Traumatic Brain Injury (TBI)
What is a traumatic brain injury (tbi).
A traumatic brain injury (TBI) can be caused by a forceful bump, blow, or jolt to the head or body, or from an object that pierces the skull and enters the brain. Not all blows or jolts to the head result in a TBI.
Some types of TBI can cause temporary or short-term problems with normal brain function, including problems with how the person thinks, understands, moves, communicates, and acts. More serious TBI can lead to severe and permanent disability, and even death.
Some injuries are considered primary, meaning the damage is immediate. Other outcomes of TBI can be secondary, meaning they can occur gradually over the course of hours, days, or appear weeks later. These secondary brain injuries are the result of reactive processes that occur after the initial head trauma.
There are two broad types of head injuries: Penetrating and non-penetrating.
- Penetrating TBI (also known as open TBI) happens when an object pierces the skull (e.g., a bullet, shrapnel, bone fragment, or by a weapon such as hammer or knife) and enters the brain tissue. Penetrating TBI typically damages only part of the brain.
- Non-penetrating TBI (also known as closed head injury or blunt TBI) is caused by an external force strong enough to move the brain within the skull. Causes include falls, motor vehicle crashes, sports injuries, blast injury, or being struck by an object.
Some accidents such as explosions, natural disasters, or other extreme events can cause both penetrating and non- penetrating TBI in the same person.
Signs and symptoms
Seek immediate medical attention if you experience any of the following physical, cognitive/behavioral, or sensory symptoms, especially within the first 24 hours after a TBI:
- Convulsions or seizures
- Blurred or double vision
- Unequal eye pupil size or dilation
- Clear fluids draining from the nose or ears
- Nausea and vomiting
- New neurologic deficit, such as slurred speech; weakness of arms, legs, or face; loss of balance
Cognitive/behavioral
- Loss of or change in consciousness anywhere from a few seconds to a few hours
- Decreased level of consciousness (e.g., hard to awaken)
- Mild to profound confusion or disorientation
- Problems remembering, concentrating, or making decisions
- Changes in sleep patterns (e.g., sleeping more, difficulty falling or staying asleep); inability to waken from sleep
- Frustration, irritability
Perception/sensation
- Light-headedness, dizziness, vertigo, or loss of balance or coordination
- Blurred vision
- Hearing problems, such as ringing in the ears
- Bad taste in the mouth
- Sensitivity to light or sound
- Mood changes or swings, agitation, combativeness, or other unusual behavior
- Feeling anxious or depressed
- Fatigue or drowsiness; a lack of energy or motivation
Headache, dizziness, confusion, and fatigue tend to start immediately after an injury but resolve over time. Emotional symptoms such as frustration and irritability tend to develop during recovery.
TBI in children
Children might be unable to let others know that they feel different following a blow to the head. A child with a TBI may display the following signs or symptoms:
- Changes in eating or nursing habits
- Persistent crying, irritability, or crankiness; inability to be consoled
- Changes in ability to pay attention
- Lack of interest in a favorite toy or activity
- Changes in sleep patterns
- Sadness or depression
- Loss of a skill, such as toilet training
- Loss of balance or unsteady walking
Effects on consciousness
A TBI can cause problems with consciousness, awareness, alertness, and responsiveness. Generally, there are four abnormal states that can result from a severe TBI:
- Minimally conscious state —People with severely altered consciousness who still display some evidence of self-awareness or awareness of one's environment (such as following simple commands, yes/no responses).
- Vegetative state —A result of widespread damage to the brain, people in a vegetative state are unconscious and unaware of their surroundings. However, they can have periods of unresponsive alertness and may groan, move, or show reflex responses. If this state lasts longer than a few weeks, it is referred to as a persistent vegetative state.
- Coma —A person in a coma is unconscious, unaware, and unable to respond to external stimuli such as pain or light. Coma generally lasts a few days or weeks after which the person may regain consciousness, die, or move into a vegetative state.
- Brain death —The lack of measurable brain function and activity after an extended period of time is called brain death and may be confirmed by studies that show no blood flow to the brain.
How TBI affects the brain
TBI-related damage can be confined to one area of the brain, known as a focal injury, or it can occur over a more widespread area, known as a diffuse injury. The type of injury also affects how the brain is damaged.
Primary effects on the brain include various types of bleeding and tearing forces that injure nerve fibers and cause inflammation, metabolic changes, and brain swelling.
- Diffuse axonal injury (DAI), one of the most common types of brain injuries, refers to widespread damage to the brain's white matter. White matter is composed of bundles of axons (the projections of nerve cells that carry electrical impulses and connect various areas of the brain to one another). DAI usually results from rotational forces (twisting) or sudden forceful stopping that stretches or tears these axon bundles. This damage commonly occurs in auto accidents, falls, or sports injuries. DAI can disrupt and break down communication among nerve cells (neurons) in the brain. It also leads to the release of brain chemicals that can cause further damage. Brain damage may be temporary or permanent and recovery can be prolonged.
- Concussion is a type of mild TBI that may be considered a temporary injury to the brain but could take minutes to several months to heal. Concussion can be caused by a number of things including a bump, blow, or jolt to the head, sports injury or fall, motor vehicle accident, weapons blast, or a rapid acceleration or deceleration of the brain within the skull, such as the person having been violently shaken. The individual either suddenly loses consciousness or has sudden altered state of consciousness or awareness. A second concussion closely following the first one causes further damage to the brain—the so-called “second hit” phenomenon—and can lead to permanent damage or even death in some instances. Post-concussion syndrome involves symptoms that last for weeks or longer.
- Epidural hematomas involve bleeding into the area between the skull and the dura mater. These can occur within minutes to hours after damage to a brain vessel under the skull and are particularly dangerous.
- Subdural hematomas involve bleeding between the dura and the arachnoid mater, and, like epidural hematomas, exert pressure on the outside of the brain. They are very common in the elderly after a fall.
- Subarachnoid hemorrhage is bleeding between the arachnoid mater and the pia mater.
- Bleeding into the brain itself is called an intracerebral hematoma and damages the surrounding tissue.
- Contusions are a bruising or swelling of the brain that occurs when very small blood vessels bleed into brain tissue. Contusions can occur directly under the impact site (a coup injury) or, more often, on the complete opposite side of the brain from the impact (a contrecoup injury). They can appear after a delay of hours to a day. Coup and contrecoup lesions generally occur when the head abruptly decelerates, which causes the brain to bounce back and forth within the skull (such as in a high-speed car crash or in shaken baby syndrome).
- Skull fractures are breaks or cracks in one or more of the bones that form the skull. They are a result of blunt force trauma and can cause damage to the membranes, blood vessels, and brain under the fracture. One main benefit of helmets is to prevent skull fractures.
- Chronic traumatic encephalopathy (CTE) is a progressive neurological disorder associated with symptoms that may include problems with thinking, understanding, and communicating; motor disorders (affecting movement); problems with impulse control and depression; confusion; and irritability. CTE occurs in those with extraordinary exposure to multiple blows to the head and as a delayed consequence after many years. Studies of retired boxers have shown that repeated blows to the head can cause issues including memory problems, tremors, and lack of coordination and dementia. Recent studies have demonstrated rare cases of CTE in other sports with repetitive mild head impacts (e.g., soccer, wrestling, football, and rugby).
- A single, severe TBI also may lead to a disorder called post-traumatic dementia (PTD), which may be progressive and share some features with CTE. Studies assessing patterns among large populations of people with TBI indicate that moderate or severe TBI in early or mid-life may be associated with increased risk of dementia later in life.
Examples of secondary damage:
- Hemorrhagic progression of a contusion (HPC) are injuries that occur when an initial contusion from the primary injury continues to bleed in and around the brain and expand over time. This creates a new or larger lesion—an area of tissue that has been damaged through injury or disease. This increased exposure to blood, which is toxic to brain cells, leads to swelling and further brain cell loss.
- A breakdown in the blood-brain barrier refers to the disruption of the network of cells that controls the movement of cells and molecules between the blood and fluid that surrounds the brain's nerve cells. Once the blood-brain barrier is disrupted, blood, plasma proteins, and other foreign substances leak into the space between neurons in the brain and trigger a chain reaction that causes brain swelling. It also causes multiple biological systems to go into overdrive, including inflammatory responses which can be harmful to the body if they continue for an extended period of time. It also permits the release of neurotransmitters, or chemicals used by brain cells to communicate, which can damage or kill nerve cells when depleted or over-expressed.
- Increased intracranial pressure is usually caused by brain swelling inside the confined area of the skull as a result of the injury. This pressure can damage brain tissue and can prevent blood flow to the brain and deprive it of the oxygen it needs to function.
- Other secondary damage can be caused by infections to the brain, low blood pressure or oxygen flow as a result of the injury, hydrocephalus (a buildup of fluid in the brain that can increase pressure on brain tissue), and seizures.
Who is more likely to get a traumatic brain injury (TBI)?
Adults age 65 and older are at greatest risk for being hospitalized and dying from a TBI, most likely from a fall. In every age group, serious TBI rates are higher for men than for women. Men are more likely to be hospitalized and are nearly three times more likely to die from a TBI than women.
The leading causes of TBI include:
- Falls—According to data from the Centers for Disease Control and Prevention (CDC), falls are the most common cause of TBIs and occur most frequently among the youngest and oldest age groups.
- Blunt trauma accidents—Accidents that involve being struck by or against an object, particularly sports-related injuries, are a major cause of TBI.
- Vehicle-related injuries—Pedestrian-involved accidents, as well as accidents involving motor vehicles and bicycles, are the third most common cause of TBI.
- Assaults/violence Assaults—Abuse-related TBIs are head injuries that result from domestic violence or shaken baby syndrome, and gunshot wounds to the head. TBI-related deaths in children age 4 and younger are most likely the result of assault.
- Explosions/blasts—TBIs caused by blast trauma from roadside bombs became a common injury to service members in military conflicts. The majority of these TBIs are classified as mild head injuries.
How is a traumatic brain injury (TBI) diagnosed and treated?
Diagnosing TBI
All TBIs require immediate assessment by a professional who has experience evaluating head injuries. A neurological exam will judge motor and sensory skills and test hearing and speech, coordination and balance, mental status, and changes in mood or behavior, among other abilities. Screening tools for coaches and athletic trainers can identify the most concerning concussions for medical evaluation.
Initial assessments may rely on standardized instruments such as the Acute Concussion Evaluation (ACE) form from the Centers for Disease Control and Prevention (CDC) or the Sport Concussion Assessment Tool 2, which provide a systematic way to assess a person who has suffered a mild TBI. Reviewers collect information about the characteristics of the injury, the presence of amnesia (loss of memory) and/or seizures, as well as the presence of physical, cognitive, emotional, and sleep-related symptoms. The ACE is also used to track symptom recovery over time. It also takes into account risk factors (including concussion, headache, and psychiatric history) that can impact how long it takes to recover from a TBI.
Diagnostic imaging. When necessary, medical providers will use brain scans to evaluate the extent of the primary brain injuries and determine if surgery will be needed to help repair any damage to the brain. The need for imaging is based on a physical examination by a doctor and a person's symptoms.
- Computed tomography (CT) is the most commonly used imaging technology to assess people with suspected moderate to severe TBI. CT creates a two-dimensional image of organs, bones, and tissues and can show a skull fracture or any brain bruising, bleeding, or swelling.
- Magnetic resonance imaging (MRI) produces detailed images of body tissue. It may be used after the initial assessment and treatment as it is a more sensitive test and picks up subtle changes in the brain that the CT scan might have missed. Significant advances have been made in the last decade to image milder TBI damage. For example, diffusion tensor imaging can image white matter tracts, more sensitive tests like fluid-attenuated inversion recovery can detect small areas of damage, and susceptibility-weighted imaging very sensitively identifies bleeding. Despite these improvements, currently available imaging technologies, blood tests, and other measures remain inadequate for detecting these changes in a way that can help diagnose mild concussive injuries.
Neuropsychological tests to gauge brain functioning are often used along with imaging in people who have suffered mild TBI. Such tests involve performing specific cognitive tasks that help assess memory, concentration, information processing, executive functioning, reaction time, and problem solving.
The Glasgow Coma Scale is the most widely used tool for assessing the level of consciousness after TBI. The standardized 15-point test measures a person's ability to open his or her eyes and respond to spoken questions or physical prompts for movement.
Many athletic organizations recommend establishing a baseline picture of an athlete's brain function at the beginning of each season, ideally before any head injuries occur. Baseline testing should begin as soon as a child begins a competitive sport. Brain function tests yield information about an individual's memory, attention, and ability to concentrate and solve problems. Brain function tests can be repeated at regular intervals (every one to two years) and also after a suspected concussion. The results may help healthcare providers identify any effects from an injury and allow them to make more informed decisions about whether a person is ready to return to their normal activities.
Treating TBI
Many factors—including the size, severity, and location of the brain injury—influence how a TBI is treated and how quickly a person might recover. One of the critical elements to a person's prognosis is the severity of the injury. Although brain injury often occurs at the moment of head impact, much of the damage related to severe TBI develops from secondary injuries which happen days or weeks after the initial trauma. For this reason, people who receive immediate medical attention at a certified trauma center tend to have the best health outcomes.
Some people with mild TBI such as concussion may not require treatment other than rest and over-the-counter pain relievers. Treatment should focus on symptom relief and “brain rest.” Monitoring by a healthcare practitioner is important to note any worsening of symptoms or new ones.
Children and teens who have a sports-related concussion should stop playing immediately and return to play only after being approved by a concussion injury specialist.
Preventing future concussions is critical. While most people recover fully from a first concussion within a few weeks, the rate of recovery from a second or third concussion is generally slower.
Even after symptoms resolve entirely, people should return to their daily activities gradually once they are given permission by a doctor. There is no clear timeline for a safe return to normal activities although there are guidelines such as those from the American Academy of Neurology and the American Medical Society for Sports Medicine to help determine when athletes can return to practice or competition. Further research is needed to better understand the effects of mild TBI on the brain and to determine when it is safe to resume normal activities.
