In this Blog category you will find articles about accidents that result in brain injuries and how to avoid them. Personal Injury suits and insurance claims may require the help of an attorney. A good lawyer can protect your rights under the law.
A traumatic brain injury (TBI) is a life-altering and costly event. Those who have had severe or repeated traumatic brain injuries may have long-lasting problems with movement, learning, or speaking, which require full initial and ongoing assessment and care. Due to the expense of obtaining assessment, evaluation, and ongoing treatment of these cases, high-dollar verdicts in traumatic brain injury (TBI) cases can reach the six- and seven-figure level.
Making the Case for TBI Reimbursement
To prepare for negotiation with defendants and insurers in court or at settlement, a plaintiff’s lawyer receiving a TBI case must produce a Cost of Future Care report, also called a Future Care Assessment or a Life Care Plan to determine the limitations and losses of the client-patient. The Cost of Future Care report considers the severity of the TBI which has been established through assessment tests, and legal reports, medical opinions and technical accident details. To produce a long term needs analysis, the lawyer then researches and consults with relevant experts regarding the client’s prognosis.
Screening and Assessment to Determine Extent of TBI Injury
A doctor initially examining a TBI patient will ask questions to test the patient’s ability to pay attention, learn, remember and solve problems, and will check the patient’s reflexes, strength, balance, coordination and sensation. The doctor may also order imaging tests, such as a CT scan or an MRI to visually assess damage. Periodic, ongoing assessment for months or longer of those with a TBI is important to monitor responses to rehabilitation and to life after the injury.
Once a diagnosis of traumatic brain injury has been established, further screening assessments are performed to evaluate the extent of damage and assist in establishing a comprehensive treatment plan. Screening is conducted by a speech-language pathologist, audiologist, or other professionals.
A speech-language pathologist tests a TBI patient’s speech, language, communication, and swallowing. The speech-language pathologist may also perform a hearing screening. If the patient shows hearing loss, an audiologist may be added to the screening team to further assess hearing loss.
Since depression can be a consequence of neurological damage or part of post-traumatic stress disorder, which often accompanies a TBI, if signs and symptoms of depression are present or suspected, the patient is referred to a neuropsychologist, clinical psychologist, or psychiatrist for further assessment.
Awareness of the link between concussions in sports activities began when former football players committed suicide after suffering the effects of traumatic brain injury on the field. New data shows that soccer players are also at high risk for traumatic brain injury.
Hockey, lacrosse, boxing, baseball, skateboarding, skiing, and horseback riding expose players to head injury, but soccer players are at greater risk of suffering degenerative damage, due to the number of repeated hits to the head.
Whether in practice games or competition, soccer players who frequently “head” the ball are three times more likely to have concussion symptoms than players who don’t experience large numbers of headers, according to a study published in the journal Neurology. When a bump or jolt to the head or a hit to the body causes the head and brain to move rapidly back and forth, the brain bounces against the inside of the skull. Soccer players routinely experience a large number of head-to-head collisions, head-to-knee collisions, and head-to-field collisions on the field, with the potential for repetitive concussions.
Research Reveals Brain Damage from Soccer Heading and Collisions
Researchers from the University College London and Britain’s National Hospital for Neurology and Neurosurgery studied 14 brains of former soccer players who developed dementia and had signs of Alzheimer’s disease. Of those 14 studied, 4 (29 percent) had chronic traumatic encephalopathy (CTE) pathology, a consequence of repeated impacts to the brain, including heading the ball and concussion from head-to-head collisions. A previous study of 268 brains from the general population in Britain found a far lower CTE detection rate of only 12 percent. Earlier studies, where researchers compared soccer players to swimmers showed that swimmers’ brains looked perfectly normal while soccer players’ brains had abnormalities in the white matter fiber tracts that carry messages throughout the brain. If the brain is violently shaken enough, there tends to be disruption of those fiber tracts. Another study from Purdue University found that heading of goal kicks and hard shots are as damaging as helmet-to-helmet impact in football.
