroph adenomas. As activin beta B-subunit is expressed in gonadotroph adenomas, we sought to determine whether activin receptor II and follistatin are also expressed. Total ribonucleic acid (RNA) was extracted from 10 gonadotroph adenomas that did not express pit-1 and was reverse transcribed. The resulting complementary DNAs for human activin receptor II and follistatin were amplified by PCR. All 10 adenomas expressed activin receptor II messenger RNA (mRNA), as did nonadenomatous pituitary tissue. Only 2 of the 10 gonadotroph adenomas expressed detectable follistatin mRNA, although all 4 nonadenomatous pituitaries did. Quantitation of follistatin mRNA by competitive reverse transcription-PCR showed that none of the 10 gonadotroph adenomas expressed as much follistatin mRNA as did the 4 nonadenomatous pituitaries, and 8 of the 10 expressed less than 10% as much. Immunospecific staining showed follistatin in the cytoplasm of the gonadotroph cells of all 5 nonadenomatous pituitaries studied, but only faintly in 1 gonadotroph adenoma and not at all in the other 9. These results suggest that pit-1-negative gonadotroph adenomas express less follistatin mRNA and follistatin peptide than do nonadenomatous gonadotroph cells. A consequence could be less binding, and thereby enhanced effectiveness, of activin, contributing to adenoma growth.

Magnetization transfer imaging of diffuse axonal injury following experimental brain injury in the pig: characterization by magnetization transfer ratio with histopathologic correlation.

PURPOSE: Our goal was to evaluate the use of the magnetization transfer ratio (MTR) in the detection of diffuse axonal injury (DAI) resulting from traumatic brain injury in a swine model. METHOD: DAI was created by applying a nonimpact, coronal plane, rotational acceleration to the heads of miniature swine (n = 4). GE imaging was performed with and without off-resonance MT saturation. Histologic correlation of axonal injury with MRI was performed 7 days postinjury. Thirty-one subcortical white matter regions and 10 deep white matter regions were selected for the direct comparison of histologic data and MTR measurements. RESULTS: Nineteen of 41 examined locations exhibited histologic evidence of axonal injury. The mean MTR in regions with axonal damage was significantly less than in regions without axonal damage. These changes were observed both in regions demonstrating high signal intensity on T2-weighted images (T2WI) (p <0.0001, n = 6) and in regions with no signal intensity change on T2WI (p < 0.05, n = 13). CONCLUSION: These results suggest that the measurement of MTR may have the potential for evaluation axonal damage in DAI following traumatic brain injury even when conventional T2WI does not demonstrate the lesion.

Transfection of human lactotroph adenoma cells with an adenovirus vector expressing tyrosine hydroxylase decreases prolactin release.

Pituitary adenomas are common intracranial neoplasms, for which surgery and radiation are usually not curative. In attempting to develop gene therapy as a better approach to treating pituitary adenomas, we chose lactotroph adenomas as a model. The rationale for the use of this model is based on the observation that dopamine agonists decrease prolactin secretion by lactotroph adenomas, and also decrease their size. We transfected primary cultures of human lactotroph adenoma cells with an adenovirus vector containing a cDNA which encodes a human tyrosine hydroxylase, the rate-limiting enzyme in the biosynthesis of dopamine. Transfection induced expression of tyrosine hydroxylase and increased production of dopamine, resulting in the predicted biologic effect of decreased prolactin secretion. These results demonstrate the potential for gene therapy of lactotroph adenomas and perhaps other pituitary adenomas, which are less amenable to pharmacologic treatment than lactotroph adenomas.

Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms.

Brain injury is the leading cause of death among individuals under the age of 45 years in the United States and Europe. Recently, the neuropathologic classification of posttraumatic brain damage has provided insight into the specific mechanisms underlying traumatically induced neuronal damage and death. Studies regarding the biomechanics of brain trauma have also provided great insight into the pathophysiologic mechanisms underlying specific patterns of posttraumatic cellular death. Based upon recent clinical evaluations and biomechanical studies, laboratory models of human brain injury have been developed that faithfully reproduce a number of important features of clinical brain trauma. Biomechanical models have been used to study both the acute sequelae of brain injury and the role of neurochemical alterations in contributing to the development of secondary or delayed cellular death and damage. This report reviews and integrates the laboratory investigations linking experimental models of brain injury to clinical diagnosis and treatment.