Continually Updated Clinical Reference
 
 
  All Sources     eMedicine     Medscape     Drug Reference     MEDLINE
 
eMedicine - Brain, Contusion : Article by

Quick Find
Authors & Editors
Introduction
Differentials
Radiograph
CT SCAN
Mri
Ultrasound
Nuclear Medicine
Angiography
Intervention
Multimedia
References




Patient Education
Back, Ribs, Neck, and Head Center

Concussion Overview

Concussion Causes

Concussion Symptoms

Concussion Treatment




Author: Denise Morales, MD, Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, Rehabilitation Institute of MI

Denise Morales is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Coauthor(s): Orlando Diaz-Daza, MD, Assistant Professor, Department of Radiology, Ben Taub General Hospital, Baylor College of Medicine; Roman Hlatky, MD, Assistant Professor, Center for Neurosurgical Sciences, The University of Texas Health Science Center; L Anne Hayman, MD, Director of Herbert J Frensley Center for Imaging Research, Professor, Departments of Radiology, Psychiatry, and Behavioral Sciences, Baylor College of Medicine

Editors: Chi-Shing Zee, MD, Chief of Neuroradiology, Professor, Departments of Radiology and Neurosurgery, University of Southern California School of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Robert L DeLaPaz, MD, Director, Professor, Department of Radiology, Division of Neuroradiology, Columbia University; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences

Author and Editor Disclosure

Synonyms and related keywords: brain injury, acute traumatic CNS damage, central nervous system injury, head trauma, head injury, skull injury, skull fracture, facial injury, facial soft tissue injury, cranial soft tissue injury, cranial fracture, concussion, brain hemorrhage, cranial contusion, laceration of the brain, punctate parenchymal hemorrhage, microhemorrhage, traumatic brain injury, TBI, coup contusion, contrecoup contusion, brain contusion, scalp hematoma

Background

Brain injury is often defined differently in published reports. Although many authors use the term brain injury to mean acute traumatic damage to the central nervous system (CNS), others use the term head injury, which allows inclusion of skull injuries, fractures, or soft tissue damage to the face or head without any obvious neurologic consequences. Kraus et al define brain injury as "physician-diagnosed physical damage from acute mechanical energy exchange resulting in concussion, hemorrhage, contusion, or laceration of the brain."1

For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education article Concussion.

Pathophysiology

Brain contusions commonly are identified in patients with traumatic brain injury (TBI) and represent regions of primary neuronal and vascular injury. These edematous lesions contain punctate parenchymal hemorrhages, which are termed microhemorrhages. By definition these parenchymal bruises are found on the surfaces of the brain. Blood may extend bidirectionally into the white matter and the subdural and subarachnoid spaces.

Contusions are formed in 2 ways: direct trauma and acceleration/deceleration injury. Direct trauma causes injury at the site of impact, which is termed a coup contusion, while deceleration causes injury at a site opposite to the site of impact, which is termed a contrecoup contusion.

In the first mechanism, direct trauma, the head is not in motion. This mechanism may result in a scalp or skull injury.

The second mechanism is related to acceleration (eg, boxing injury) or deceleration (eg, motor vehicle accident), which causes the brain to strike the skull. In an event in which the head is in motion, cortical injury occurs adjacent to the floor of the anterior or posterior cranial fossa, the sphenoid wing, the petrous ridge, the convexity of the skull, and the falx or tentorium. The inferior frontal and temporal lobes are particularly vulnerable.

Gliding contusions are due to sagittal angular acceleration with abrupt stretching and tearing of the parasagittal veins, arachnoid membrane, and adjacent cerebrum. Gliding contusions occur along the superior margin of the cerebral hemispheres. Sganzerla et al concluded that the gliding contusion should be considered another type of primary brain damage brought about by acceleration/deceleration shear strains. Therefore, these authors believe that a patient with a gliding contusion will most likely have diffuse axonal injury as well.

Contusions may progress with time. CT scans often demonstrate progression over time in the size and number of contusions and the amount of hemorrhage within the contusions. Such changes are most evident over the first 24-48 hours, with one fourth of cases demonstrating delayed hemorrhage in areas that were previously free of hemorrhage.