When Is Concussion More Likely to Occur
A number of biological factors determine whether or not a hit to the head will lead to a concussion:
- How many concussions a person has had before
- How severe those previous concussions were and how close together they occurred
- Neck strength (a strong neck supporting the head reduces the chance of concussion)
- Hydration status (if you are dehydrated you are more likely to have a concussion)
- Gender (women are more easily concussed than men)
- Age (it is easier to concuss at an earlier age than at an adult age and recovery is slower)
Myelin that coats white matter fibers carrying brain messages is not as thick and strong in youngsters as in adults. Youngsters also have bigger heads in proportion to their bodies with very weak necks, compared to adults, giving them a bobblehead-doll effect that tends to cause damage.
Stroke-detecting technology using microwaves shows promise in detecting intracranial bleeding from traumatic brain injury.
Treatment for severe traumatic brain injuries (TBIs) characterized by bleeding in the brain (intracranial) requires opening the skull to release pressure and remove clotted blood, called a hematoma. The survival rate is only ten percent if the hematoma is not removed within four hours. Getting a patient with an intracranial hematoma to a neurosurgical center with radiology facilities for a CT scan in the shortest amount of time then becomes a matter of life and death.
“It’s not so much an issue of being able to do more for them (TBI patients) pre-hospital wise, it’s a question of triage, of transporting them to the right hospital, and that’s a huge problem,” said Mikal Elam, chair of clinical neurophysiology at the University of Gothenburg.
Stroke Detecting Device May Detect Hematoma from TBI
The goal has been to find a portable device to detect bleeding from TBI at low cost to convey diagnostic information in a fast, non-invasive, and safe manner. Researchers at Chalmers University of Technology in Sweden are now considering applying an already existing, light-weight (under 10 pounds), portable stroke-detecting device called a Strokefinder to quickly diagnose intracranial bleeding at the site of a traumatic brain injury.
Built by Medfield Diagnostics, the Strokefinder is a tool already used to differentiate between strokes without a clot blocking blood flow and those that involve bleeding. Medfield is collaborating with Chalmers’ and Gothenburg’s Sahlgrenska University Hospital on projects featuring the Strokefinder, believing doctors there would have a better idea of what they need than engineers at the company.
Here’s How It Works
The Strokefinder device a patient’s head is placed inside has eight microwave antennas on it, each one firing a small amount of microwave radiation through the brain (between 1/100th and 1/10th what you receive from a cell phone conversation), while the other antennas pick it up. The process is repeated at several different frequencies. The microwaves quietly progress through the tissue in different ways, depending on the consistency of the tissue, and are then filtered via an algorithm instead of an image, to enable the hematoma to stand out as either a stroke or a TBI. The patient can’t feel it working, and the entire process takes only 45 seconds. Once a hematoma is detected, the patient can be quickly transported to the correct hospital with a neurosurgical center.
Since Washington State passed the Zachery Lystedt law in 2009, each state has enacted legislation to protect young athletes from the risks associated with concussion in sport.
On October 2006, 13-year old Zachery Lystedt collapsed from a traumatic brain injury when he was allowed back into the game just fifteen minutes after suffering from a concussion and then spent months in a coma followed by years of rehabilitation. As a result of that event, Washington State enacted the first youth sports concussion safety law to address management in youth athletics, called the Zachery Lystedt law.
The key provisions of the Zachery Lystedt law are:
- School districts board of directors and state interscholastic activities associations must develop concussion guidelines and education programs.
- Youth athletes and a parent and/or guardian must sign and return a concussion and head injury information sheet on a yearly basis before the athlete’s first practice or before being allowed to compete.
- Youth athletes suspected of having sustained a concussion in a practice or game must be immediately removed from competition.
- Youth athletes who have been taken out of a game because of suspected concussion are not allowed to return to play until after:
- Being evaluated by a health care provider with specific training in the evaluation and management of concussions
- Receiving written clearance to return to plan from that health care provider
- A school district complying with the law is immune from liability for injury or death of an athlete participating in a private, non-profit youth sports program due to action or inaction of persons employed by or under contract with the sports program if:
- The action or inaction occurs on school property.