People with a mild TBI should:
- Make an appointment for a follow-up visit with their healthcare provider to confirm the progress of their recovery
- Inquire about new or persistent symptoms and how to treat them
- Pay attention to any new signs or symptoms even if they seem unrelated to the injury (for example, mood swings, unusual feelings of irritability)
These symptoms may be related even if they occurred several weeks after the injury.
Medications to treat some of the symptoms of TBI may include:
- Over-the-counter or prescribed pain medicines
- Anticonvulsant drugs to treat seizures
- Anticoagulants to prevent blood clots
- Diuretics to help reduce fluid buildup and reduce pressure in the brain
- Stimulants to increase alertness
- Antidepressants and anti-anxiety medications to treat depression and feelings of fear and nervousness
Immediate treatment for someone who has suffered a severe TBI focuses on preventing death; stabilizing the person's spinal cord, heart, lung, and other vital organ functions; ensuring proper oxygen delivery and breathing; controlling blood pressure; and preventing further brain damage. Emergency care staff will monitor the flow of blood to the brain, brain temperature, pressure inside the skull, and the brain's oxygen supply.
Surgery may be needed to for emergency medical care and to treat secondary damage, including:
- Relieving pressure inside the skull (inserting a special catheter through a hole drilled into the skull to drain fluids)
- Removing debris or dead brain tissue (especially for penetrating TBI)
- Removing hematomas
- Repairing skull fractures
In-hospital strategies for managing people with severe TBI aim to prevent conditions including:
- Infection, particularly pneumonia
- Deep vein thrombosis (blood clots that occur deep within a vein; risk increases during long periods of inactivity)
People with TBIs may need nutritional supplements to minimize the effects that vitamin, mineral, and other dietary deficiencies may cause over time. Some individuals may even require tube feeding to maintain the proper balance of nutrients.
Rehabilitation
After the acute care period of in-hospital treatment, people with severe TBI are often transferred to a rehabilitation center where a multidisciplinary team of health care providers help with recovery.
The rehabilitation team includes neurologists, nurses, psychologists, nutritionists, as well as physical, occupational, vocational, speech, and respiratory therapists.
Therapy is aimed at improving the person's ability to handle activities of daily living and to address cognitive, physical, occupational, and emotional difficulties. Treatment may be needed on a short-term basis or throughout a person's life. Some therapy is provided through outpatient services.
Cognitive rehabilitation therapy (CRT) is a strategy aimed at helping individuals regain their normal brain function through an individualized training program. Using this strategy, people may also learn compensatory strategies for coping with persistent deficiencies involving memory, problem solving, and the thinking skills to get things done. CRT programs tend to be highly individualized and their success varies. A 2011 Institute of Medicine report concluded that cognitive rehabilitation interventions need to be developed and assessed more thoroughly.
Other factors that influence recovery include genes and age.
Genes— Genetics may play a role in how quickly and completely a person recovers from a TBI. For example, researchers have found that apolipoprotein E ε4 (ApoE4) — a genetic variant associated with higher risks for Alzheimer's disease — is associated with worse health outcomes following a TBI. Much work remains to be done to understand how genetic factors, as well as how specific types of head injuries, affect recovery. This research may lead to new treatment strategies and improved outcomes for people with TBI.
Age— Studies suggest that age and the number of head injuries a person has suffered over his or her lifetime are two critical factors that impact recovery. For example, TBI-related brain swelling in children can be very different from the same condition in adults, even when the primary injuries are similar. Brain swelling in newborns, young infants, and teenagers often occurs much more quickly than it does in older individuals. Evidence from very limited CTE studies suggest that younger people (ages 20 to 40) tend to have behavioral and mood changes associated with CTE, while those who are older (ages 50+) have more cognitive difficulties.
Compared with younger adults with the same TBI severity, older adults are likely to have less complete recovery. Older people also have more medical issues and are often taking multiple medications that may complicate treatment (e.g., blood-thinning agents when there is a risk of bleeding into the head). Further research is needed to determine if and how treatment strategies may need to be adjusted based on a person's age.
Preventing TBI
The best treatment for TBI is prevention. Unlike most neurological disorders, head injuries can be prevented. According to the CDC, the following actions can help prevent TBIs:
- Wear a seatbelt when you drive or ride in a motor vehicle
- Wear the correct helmet and make sure it fits properly when riding a bicycle, skateboarding, and playing sports like hockey and football
- Install window guards and stair safety gates at home for young children
- Never drive under the influence of drugs or alcohol
- Improve lighting and remove rugs, clutter, and other trip hazards in the hallway
- Use nonslip mats and install grab bars next to the toilet and in the tub or shower for older adults
- Install handrails on stairways
- Improve balance and strength with a regular physical activity program
- Ensure children's playgrounds are made of shock-absorbing material, such as hardwood mulch or sand
What are the latest updates on traumatic brain injuries (TBI)?
The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and use that knowledge to reduce the burden of neurological disease. NINDS, a component of NIH, supports research across the full range of TBI severity. Here is a list of efforts and developments.
- Transforming Research and Clinical Knowledge in TBI, or TRACK TBI, is an observational study of adults and children with TBI across the spectrum of injury severity. It is creating a TBI database and provides tools and resources to establish more precise methods to diagnose TBI, improve outcome assessment, and compare the effectiveness and costs of tests, treatments, and services. The data from this study will be available in the Federal Interagency TBI Research database (which enables comparisons across clinical trials and clinical studies.
- Scientists can now look in real time at how head injury affects thousands of individual cells and genes simultaneously in mice. Using a novel sequencing technique that can quickly analyze the gene activity of a cell, scientists were able to look individual brain cells in the hippocampus, a region of the brain involved in learning and memory, after TBI or in uninjured control animals. Scientists can now pinpoint which genes to treat with new therapies.
- Researchers are conducting studies to better understand the lasting effects of a single head injury vs. repetitive injuries to the brain, how repetitive TBI might lead to chronic traumatic encephalopathy, and how commonly these changes occur among adults. NINDS researchers are currently working to identify biomarkers (signs that may indicate risk of a disease and aid in diagnosis) for chronic traumatic encephalopathy in order to detect this and similar disorders in living people rather than through brain studies after death.
- Researchers are exploring ways to promote the brain's innate ability to adapt and repair itself, known as neuroplasticity.
- A developed mouse model of TBI is enabling researchers to look at potential treatments for concussion. Using the model, they found that applying glutathione (an antioxidant that is normally found in our cells) directly on the skull surface after brain injury reduced the amount of brain cell death.
- The NINDS-funded Translational Outcomes Project in Neurotrauma (-NT) consortium supports development and creation of better assessment tools for preclinical studies in TBI and spinal cord injury and to support data sharing to improve preclinical studies and clinical trial design.
- In February 2018 the U.S. Food and Drug Administration (FDA) authorized marketing the first blood test to help diagnose concussion. NINDS funded the early work on the project and the Department of Defense supported its later development.
Clinical research
Despite recent progress in understanding what happens in the brain following TBI, more than 30 large clinical trials have failed to identify specific treatments that make a dependable and measurable difference in people with TBI. A key challenge facing doctors and scientists is the fact that each person with a TBI has a unique set of circumstances based on such multiple variables as the location and severity of the injury, the person's age and overall heath, and the time between the injury and the initiation of treatment. These factors, along with differences in care across treatment centers, highlight the importance of coordinating research efforts so that the results of potential new treatments can be confidently measured.
NINDS co-leads the Strategies to Innovate EmeRgENcy Care Clinical Trials (SIREN) network, with projects that include TBI trials — one of which is looking at brain tissue oxygen monitoring to improve neurologic outcome in the most severely injured people with TBI.
Harnessing the efforts of the many physicians and scientists working on developing better treatments for TBI requires everyone to collect the same types of information from people, including details about injuries and treatment results. To lay the groundwork for these studies, NINDS started the Common Data Elements project. This effort brings the research community together to develop data collection standards.
Interagency and international research collaboration
- NINDS and the European Commission conduct studies through the International Initiative for TBI research (InTBIR) to collect data and encourage new collaborations to improve diagnosis and evaluate which types of care are associated with the best outcomes in children and adults.
- NIH and the Department of Defense together lead the Federal Interagency TBI Research (FITBIR) database, which includes both new observational studies and other studies, such as the Child Health After Injury Study.
- NIH investigators and the FDA are active collaborators in the Department of Defense-led TBI Endpoints Initiative to advance diagnosis and treatment of TBI.
- NINDS also works with Department of Defense and the Departments of Health and Human Services, Veterans Affairs, and Education to coordinate TBI research for military members. This National Research Action Plan (NRAP) aims to improve prevention, diagnosis, and treatment of TBI and other mental health conditions such as PTSD that affect veterans and their families. The findings resulting from NRAP will be rapidly translated into new effective prevention strategies and clinical innovations, as well as identify biomarkers to detect these disorders early and accurately.
NIH research projects on TBI and other disorders can be found using NIH RePORTER , a searchable database of current and past research projects supported by NIH and other federal agencies. RePORTER also includes links to publications from these projects and other resources.
How can I or my loved one help improve care for people with a traumatic brain injury (TBI)?
Consider participating in a clinical trial so clinicians and scientists can learn more about TBI and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.
All types of volunteers are needed— those who are healthy or may have an illness or disease— of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.
For information about participating in clinical research visit NIH Clinical Research Trials and You . Learn about clinical trials currently looking for people with TBI at Clinicaltrials.gov .
People with a TBI also can support TBI research by designating the donation of brain tissue before they die. The study of human brain tissue is essential to increasing the understanding of how the nervous system functions.
The NIH NeuroBioBank is an effort to coordinate the network of brain banks it supports across the country to advance research through the collection and distribution of post-mortem brain tissue. Stakeholder groups include brain and tissue repositories, researchers, NIH program staff, information technology experts, disease advocacy groups, and most importantly individuals seeking information about opportunities to donate. It ensures protection of the privacy and wishes of donors.
Where can I find more information about traumatic brain injury (TBI)? Information may be available from the following resources: Brain Injury Association of America Phone: 703-761-0750 or 800-444-6443 Brain Injury Resource Center Phone: 206-621-8558 Brain Trauma Foundation Phone: 212-772-0608 Defense and Veterans Brain Injury Center Phone: 800-870-9244 National Library of Medicine Phone: 301-594-5983 or 888-346-3656 National Rehabilitation Information Center Phone: 800-346-2742 ThinkFirst Phone: 630-961-1400 or 800-844-6556 Uniformed Services University of the Health Sciences (USUHS) U.S. Centers for Disease Control and Prevention (CDC) - Heads Up to Concussion Phone: 800-232-4636 or 888-232-6348 U.S. Centers for Disease Control and Prevention (CDC) - TBI & Concussion Phone: 800-232-4636 or 888-232-6348
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Successful outcome in severe traumatic brain injury: a case study
Affiliation.
- 1 Neurotrauma Intensive Care Unit, Hospital of the University of Pennsylvania in Philadelphia, PA, USA.
- PMID: 16379129
- DOI: 10.1097/01376517-200510000-00002
This case study describes the management of a 54-year-old male who presented to the Hospital of the University of Pennsylvania (HUP) with a traumatic brain injury (TBI) after being assaulted. He underwent an emergent bifrontal decompressive hemicraniectomy for multiple, severe frontal contusions. His postoperative course included monitoring of intracranial pressure, cerebral perfusion pressure, partial pressure of brain oxygen, brain temperature, and medical management based on HUP's established TBI algorithm. This case study explores the potential benefit of combining multimodality monitoring and TBI guidelines in the management of severe TBI.
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Traumatic Brain Injury - Case Study Part 1
- 1 Presenting Condition
- 2 History of Presenting Condition
- 3 Social History
- 4 Past Medical History
- 5 Investigations
Presenting Condition [ edit | edit source ]
Traumatic brain injury with intracranial bleed, skull fracture, and diffuse brain oedema.
Intubated and ventilated.
History of Presenting Condition [ edit | edit source ]
Sustained a traumatic brain injury following a road traffic accident on his bicycle. His bicycle was hit side on by a car, which propelled James off the bicycle and into oncoming traffic. His helmet was broken during the impact. GCS 6 at the scene and required intubation prior to transfer to the emergency room.
Social History [ edit | edit source ]
James is a 43 year old computer programmer. He lives with his wife, one son and one daughter (age 9 & 12 respectively) in a two storey house. He is a sports enthusiast, playing social 5-a-side football with work colleagues weekly, and in his spare time enjoys running and biking. He also has an interest in gaming, and in making or modifying computers and helps out at his local Coder Do Jo, where his children learn about computers.
Past Medical History [ edit | edit source ]
No significant past medical history.
ORIF left radial fracture 3 years ago following fall from bicycle
Investigations [ edit | edit source ]
- Mild subdural heamatoma
- Moderate right intracranial bleed with ventricular and peri-mesencephalic cistern obliteration consistent with a trans-tentorial herniation.
- Large depressed fracture right temperoparietal area and large scalp wound
- Right clavicle fracture and 4th rib fracture
- Diffuse brain swelling
Surgery [ edit | edit source ]
- Right hemi-craniectomy for removal of epidural and subdural haematoma to manage intracranial pressure
- Left craniotomy for the placement of an external ventricular drain, which remained in situ for 14 days
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Case Study Traumatic Brain Injury (TBI)
Clinician Name: Robert Longo, MRC, LPC, BCN
Clinic Name & Location: Serendipity, Lexington, North Carolina
Professional Status: Masters Rehabilitation Counseling. Licensed Professional Counselor. Board Certified Neurofeedback
- Abstract: This case study reviews Ms. B., a 56 year-old female with a history of multiple head injuries. She is a nurse practitioner who contracts her services to several organizations and companies. She presented for treatment due to symptoms that included, anxiety, insomnia, and cognitive deficits.
The patient has a history of multiple head injuries, sleep problems, high blood pressure, and thyroid problems and reports diagnosis of anxiety, depression, insomnia, seizure disorder, panic attack, migraine, TMJ and memory problems.
She was taking prescriptions of Tegretol, Lithium, and Gabapentin which combined reduces alpha power and decreases alpha peak frequency, increases delta and theta and results in diffuse slowing of the EEG
Physiology problems included, but were not limited to, insomnia, depression, anxiety, headaches, dizziness, shaking & tremors, fainting spells, agitation, visual blurring, and nausea.