Frequency

United States

Variations in the reported incidence may be due to different data collection methods and the diversity of the populations studied. Each year, TBI occurs in more than 800,000 people in the United States. Although 90% of patients survive the injury, 25% or more have significant residual complaints.2 The National Institutes of Health (NIH) Consensus Statement 1998 estimates that 1.5-2 million Americans have a TBI each year, or an annual incidence of 100 cases per 100,000 persons.3

The National Health Interview Survey (NHIS) estimates that 1.5-2 million people have a TBI each year in the United States. Approximately 1 million of these individuals are treated in hospital emergency departments (EDs). Using self-reported data from the 1991 NHIS Injury Supplement (NHIS-I), Sosin et al estimated that 1.5 million persons had TBIs in 1991.4 Among these, 35% (525,000, or 216 cases per 100,000 population) received medical attention in EDs and were not admitted to the hospital.

Mortality/Morbidity

  • Mortality: In 1994, more than 147,500 Americans died of traumatic injury. This figure represents approximately 6.5% of all deaths in the United States. The exact mortality rate involving significant TBI is not known, and estimates of mortality rates vary. The reported TBI mortality rate varies from 14-30 cases per 100,000 population. Thurman et al estimate the 1994 incidence rate of fatalities and hospital admissions in patients with TBIs was 91 cases per 100,000 population.5 Annegers et al note that the elderly population has the highest mortality rate.6 However, Woo et al note that the mortality rates for TBI are highest in persons aged 15-24 years.7 The mortality rates are as follows:

    • Persons aged 15-24 years - 33 cases per 100,000 population


    • Persons aged 65 years or older - 31 cases per 100,000 population
       
  • Morbidity: A national estimate of all hospitalized and nonhospitalized nonfatal TBIs in the United States was derived from NHIS data for the years 1985-1987. Extrapolated to the 1990 US Census figure of approximately 249 million residents, the NHIS reports approximately 2 million incidents of TBIs per year. Fife concluded that only 1 of 6 persons with head injuries had an injury severe enough to warrant admission to a hospital.8 Since the number of individuals who seek some form of medical care from non-ED facilities is unknown, the NHIS figure of 1.975 million injuries remains an uncertain estimate of the true incidence of TBI in the entire population.

Race

Rosenthal et al note that hospital data vary widely in noting ethnicity or race in medical records; hence, the true incidence of TBI in racial or ethnic groups has yet to be determined accurately. Several studies have noted that TBI tends to occur with slightly greater frequency among minority groups.

Sex

In all studies of TBIs, men outnumber women by a ratio of at least 2:1. TBI fatalities in males are 3-4 times more frequent than in females. Rosenthal et al report a male-to-female ratio of approximately 2.0-2.8:1. Injuries from motor vehicle accidents, contact sports, and interpersonal violence are more common among males, who also have a higher rate of alcohol abuse.

Age

Studies of brain injury rates in the United States show that people aged 15-24 years are at the highest risk. Patterns in age-specific rates illustrate 2 generally high rates. Rates generally peak after age 15 years, decline after age 24 years, and continue to decline in the middle-aged years. Rates increase again in persons aged 60-65 years.

Anatomy

Anatomic diagrams depict typical locations of brain contusions. See Image 1 for schematic diagrams of sagittal, lateral, and base views of the brain depicting the areas most commonly affected by contusions and the areas occasionally affected by contusions.

Clinical Details

The uniform use of a clinical grading scale has improved comparisons between studies and assessment of outcome measurements. The rating system is termed the Glasgow Coma Scale (GCS).

After TBI, the first grade usually applied is a scale indicating depth of coma. The GCS has gained wide acceptance as a method of assessing severity of injury. The GCS has been tested extensively for interrater reliability and shows a high level of agreement, an issue of obvious importance when multiple observers may be observing the same patient sequentially.

On the basis of the GCS, patients may rapidly be assigned to a category of severe (score 3-8), moderate (score 9-12), or mild (score 13-15) brain injury. These categories determine the urgency of subsequent investigation and treatment. Total scores range from the lowest possible, 3, to the highest possible, 15.

The GCS is intended to assess level of consciousness and is not designed for following neurologic deficits.

GCS test response scoring is as follows:

  • Eye opening

    • Opens eyes on own (spontaneous) - 4

    • Opens eyes on request (responds to speech) - 3

    • Opens eyes in response to pain - 2

    • Does not open eyes in response to pain - 1

  • Best motor response

    • Follows simple commands - 6

    • Localizes pain - 5

    • Withdraws to pain - 4

    • Abnormal flexion (decorticate) - 3

    • Abnormal extension (decerebrate) - 2

    • No response to pain stimuli - 1

  • Verbal response (speech)

    • Converses, is oriented - 5

    • Confused, disoriented - 4

    • Speaks, makes no sense - 3

    • Makes sounds only, no words - 2

    • Makes no noise (no speech) - 1

Preferred Examination

CT imaging is the preferred acute imaging modality because scans can be performed quickly; newer CT scanners can complete a scan within 5 minutes, with virtually no motion artifacts. CT findings help identify abnormalities that may need acute intervention. CT can be performed in the presence of life support equipment.