- The non-profit provides proof of insurance.
- The non-profit provides a statement of compliance with the policies for management of concussion and head injury in youth sports.
NFL Commissioner Urges State Governors to Enact Youth Concussion Laws
Following passage of the Zachery Lystedt law, in the spring of 2010, NFL Commissioner Roger Goodell sent a letter to 77 U.S. Governors to encourage them to push for concussion legislation to protect youth athletes in their states.
He said: “Given our experience at the professional level, we believe a similar approach is appropriate when dealing with concussions in all youth sports. That is why the NFL and its clubs urge you to support legislation that would better protect your state’s young athletes by mandating a more formal and aggressive approach to the treatment of concussions.”
States Pass Youth Concussion Laws Modeled after Zachery Lystedt Law
By 2013, all states except Mississippi had enacted youth sports concussion safety laws modeled after Washington State’s Zachery Lystedt law. Finally, in 2014 Mississippi became the 50th state to respond by passing legislation to protect young athletes from the risks associated with concussion in sport.
The three main tenets of each state’s concussion legislation are:
- To mandate educational outreach to coaches, parents and athletes
- To mandate immediate removal from play of any athlete who sustains a concussion or who exhibits signs, symptoms or behaviors consistent with the injury
- To only allow those athletes who exhibit such signs, symptoms, or behaviors to return to physical activity after receiving written clearance from an appropriate health care provider who is trained in concussion management
Many state laws also require parents to sign an acknowledgement form prior to allowing their child to play a contact sport after they have received information on concussion and acknowledged concussion risks involved with that sport.
Although nearly all laws include those three tenets, based on their own individual needs, many state laws vary on what sport programs must comply, what penalties exist for those who do not comply, and what medical providers are “appropriate” to make return to play decisions.
The 2017 lawsuit stated that Akorn Pharmaceuticals failed to note in its prescription warning labeling that its drug methylene blue would react adversely with antidepressant Effexor UR, which the woman was already taking when she was given methylene blue during a surgery. The adverse drug interaction caused her to go into a coma and suffer permanent brain damage.
FDA Drug Labeling Requirements
In 2006, the Federal Drug Administration (FDA) issued a prescription drug product labeling guidance for industry Drug makers, requiring them to list any adverse reactions that occur with a drug and with drugs in the same pharmacologically active and chemically related class. This is to ensure that information about adverse reactions are readily accessible for health care practitioners, to make correct prescribing decisions.
Drug makers and distributors are required to submit documentation about their products to the FDA. Product documentation must contain a summary of essential scientific information needed for the safe and effective use of the drug. The FDA then returns data from drug maker submissions to use for product labeling, including when to use the product and adverse reactions to it when used alone or with drugs in the same pharmacologically active and chemically related class.
Reported Adverse Events Trigger Methylene Blue Warning
Following adverse event reports from the FDA Adverse Event Reporting System (AERS) of serious central nervous system (CNS) reactions in patients administered methylene blue who were also taking serotonergic psychiatric medications, in 2011 the Federal Drug Administration (FDA) warned that “methylene blue should generally not be given to patients taking serotonergic drugs (antidepressants).” Reported adverse events were lethargy, confusion, delirium, agitation, aggression, and coma. They were frequently accompanied by the following neurological symptoms: muscle spasms, loss of ability to communicate, seizures, fever, and high blood pressure.
The FDA reports indicated that methylene blue could adversely react with serotonin-norepinephrine reuptake inhibitors (SNRIs) and other monoamine oxidase inhibitors (MAOIs) and psychiatric drugs, including Paxil, Zoloft, Prozac, Lexapro, Cymbalta, Celexa, Effexor, Wellbutrin, and Zyban.
Methylene Blue with Antidepressants Causes Serotonin Syndrome
Methylene blue inhibits the action of monoamine oxidase-A, an enzyme that breaks down serotonin, a naturally-occurring chemical in the brain that acts as an antidepressant. The FDA concluded that methylene blue administered along with antidepressants causes high levels of serotonin to build up in the brain, creating what is known as Serotonin Syndrome. Signs and symptoms of Serotonin Syndrome include mental changes (confusion, hyperactivity, and memory problems), muscle twitching, excessive sweating, shivering or shaking, diarrhea, trouble with coordination, and/or fever.