- Description of Case Study:
The patient underwent an initial QEEG on November 5, 2014, and a subsequent remapping on March 2, 2015 to ascertain her status/progress after it was learned that she had sustained a head injury from falling on ice sometime around February 17, 2015.
When the patient indicated that she wanted to continue Neurofeedback (despite potential caveats about starting Neurofeedback immediately following a TBI), an additional map was acquired on March 16, 2015 (her ‘new’ training map).
A subsequent head injury occurred via a bicycle accident on April 17, 2015. At that point, the patient completed a formal acknowledgement/consent to continue Neurofeedback treatment in spite of the new head injury, because she felt that the training was beneficial and wanted to continue.
QEEG maps were acquired via a 19 channel simultaneous acquisition process using the Brainmaster Discovery hardware and software. Artifacted data sets (eyes closed condition; eyes open condition) were then uploaded to the NewMind Expert QEEG Interpretive system for statistical analysis and spectral mapping. NewMind assessment questionnaires, such as the Cognitive-Emotional Checklist (CEC), Interpersonal Style Inventory (ISI), and Metabolic (Physiological symptom) Checklist, were also administered and scored as part of the QEEG interpretive report.
Overall, the patient received 36 sessions of neurofeedback over the course of 11 months. Sessions were conducted 1-2 times per week. Each neurofeedback session lasted an average of 30 minutes. The patient progressed well despite incurring 2 additional head injuries after NFB training started.
III. Literature Review:
The Brain Injury Association of America notes that 1-5 million traumatic brain injuries are sustained annually (Morkides, 2009.) Each year, traumatic brain injuries (TBI) contribute to a substantial number of deaths and cases of permanent disability. A TBI is caused by a bump, blow or jolt to the head, or a penetrating head injury, that disrupts the normal function of the brain. The severity of a TBI may range from “mild” (e.g. concussion), to “severe” (e.g. involving midline shift), based upon variables such as duration of loss of consciousness and/or duration of post-traumatic amnesia. Objectively-derived empirical data from various sources (physiological, psychological, occupational, socioeconomic, psychosocial, socio-legal, sports-related, etc.) are critical to understanding the impact of this important public health problem. This information can help inform TBI prevention strategies, identify research and education priorities, and support the need for services among those living with a TBI (http://www.cdc.gov/traumaticbraininjury/pdf/BlueBook_factsheet-a.pdf)
Cognitive functioning is thus often overshadowed by psychiatric problems. The question often posed, with regard to TBI patients, concerns whether persistent dysfunction can be attributed to an underlying acquired neurologic disorder, versus whether problematic sequelae are primarily psychologically-mediated. Recent findings are that many TBI patients (e.g. NFL football players) have treatment-resistant depression. Endocrinological research and clinical practice in the treatment of TBI indicates that ½ or more of patients referred for treatment become clinically depressed within one year post-injury. (Mark Gordon, MD, Personal Communication)
IV Procedure:
(1)Subject Information :
Client Gender: Female
Socioeconomic status: Middle Class
Public or Private School: N/A
Grades: N/A
Years in School: 16 / college undergraduate degree
Started Dating at Age: N/A
Number of Friends: several
Social Groups: N/A
Frequency of Dating: N/A
Sports Played: cycling, kayaking, hiking
Parental Status: N/A
Amount of Parental Discord: N/A
Sexual or Physical Abuse: N/A
Family Substance Abuse: unknown
History of Head Trauma: Multiple head injuries and TBIs from playing sports and falling.
(2) Presenting Symptoms :
Insomnia: Sleep onset
Attention: Difficulty focusing at work
Memory: Working Memory and Short Term Memory Problems
Headaches: Frequent
Rumination: Constant
Worry: Constant- Especially at work.
Suicidal Thoughts: Yes
CPT (add here) N/A
(3) NewMind Assessment Data:
- Cognitive-Emotional Checklist (CEC): Patient acknowledges problems with attention, memory, impulsivity and anxiety, as indicated below.
- Interpersonal Style Inventory (ISI): The patient scored above the norm on scales assessing Depression (score = 27) and Anxiety (score = 22). The ISI inventory data are consistent with the patient’s self-report in interview of feeling depressed (with suicidal thoughts); anxious (with panic attacks); stressed at work with difficulty completing work tasks; and experiencing ongoing difficulties focusing and sustaining attention, with a tendency to behave impulsively.
- Metabolic Checklist:
This patient obtained a total score of 195 on the Metabolic Checklist. Her most elevated scores were on item clusters associated with dysfunction in the following bodily systems: Kidney (27); Thyroid (e.g. Hypothyroidism; 26); Adrenals (25); Thyroid (e.g. Hyperthyroidism 24); Blood Sugar (22); Cardiovascular (18); Pituitary (20); and Blood Sugar (18). It was recommended that she share this information with her Primary Care Physician.
The Metabolic Checklist data raise the possibility of that a metabolic/medical load on the bodily system could potentially attenuate the rate (speed) of effectiveness of Neurofeedback training. This metabolic load may correlate with hypothesized neuroinflammatory and endocrinological changes in the brain in response to repetitive insults to the brain; processes which initially are intended to be protective, but which over time have a degrading effect upon the brain’s structural and functional integrity.
(4) Neurofeedback Training Sessions:
- Patient began NFB on November 7, 2014. A two-channel Bipolar Montage was used: New Mind Protocol #3 (2-12d, 15-20u on the Left and 2-12down, 13-15u on the Right) at Active sites C3 & C4, in the Eyes Closed condition. Reference sites used were A1 and A2, and Ground was placed at Cz.
- On January 30, 2015, an alternate two-channel Bipolar Montage was used: New Mind Protocol #17 (2-7d, 15-20u on the left and 2-7d, 9-11u on the right) at Active sites P3 & P4 in the Eyes Closed condition, for 4 sessions. . Reference sites used were A1 & A2, and Ground was placed at Cz.
- On February 17, 2015, Ms. B. slipped on the ice and sustained another head injury. A second QEEG was performed on March 2, 2015 to assess impact of injury.
- On March 16, 2015, 4 weeks post injury, a third QEEG map was done, as the patient requested to continue NFB.
- On March 27, 2015 (over one month after falling on the ice and sustaining a TBI), as a condition of continuing Neurofeedback, she read and signed the following acknowledgement of new TBI and consent to continue treatment, indicating that she did not want to stop her neurofeedback training due to the benefits she was receiving from the intervention”
I, _________, acknowledge that approximately 6 weeks ago, I slipped on the ice and sustained a new head injury. My subsequent QEEG brain maps reveal that my EEG has changed; and those indicated changes are likely from that injury; and are signs consistent with a new brain injury. I understand that neurofeedback is not conventionally recommended until at least three months following a head injury, to allow sufficient time for the brain’s intrinsic healing processes to occur (e.g. the brain’s neuro-plastic compensatory processes involving reorganization).
I consent to continuation of Neurofeedback training with the understanding that participating in Neurofeedback sooner than the customary 3 month wait period might potentially result in negative symptoms or side effects. In the event that I (or my family) begin to notice any unusual or lasting negative effects during my neurofeedback training over the next few months, I agree to inform Robert Longo immediately.
- On March 27, 2015, she began a “Squash” Protocol for 15 sessions, in the Eyes Closed condition: A single-channel Monopolar Montage (2-30d) at Active site Cz , with Ground at A1 and Reference at A2.
- On July 3, 2015, she began a different two-channel Bipolar Montage: NewMind Protocol #10 (2-12d, 15-20u on the Left and 13-15u, 16-30d on the Right) at Active sites Fp1 and Fp2 in the Eyes Open condition for 2 sessions. Reference sites used were A1 & A2, and Ground was placed at Cz. Each session was approximately 30 minutes in length.
- On July 17, 2015, she began another two-channel Bipolar Montage: NewMind Protocol #4 (2-7d, 15-20u on the Left and 2-7d, 13-15u, on the Right) at Active sites F3 & F4 in the Eyes Open condition for 4 sessions. . Reference sites used were A1 and A2, and Ground was placed at Cz.
- Pre-Post Trend Screens:
NewMind Protocol #3: 11 Sessions
Pre-Protocol Trend Screen
Post-Protocol Trend Screen
NewMind Protocol #17: 4 Sessions
“Squash” Protocol: 15 Sessions
NewMind Protocol #17: 2 Sessions
- Pre-Post QEEG Map Comparisons:
After 15 sessions, a remap revealed a 28% overall change in the Eyes Closed condition with 45% reorganization and 55% normalization. The Eyes Open condition revealed a 24% overall change with 45% reorganization and 55% normalization.
- Eyes-Closed Map Comparison: 11/5/2014 versus 3/2/2015
- Eyes-Open Map Comparison: 11/5/2014 versus 3/2/2015
- Eyes-Closed Map Comparison: 3/2/2015 versus 3/16/2015
After her head injury, remapping between 2nd and 3rd remap EC revealed 21% overall change with 50% reorganization and 50% normalization EO revealed 30% overall change with 53% reorganization and 44% normalization.
- Eyes-Open Map Comparison: 3/2/2015 versus 3/16/2015
- Results: Weekly Symptom Tracker
Patient tracked progress for 11 symptoms. The trend suggests a reduction in severity in all symptoms. The most pressing symptoms (identified by the patient) below reflect the reductions in sleep disturbance, depression, anxiety, panic attacks, and suicidal thoughts.
Discussion:
Neurofeedback began on November 7, 2014 and was terminated on September 11, 2015 (after roughly 10 consecutive months). A total of 36 sessions using five different protocols involving single-channel Monopolar and two-channel Bipolar protocols were used during the course of her neurofeedback training. The patient’s overall progress ranged from good to excellent, and her self-report indicated that all symptoms had improved. The patient was encouraged to practice diaphragmatic breathing multiple times per day.
The patient was asked to track her progress weekly for the following symptoms: Dysregulated sleep cycle, difficulty organizing personal time or space, reading difficulty, auditory hypersensitivity, trouble doing anything because felt bad, anxiety, depression, mood swings, panic attacks, suicidal thoughts, and poor balance. The patient reported overall symptom reduction and improved higher quality of life.
Changes in reorganization and normalization occurred with each QEEG remapping. Unfortunately, it is not possible to ascertain what proportion of change in the map(s) (corresponding to neuro-physiological changes in the brain) was potentially attributable to neurofeedback intervention (e.g. between the November 5, 2014 and March 2, 2015 map). The QEEG map comparison data are included primarily to demonstrate how the brain reorganizes itself: whether with positive intervention, such as neurofeedback, as well as in response to new insults to the brain (such as repeat TBIs).
In this respect, it is noteworthy that the patient sustained a TBI (slipping on ice and falling, hitting her head) in mid-February, which is a confounding factor (potentially likely to undo some of the beneficial effects of the neurofeedback). The patient also began to make other important lifestyle changes, which likely contributed to changes in the maps. Other uncontrolled factors (e.g. work and family stress, sleep patterns, even light cycle changes such as reduced daylight hours in midst of winter, etc.) may potentially contribute to changes in QEEG maps. This is why subsidiary measures, such as the weekly symptom tracker are so vital in ascertaining positive change (based upon self-report) in neurofeedback training.
Editor’s Note: This case study provides an important training lesson for practitioners, particularly new neurofeedback clinicians. On March 2 nd , 2015, as soon as it was learned that the patient had sustained a new TBI (from slipping on ice and falling, hitting her head in mid-February), the neurofeedback sessions were put on hold, and a remap was done at that very session (which would have been about 2 weeks, post-injury). The patient was wanting to continue the neurofeedback right away, but the author wisely waited until one month had transpired since the accident, and did a second remap. Waiting a month allowed some brain organization/ reconsolidation to occur as part of neuroplastic compensatory processes. Waiting 3 months could have too long a period of dysfunction for this distressed client to endure before resuming.
In a very pragmatic fashion, the practitioner educated the patient about the rationale for customarily waiting 3 months before re-engaging in neurofeedback, and potential risks of resuming training sooner. She was agreeable to taking this risk, because she had found the neurofeedback to be so helpful. The author had the patient sign an acknowledgement statement (that she had sustained a new TBI, and an understanding of how the new TBI may have interfered with previous progress, and how opting to continue neurofeedback might interfere with the brain’s neuroplastic recovery processes). He obtained her consent to continue neurofeedback, and used the 1 month post-injury map as the new starting place to determine the most effective protocol. Initially, he opted to do a “squash protocol” at Cz via Monopolar Montage, presumably because of across-the-board excessively high amplitudes of most or all of the frequency bands. Once the amplitudes began to reduce, he then shifted to a different two-channel Bipolar Montage with more specific targeting of problematic amplitudes in select frequency bands. Again, the use of a weekly symptom tracking system proved invaluable, as it demonstrated that despite new TBIs (which could confound the interpretation of pre-post maps), the overall trajectory of neurofeedback intervention was to reduce symptoms across the board appreciably from baseline, and allow for a very positive outcome for this complex patient. By the end of 10 months of treatment, her depression and anxiety had significantly improved, her TBI symptoms had improved, and she was very pleased with the improvement in her functioning and quality of life. This case example represents flexible, informed neurofeedback at work.
Morkides, C. (2009). A silent epidemic. Counseling Today, October, 2009, 40-42.
Pascual-Leone, A., Amedi, A., Fregni, F., and Merabet, L (2005). The plastic human brain cortex. Annual Review of Neuroscience , 28 , 377-401.
Science Daily (February 14, 2012). Traumatic brain injuries are likely more common than previously thought. http://www.sciencedaily.com/releases/2012/02/120214170906.htm.
Silver, J.M., McAllister, T.W., & Yudofsky, S.C. (2011). Textbook of traumatic brain injury. Washington, DC: American Psychiatric Publishing, Inc.
Soutar, R., & Hopson, J. (2017). Depression and QEEG Asymmetry, NewMind Online Journal, Volume 1. www.nmindjournal.com
Soutar, R., & Longo, R.E. (2011). Doing neurofeedback. San Rafael, CA: ISNR Research
Foundation.