Limitations of Techniques

With CT scans, the true volume of neuronal damage in the contused tissue can be underestimated. The detection of superficial contusions using CT scans is hampered by artifacts from adjacent bone. MRI is more sensitive and accurate than CT for detecting contusions because of its multiplanar capability and greater sensitivity for edema.9

Imaging findings in brain contusions tend to vary because of the stages of evolution common to these lesions. Initially, CT findings can be normal or minimally abnormal because the partial volumes between the dense microhemorrhages and the hypodense edema can render contusions isoattenuating relative to the surrounding brain.

MRI findings typically demonstrate the lesions from the onset of injury, but many facilities cannot perform MRI on an emergent basis. In addition, MRI examination can take up to an hour to perform, and patients may require sedation to minimize motion artifacts. Not all hospitals have MRI-compatible life-support devices, and the patient's body habitus must be physically compatible with the size of the machine.



Other Problems to Be Considered

In the setting of trauma, radiologic findings are almost always diagnostic. Injuries to other parts of the body must not be overlooked. Accompanying diffuse intravascular coagulopathy may worsen intracranial bleeding.



Findings

Skull radiographs are notoriously unhelpful in predicting underlying brain injury. However, scalp hematomas or skull fractures are usually good indicators of a significant direct force to a focal region. As such, the radiographic findings are usually associated with underlying brain contusions, although significant brain injury may occur without these findings.

Degree of Confidence

Skull radiographs are unreliable.

False Positives/Negatives

The rate of false-negative findings is high, but few false-positive findings occur.



Findings

Contusions may progress with time. Imaging findings in brain contusions tend to vary because of the stages of evolution common to these lesions.

Acute CT initially demonstrates isoattenuating contusions that become more evident on follow-up CT (see Image 4). CT scans often demonstrate progression over time in the size and number of contusions and the amount of hemorrhage in the contusions (see Images 4-6). Initially, CT findings can be normal or minimally abnormal because the partial volumes between the dense microhemorrhages and the hypodense edema can render contusions isoattenuating relative to the surrounding brain tissue (see Images 2-4).

Gliding contusions are due to sagittal angular acceleration with stretching and tearing of the parasagittal veins (see Image 6). Gliding contusions are often hemorrhagic, not only from the differential motion of subcortical structures (commonly referred to as shear injury), but also from tearing of parasagittal veins. When the brain abruptly shifts at the time of impact, the subcortical tissues glide more than the cortex. The convexities of each hemisphere are anchored to the dura by arachnoid granulations. Gliding contusions also tend to be bilateral.

Image 7 shows a CT scan compared with a xenon blood-flow image. On CT scan, the contusions are seen in the bifrontal regions as hyperintense areas. The corresponding xenon blood-flow image shows dark regions that indicate decreased perfusion in the contused areas of the brain.

Image 8 shows CT and MRI of acute contusions.

Degree of Confidence

CT is an excellent modality for defining contusions. Contusions often are not appreciated on the first CT scan obtained immediately after trauma, but they become obvious on follow-up scans.

False Positives/Negatives

Initially, the false-negative rate is high, but false-positive findings are negligible.

Contusions often are not appreciated on the first CT scan obtained immediately after trauma, but they become obvious on follow-up scans.



Findings

MRIs typically demonstrate brain contusions from the onset of injury. MRI is sensitive to hyperacute hemorrhagic contusions ( <12 h).

On MRI, contusions are isointense to hyperintense on T1-weighted (see Images 8-11) and hyperintense on T2-weighted images (see Images 9-11). Gradient-echo MRIs (see Image 11) may reveal hypointensity, which is critical to the detection and delineation of contusions. Image 12 shows a T2-weighted MRI on which the subdural hematoma is inconspicuous. Image 12 also demonstrates how the gradient-echo MRI reveals the hypointensity of the subdural hematoma.