UCLA researchers have found a biological marker that can predict early on whether a child will experience further cognitive decline after a traumatic brain injury (TBI).
Children and adolescents who sustain traumatic brain injuries may either steadily progress toward normal, pre-injury functioning or suffer progressive cognitive decline. Nearly half of children who experience moderate to severe traumatic brain injuries show this decline, with resulting poor academic outcomes.
UCLA Study Finds TBI Outcomes Link
In a University of California at Los Angeles (UCLA) study published in the online issue of the medical journal Neurology, senior author Robert Asarnow from UCLA Department of Psychiatry and Behavioral Sciences reported that scientists are able to predict the outcomes of those who experience a traumatic brain injury. Using special MRIs and electroencephalograms (EEGs), scientists can now measure brain function by examining the speed of brain signals passing from one part of the brain to another. Asarnow said that, by understanding why and how kids develop neurodegeneration, doctors can use existing treatments or new ways to delay the process.
The researchers conducted the study on 21 children aged eight to 18 with moderate to severe traumatic brain injuries acquired through auto-pedestrian accidents, motor vehicle accidents, and falls. The subjects were assessed twice using MRI and EEG: the first assessment was two to five months after injury and the second was 13 to 19 months post-injury. The results of the assessments were compared with children of the same age who did not experience traumatic brain injury.
TBI patients who had healthy white matter or normal signaling between brain hemispheres shown on MRI progressed more favorably compared to those with significantly slower signaling, who showed progressive decline. Progressive decline would cause poor academic outcomes and adverse effects on other areas of their lives.
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Recent studies indicate that the harmful effects of a traumatic brain injury are more severe when there have been previous brain injuries, and the life altering damage from multiple TBIs can lead to suicide immediately after the event or even years later.
Study Links Multiple TBIs with Suicide
Craig Bryan, assistant professor of psychology at the University of Utah and associate director of the National Center for Veterans Studies, studying active-duty soldiers in Iraq in 2009, gathered data about their suicidal thoughts after returning to base with traumatic brain injuries. Bryan’s study, published in the medical journal JAMA Psychiatry in 2013, found that one in five patients, about 22 percent, who had experienced more than one traumatic brain injury (TBI) reported thoughts or preoccupation with suicide, compared to 6 percent of patients with only one TBI.
Soldiers in Bryan’s study with multiple TBIs were injured either in previous deployments or before enlistment, with some reporting as many as six sports related head injuries before enlisting. About 20 percent of service members sustained concussions during basic training. While deployed, some service members experienced as many as 15 TBIs, usually in an IED attack.
The Defense Department has estimated that 266,810 of the 1.6 million service members who served in Iraq and Afghanistan received a traumatic brain injury between 2000 and 2012. A 2008 Rand Corporation study estimated the number of TBIs much higher at 400,000. All five branches of the service have dealt with high suicide rates in recent years. In 2011, 303 active-duty service members killed themselves, and in 2012 the number increased to 349. Considering those statistics, a soldier is more likely to die from suicide than from war injuries.
Risk of Suicide Greater with Mild TBI
Bryan said his data and other studies also suggest that mild head injuries tend to be more likely to lead to suicidal thoughts than more severe ones, possibly because those who sustain a mild TBI don’t take time for a complete recovery. Although the military screens all at-risk service members for concussions, according to its protocol for handling TBI, those with mild head injuries return to the field within five days. Bryan concluded that the military needs to allow more time for recovery and do more to screen those with TBIs for personal risk factors for suicide.
Data recently collected and reviewed from soldiers serving in Afghanistan and Iraq who sustained a traumatic brain injury reveals a correlation between Traumatic Brain Injury (TBI) and Post-traumatic Stress Disorder (PTSD).