Surprising Link Between TBI and ADHD. Neuroscience News August 23, 2015. http://neurosciencenews.com/tbi-adhd-neurology-psychology-2485
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Adults With Traumatic Brain Injury: Three Case Studies of Cognitive Rehabilitation in the Home Setting
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Susan Miron Schwartz; Adults With Traumatic Brain Injury: Three Case Studies of Cognitive Rehabilitation in the Home Setting. Am J Occup Ther July/August 1995, Vol. 49(7), 655–667. doi: https://doi.org/10.5014/ajot.49.7.655
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This article discusses the use of occupational therapy in the home setting and the individual application of treatment methods. Three case studies are presented that involve adults with acquired brain injury with memory deficits. The treatment methods used were (a) saturational cuing with behavioral chaining and positive reinforcement, (b) a coordinated team approach incorporating family or significant others and other therapists, and (c) environmental adaptations. A decision-making model and the dynamic assessment approach were used as a framework for treatment planning.
The treatment technique chosen depended on the skill to be learned and the patient’s learning style. Each case required the selection of environmental adaptations including (a) use of family and attendants as cotherapists; (b) a tape-recorded message, played daily; and (c) an appointment book for daily things to do. Each case demonstrated prolonged therapy for skill acquisition with this patient population.
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Case Study: Traumatic Brain Injury
APP3037 Case Study 2 – Traumatic Brain Injury Miriam is a 35 year old woman living in the suburbs of Melbourne who suffered a traumatic brain injury in a head on motor vehicle accident (MVA) 12 months ago. At the time of her injury she was working as a senior manager in for a large bank. She is married to Jake who works as a logistics manager for a large transport company. Together they have two children, Josh, aged 6, who is currently in grade 1 at the local primary school, and Kayla, aged 2. Miriam was alone in her car travelling at 100kms per hour on a freeway when a drunk driver crossed to the opposite side of the road, causing the head on collision. Her head contacted with the windscreen and she suffered facial contusions and severe trauma to her right leg. She sustained a closed head injury causing damage to her frontal lobes, specifically to the premotor and supplementary motor areas of the left hemisphere, and the prefrontal cortex, dorsolateral prefrontal cortex and the orbitofrontal cortex bilaterally. She also suffered a series of small bleeds and white matter damage to her temporal lobes bilaterally. Following the accident Miriam spent 6 weeks in an acute care hospital. She was unconscious for three days, and suffered a period of 1 month post-traumatic amnesia. She displays a retrograde amnesia for the period of 6 months prior to the accident that persists to the current time (1 year later). From the acute care setting she was transferred as an inpatient to a rehabilitation facility for a period of a further 3 months where she underwent intensive therapy to learn to walk and talk again. Since discharge she has continued her rehabilitation program as an outpatient, and persistent weakness remains in her right limbs. Her speech production also remains effortful and telegraphic, and a dysarthria remains evident. As a consequence of the MVA Miriam has been unable to return to her demanding work role. Although her post-traumatic amnesia is resolved, she continues to have problems with memory, concentration and reasoning. Although she does not suffer anterograde amnesia, she does suffer impairments in her short term memory. Her husband reports that she constantly repeats the same anecdotes and has trouble remembering to take her medication and to assist her children beyond their basic care. Jake also reports a personality change in Miriam. He says that she is becoming increasingly frustrated and has started to have anger outbursts, and it is not unusual for her to move from laughter to anger very quickly. Despite being described as a bubbly and fun person before the MVA, she now presents as flat and detached from her emotions most of the time. Since she has a six month retrograde amnesia for the time prior to the MVA she has no recollection of Kayla learning to walk and talk, and her physical impairments make it difficult for her to pick or hold her young daughter. After reading the case study, respond to the following, using references to support your conclusions: 1. Using information from the case study regarding Miriam’s injuries, describe the relationship between the location of the damage in her brain to her symptoms. (approx. 400 words). 2. Considering the information from the case study and using Erikson’s theory of psychosocial development as a framework, describe the implications for the lived experience of Miriam (e.g. in relation to family, work/school, friends etc.; approx. 600 words). 3. Considering the information from the case study and using Erikson’s theory of psychosocial development as a framework, describe the implications for the lived experience of Miriam’s family (e.g. in relation to family, work/school, friends etc.; approx. 400 words). — Case Study: Traumatic Brain Injury Student Name Institution Course
Case Study: Traumatic Brain Injury Using information from the case study regarding Miriam’s injuries, describe the relationship between the location of the damage in her brain to her symptoms. (approx. 500 words). Question One Premotor and Supplementary Motor Cortex The premotor and supplementary motor regions of the brain are responsible for the planning and preparation of movement, respectively. Research shows that damaged sustained to these sub-regions of the motor cortex impaires ………. In Miriams case, she has muscle weakness in her right region …. Which is the result of injuries sustained too xxx sub-region …. Prefrontal Cortex (Broca’s) Dorsolateral Cortex – Orbital frontal Cortex The prefrontal cortex (PFC) and its sub regions; dorsolateral (DLPFC) orbitofrontal (OFC), ventrolateral (VLPFC) are responsible for “executive functioning” and acts as a receiver of information from other regions of the brain. Damaged sustained to the PFC In Miriam’s case Temporal lobe (Wernicke’s) White Matter (Arcuate Fasciculus) – Maybe incorporate the implication of the bi-lateral damage sustained in the temporal lobe into the above two sub headings please. The white matter damage causes impaired message delivery to the frontal lobe region so it can be linked in.
Question Two – Lived experience of Miriam in three context and the implications Considering the information from the case study and using Erikson’s theory of psychosocial development as a framework, describe the implications for the lived experience of Miriam (e.g. in relation to family, work/school, friends etc.; approx. 600 words).
Family Work/School Friends
Question Three – Lived experience of those around Miriam and the implications Considering the information from the case study and using Erikson’s theory of psychosocial development as a framework, describe the implications for the lived experience of Miriam’s family (e.g. in relation to family, work/school, friends etc.; approx. 400 words).
Family (Husband Jake 35 years old / Son Josh 6 years old / Daughter Kayla 2 years old) Work Friends
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Progress in the years after a severe anoxic brain
This 30 year-old, mother of two children and former medical secretary was admitted to the Neurologic Rehabilitation Institute (NRI) program in May of 2009. Mary Anne had an anoxic brain injury as a result of ventricular fibrillation in November 2004.
Following her injury, Mary Anne had significant problems with short-term memory, auditory processing, problem solving, insight, confusion, orientation, organization, and attention. Additionally, she had neurobehavioral problems which included aggression, hypersexuality, obsessive and ritualized behaviors, elopement attempts, verbal outbursts, impulsivity, and severe mood swings. Following her initial injury Mary Anne had also developed medical problems such as incontinence, seizures, hypothyroidism, hypertension, hypokalemia, and episodes of choking and weight loss.
Prior to her admission to the NRI program Mary Anne was in a locked psychiatric hospital due to severe aggression and impulsive/risky behaviors (she had once attempted to jump out of a moving automobile, for example). She was unable to care for herself and her children, which resulted in her parents assuming guardianship and parenting responsibilities for her children, then 6 and 8.
In the NRI program, Mary Anne’s rehabilitation addressed her medical, cognitive and behavioral problems. Her rehabilitation focused on regaining skills related to activities of daily living; improving her cognitive functions; reducing the frequency and severity of aggressive physical and behavioral outbursts; reducing her inappropriate sexual behaviors and promoting pro-social, cooperative activities with peers; and learning about how she could better self-manage the deficits related to her brain injury to support her return to home and parenting.
In October 2010, Mary Anne progressed into the Transitional Living Center program where she lived with six other peers in a large, 6- bedroom, ranch style home located approximately two miles from the hospital campus. In the TLC program, Mary Anne participated in improving her independent living skills and reducing her reliance on staff for constant cues and direction. Her hospital-based rehabilitation program continued on a Monday to Friday schedule and became more focused on functional skills and pre-vocational training to support her planned return home to live with her children and parents.
Mary Anne’s return home was celebrated in March 2011. Her family was involved in extensive planning, education and trial visits home in the months prior to her discharge. Mary Anne was referred to a vocational training program near her home where she could be in a supported work setting for 30 hours a week. Additional services for her health needs were established with a home health agency and an outpatient therapist was secured to help Mary Anne with personal adjustment issues.
Since her discharge home, Mary Anne’s family has kept us up-to-date on her progress. They report that people who haven’t seen her since her injury “can’t believe it’s the same person.” Mary Anne has re-established her relationship with her children and has rejoined her family and community. Her progress in the NRI program is a testament to the real changes which can be made years after brain injury
©2023 Neurologic Rehabilitation Institute. All Rights Reserved.
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Phineas Gage: His Accident and Impact on Psychology
Kendra Cherry, MS, is an author and educational consultant focused on helping students learn about psychology.
:max_bytes(150000):strip_icc():format(webp)/IMG_9791-89504ab694d54b66bbd72cb84ffb860e.jpg "a case study traumatic brain injury")
Emily is a board-certified science editor who has worked with top digital publishing brands like Voices for Biodiversity, Study.com, GoodTherapy, Vox, and Verywell.
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- Phineas Gage's Accident
- Effects of Injury
- Severity of Brain Damage
- Impact on Psychology
- Post-Accident Life
Frequently Asked Questions
Phineas Gage is often referred to as the "man who began neuroscience." He experienced a traumatic brain injury when an iron rod was driven through his skull, destroying much of his frontal lobe .
Gage miraculously survived the accident. However, his personality and behavior were so changed as a result of the frontal lobe damage that many of his friends described him as an almost different person entirely. The impact that the accident had has helped us better understand what the frontal lobe does, especially in relation to personality .
Phineas Gage's Accident
On September 13, 1848, 25-year-old Gage was working as the foreman of a crew preparing a railroad bed near Cavendish, Vermont. He was using an iron tamping rod to pack explosive powder into a hole.
Unfortunately, the powder detonated, sending the 43-inch-long, 1.25-inch-diameter rod hurling upward. The rod penetrated Gage's left cheek, tore through his brain , and exited his skull before landing 80 feet away.
Gage not only survived the initial injury but was able to speak and walk to a nearby cart so he could be taken into town to be seen by a doctor. He was still conscious later that evening and able to recount the names of his co-workers. Gage even suggested that he didn't wish to see his friends since he would be back to work in "a day or two" anyway.
The Recovery Process
After developing an infection, Gage spent September 23 to October 3 in a semi-comatose state. On October 7, he took his first steps out of bed, and, by October 11, his intellectual functioning began to improve.
Descriptions of Gage's injury and mental changes were made by Dr. John Martyn Harlow. Much of what researchers know about the case is based on Harlow's observations.
Harlow noted that Gage knew how much time had passed since the accident and remembered clearly how the accident occurred, but had difficulty estimating the size and amounts of money. Within a month, Gage was well enough to leave the house.
In the months that followed, Gage returned to his parent's home in New Hampshire to recuperate. When Harlow saw Gage again the following year, the doctor noted that while Gage had lost vision in his eye and was left with obvious scars from the accident, he was in good physical health and appeared recovered.
Theories About Gage's Survival and Recovery
The type of injury sustained by Phineas Gage could have easily been fatal. While it cannot be said with certainty why Gage was able to survive the accident, let alone recover from the injury and still function, several theories exist. They include:
- The rod's path . Some researchers suggest that the rod's path likely played a role in Gage's survival in that if it had penetrated other areas of the head—such as the pterygoid plexuses or cavernous sinus—Gage may have bled to death.
- The brain's selective recruitment . In a 2022 study of another individual who also had an iron rod go through his skull—whom the researchers referred to as a "modern-day Phineas Gage"—it was found that the brain is able to selectively recruit non-injured areas to help perform functions previously assigned to the injured portion.
- Work structure . Others theorize that Gage's work provided him structure, positively contributing to his recovery and aiding in his rehabilitation.
The Effects of Gage's Injury
Popular reports of Gage often depict him as a hardworking, pleasant man prior to the accident. Post-accident, these reports describe him as a changed man, suggesting that the injury had transformed him into a surly, aggressive heavy drinker who was unable to hold down a job.
Harlow presented the first account of the changes in Gage's behavior following the accident. Where Gage had been described as energetic, motivated, and shrewd prior to the accident, many of his acquaintances explained that after the injury he was "no longer Gage."
Since there is little direct evidence of the exact extent of Gage's injuries aside from Harlow's report, it is difficult to know exactly how severely his brain was damaged. Harlow's accounts suggest that the injury did lead to a loss of social inhibition, leading Gage to behave in ways that were seen as inappropriate.
Some evidence suggests that many of the supposed effects of the accident may have been exaggerated and that Gage was actually far more functional than previously reported.
Severity of Gage's Brain Damage
In a 1994 study, researchers utilized neuroimaging techniques to reconstruct Phineas Gage's skull and determine the exact placement of the injury. Their findings indicate that he suffered injuries to both the left and right prefrontal cortices, which would result in problems with emotional processing and rational decision-making .
Another study conducted in 2004 used three-dimensional, computer-aided reconstruction to analyze the extent of Gage's injury. It found that the effects were limited to the left frontal lobe.
In 2012, new research estimated that the iron rod destroyed approximately 11% of the white matter in Gage's frontal lobe and 4% of his cerebral cortex.
Phineas Gage's Impact on Psychology
Gage's case had a tremendous influence on early neurology. The specific changes observed in his behavior pointed to emerging theories about the localization of brain function, or the idea that certain functions are associated with specific areas of the brain.
In those years, neurology was in its infancy. Gage's extraordinary story served as one of the first sources of evidence that the frontal lobe was involved in personality.
Today, scientists better understand the role that the frontal cortex has to play in important higher-order functions such as reasoning , language, and social cognition .
What Happened to Phineas Gage?
After the accident, Gage was unable to continue his previous job. According to Harlow, Gage spent some time traveling through New England and Europe with his tamping iron to earn money, supposedly even appearing in the Barnum American Museum in New York.
He also worked briefly at a livery stable in New Hampshire and then spent seven years as a stagecoach driver in Chile. He eventually moved to San Francisco to live with his mother as his health deteriorated.
After a series of epileptic seizures, Gage died on May 21, 1860, almost 12 years after his accident. Seven years after his death, Gage's body was exhumed. His brother gave his skull and the tamping rod to Dr. Harlow, who subsequently donated them to the Harvard University School of Medicine. They are still exhibited in its museum today.