Use of fast fluid-attenuated inversion recovery (FLAIR) sequences has made detection of accompanying subarachnoid hemorrhage possible, with a sensitivity that is equal to or greater than that of CT. The use of FLAIR in identifying brain contusions is shown in Images 8-10). Using FLAIR sequences, subarachnoid hemorrhage produces dramatic hyperintensity in the normally hypointense cerebrospinal fluid. Additionally, companion FLAIR images show the extent of contusions better than most traditional MRIs.

Image 8 shows the ability of traditional MRIs to depict the site of the cortical contusion. The companion FLAIR image shows the full extent of the hyperintense cortical contusion more clearly. This advantage is also demonstrated in Image 9, which shows traditional MRIs and a comparison FLAIR image that shows the subdural hemorrhage and its' extension into the brain more clearly.

Use of diffusion-weighted imaging (DWI) in acute brain trauma has not been described in depth in the literature. DWI allows the rapid detection of an ischemic region after the onset of brain injury. The signal intensity is increased in the affected region on DWIs. The use of DWI to identify cerebral contusions is demonstrated in Images 9-11). DWIs show areas of restricted diffusion in areas associated with cerebral contusions.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble

movingor straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

The degree of confidence is excellent with FLAIR imaging.

False Positives/Negatives

MRI is sensitive but nonspecific for brain injuries. MRI is the criterion standard for defining contusions. Ischemic lesions often depicted in the normal aging brain may be difficult to distinguish from traumatic injuries in the acute phase.



Findings

Ultrasound has no role in acute brain injury.



Findings

Umile et al note that single-photon emission computed tomography (SPECT) blood-flow imaging with technetium-99m hexamethylpropyleneamine oxime (HMPAO) uptake is sensitive enough to detect diffuse changes in patients with decreased blood flow due to depression. Many studies of mild, moderate, and severe TBI in the acute, subacute, and chronic stages have shown that SPECT is more sensitive than CT and MRI, and scans can depict changes even when findings are normal.10 SPECT findings are particularly sensitive in patients with mild postconcussive symptoms. SPECT scans can depict focal changes in 53% of patients with mild head injury who showed few abnormal findings on MRI and CT scans.11

SPECT results are correlated with the severity of injury. A negative finding on SPECT in the first 4 weeks is predictive of a good outcome. SPECT findings also can help in predicting a poor outcome, posttraumatic headaches, and clinical deterioration in patients with intracerebral hematomas. Studies correlating SPECT with neuropsychologic testing have been inconsistent. One study reported that SPECT can reveal significant increases in blood flow following cognitive rehabilitation therapy 2 years after TBI; these findings were correlated with improvements on neuropsychological tests.12

Xenon is an inert noble gas that is diffusible across the blood brain barrier. The inhalation of nonradioactive xenon can be used to calculate physiologic aspects of brain function, including regional cerebral blood flow, by using CT. Xenon imaging has been used for the documentation of brain death. Brain trauma is a potential application for xenon CT scanning.

At the current time, xenon blood-flow imaging has not achieved widespread use because of a number of factors. Xenon gas is expensive; without a rebreathing apparatus, approximately 10 L of xenon is required for each study, adding additional costs to each examination. Also, anesthetic equipment must be used, and special software must be purchased for the CT scanner. The anesthetic effects of xenon are somewhat worrisome as well. Multiple, rapid-sequence images must be obtained at the same level, limiting the total number of section levels that can be obtained. This factor may limit the scan to a few regions, when a given patient may have multiple pathologic areas.

Degree of Confidence

SPECT blood flow imaging has excellent sensitivity.

False Positives/Negatives

Caution must be taken not to mistakenly attribute the diffuse changes seen in psychiatric disorders with focal TBI changes.



Findings

Focal vascular spasm may be seen in the acute/subacute injury phase.

Traumatic aneurysms are rare, but may occur as a result of either blunt or penetrating brain trauma. Intracranial aneurysms may result from fracture, with laceration of the adjacent artery by bone spicules, or by shearing forces secondary to rapid deceleration injury. Penetrating wounds, usually from bullets or shrapnel, are another etiology. Most traumatic aneurysms are pseudoaneurysms, meaning that they are hematoma cavities contained by the soft tissues adjacent to an arterial laceration. As the hematoma organizes and resolves, it becomes surrounded by a fibrous pseudocapsule, which is highly prone to rupture.

Cerebral aneurysms are potentially catastrophic lesions and many persons who do survive aneurysms rupture are permanently disabled. Treatment of unruptured aneurysms has low morbidity and mortality, which makes accurate and timely diagnosis important.