In observance of March 2017 Brain Injury Awareness Month, researchers at the Uniformed Services University of the Health Sciences (USU) and the Defense and Veterans Brain Injury Center published this month in the journal Neurology results of their study “Epidemiology and Prognosis of mTBI in Returning Soldiers: A Cohort Study.”
Reviewing data from screenings for Traumatic Brain Injury (TBI) of about 1,500 soldiers returning from Afghanistan and Iraq between 2009 and 2014, the researchers found that nearly 50% of recently-deployed soldiers who sustained TBI reported at least one severe or very severe post-concussive symptom three months after returning home. Symptoms included headaches, sleep disturbances, forgetfulness, irritability, and trouble concentrating. Consistent with prior research, the study found that many of the soldiers with TBI also reported concurrent health issues such as post-traumatic stress.
Earlier Study First to Establish TBI PTSD Link
Findings published February 15, 2012 in the journal Biological Psychiatry following data collected from the 2012 Marine Resiliency Study (MRS), funded by the National Institutes of Health, US Department of Defense, and UCLA Brain Injury Research Center, showed the first evidence of a causal link between TBI and increased susceptibility to Post-traumatic Stress Disorder (PTSD). The researchers theorized that PTSD could be a reaction to the same event that caused the TBI. Findings from lab research in the study showed that brain injury effects a part of the brain called the Amygdala, leaving it in a more excitable state, in preparation for more trauma.
The main causes of TBI in the military are blasts, motor vehicle accidents, and gunshot wounds. Most soldiers in the study reported having experienced one or more TBI before their most recent deployment, either before joining the military or during an earlier deployment. The rate of PTSD after brain injury is much higher in veterans than civilians due to multiple and prolonged exposure to combat, and symptoms last much longer (18-24 months on average) after the TBI.
Comparing TBI with PTSD Symptoms
While TBI is a neurological disorder caused by trauma to the brain, PTSD is a mental disorder. In civilian life, anyone (child, adolescent, adult, or elderly) who is exposed to a life-threatening trauma such as from a
Objectively proving brain injury is the best and quickest way to win or settle a brain injury case. However, objective evidence of brain injury is not always present on MRI or CT scan, and patient symptoms alone such as confusion and memory loss may not be sufficient evidence of injury. A new technology added to traditional MRI called “Diffusion Tensor Imaging,” or MRI/DTI, is more sensitive to injury than traditional MRI and has helped to prove traumatic brain injury.
Juries tend to be sympathetic to brain injuries that can be objectively proved. However, imaging tools such as MRI and CT scans don’t always show evidence of brain injury, causing doctors to diagnose concussions more often based on the signs and symptoms a patient demonstrates, which insurance companies can often easily disprove.
Insurance companies, attempting to disprove an injury, will assume a patient is faking injuries or has psychological problems that pre-existed the accident. Grade school records, medical records from childhood, psychological and psychiatric records, and anything else through the years that insurance companies can obtain can be brought out as defense against litigation.
DTI Provides Better Evidence of TBI
DTI (Diffusion Tensor Imaging) is giving doctors objective evidence missing with traditional MRI. Invented 20 years ago, DTI is an imaging method that grew out of and is part of MRI. It is performed on a normal MRI machine with special “Diffusion Tensor Imaging” software that records damage in the white matter tracts inside the brain. White matter, like telegraph wires, connects different lobes of the brain. When white matter is injured, communication between areas of the brain it connects is decreased.
MRI/DTI tracks movement of water molecules within white matter fibers, and can detect interference with that movement. DTI can show injury to the white matter of the brain which cannot be seen on MRI, CT scan, PET scan, or SPECT, and can provide objective evidence of continued cognitive decline associated with confusion and memory loss.
A radiologist reading an MRI/DTI will perform a differential diagnosis to rule out other possible causes of an abnormality seen on DTI, such as an old stroke, a prior TBI, a prior brain surgery, prior infectious process such as encephalopathy, or history of MS. Other possible causes of abnormality on DTI could be a congenital process or degeneration due to advanced age of the patient. In those cases, DTI evidence would be