By Matt Lalande in Brain Injuries on April 15, 2021
CTE is a progressive degenerative brain disease caused by repeated blows to the head and traumatic brain injury. It is characterized by the loss of normal brain matter as well as an unusual buildup of tau, a protein in the brain cells that is responsible for transporting nutrients through the nervous system via a structure called the microtubule. When tau builds up in clumps in the brain, it can begin to destroy surrounding brain cells.
CTE’s location of tau plaque build-up is uniquely different than the location of plaque build-up present in all other neurodegenerative diseases. Concussions, or (TBI’s), influence the risk of acquiring CTE along with all neurodegenerative diseases.
Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease characterized as a variant of dementia pugilistica also referred to as punch-drunk syndrome, coined by forensic pathologist Harrison Martland in the early 20th century. The syndrome was common among boxers and professional athletes.
CTE itself was first described by Dr. Omalu, a forensic pathologist at the University of Pittsburgh around 2005. Among the many symptoms of CTE are confusion, headaches, memory loss, impulsive behaviour, poor judgement, dementia, tremors, vertigo, depression and suicidality. Today, much of the research on CTE is conducted on the brains of deceased CFL and NFL players – and soon to be, MMA fighters.
CTE is a significant cause of concern among professional athletes in contact-based sports such as hockey, football, and MMA, as well as in combat veterans in the military. To date there have been two MMA fighters who have been officially linked to CTE. One well known UFC veteran, Tim Hague, tragically passed away at the age of 34 after suffering a cerebral hemorrhage in a UFC bout held in Edmonton several years ago. CTE was diagnosed by autopsy – which meant that he would have been suffering from progressive brain damage prior to his fight.
Spencer Fisher, a former popular UFC lightweight fighter has reportedly been suffering symptoms that may lead to a future diagnosis of CTE. MMAFIGHTING.com did an extensive piece on Spencer Fisher, entitled “The Cost of Being the King” which outlines the damage he now suffered after fighting in the UFC for ten years. The read is quite amazing.
NFL players appear to be prone to the particular neurodegenerative disease because of their sport repeatedly engaging in action causing extensive trauma to the head. According to Wikipedia, Dr. Bennet Omalu is the neuropathologist credited for sparking re-awareness of Chronic traumatic encephalopathy through autopsy and final diagnosis of former NFL Player Mike Weber. Mike Weber remarkably showed the necessary evidence of Mike Weber’s brain indeed affected by CTE in the year of 2002. In the summer of 2017 a study showed concerning results after analyzing 111 deceased football players brains during autopsy. The study showed evidence of CTE in the brain matter of 110 of the 111 NFL subjects. Oftentimes CTE is left undiagnosed due to the unfamiliarity of healthcare professionals. Moreso, CTE is commonly misdiagnosed as ALS or other neurodegenerative diseases which skewes percentages of individuals affected. Thus growing awareness and attention for the condition must change for the best in hopes to eventually exploit all dementia related diseases.
CTE is medically described as progressive brain degeneration which is likely caused by “repeated” head trauma. Any time the brain can be jostled inside the skull, a person could potentially experience CTE, especially a person with a concussion history or who is pre-disposed to a head injury due to repeated concussion. With that being said, however, both frequency and cause of the disease remain unknown and controversial today.
We do know that diagnosis of the condition is only available postmortem. CTE autopsy will normally show aggravated clusters of the tau protein which is found in other neurodegenerative diseases. The clusters of the tau protein found in CTE patients is unique in regards to the location of the brain they are found. Clusters of the protein found in CTE patients are apparent near blood vessels and most commonly found in the deep sulci of the brain Sulci, according to the medical-dictionary online, are the deep grooves or furrows in the brain. CTE’s location of tau plaque build-up is uniquely different than the location of plaque build-up present in all other neurodegenerative diseases.
According to the Northern Brain Injury Association, 452 Canadians suffer a brain injury every day, and brain injuries in Canada are more common than spinal cord injury, Multiple Sclerosis, breast cancer, and HIV/AIDS combined. The Boston University-based VA Boston Healthcare System, which houses the largest CTE brain bank in the world, has assessed approximately 600 brains with injuries and discovered CTE in over 50% of the specimens.
Concussions are a common injury sustained from car accidents, particularly rear-end collisions, and are directly linked to CTE and post-concussive syndrome (PCS). When a victim suffers a mild concussion, it may heal on its own after a few weeks or months. However, when the victim suffers a major concussion, or if the concussion does not heal properly, the victim becomes more prone to second-impact syndrome, progressive concussions and eventually, CTE, which can have catastrophic, fatal consequences. Research from the Canadian House of Commons Health Committee has indicated that up to 20% of people who suffer concussions experience prolonged or permanent consequences.
Over time, the brain tissue begins to degenerate, causing a progressive loss of cognitive function. This can lead to early onset Alzheimer’s disease and dementia, as well as a variety of other permanent, life-altering symptoms.
Symptoms of CTE develop slowly over time, and often do not present immediately in a victim after an accident. The severity of CTE symptoms depends on how many times the brain has been injured and the severity of the initial injury itself. When the symptoms are severe, they can have a substantial impact on the victim’s life, limiting their ability to work, their quality of life, and their overall enjoyment of life.
Long-term symptoms that have been identified and linked to CTE include:
One of the complexities with CTE is that it can be difficult to receive a diagnosis. Diagnosis cannot be made until the victim is deceased as the current technologies for testing are not equipped to detect CTE while the victim is alive.