Conventional angiography remains the definitive procedure for the preoperative evaluation of aneurysms. However, the cross-sectional imaging modalities, including computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), add indispensable information concerning the size of the lesion, location, presence of thrombus, associated hemorrhage, and the condition of surrounding brain tissue.

Degree of Confidence

Spasm is a good indicator of subarachnoid hemorrhage and underlying brain injury.

False Positives/Negatives

Few false-positive findings occur, but angiography may not reveal the true extent of injury.



No radiologic interventions exist.

Surgical resection of contused brain tissue is indicated when the patient has brain swelling that increases the intracranial pressure above an acceptable degree. Above this level, increased pressure threatens to diminish cerebral perfusion of the remaining viable brain tissue.

Medical/Legal Pitfalls

  • Potentially, initial CT scan can fail to reveal a contusion that is revealed on subsequent scans.
  • The clinician bears the responsibility for ordering follow-up scans to better estimate the extent of injury.

Special Concerns

  • Patients with bleeding disorders (eg, patients receiving anticoagulant agents or patients with disseminated intravascular coagulopathy or liver disease) or platelet disorders present a special concern.
  • High blood alcohol content is associated with increased morbidity.



Media file 1:  Schematic diagrams of contusion locations in sagittal midline (A), lateral (B), and base (C) views show the areas most commonly affected by contusions (red) and those that are occasionally affected by contusions (blue). Areas that are predominantly affected by contusions include the orbitofrontal cortex, anterior temporal lobe, and posterior portion of the superior temporal gyrus area, with the adjacent parietal opercular area. Areas that are less commonly affected include the lateral midbrain, inferior cerebellum and adjacent tonsil, and the midline superior cerebral cortex.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Image

Media file 2:  Acute brain contusion. Axial CT scan obtained in a patient immediately after a high-speed motor vehicle accident demonstrates a large, right frontal contusion with hemorrhage and surrounding edema. A smaller, subtle, right temporal cortical contusion (short arrow) is noted, as well as a small, left frontal subdural hematoma (long arrow).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 3:  Enlargement of an acute brain contusion. (A) Axial CT scan obtained on day 1 after head trauma shows a subtle area of slightly hypoattenuating right frontal lobe contusion (arrows) with a small, overlying, right frontal subdural hematoma. Note that the scalp hematomas in the frontal and temporal regions indicate areas of direct force. (B) Companion axial CT scan obtained on day 2 shows a large, right frontal contusion (arrow) and a new, large, left temporal contusion (arrow). Note that the scalp hematomas have increased in size.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 4:  Evolution of an acute brain contusion. (A) Axial CT scan obtained immediately following severe blunt trauma to the head shows a small, left frontal epidural hematoma (arrow). Extensive subgaleal bicranial hematomas are seen. (B) Companion CT scan obtained 6 days after trauma shows the small, left frontal epidural hematoma (long arrow) and smaller areas of subgaleal bicranial hematomas. Note that the previously isoattenuating contusion in the right posterior temporal area is now evident (short arrows in B).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 5:  Resolution of a brain contusion. (A) Axial CT scan obtained on day 1 after a high-speed motor vehicle accident shows subtle evidence of bifrontal hemorrhagic contusions (arrows). (B) Axial CT scan obtained on day 2 shows increased hemorrhage within the inferior frontal cortex bilaterally (arrows). (C) Axial CT scan obtained on day 14 shows resolution of the bright blood (upper arrows) and residual areas of dark edema in both frontal lobes and a subtle area throughout the right temporal lobe (lower arrows).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 6:  Acute gliding brain contusions. Axial CT scan obtained immediately after blunt trauma to the left convexity of the skull resulted in severe swelling of the entire left cerebral hemisphere with loss of the gyral pattern secondary to edema. A small collection of subarachnoid blood is present (up arrow). The right hemisphere shows contrecoup gliding contusions (down arrows).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 7:  Comparison of a CT scan with a xenon blood-flow radionuclide scan. (A) CT scan shows bifrontal contusions following severe head trauma (arrows). (B) Companion CT scan showing xenon uptake demonstrates dark regions (arrows), indicating decreased perfusion in the contused brain.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 8:  Comparison of a CT scan and MRIs showing acute contusions. (A) Contrast-enhanced axial CT scan obtained immediately after head trauma shows a foreign body in the scalp (arrow) that marks the site of direct impact. Blood is noted in the right lateral ventricle. Chronic white-matter changes are present. (B) Axial T1-weighted MRI obtained on the same day shows the scalp changes at the site of the trauma (arrow). There is minimal underlying superficial cortical hyperdensity consistent with cortical contusion. (C) Comparison gadolinium-enhanced T1-weighted MRI shows minimal enhancement of the left posterior temporal-occipital cortex below the site of the scalp trauma (arrow). (D) Companion fluid-attenuated inversion recovery (FLAIR) MRI shows the extent of the left cortical contusion (arrow). Note the hyperintense signal from blood in cerebrospinal fluid and the displaced right lateral ventricle with surrounding signal intensity changes in the adjacent optic radiations (arrow).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  CT