Phineas Gage Summary
In 1948, Phineas Gage had a workplace accident in which an iron tamping rod entered and exited his skull. He survived but it is said that his personality changed as a result, leading to a greater understanding of the brain regions involved in personality, namely the frontal lobe.
A Word From Verywell
Gage's accident and subsequent experiences serve as a historical example of how case studies can be used to look at unique situations that could not be replicated in a lab. What researchers learned from Phineas Gage's skull and brain injury played an important role in the early days of neurology and helped scientists gain a better understanding of the human brain and the impact that damage could have on both functioning and behavior.
Gage died from an epileptic seizure almost 12 years after the accident. These seizures started a few months before his passing, though his health had started to decline several months before the seizures began.
The damage occurred to Phineas Gage's frontal lobe, the region of the brain at the front of the head. The frontal lobe plays a role in our ability to speak, make decisions, and move. It is also partially responsible for our personality.
Post-accident, Gage's demeanor was said to have changed from pleasant to surly and he went from being a hardworking, motivated man to a man who had trouble keeping a steady job. Some reports suggest that Gage's personality changes were exaggerated, and that they may also have been temporary, fading a couple of years after the accident.
Phineas Gage lived almost 12 years after the rod pierced his skull. He died on May 21, 1860. This would make him just short of 37 years old at the time of his death.
Gage's accident helped teach us that different parts of the brain play a role in different functions. Through studying Gage's frontal lobe damage, we gained a better understanding of what the frontal cortex does with regard to personality. We also began to know more about the effects of frontal lobe damage and how it may change a person.
Sevmez F, Adanir S, Ince R. Legendary name of neuroscience: Phineas Gage (1823-1860) . Child's Nervous System . 2020. doi:10.1007/s00381-020-04595-6
Twomey S. Phineas Gage: Neuroscience's most famous patient . Smithsonian Magazine.
Harlow JM. Recovery after severe injury to the head . Bull Massachus Med Soc . 1848. Reprinted in Hist Psychiat. 1993;4(14):274-281. doi:10.1177/0957154X9300401407
Harlow JM. Passage of an iron rod through the head . 1848. J Neuropsychiatry Clin Neurosci . 1999;11(2):281-3. doi:10.1176/jnp.11.2.281
Itkin A, Sehgal T. Review of Phineas Gage's oral and maxillofacial injuries . J Oral Biol . 2017;4(1):3.
de Freitas P, Monteiro R, Bertani R, et al. E.L., a modern-day Phineas Gage: Revisiting frontal lobe injury . The Lancet Regional Health - Americas . 2022;14:100340. doi:10.1016/j.lana.2022.100340
Macmillan M, Lena ML. Rehabilitating Phineas Gage . Neuropsycholog Rehab . 2010;20(5):641-658. doi:10.1080/09602011003760527
O'Driscoll K, Leach JP. "No longer Gage": An iron bar through the head. Early observations of personality change after injury to the prefrontal cortex . BMJ . 1998;317(7174):1673-4. doi:10.1136/bmj.317.7174.1673a
Macmillan M. An Odd Kind of Fame: Stories of Phineas Gage . MIT Press.
Damasio H, Grabowski T, Frank R, Galaburda AM, Damasio AR. The return of Phineas Gage: Clues about the brain from the skull of a famous patient . Science . 1994;264(5162):1102-5. doi:10.1126/science.8178168
Ratiu P, Talos IF. Images in clinical medicine. The tale of Phineas Gage, digitally remastered . N Engl J Med . 2004;351(23):e21. doi:10.1056/NEJMicm031024
Van Horn JD, Irimia A, Torgerson CM, Chambers MC, Kikinis R, Toga AW. Mapping connectivity damage in the case of Phineas Gage . PLoS One . 2012;7(5):e37454. doi: 10.1371/journal.pone.0037454
Shelley B. Footprints of Phineas Gage: Historical beginnings on the origins of brain and behavior and the birth of cerebral localizationism . Archives Med Health Sci . 2016;4(2):280-6. doi:10.4103/2321-4848.196182
Garcia-Molina A. Phineas Gage and the enigma of the prefrontal cortex . Neurologia . 2012;27(6):370-5. doi:10.1016/j.nrleng.2010.03.002
Johns Hopkins Medicine. Brain anatomy and how the brain works .
By Kendra Cherry Kendra Cherry, MS, is an author and educational consultant focused on helping students learn about psychology.
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What is traumatic brain injury?
Traumatic brain injury (TBI) happens when a sudden, external, physical assault damages the brain. It is one of the most common causes of disability and death in adults. TBI is a broad term that describes a vast array of injuries that happen to the brain. The damage can be focal (confined to one area of the brain) or diffuse (happens in more than one area of the brain). The severity of a brain injury can range from a mild concussion to a severe injury that results in coma or even death.
What are the different types of TBI?
Brain injury may happen in one of two ways:
Closed brain injury. Closed brain injuries happen when there is a nonpenetrating injury to the brain with no break in the skull. A closed brain injury is caused by a rapid forward or backward movement and shaking of the brain inside the bony skull that results in bruising and tearing of brain tissue and blood vessels. Closed brain injuries are usually caused by car accidents, falls, and increasingly, in sports. Shaking a baby can also result in this type of injury (called shaken baby syndrome).
Penetrating brain injury. Penetrating, or open head injuries happen when there is a break in the skull, such as when a bullet pierces the brain.
What is diffuse axonal injury (DAI)?
Diffuse axonal injury is the shearing (tearing) of the brain's long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull. DAI usually causes coma and injury to many different parts of the brain. The changes in the brain are often microscopic and may not be evident on computed tomography (CT scan) or magnetic resonance imaging (MRI) scans.
What is primary and secondary brain injury?
Primary brain injury refers to the sudden and profound injury to the brain that is considered to be more or less complete at the time of impact. This happens at the time of the car accident, gunshot wound, or fall.
Secondary brain injury refers to the changes that evolve over a period of hours to days after the primary brain injury. It includes an entire series of steps or stages of cellular, chemical, tissue, or blood vessel changes in the brain that contribute to further destruction of brain tissue.
What causes a head injury?
There are many causes of head injury in children and adults. The most common injuries are from motor vehicle accidents (where the person is either riding in the car or is struck as a pedestrian), violence, falls, or as a result of shaking a child (as seen in cases of child abuse).
What causes bruising and internal damage to the brain?
When there is a direct blow to the head, the bruising of the brain and the damage to the internal tissue and blood vessels is due to a mechanism called coup-contrecoup. A bruise directly related to trauma at the site of impact is called a coup lesion (pronounced COO ). As the brain jolts backward, it can hit the skull on the opposite side and cause a bruise called a contrecoup lesion. The jarring of the brain against the sides of the skull can cause shearing (tearing) of the internal lining, tissues, and blood vessels leading to internal bleeding, bruising, or swelling of the brain.
What are the possible results of brain injury?
Some brain injuries are mild, with symptoms disappearing over time with proper attention. Others are more severe and may result in permanent disability. The long-term or permanent results of brain injury may need post-injury and possibly lifelong rehabilitation. Effects of brain injury may include:
Shortened attention span
Memory problems and amnesia
Problem-solving deficits
Problems with judgment
Inability to understand abstract concepts
Loss of sense of time and space
Decreased awareness of self and others
Inability to accept more than one- or two-step commands at the same time
Paralysis or weakness
Spasticity (tightening and shortening of the muscles)
Poor balance
Decreased endurance
Inability to plan motor movements
Delays in getting started
Swallowing problems
Poor coordination
Changes in hearing, vision, taste, smell, and touch
Loss of sensation or heightened sensation of body parts
Left- or right-sided neglect
Difficulty understanding where limbs are in relation to the body
Vision problems, including double vision, lack of visual acuity, or limited range of vision
Difficulty speaking and understanding speech (aphasia)
Difficulty choosing the right words to say (aphasia)
Difficulty reading (alexia) or writing (agraphia)
Difficulty knowing how to perform certain very common actions, like brushing one's teeth (apraxia)
Slow, hesitant speech and decreased vocabulary
Difficulty forming sentences that make sense
Problems identifying objects and their function
Problems with reading, writing, and ability to work with numbers
Impaired ability with activities of daily living (ADLs), such as dressing, bathing, and eating
Problems with organization, shopping, or paying bills
Inability to drive a car or operate machinery
Impaired social capacity resulting in difficult interpersonal relationships
Difficulties in making and keeping friends
Difficulties understanding and responding to the nuances of social interaction
Changes in sleep patterns and eating habits
Loss of bowel and bladder control
Decreased motivation
Emotional lability
Irritability
Anxiety and depression
Disinhibition, including temper flare-ups, aggression, cursing, lowered frustration tolerance, and inappropriate sexual behavior
Certain psychiatric disorders are more likely to develop if damage changes the chemical composition of the brain.
- Epilepsy can happen with a brain injury, but more commonly with severe or penetrating injuries. While most seizures happen immediately after the injury, or within the first year, it is also possible for epilepsy to surface years later. Epilepsy includes both major or generalized seizures and minor or partial seizures.
Can the brain heal after being injured?
Most studies suggest that once brain cells are destroyed or damaged, for the most part, they do not regenerate. However, recovery after brain injury can take place, especially in younger people, as, in some cases, other areas of the brain make up for the injured tissue. In other cases, the brain learns to reroute information and function around the damaged areas. The exact amount of recovery is not predictable at the time of injury and may be unknown for months or even years. Each brain injury and rate of recovery is unique. Recovery from a severe brain injury often involves a prolonged or lifelong process of treatment and rehabilitation.
What is coma?
Coma is an altered state of consciousness that may be very deep (unconsciousness) so that no amount of stimulation will cause the patient to respond. It can also be a state of reduced consciousness, so that the patient may move about or respond to pain. Not all patients with brain injury are comatose. The depth of coma, and the time a patient spends in a coma varies greatly depending on the location and severity of the brain injury. Some patients emerge from a coma and have a good recovery. Other patients have significant disabilities.
How is coma measured?
Depth of the coma is usually measured in the emergency and intensive care settings using a Glasgow coma scale. The scale (from 3 to 15) evaluates eye opening, verbal response, and motor response. A high score shows a greater amount of consciousness and awareness.
In rehabilitation settings, here are several scales and measures used to rate and record the progress of the patient. Some of the most common of these scales are described below.
Rancho Los Amigos 10 Level Scale of Cognitive Functioning. This is a revision of the original Rancho 8 Level Scale, which is based on how the patient reacts to external stimuli and the environment. The scales consist of 10 different levels and each patient will progress through the levels with starts and stops, progress and plateaus.
Disability Rating Scale (DRS). This scale measures functional change during the course of recovery rating the person's disability level from none to extreme. The DRS assesses cognitive and physical function, impairment, disability, and handicap and can track a person's progress from "coma to community."
Functional Independent Measure (FIM). The FIM scale measures a person's level of independence in activities of daily living. Scores can range from 1 (complete dependence) to 7 (complete independence).
Functional Assessment Measure (FAM). This measure is used along with FIM and was developed specifically for people with brain injury.
The Brain Injury Rehabilitation Program
Rehabilitation of the patient with a brain injury begins during the acute treatment phase. As the patient's condition improves, a more extensive rehabilitation program is often begun. The success of rehabilitation depends on many variables, including the following:
Nature and severity of the brain injury
Type and degree of any resulting impairments and disabilities
Overall health of the patient
Family support
It is important to focus on maximizing the patient's capabilities at home and in the community. Positive reinforcement helps recovery by improving self-esteem and promoting independence.
The goal of brain injury rehabilitation is to help the patient return to the highest level of function and independence possible, while improving the overall quality of life— physically, emotionally, and socially.
Areas covered in brain injury rehabilitation programs may include:
- Self-care skills, including activities of daily living (ADLs) : feeding, grooming, bathing, dressing, toileting, and sexual functioning
- Physical care : nutritional needs, medicines, and skin care
- Mobility skills : walking, transfers, and self-propelling a wheelchair
- Communication skills : speech, writing, and alternative methods of communication
- Cognitive skills : speech, writing, and alternative methods of communication
- Socialization skills : interacting with others at home and within the community
- Vocational training : work-related skills
- Pain management : medicines and alternative methods of managing pain
- Psychological testing and counseling : identifying problems and solutions with thinking, behavioral, and emotional issues
- Family support : assistance with adapting to lifestyle changes, financial concerns, and discharge planning
- Education : patient and family education and training about brain injury, safety issues, home care needs, and adaptive techniques
The Brain Injury Rehabilitation Team
The brain injury rehabilitation team revolves around the patient and family and helps set short- and long-term treatment goals for recovery. Many skilled professionals are part of the brain injury rehabilitation team, including any or all of the following:
Neurologist/neurosurgeon
Physiatrist
Internists and specialists
Rehabilitation nurse
Social worker
Physical therapist
Occupational therapist
Speech/language pathologist
Psychologist/neuropsychologist/psychiatrist
Recreation therapist
Audiologist
Vocational counselor
Case manager
Respiratory therapist
Types of Brain Injury Rehabilitation Programs
There are a variety of brain injury treatment programs, including the following:
Acute rehabilitation programs
Subacute rehabilitation programs
Long-term rehabilitation programs
Transitional living programs
Behavior management programs
Day-treatment programs
Independent living programs
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- DOI: 10.1081/CRP-120018744
- Corpus ID: 72384276
Implementing Scientific Evidence-Based Guidelines: Case Study of Severe Traumatic Brain Injuries
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- Traumatic brain injury
Traumatic brain injury usually results from a violent blow or jolt to the head or body. An object that goes through brain tissue, such as a bullet or shattered piece of skull, also can cause traumatic brain injury.
Mild traumatic brain injury may affect your brain cells temporarily. More-serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain. These injuries can result in long-term complications or death.
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Traumatic brain injury can have wide-ranging physical and psychological effects. Some signs or symptoms may appear immediately after the traumatic event, while others may appear days or weeks later.