This is largely due to the fact that many of the symptoms of CTE often overlap with other degenerative brain diseases such as Alzheimer’s disease, Parkinson’s disease, or dementia. The presence of the tau protein is the key indicator that differentiates CTE from other brain diseases; however, this protein can typically only be found by dissecting the brain after the victim is deceased.
Some MRI-based technologies, such as Diffusion Tensor Imaging (DTI), can detect abnormalities in white matter tracts that may indicate signs of CTE. Further, with more attention in the mainstream media on CTE and PCS in professional athletes, more research has been focused on developing diagnostic testing for living people. At present, a CTE diagnosis is given presumptively by a medical care professional by assessing various factors such as the patient’s history, lifestyle, age, and any abnormalities shown on diagnostic imaging scans.
Complications in receiving a diagnosis for CTE can make life especially unfair when your traumatic brain injuries have been caused by someone else’s negligence, and you are living with the long-term consequences of someone’s poor decisions. It can also cause difficulty in determining the future cost of your pain and suffering when filing a personal injury claim as you cannot predict CTE.
Since 2003, our firm has been representing victims with severe brain injuries in both personal injury claims and denied long-term disability claims. We work with victims across Ontario who have suffered unbearable pain, stress, and psychological distress due to others’ careless actions. Over the years, we have been fortunate to represent victims and disability claimants who have suffered head injuries such as:
Diffuse Axonal Injuries: Axons, which compose what is also known as the white matter of the brain, connect nerve cells throughout the brain. When the brain reverberates (quickly moves back and forth inside the skull), the nerve axons are torn and damaged. During automobile accidents, for example, rapid rotation or deceleration of the brain causes stretching of these nerve cells on a cellular level, the brain’s normal transmission of signals (information) is disrupted, and this can dramatically impact the person’s alertness and wakefulness.
Ischemia is another form of diffuse injury. This happens when certain parts of the brain are cut off from an adequate supply of blood. A marked decrease in blood supply is especially perilous for a TBI patient because the brain becomes extremely sensitive even the smallest decreases in blood supply after a traumatic injury. Changes in blood pressure during the first-week post-head injury can have adverse effects.
Brain Hematoma – when a blood vessel in the brain is ruptured, bleeding starts and the blood naturally clots. Sometimes these hematomas are very small. When a hematoma is large, it might compress the brain. Symptoms will depend on the location of the hematoma and hematomas are named for their location. A hematoma that forms between the skull and the dura (the tough outermost membrane enveloping the brain and spinal cord) is named an epidural hematoma. When the hematoma forms between the brain and the dura, it is named a subdural hematoma. When the hematoma forms deep inside the brain, it is named an intracerebral hematoma. Under fortunate circumstances, the body will reabsorb the hematoma. Large clots (hematomas) are periodically removed by surgery.
Second Impact Syndrome (SIS) – SIS causes the brain to swell catastrophically. SIS is not strictly speaking a type of injury, rather an extreme response of the brain to a second blow to the head/brain (even a very mild blow) after a first impact (seconds up to days after the first blow) already changed the brains functioning and left it in a vulnerable state. A second blow to the head during concussion unleashes a series of metabolic events that might start within 15 seconds. One of the ramifications is a very large increase in blood flow due to a loss of autoregulation of the brain’s blood vessels. Huge increases in intracranial pressure follow, and this might cause cerebellar herniation (the brain is squeezed past structures within the skull) which is very often fatal.
Skull Fractures – Linear skull fractures are simple cracks or breaks in the skull. The bigger concern when this happens is the fear that the underlying force that created the fracture might have caused damage to the brain itself. Fractures to the base of the skull can be very problematic because it may cause damage to arteries, nerves and other structures. If a fracture reaches down to the sinuses, this may cause cerebrospinal fluid to leak from the nose and ears. Sometimes this might require intervention to insert a lumbar drain. Depressed skull fractures are more problematic. These fractures happen when a part of the bone presses on or into the brain itself. This more often than not requires surgical intervention. The specific damage caused will be dependent upon the region where this fracture happens as well as its interaction/coexistence with any diffuse brain injuries.
Traumatic Subarachnoid Hemorrhage – When an escape of blood from a ruptured blood vessel leaks into the space that surrounds the brain, this kind of stroke caused by an external impact on the brain, is described as a subarachnoid hemorrhage. The subarachnoid space is the fluid-filled space around the brain between the arachnoid membrane and the pia mater (the delicate innermost membrane enveloping the brain and spinal cord) through which major blood vessels pass. The cerebrospinal fluid in this space forms a floating cushion the brain hovers in for protection. When an injury causes some of the small arteries to tear, the blood flow spreads all over the surface of the brain, causing widespread traumatic effects.
Our brain injury lawyers offer free consultations, with no up front fees and no obligation to retain our services after we meet. During your consultation, we will provide you with helpful, transparent advice and go over your options with you to ensure you have the information you need to make a decision about your future. Our firm operates on a contingency basis, which means we do not charge you until we win your case, and if you don’t win, we don’t charge.
Call us at province wide at 1-844-LALANDE (525-2633) or locally in the Hamilton / GTA at at 905-333-8888. You can also request a private call back by filling out our online contact form, and we will be in touch as soon as we can (usually within one business day).
LALANDE PERSONAL INJURY LAWYERS – HAMILTON OFFICE
1 King Street East, Suite 1705
Hamilton, On L8P 1A4
905-333-8888
www.brainline.org
https://www.mmafighting.com/2021/1/12/21554602/the-cost-of-being-the-king-spencer-fisher-ufc
www.medical-dictionary.com
www.cdc.gov
https://pubmed.ncbi.nlm.nih.gov/10671706
https://pubmed.ncbi.nlm.nih.gov/25904048
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255271/
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