Media file 9:  MRI in a 2-day-old brain contusion. (A) T1-weighted image shows obliteration of the left temporal horn due to subdural hemorrhage (arrows). (B) T2-weighted and (C) fluid-attenuated inversion recovery (FLAIR) images show hyperintense signal surrounding isointense blood in the left temporal lobe. The FLAIR image shows the left anterior temporal subdural hemorrhage and a posterior extension more clearly (arrow). (D) Diffusion-weighted MRI shows areas of restricted diffusion in the left temporal lobes and 2, small, abnormal areas in the right midbrain (arrows). The bilateral anterior frontal and temporal hyperintense areas represent artifacts (arrows).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  MRI

Media file 10:  Comparison of a CT scan and MRIs obtained 1 day after acute trauma. (A) Acute CT scan shows a large, temporal-lobe contusion lateral to the displaced left temporal horn (arrows). (B) T1-weighted MRI shows hypointense signal in the left temporal lobe, with mass effect causing a clear loss of sulcal pattern (arrows). (C) Spin-density MRI shows mixed signals within the contusion with predominant isointensity. Note partial volume artifacts surrounding the brainstem.(D) Spin-echo T2-weighted MRI shows mixed intensity throughout the large left temporal contusion. (E) Fluid-attenuated inversion recovery (FLAIR) MRI demonstrates petechial hemorrhages that are isointense to the brain. Note the accompanying abnormally bright signal in the left optic radiations (arrows); one of many small shearing injuries is seen at the right occipital cortex/gray matter junction (arrow). (F) Diffusion-weighted MRI shows mixed signals with restricted diffusion in the most posterior aspect of the large left temporal contusion. An artifact appears in the right temporal lobe.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  MRI

Media file 11:  Comparison of a CT scan and MRIs obtained 4 hours after acute trauma. (A) CT scan shows focal contusion in the left superior temporal gyrus (arrow) and a posterior falx subdural hematoma (arrows). Incidental white matter changes are present in both hemispheres. Incidental left parietal bone postsurgical changes are present. (B) T1-weighted MRI shows slight hypointensity in the contusion (arrows) and isointense signal in the subdural (arrows). Incidentally noted in the anterior corpus callosum is a small, hypointense scar from a prior intraventricular shunt (white arrow). Postsurgical changes in the left parietal bone are depicted. (C) Spin-density MRI shows a large area of hyperintense signal at the contusion site (arrows) and hyperintensity in the subdural blood (arrows).(D) T2-weighted MRI shows hyperintense edema surrounding the hemorrhagic area, which has a hypointense ring (arrow) and an isointense center. The subdural blood is inconspicuous on this image. Chronic white-matter signal abnormalities match those seen on the CT scan (A). (E) Gradient-echo MRI shows marked hypointense signal in the falcine subdural hematoma (arrows), contusion (arrow), and right frontal region, representing magnetic susceptibility products due to subacute hemorrhage. (F) Diffusion-weighted MRI shows restricted diffusion in a zone surrounding the contusion (arrows). Artifacts are depicted in the cortex of both hemispheres (red and yellow arrows).
Click to see larger pictureClick to see detailView Full Size Image
Media type:  MRI