Mild traumatic brain injury
The signs and symptoms of mild traumatic brain injury may include:
Physical symptoms
- Nausea or vomiting
- Fatigue or drowsiness
- Problems with speech
- Dizziness or loss of balance
Sensory symptoms
- Sensory problems, such as blurred vision, ringing in the ears, a bad taste in the mouth or changes in the ability to smell
- Sensitivity to light or sound
Cognitive, behavioral or mental symptoms
- Loss of consciousness for a few seconds to a few minutes
- No loss of consciousness, but a state of being dazed, confused or disoriented
- Memory or concentration problems
- Mood changes or mood swings
- Feeling depressed or anxious
- Difficulty sleeping
- Sleeping more than usual
Moderate to severe traumatic brain injuries
Moderate to severe traumatic brain injuries can include any of the signs and symptoms of mild injury, as well as these symptoms that may appear within the first hours to days after a head injury:
- Loss of consciousness from several minutes to hours
- Persistent headache or headache that worsens
- Repeated vomiting or nausea
- Convulsions or seizures
- Dilation of one or both pupils of the eyes
- Clear fluids draining from the nose or ears
- Inability to awaken from sleep
- Weakness or numbness in fingers and toes
- Loss of coordination
Cognitive or mental symptoms
- Profound confusion
- Agitation, combativeness or other unusual behavior
- Slurred speech
- Coma and other disorders of consciousness
Children's symptoms
Infants and young children with brain injuries might not be able to communicate headaches, sensory problems, confusion and similar symptoms. In a child with traumatic brain injury, you may observe:
- Change in eating or nursing habits
- Unusual or easy irritability
- Persistent crying and inability to be consoled
- Change in ability to pay attention
- Change in sleep habits
- Sad or depressed mood
- Loss of interest in favorite toys or activities
When to see a doctor
Always see your doctor if you or your child has received a blow to the head or body that concerns you or causes behavioral changes. Seek emergency medical care if there are any signs or symptoms of traumatic brain injury following a recent blow or other traumatic injury to the head.
The terms "mild," "moderate" and "severe" are used to describe the effect of the injury on brain function. A mild injury to the brain is still a serious injury that requires prompt attention and an accurate diagnosis.
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Traumatic brain injury is usually caused by a blow or other traumatic injury to the head or body. The degree of damage can depend on several factors, including the nature of the injury and the force of impact.
Common events causing traumatic brain injury include the following:
- Falls. Falls from bed or a ladder, down stairs, in the bath, and other falls are the most common cause of traumatic brain injury overall, particularly in older adults and young children.
- Vehicle-related collisions. Collisions involving cars, motorcycles or bicycles — and pedestrians involved in such accidents — are a common cause of traumatic brain injury.
- Violence. Gunshot wounds, domestic violence, child abuse and other assaults are common causes. Shaken baby syndrome is a traumatic brain injury in infants caused by violent shaking.
- Sports injuries. Traumatic brain injuries may be caused by injuries from a number of sports, including soccer, boxing, football, baseball, lacrosse, skateboarding, hockey, and other high-impact or extreme sports. These are particularly common in youth.
Explosive blasts and other combat injuries. Explosive blasts are a common cause of traumatic brain injury in active-duty military personnel. Although how the damage occurs isn't yet well understood, many researchers believe that the pressure wave passing through the brain significantly disrupts brain function.
Traumatic brain injury also results from penetrating wounds, severe blows to the head with shrapnel or debris, and falls or bodily collisions with objects following a blast.
Risk factors
The people most at risk of traumatic brain injury include:
- Children, especially newborns to 4-year-olds
- Young adults, especially those between ages 15 and 24
- Adults age 60 and older
- Males in any age group
Complications
Several complications can occur immediately or soon after a traumatic brain injury. Severe injuries increase the risk of a greater number of and more-severe complications.
Altered consciousness
Moderate to severe traumatic brain injury can result in prolonged or permanent changes in a person's state of consciousness, awareness or responsiveness. Different states of consciousness include:
- Coma. A person in a coma is unconscious, unaware of anything and unable to respond to any stimulus. This results from widespread damage to all parts of the brain. After a few days to a few weeks, a person may emerge from a coma or enter a vegetative state.
Vegetative state. Widespread damage to the brain can result in a vegetative state. Although the person is unaware of surroundings, he or she may open his or her eyes, make sounds, respond to reflexes, or move.
It's possible that a vegetative state can become permanent, but often individuals progress to a minimally conscious state.
- Minimally conscious state. A minimally conscious state is a condition of severely altered consciousness but with some signs of self-awareness or awareness of one's environment. It is sometimes a transitional state from a coma or vegetative condition to greater recovery.
- Brain death. When there is no measurable activity in the brain and the brainstem, this is called brain death. In a person who has been declared brain dead, removal of breathing devices will result in cessation of breathing and eventual heart failure. Brain death is considered irreversible.
Physical complications
- Seizures. Some people with traumatic brain injury will develop seizures. The seizures may occur only in the early stages, or years after the injury. Recurrent seizures are called post-traumatic epilepsy.
- Fluid buildup in the brain (hydrocephalus). Cerebrospinal fluid may build up in the spaces in the brain (cerebral ventricles) of some people who have had traumatic brain injuries, causing increased pressure and swelling in the brain.
- Infections. Skull fractures or penetrating wounds can tear the layers of protective tissues (meninges) that surround the brain. This can enable bacteria to enter the brain and cause infections. An infection of the meninges (meningitis) could spread to the rest of the nervous system if not treated.
- Blood vessel damage. Several small or large blood vessels in the brain may be damaged in a traumatic brain injury. This damage could lead to a stroke, blood clots or other problems.
- Headaches. Frequent headaches are very common after a traumatic brain injury. They may begin within a week after the injury and could persist for as long as several months.
- Vertigo. Many people experience vertigo, a condition characterized by dizziness, after a traumatic brain injury.
Sometimes, any or several of these symptoms might linger for a few weeks to a few months after a traumatic brain injury. When a combination of these symptoms lasts for an extended period of time, this is generally referred to as persistent post-concussive symptoms.
Traumatic brain injuries at the base of the skull can cause nerve damage to the nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:
- Paralysis of facial muscles or losing sensation in the face
- Loss of or altered sense of smell or taste
- Loss of vision or double vision
- Swallowing problems
- Ringing in the ear
- Hearing loss
Intellectual problems
Many people who have had a significant brain injury will experience changes in their thinking (cognitive) skills. It may be more difficult to focus and take longer to process your thoughts. Traumatic brain injury can result in problems with many skills, including:
Cognitive problems
- Attention or concentration
Executive functioning problems
- Problem-solving
- Multitasking
- Organization
- Decision-making
- Beginning or completing tasks
Communication problems
Language and communications problems are common following traumatic brain injuries. These problems can cause frustration, conflict and misunderstanding for people with a traumatic brain injury, as well as family members, friends and care providers.
Communication problems may include:
- Difficulty understanding speech or writing
- Difficulty speaking or writing
- Inability to organize thoughts and ideas
- Trouble following and participating in conversations
Communication problems that affect social skills may include:
- Trouble with turn taking or topic selection in conversations
- Problems with changes in tone, pitch or emphasis to express emotions, attitudes or subtle differences in meaning
- Difficulty understanding nonverbal signals
- Trouble reading cues from listeners
- Trouble starting or stopping conversations
- Inability to use the muscles needed to form words (dysarthria)
Behavioral changes
People who've experienced brain injury may experience changes in behaviors. These may include:
- Difficulty with self-control
- Lack of awareness of abilities
- Risky behavior
- Difficulty in social situations
- Verbal or physical outbursts
Emotional changes
Emotional changes may include:
- Mood swings
- Irritability
- Lack of empathy for others
Sensory problems
Problems involving senses may include:
- Persistent ringing in the ears
- Difficulty recognizing objects
- Impaired hand-eye coordination
- Blind spots or double vision
- A bitter taste, a bad smell or difficulty smelling
- Skin tingling, pain or itching
- Trouble with balance or dizziness
Degenerative brain diseases
The relationship between degenerative brain diseases and brain injuries is still unclear. But some research suggests that repeated or severe traumatic brain injuries might increase the risk of degenerative brain diseases. But this risk can't be predicted for an individual — and researchers are still investigating if, why and how traumatic brain injuries might be related to degenerative brain diseases.
A degenerative brain disorder can cause gradual loss of brain functions, including:
- Alzheimer's disease, which primarily causes the progressive loss of memory and other thinking skills
- Parkinson's disease, a progressive condition that causes movement problems, such as tremors, rigidity and slow movements
- Dementia pugilistica — most often associated with repetitive blows to the head in career boxing — which causes symptoms of dementia and movement problems
Follow these tips to reduce the risk of brain injury:
- Seat belts and airbags. Always wear a seat belt in a motor vehicle. A small child should always sit in the back seat of a car secured in a child safety seat or booster seat that is appropriate for his or her size and weight.
- Alcohol and drug use. Don't drive under the influence of alcohol or drugs, including prescription medications that can impair the ability to drive.
- Helmets. Wear a helmet while riding a bicycle, skateboard, motorcycle, snowmobile or all-terrain vehicle. Also wear appropriate head protection when playing baseball or contact sports, skiing, skating, snowboarding or riding a horse.
- Pay attention to your surroundings. Don't drive, walk or cross the street while using your phone, tablet or any smart device. These distractions can lead to accidents or falls.
Preventing falls
The following tips can help older adults avoid falls around the house:
- Install handrails in bathrooms
- Put a nonslip mat in the bathtub or shower
- Remove area rugs
- Install handrails on both sides of staircases
- Improve lighting in the home, especially around stairs
- Keep stairs and floors clear of clutter
- Get regular vision checkups
- Get regular exercise
Preventing head injuries in children
The following tips can help children avoid head injuries:
- Install safety gates at the top of a stairway
- Keep stairs clear of clutter
- Install window guards to prevent falls
- Use playgrounds that have shock-absorbing materials on the ground
- Make sure area rugs are secure
- Don't let children play on fire escapes or balconies
- Traumatic brain injury: Hope through research. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Traumatic-Brain-Injury-Hope-Through. Accessed Dec. 17, 2020.
- Traumatic brain injury (TBI). American Speech-Language-Hearing Association. https://www.asha.org/public/speech/disorders/traumatic-brain-injury/. Accessed Dec. 17, 2020.
- Goldman L, et al., eds. Traumatic brain injury and spinal cord injury. In: Goldman-Cecil Medicine. 26th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Dec. 17, 2020.
- Traumatic brain injury. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury. Accessed Dec. 17, 2020.
- Evans RW, et al. Acute mild traumatic brain injury (concussion) in adults. https://www.uptodate.com/contents/search. Accessed Dec. 17, 2020.
- Kasper DL, et al., eds. Concussion and other traumatic brain injuries. In: Harrison's Principles of Internal Medicine. 20th ed. McGraw-Hill Education; 2018. https://accessmedicine.mhmedical.com. Accessed Dec. 17, 2020.
- Hemphill JC. Traumatic brain injury: Epidemiology, classification, and pathophysiology. https://www.uptodate.com/contents/search. Accessed Jan. 6, 2021.
- Weinhouse GL. Hypoxic-ischemic brain injury: Evaluation and prognosis. https://www.uptodate.com/contents/search. Accessed Oct. 16, 2017.
- McCrory P, et al. Consensus statement on concussion in sport — The 5th international conference on concussion in sport held in Berlin, October 2016. British Journal of Sports Medicine. 2017;51:838.
- Adams JG, et al., eds. Traumatic brain injury (adult). In: Emergency Medicine: Clinical Essentials. 2nd ed. Philadelphia, Pa.: Saunders Elsevier; 2013. https://www.clinicalkey.com. Accessed Jan. 6, 2021.
- Hemphill JC. Management of acute severe traumatic brain injury. https://www.uptodate.com/contents/search. Accessed Jan. 6, 2021.
- Traumatic brain injury & concussion prevention. Centers for Disease Control and Prevention. http://www.cdc.gov/traumaticbraininjury/prevention.html. Accessed Jan. 6, 2021.
- Schultz BA (expert opinion). Mayo Clinic. DATE.
- Schultzman S. Minor blunt head trauma in children (≥2 years): Clinical features and evaluation. https://www.uptodate.com/contents/search. Accessed Jan. 6, 2021.
- Traumatic brain injury. Family Caregiver Alliance. https://www.caregiver.org/traumatic-brain-injury. Accessed Jan. 6, 2021.
- Carney N, et al. Guidelines for the management of severe traumatic brain injury. Neurosurgery. 4th ed. 2017; doi:10.1227/NEU.0000000000001432.
- Heads up to youth sports: Clipboard concussion information sheet. Centers for Disease Control and Prevention. https://www.cdc.gov/headsup/youthsports/coach.html. Accessed Jan. 6, 2021.
- What can I do to help feel better after a traumatic brain injury? Centers for Disease Control and Prevention. https://www.cdc.gov/traumaticbraininjury/recovery.html. Accessed Jan. 6, 2021.
- Traumatic brain injury & concussion: Signs and symptoms. Centers for Disease Control and Prevention. https://www.cdc.gov/traumaticbraininjury/symptoms.html. Accessed Jan. 6, 2021.
- Bellamkonda E (expert opinion). Mayo Clinic. DATE.
- Pediatric traumatic brain injury. American Speech-Language-Hearing Association. https://www.asha.org/practice-portal/clinical-topics/pediatric-traumatic-brain-injury/#collapse_2. Accessed Jan. 6, 2021.
- Mendez MF. What is the relationship of traumatic brain injury to dementia? Journal of Alzheimer's disease. 2017; doi:10.3233/JAD-161002.
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$3,000,000 Personal Injury Settlement Claim
Our law firm established prior water damage., personal injury case: background.
Phil had built a reputation as a top-notch plumber and successfully started his own plumbing company. He worked long hours starting early each morning.
He was contacted by a long-time client to do plumbing work in a new business that was opening in a strip mall in Kirkland, Washington. The lease space had been partially demolished, and he needed to install some piping in one of the back walls of the space. He arrived very early one morning to accomplish the task.
He went to the back corner of the space and began his work. Without warning or any notice, the floor gave way beneath him. Phil landed on the concrete garage floor beneath the lease space, a drop of about 30 feet.
Personal Injury Sustained
Landing directly on both feet, he suffered serious injuries and multiple fractures. He could not move and was in extreme pain. He called for help and finally after over an hour, a person walking by the area heard him and came to his aid. He was rushed to a local hospital.
Most personal injury cases investigate the possibility of traumatic brain injury, regarded as severe harm or serious injury under injury law.
What is Considered Traumatic Brain Injury?
Traumatic brain injury law deals specifically with cases where an accident or incident has led to traumatic brain injury. This may be of a result of a car accident, personal injury or physical assault for example. Traumatic brain injury lawyers are experienced with handling these cases and ensuring a favorable outcome for the victim and/or the family of the brain injury victim.
Contact Personal Injury Lawyers Immediately
Although this was not an intentional act, an injured person in such a case has a right to a personal injury claim settlement.
Phil turned to our law firm for representation from our proactive personal injury lawyers, who have represented several personal injury cases.
After several surgeries and medical treatment, he began the process of healing and rehabilitation from his serious injury.
Tough and determined, Phil returned to work in a wheelchair and supervised his employee, continuing his job commitments.
A Personal Injury Law Firm Determines Liability
After being retained, our personal injury law firm immediately went to the strip mall to talk with other business owners about the lease space.
Sure enough, we found out that there had been major water leaks in the space over the past several years.
Those leaks and the failure of the landlord to inspect and maintain the wood flooring resulted in a substantial amount of rot in the flooring and subflooring.
Structural Damage Discovered
It was the structural weaknesses and subsequent property damage that caused Phil to fall through the floor and onto the concrete below and his injuries.
Successful Personal Injury Claims
With the discovery of said structural negligence, the deposition of the landlord, and retained experts, we were able to reach a compensation settlement of nearly $3,000,000 for personal injury, associated medical expenses, and other punitive damages.
Phil returned to his successful plumbing business after his personal injury case, which has continued to grow, despite his serious injury.
Free case evaluation with Personal Injury Lawyers
At Coluccio Law firm , we offer free case evaluation for personal injury cases due to a car accident, medical malpractice, or personal injury cases due to other types of negligence.
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AI offers ‘paradigm shift’ in Stanford study of brain injury
By helping researchers choose among thousands of available computational models of mechanical stress on the brain, AI is yielding powerful new insight on traumatic brain injury.
From the gridiron to the battlefield, the study of traumatic brain injury has exploded in recent years. Crucial to understanding brain injury is the ability to model the mechanical forces that compress, stretch, and twist the brain tissue and causing damage that ranges from fleeting to fatal.
Models discovered by the Constitutive Artificial Neural Network outperform existing models for brain tissue. (Image credit: Ellen Kuhl)
Researchers at Stanford University now say they have tapped artificial intelligence to produce a profoundly more accurate model of how deformations translate into stresses in the brain and believe that their approach could reveal a more definitive understanding of when and why concussion sometimes leads to lasting brain damage, and other times not.
“The problem in brain modeling to date is that the brain is not a homogeneous tissue – it’s not the same in every part of the brain. Yet, trauma is often pervasive,” said Ellen Kuhl , professor of mechanical engineering, director of the Living Matter Lab , and senior author of a new study appearing in the journal, Acta Biomaterialia . “The brain is also ultrasoft, much like Jell-O, which makes both testing and modeling physical effects on the brain very challenging.”
Going to the library
Researchers who want to study brain trauma are forced to select from a library of dozens of material models, some dating back almost a century, to help calculate the stresses on the brain.
For decades, scientists have developed these models for soft materials with inscrutable names like the “neo-Hookean Model for Plastics and Rubber,” the “Demiray Model for Soft Tissues,” and the “Ogden Model for Rubber-like Solids.” But a model that works for a certain type of stress – tension, compression, or shear – may not work for another. Or, a model that might work for one region of the brain, might not for another.
The new approach takes a model-of-models tack, using artificial intelligence to discover which model, out of more than 4,000 possibilities, best explains the behavior of the brain. In the past, selecting the best model was a hit-or-miss process that depended largely on user experience and personal preference.
“We take user selection out of the equation by allowing machine learning to examine the data and decide which model works best,” adds Sarah St. Pierre , a doctoral scholar in Kuhl’s lab and a co-author of the paper. “Automating this process lowers barriers to model the brain. Now, every Stanford student can do this!” Once machine learning has discovered the best model, it’s easy to relate it back to the models that generations of researchers have proposed.
Transformative insights
The approach, known as a Constitutive Artificial Neural Networks, was developed by Kevin Linka before he joined the Living Matter Lab as a postdoc to apply his method to the brain.
Out of 4095 possible models, the network autonomously discovers the model and parameters that best explain the stresses in human brain tissue. (Image credit: Sarah St. Pierre)
“We provide the network all existing constitutive models developed over the last century. And the AI does a mix-and-match to find the best option. This is impossible to do by hand,” Linka said. “Now, we’ve effectively discovered a new model that makes us more confident in studying the mechanical stress in the brain.”
Unlike conventional off-the-shelf neural networks, Constitutive Artificial Neural Networks provide novel insights into the physics of the brain. As but one example, the team notes that they have pinpointed physically meaningful parameters, such as varying shear stiffnesses in four different regions of the brain – the cortex, basal ganglia, corona radiata, and corpus callosum – at precisely 1.82, 0.88, 0.94, and 0.54 kilopascals each.
The shear modulus relates the force from a hit to the head, for instance, to the resulting deformation of the brain tissue. By these measures, the cortex – the gray, outer layer of the brain – is more than three times as stiff as the corpus callosum, the network of nerves connecting the two hemispheres of the brain.
With such improved knowledge, brain trauma researchers can more accurately simulate and understand where in the brain trauma originates. This could inspire the design of new protective equipment or treatments that promote healing. To translate this knowledge into engineering practice, Kuhl’s group has collaborated with a major simulation software company, Dassault Systemès Simulia, to integrate automated model discovery directly into their analysis workflow.
“What’s really most exciting about this research,” Kuhl said, “is that Constitutive Artificial Neural Networks could induce a paradigm shift in soft tissue modeling, from user-defined model selection to automated model discovery. This could forever change how we simulate materials and structures.”
This work was supported by a German Academic Exchange Service (DAAD) Fellowship, by a National Science Foundation Graduate Research Fellowship, by the Stanford School of Engineering Covid-19 Research and Assistance Fund, and by a Stanford Bio-X IIP seed grant.
To read all stories about Stanford science, subscribe to the biweekly Stanford Science Digest .
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March 1, 2023
AI offers 'paradigm shift' in study of brain injury
by Andrew Myers, Stanford University
Going to the library
Transformative insights
More information: Kevin Linka et al, Automated model discovery for human brain using Constitutive Artificial Neural Networks, Acta Biomaterialia (2023). DOI: 10.1016/j.actbio.2023.01.055 Journal information: Acta Biomaterialia
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Does the Addition of a “Black Bone” Sequence to a Fast Multisequence Trauma MR Protocol Allow MRI to Replace CT after Traumatic Brain Injury in Children?
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BACKGROUND AND PURPOSE: Head CT is the current neuroimaging tool of choice in acute evaluation of pediatric head trauma. The potential cancer risks of CT-related ionizing radiation should limit its use in children. We evaluated the role of MR imaging, including a “black bone” sequence, compared with CT in detecting skull fractures and intracranial hemorrhages in children with acute head trauma.
MATERIALS AND METHODS: We performed a retrospective evaluation of 2D head CT and brain MR imaging studies including the black bone sequence of children with head trauma. Two experienced pediatric neuroradiologists in consensus created the standard of reference. Another pediatric neuroradiologist blinded to the diagnosis evaluated brain MR images and head CT images in 2 separate sessions. The presence of skull fractures and intracranial posttraumatic hemorrhages was evaluated. We calculated the sensitivity and specificity of CT and MR imaging with the black bone sequence in the diagnosis of skull fractures and intracranial hemorrhages.
RESULTS: Twenty-eight children (24 boys; mean age, 4.89 years; range, 0–15.5 years) with head trauma were included. MR imaging with the black bone sequence revealed lower sensitivity (66.7% versus 100%) and specificity (87.5% versus 100%) in identifying skull fractures. Four of 6 incorrectly interpreted black bone MR imaging studies showed cranial sutures being misinterpreted as skull fractures and vice versa.
CONCLUSIONS: Our preliminary results show that brain MR imaging complemented by a black bone sequence is a promising nonionizing alternative to head CT for the assessment of skull fractures in children. However, accuracy in the detection of linear fractures in young children and fractures of aerated bone remains limited.
- ABBREVIATIONS:
CT is the initial neuroimaging technique of choice for the acute evaluation of pediatric head trauma due to its wider availability, lower cost, and short acquisition time. In addition, CT identifyies most traumatic injuries that require urgent treatment and correlates well with clinical scales and outcome. 1 However, CT-related ionizing radiation involves the potential risk of patients developing cancer and strongly argues in favor of alternative neuroimaging techniques such as MR imaging. 2 The lifetime cancer mortality risk attributable to the radiation from a single CT scan of the head in a 1-year-old child has been estimated as 0.07%. This small risk translates into a large population-level risk, especially because head trauma in children from 0 to 14 years of age accounts for nearly half a million emergency department visits in the United States annually. 3 , 4
MR imaging is a nonionizing technique that provides superior contrast resolution and has a higher sensitivity and specificity for parenchymal lesions compared with CT. 3 , 4 Especially, advanced MR imaging techniques (DWI, SWI) provide additional information that correlates well with outcome. 5 , 6 Nonhemorrhagic shear injuries and subtle microhemorrhages are typically seen with higher sensitivity by MR imaging compared with CT. Nevertheless, the role of MR imaging in the acute diagnostic work-up of head trauma in children is still limited. 2 , 7 , 8 This limitation may be partially explained by longer acquisition times and the subsequent need for sedation as well as the low sensitivity of MR imaging for skull fractures. 2 , 8 Recently, black bone MR images have been introduced as a new sequence for the evaluation of structural bony abnormalities such as craniosynostosis. 9
On the basis of the inherent diagnostic quality of the black bone sequence, we aimed to determine whether a trauma brain MR imaging protocol with an included black bone MR image could be an alternative to head CT in the acute work-up of children with head trauma. To address our goal, we compared the diagnostic accuracy of brain MR imaging including the black bone sequence with CT for the detection of skull fractures after traumatic brain injury in children. Images were also studied for coexisting intracranial lesions.
- Materials and Methods
This single-center retrospective study was approved by the Johns Hopkins Hospital institutional research ethics board, which waived informed consent.
Study Population
Inclusion criteria were the following: 1) a history of head trauma; 2) the availability of thin-section (≤3 mm) 2D head CT data and a brain MR imaging study including a black bone sequence acquired within 7 days of each other, and 3) age at neuroimaging younger than 18 years. The exclusion criteria were the following: 1) susceptibility artifacts on a black bone sequence due to implanted materials, and 2) a brain MR imaging study acquired after craniotomy. Data from eligible children were obtained through an electronic search of our pediatric neuroradiology data base covering the period between January 1, 2015 (date when black bone MR imaging was introduced in our hospital), and November 15, 2015.
Image Acquisition
All CT studies performed at our radiology department were acquired on a commercially available 2 × 128 detector system (Somatom Definition Flash; Siemens, Erlangen, Germany) using the institutional pediatric head CT protocol, including the following parameters: tube voltage,120 kV; tube current, 380 reference mA; rotation time, 1.0 second; axial acquisition; 0.75-mm section thickness; FOV, 160 × 160 to 250 × 250 mm. No intravenous injection of a contrast agent was performed. The CT studies imported to our neuroradiology data base from outside hospitals and officially reviewed by our pediatric neuroradiologists met the inclusion criteria if the studies were performed with a section thickness of ≤3 mm.
The brain MR imaging studies were performed on a 1.5T (Magnetom Aera; Siemens) or 3T (Magnetom Skyra; Siemens) clinical scanner using a standard pediatric 16-channel head coil. The institutional pediatric head trauma MR imaging protocol includes a 3D T1-weighted sequence with a sagittal acquisition, an axial T2-weighted sequence, axial FLAIR, DTI, and SWI. In addition, a black bone sequence was acquired in the axial plane from above the skull vertex to below the mandible, with 2D reconstruction in the coronal and sagittal planes. The black bone sequence is a gradient-echo sequence with short TEs and TRs and an optimal flip angle for the differentiation of bone from soft-tissue contrast (TE, 4.20 ms; TR, 8.60 ms; flip angle, 5°; FOV, 240 mm; section thickness, 1.00 mm; section spacing, 0.2 mm). 10 Signal from fat and water is suppressed to provide uniform soft-tissue contrast, thereby optimizing the visualization of the bone–soft tissue margin. 10 , 11
Image Analysis
Both the CT and MR imaging datasets were evaluated for the presence of skull fractures and intracranial hemorrhages. Additionally, the fracture type was classified into linear, depressed, or basilar, and the type of intracranial hemorrhage was subdivided into subdural, epidural, subarachnoid, intraparenchymal, intraventricular, and mixed (>1 type of intracranial hemorrhage). 3 , 4
The standard of reference for the diagnosis of a skull fracture and/or posttraumatic intracranial hemorrhage was established by consensus interpretation of 2 experienced pediatric neuroradiologists with 14 and 22 years of experience (A.T. and T.A.G.M.H.). The complete CT datasets, including 2D and, if available, 3D images, and the full MR imaging datasets were reviewed to create the standard of reference.
The study reader was a pediatric neuroradiologist with 7 years of experience (T.B.). The reader was blinded to the medical records, clinical examination findings, previous neuroimaging studies, and final diagnosis. In a first reading session, he evaluated the available MR imaging studies of all patients in a random order. The reader first assessed the presence, location, and type of skull fractures using only the black bone sequence. After this initial assessment, the reader could use the other available sequences to identify posttraumatic intracranial lesions. No adjustments were made to the black bone interpretation score after the assessment of the intracranial lesions. In a second independent reading session 30 days after the first session, the 2D-CT studies were evaluated in a different random order. The first author (M.H.G.D.) assisted the study reader by opening only the relevant images for each reading session and entering the results of the evaluation on an anonymized data sheet. The black bone images were reviewed in regular and inverted format. Empirically, the inverted MR imaging window level setting resembles the classic bone CT appearance best.