  1. Kraus JF, Black MA, Hessol N, et al. The incidence of acute brain injury and serious impairment in a defined population. Am J Epidemiol. Feb 1984;119(2):186-201. [Medline].
  2. Giles GM, Clark-Wilson J. Brain Injury Rehabilitation: A Neurofunctional Approach. San Diego, CA: Singular Publishing Group; 1993.
  3. NIH. Rehabilitation of persons with traumatic brain injury. NIH Consensus Statement. Oct 26-28 1998;16(1):1-41. [Medline].
  4. Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj. Jan 1996;10(1):47-54. [Medline].
  5. Thurman DJ, Alverson C, Dunn KA, et al. Traumatic brain injury in the United States: A public health perspective. J Head Trauma Rehabil. Dec 1999;14(6):602-15. [Medline].
  6. Annegers JF, Grabow JD, Kurland LT, Laws ER Jr. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology. Sep 1980;30(9):912-9. [Medline].
  7. Woo B. The Rehabilitation of People with Traumatic Brain Injury. Malden, MA:. Blackwell Science;2000.
  8. Fife D. Head injury with and without hospital admission: comparisons of incidence and short-term disability. Am J Public Health. Jul 1987;77(7):810-2. [Medline].
  9. Zimmerman RA, Gibby WA, Carmody RF. Head and brain trauma. In: Neuroimaging: Clinical and Physical Principles. New York:. Springer-Verlag;2001: 699-729.
  10. Umile EM, Plotkin RC, Sandel ME. Functional assessment of mild traumatic brain injury using SPECT and neuropsychological testing. Brain Inj. Jul 1998;12(7):577-94. [Medline].
  11. Kant R, Smith-Seemiller L, Isaac G, Duffy J. Tc-HMPAO SPECT in persistent post-concussion syndrome after mild head injury: comparison with MRI/CT. Brain Inj. Feb 1997;11(2):115-24. [Medline].
  12. Laatsch L, Pavel D, Jobe T, et al. Incorporation of SPECT imaging in a longitudinal cognitive rehabilitation therapy programme. Brain Inj. Aug 1999;13(8):555-70. [Medline].
  13. Bigler ED. Neuroimaging in pediatric traumatic head injury: diagnostic considerations and relationships to neurobehavioral outcome. J Head Trauma Rehabil. Aug 1999;14(4):406-23. [Medline].
  14. Collins JG. Types of injuries by selected characteristics. Vital Health Stat 10. Dec 1990;(175):1-68. [Medline].
  15. Fife D, Faich G, Hollinshead W, Boynton W. Incidence and outcome of hospital-treated head injury in Rhode Island. Am J Public Health. Jul 1986;76(7):773-8. [Medline].
  16. Frankowski RF. The demography of head injury in the US. In: Miner M, Wagner KA, eds. Neurotrauma. Vol 1. Boston:. Butterworths;1986:1-17.
  17. Gean AD. Imaging of Head Trauma. New York: Raven Press Ltd;1994.
  18. Grossman RI, Yousem DM. Head trauma. In: Neuroradiology: The Requisites. St. Louis, Mo:. Mosby-Year Book;1994:156-7.
  19. Kraus JF, McArthur DL. Incidence and prevalence of, and costs associated with, traumatic brain injury. In: Rehabilitation of the Adult and Child with TBI. 3rd ed. Philadelphia: FA Davis; 1999.
  20. Kraus JF, Sorenson SB. Epidemiology. In: Silver JM, Yudofsky SC, Hales RE, eds. Neuropsychiatry of TBI. Washington, DC:. American Psychiatric Press;1994: 3-41.
  21. Orrison WW Jr, Moore KR. Neuroimaging & head trauma. In: Neuroimaging. Philadelphia, Pa:. WB Saunders Co;2000: 901-2.
  22. Osborne AG. Craniocerebral trauma. In: Diagnostic Neuroradiology. St. Louis, Mo:. Mosby-Year Book;1994:217.
  23. Rose FD, Johnson DA. Brain Injury and After: Towards Improved Outcome. West Sussex, England:. John Wiley & Sons;1996.
  24. Rosenthal M, Griffith E, Kreutzer J, et al. Rehabilitation of the adult and child with traumatic brain injury. 3rd ed. Philadelphia:. FA Davis;1999: 8-9.
  25. Sganzerla EP, Tomei G, Rampini P. A peculiar intracerebral hemorrhage: the gliding contusion, its relationship to diffuse brain damage. Neurosurg Rev. 1989;12 Suppl 1:215-8. [Medline].
  26. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. Jul 13 1974;2(7872):81-4. [Medline].
  27. Whitman S, Coonley-Hoganson R, Desai BT. Comparative head trauma experiences in two socioeconomically different Chicago-area communities: a population study. Am J Epidemiol. Apr 1984;119(4):570-80. [Medline].

Brain, Contusion excerpt

Article Last Updated: Apr 3, 2007