Statistical Analysis
The independent evaluations of the CT images and MR imaging datasets (including the black bone sequence) from the study reader were compared with the standard of reference to analyze the diagnostic accuracy. To compare the CT and MR imaging data for the presence of skull fractures and intracranial hemorrhages, we used 2 × 2 contingency tables. The decision to report the presence or absence of skull fractures or intracranial hemorrhages was considered as, respectively, a true-positive or true-negative result when it matched the consensus reading of the standard of reference or as, respectively, a false-positive or a false-negative result when it did not match the reading of the standard of reference. To calculate sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), we correlated the specific decisions (true-positive, false-positive, true-negative, or false-negative) with the total decisions for the study reader. For both 2D head CT and brain MR imaging including the black bone sequence, the sensitivity, specificity, PPV, and NPV were calculated for the detection of skull fractures only, intracranial hemorrhages only, and skull fractures and/or intracranial hemorrhages combined (representing whether the neuroimaging study findings were normal for fractures and hemorrhages). Finally, the sensitivity, specificity, PPV, and NPV of brain MR imaging including the black bone sequence in the detection of skull fractures were calculated for 2 different age groups, children up to 2 years of age (with relatively wide cranial sutures) and older than 2 years of age, and for children with MR imaging studies performed on 1.5T and 3T MR imaging scanners, respectively.
Twenty-eight children (24 boys and 4 girls) with acute head trauma met the inclusion criteria for this study. The mean age of the children at the first neuroimaging study was 4.89 years (range, 6 days to 15.5 years). None of the patients died. Fourteen children (50%) were younger than of 2 years of age. The field strength of the MR imaging scanner was 1.5T in 12 children and 3T in 16 children. For 7 children (25%), anesthesia was necessary to perform MR imaging. The mean time interval between the CT and MR imaging was 2 ± 1.43 days (range, 0–6 days).
Imaging Analysis
On the basis of the standard of reference, 12 children had skull fractures (43%) and 22 children (79%) had intracranial hemorrhages. The different types of skull fractures and intracranial hemorrhages are shown in Table 1 . Six children with a skull fracture were younger than 2 years of age. Twenty-two of 28 children (79%) had at least a skull fracture and/or an intracranial hemorrhage (all children with a skull fracture had an intracranial hemorrhage).
- View inline
Number and types of skull fractures and intracranial hemorrhages detected on axial 2D head CT and brain MRI including the black bone sequence in 28 children with head trauma
The sensitivity, specificity, PPV, and NPV for 2D head CT and brain MR imaging including the black bone sequence for detecting skull fractures, intracranial hemorrhages, and skull fractures and/or intracranial hemorrhages combined are shown in Table 2 . The 2D head CT had a higher sensitivity, specificity, PPV, and NPV compared with brain MR imaging including the black bone sequence for the detection of skull fractures, while brain MR imaging including the black bone sequence had a higher sensitivity, specificity, PPV, and NPV compared with 2D head CT for the detection of skull fractures and/or intracranial hemorrhages combined.
Diagnostic accuracy of axial 2D head CT compared with brain MRI including the black bone sequence for the detection of skull fractures, intracranial hemorrhages, and skull fractures and/or intracranial hemorrhages combined in 28 children with head trauma
The sensitivity, specificity, PPV, and NPV for brain MR imaging including the black bone sequence in detecting skull fractures dependent on the age of the children at neuroimaging and the magnetic field strength of the MR scanner are shown in Table 3 . In children younger than 2 years of age, the sensitivity and NPV for brain MR imaging including the black bone sequence in detecting skull fractures were higher and the specificity and PPV were lower compared with children older than 2 years of age. In children with brain MR imaging acquired on a 1.5T MR imaging scanner, the sensitivity, PPV, and NPV for brain MR imaging including the black bone sequence in detecting skull fractures were higher and the specificity was lower compared with children with brain MR imaging acquired on a 3T MR imaging scanner.
Differences in diagnostic accuracy of brain MRI including the black bone sequence for the detection of skull fractures in 28 children with head trauma, depending on the age of the child and MR imaging field strength
Skull fractures are relatively common in children with head trauma (up to 30%), particularly in the younger age groups. 12 , 13 Morphologically, skull fractures can be described as linear, depressed, or basilar (skull base). Most skull fractures are linear (66%–75%). 14 , 15 Although isolated fractures themselves rarely require intervention, a neuroimaging study may be needed to describe the full extent of calvarial and intracranial injuries. 16
Black bone is a novel MR imaging sequence that uses short TEs and TRs as well as an optimal flip angle to minimize soft-tissue contrast and enhance the bone–soft-tissue boundary. 9 ⇓ – 11 , 17 Signal from fat and water is suppressed to provide uniform soft-tissue contrast, thereby optimizing the visualization of the bone–soft-tissue interface. 10 , 11 The short TEs and TRs and the volume acquisition result in short imaging times. Black bone MR imaging has been shown to be useful and accurate in the evaluation of cranial bones and sutures in children with craniosynostosis. This finding reveals a considerable clinical potential in the assessment of osseous abnormalities as a nonionizing alternative to CT. 9 ⇓ – 11 , 17
Our study evaluated the diagnostic accuracy of black bone MR imaging in detecting skull fractures in children with head trauma compared with CT. The black bone MR imaging sequence showed a sensitivity of 66.7% and a specificity of 87.5% in the detection of skull fractures ( Fig 1 ). The specificity is acceptable, while the sensitivity is low. To determine the reasons for the low sensitivity of the black bone MR imaging sequence, we studied the 4 false-negative linear fractures and the 2 false-positive linear fractures. In 2 children younger than 2 years of age, false-negative linear fractures were misinterpreted as cranial sutures (2 false-negative cases). Furthermore, the 2 false-positive cases were children in the younger age group (younger than 2 years), with cranial sutures being falsely identified as linear fractures. In young children, the presence of open sutures is known to increase the diagnostic uncertainty of skull fractures on 2D images as recently shown by a head CT study. 14 In head CT studies, the addition of 3D reconstructions to the 2D dataset has been shown to increase the reader's confidence for correct differentiation of sutures and other nonfracture-related linear lucencies such as vascular channels versus linear fractures. 14 The addition of 3D reconstruction to the 2D black bone MR images as shown for the study of craniosynostosis 9 could potentially decrease the misinterpretation as shown for head CT.
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A , Axial CT image shows a nondisplaced linear fracture of the right parietal bone ( arrow ) with extracranial soft-tissue swelling. Black bone ( B ) and inverted black bone ( C ) MR images reveal equivalent visualization of the right parietal fracture ( arrows ), as well as overlying soft-tissue swelling.
The third false-negative case was an older child in whom a linear fracture was misinterpreted as a venous transosseous vascular channel. More familiarity with the black bone sequence and the use of 3D reconstruction could potentially help overcome this problem. The fourth case of a missed linear fracture on black bone MR imaging was a fracture in the mastoid region ( Fig 2 ). This case highlights the main limitation of black bone MR imaging: In anatomic regions where bone abuts air (mastoid, craniofacial sinuses), the distinction between air and bone is difficult because both have low signal intensity on this sequence. 10 The application of black bone MR imaging at air-bone interfaces is challenging and requires experience with the technique and careful review of the images.
A , Axial CT image shows 2 small nondisplaced linear fractures of the mastoid ( arrows ). On black bone ( B ) and inverted black bone ( C ) MR images, these fractures are barely visible ( arrows ).
The fractures missed on black bone MR images were linear and nondisplaced and did not require specific treatment. Fractures of the mastoid air cells and temporal bone region are potentially of major clinical concern; in case of suspected CSF leaks, damage to inner/middle ear structures, and vascular injury, CT is needed. Further improvement of the black bone imaging technique is necessary for implementation of this technique to all neurotrauma patients. Isolated, linear, nondisplaced skull fractures are known to have a low clinical significance: They are not associated with neurologic deterioration, affected children can be appropriately managed as outpatients, and neurologic outcome is excellent. 2 , 18 A precise and complete diagnosis in children with head trauma is important (eg, for medical legal purposes); therefore for the work-up of nonaccidental trauma or for other carefully selected pediatric patients, an additional head CT study may be necessary if the black bone MR images are negative for identification of skull fractures. In most cases, the missed diagnosis of an isolated, linear skull fracture appears to have low clinical significance and no impact on the management of the affected children.
By using MR imaging including the black bone sequence as a primary screening tool in patients with neurotrauma, the number of CT studies in the pediatric population can be decreased. The identification of intracranial hemorrhages, on the other hand, has important implications for acute management and long-term outcome of children with head trauma. 3 , 4 , 19 Our study reveals a higher sensitivity (100% versus 72.7%) and specificity (100% versus 83.3%) of MR imaging including black bone sequence compared with head CT in detecting intracranial hemorrhages in children with head trauma ( Fig 3 ). The higher sensitivity and specificity of MR imaging is not surprising: The superior contrast resolution of MR imaging compared with CT results in a higher sensitivity for parenchymal lesions. 20 The implementation of SWI as part of the MR imaging protocol for children with head trauma further increases the sensitivity for detection of intracranial hemorrhages. Additionally, a strong correlation has been shown between the number and volume of SWI lesions and the severity of injury (determined by the initial Glasgow Coma Scale score and the duration of the coma) as well as neurologic outcome 6–12 months after the injury. 21 These results emphasize the importance of MR imaging in the acute work-up of children with head trauma. In our opinion, MR imaging as a nonionizing imaging technique should not only be an important alternative to CT in the acute evaluation of pediatric head trauma but also gradually become the main neuroimaging technique for the evaluation of traumatic skull and brain injury in the pediatric population. Specifically, the combination of highly sensitive MR imaging sequences for identification of intracranial and intra-axial lesions with a relatively sensitive MR image for clinically relevant fractures offers a diagnostically important “one-stop shopping” imaging approach. In our institution, we currently use a fast trauma head MR imaging, which combines the black bone MR image with 3D T1-weighted, axial HASTE T2-weighted, axial DWI, and SWI sequences.
A , Axial CT image does not show intracranial hemorrhage. A matching axial T2-weighted MR image ( B ), axial trace of diffusion ( C ), ADC map ( D ), minimal intensity projection–SWI ( E ), and inverted black bone MR image ( F ) reveal areas of T2-hyperintense signal and restricted diffusion within the temporal white matter ( arrows in B–D ), areas of restricted diffusion within the right frontal lobe and splenium of the corpus callosum ( arrows in C and D ), and foci of hypointense SWI signal within the right frontal white matter ( arrows in E ), suggestive of intracranial hemorrhages and diffuse axonal injury not seen on axial CT.
Our results show a negative correlation between the sensitivity of black bone MR imaging and the magnetic field strength of the MR imaging scanner: 83% in 1.5T versus 50% in 3T. The short TE and TR cause the black bone sequence to be a gradient-echo sequence, hence susceptible to artifacts. Movement artifacts, dental braces, and implanted materials (ie, ventriculoperitoneal shunt reservoirs) can potentially degrade image quality and decrease the sensitivity of the study, particularly at 3T due to higher amenability to susceptibility artifacts in 3T datasets. In addition, our study reveals a lower specificity for black bone MR imaging in children younger than 2 years of age compared with older children. This difference is most likely due to the confounding role of open cranial sutures in younger children as shown for head CT data. 14
We acknowledge the limitations of our study, including the small number of patients and its retrospective nature. In addition, the standard of reference was established by experienced pediatric neuroradiologists using all available images (CT and MR imaging), as is typical in daily routine. We had no postmortem studies because all patients survived. Furthermore, head CT and brain MR imaging data were not acquired on the same day in some patients. The optimal study design to compare the diagnostic accuracy of CT and MR imaging datasets would require the acquisition of CT and MR imaging studies on the same day. However, in this retrospective study, this was not feasible due to both practical and ethical reasons. Future prospective research should focus on optimizing the study design to avoid selection bias. For 7 children, anesthesia was necessary to perform brain MR imaging. This was partly because most of the study population was younger than 6 months of age or older than 5 years and the MR imaging examination could be performed with the patient in a vacuum cushion or after preparing and coaching the child and the parents/caregivers, respectively. The increasing availability of child life specialists may further help decrease the need for anesthesia for brain MR imaging in the future. Finally, brain MR imaging examinations were obtained for clinical indications on the basis of the head CT findings or neurologic symptoms not explained by the head CT findings. This choice may have been a potential source of selection bias in our study population. A prospective study design in which CT and MR imaging studies are performed in all pediatric trauma patients is needed for further evaluation of MR imaging as a primary neuroimaging screening tool in the pediatric population.
- Conclusions
Our preliminary results show that brain MR imaging including the black bone sequence may be a promising alternative to head CT as a primary screening tool for the acute diagnostic work-up of children with head trauma. The higher sensitivity and specificity of MR imaging in detecting intracranial hemorrhages compared with CT highlights the key role of MR imaging for acute management and prognosis of long-term outcome of children with head trauma. The lack of ionizing radiation further supports the use of brain MR imaging as the primary neuroimaging tool for acute head trauma in the pediatric population. Currently, additional head CT studies are indicated for patients without identifiable skull fracture on the black bone sequence because of the possibility of missing certain types of skull fractures. Prospective studies with a larger number of children are needed to further evaluate the diagnostic role of black bone MR imaging in children with acute head trauma. Furthermore, the value of a fast trauma MR imaging protocol should be prospectively evaluated for the wide range of posttraumatic lesions that may be encountered in the brain, including diffuse axonal injury, nonhemorrhagic contusions, and tissue lacerations.
- Acknowledgments
We thank and dedicate this study to our friend and exceptionally gifted and talented colleague Dr Andrea Poretti for providing his insight and expertise. We are immensely grateful for his dedication to the field of pediatric neuroimaging. He left us too early, and we will miss his sharp intellect, humble character, and relentless effort to advance our understanding of pediatric neurologic diseases.
Disclosures: Marjolein H.G. Dremmen— UNRELATED : Employment : Pediatric Radiologist, Erasmus Medical Center Rotterdam, Comments : 3-month observing fellowship in pediatric neuroradiology, Johns Hopkins Hospital (unpaid). Thangamadhan Bosemani— UNRELATED : Consultancy : Alexion Pharmaceutical. Thierry A.G.M. Huisman— UNRELATED : Board Membership : Editorial Board American Journal of Neuroradiology .
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- Received September 6, 2016.
- Accepted after revision June 10, 2017.
- © 2017 by American Journal of Neuroradiology
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