Where is cte located in the brain?
Among individuals diagnosed with CTE, some report mood and behavior symptoms that can appear as early as the patient’s 20s. Disorders reported include:
However, these reported symptoms may not necessarily be caused by CTE. Experts believe these symptoms could also be caused by concussions, other consequences of repetitive head impacts like white matter changes - or could be completely unrelated to head impacts.
No matter the cause, these symptoms can be treated, and the CLF HelpLine is here to connect you with a doctor who can help treat these symptoms and provide additional support.
Cognitive symptoms
Most patients with CTE eventually experience progressive disorders of thinking and memory, including problems with:
Progressive cognitive symptoms related to CTE tend to appear later in life, sometimes in midlife, but more frequently in a patient’s 60s or 70s. Patients may exhibit one or both symptom clusters. In some cases, symptoms worsen with time (even if the patient suffers no additional head impacts). In other cases, symptoms may be stable for years before worsening.
If cognitive symptoms appear in early or midlife, they could have another, more treatable cause than CTE. Sleep disorders and neuroendocrine disorders from damage to the pituitary gland can cause treatable cognitive changes. Learn what you can do to improve your lifelong brain performance at Operation Brain Health.
Sleep symptoms
A 2020 study from the UNITE Brain Bank suggests that problems with sleep, specifically symptoms associated with REM behavior disorder, may be related to CTE pathology. Watch the study's corresponding author describe the findings by clicking here.
Unfortunately, there is currently no treatment for CTE. Prevention, therefore, is of great importance.
There are symptoms that are highly suggestive of CTE, including the following:
In addition, there are some physical signs of CTE that may be present, including:
A small subset of patients with CTE have chronic traumatic encephalomyelopathy (CTEM). This disorder mimics the symptoms of Lou Gehrig’s disease (ALS), with muscle weakness and wasting, difficulty swallowing, and hyperactive reflexes.
Later on, in the course of CTE, patients will experience from dementia. Rather than Alzheimer’s disease, the symptoms of chronic traumatic encephalopathy more closely resemble the behavioral variant of frontotemporal dementia (bvFTD).
However, typical bvFTD behavioral symptoms, such as apathy and disinhibition, are often not seen in CTE patients.
A history of repetitive brain trauma is necessary for the development of CTE. Even mild traumatic brain injuries (mTBIs) or less minor head injuries can contribute to the development of this degenerative brain disease.
Besides athletes who engage in contact sports such as football, soccer, boxing, and hockey (professionally or otherwise), other groups of people at risk for developing CTE include military personnel, victims of domestic abuse, and people with a seizure disorder.
It's unclear why some individuals with repetitive head traumas develop CTE and others do not. Experts are looking into whether certain genes, age, or lifestyle habits (e.g., substance abuse) are involved.
Gender may also play a role. Women seem to have a more prolonged recovery from a concussion than men, but it's not known if this leads to a different risk of developing CTE. Most of the brains with CTE that have been studied have been male, as they came from individuals in the male-dominated fields of professional sports and combative military service.
Lastly, it's important to distinguish post-concussive syndrome (PCS) from CTE. PCS occurs after a concussion in some people and causes symptoms like nausea, headache, and confusion. But CTE is more than just a prolonged period of the post-concussive syndrome—it occurs years later, unlike PCS, which usually comes on very shortly after the head injury.
While various emotional, cognitive, and physical symptoms (for example, depression, anger, concentration loss, and impaired balance) can provide clues to this underlying disease while a person is alive, as may some imaging tests, an official CTE diagnosis can only be made after conducting an autopsy.
While public awareness of CTE has grown rapidly, science is slower to develop tests that are specific to the problem. Magnetic resonance imaging (MRI) can help rule out other diseases and may show abnormal wasting of the amygdala, which could suggest CTE as a diagnosis.
Other more experimental techniques such as functional MRI, positron emission tomography (PET), and diffusion tensor imaging are also being explored.
There are several brain findings of CTE on autopsy. Most notably, there is accumulation in various areas of the brain of certain proteins, such as tau and TDP-43. This is distinct from Alzheimer’s disease, which shows beta-amyloid plaques, which are not present in most cases of CTE.
In addition to specific protein accumulation, in CTE, there is reduced brain weight and thinning of the corpus callosum, which connects the brain's two hemispheres. There is also frequent atrophy of the frontal lobes in CTE. The frontal lobes control your ability to make good decisions and plan, as well retrieve memories.
Other affected areas of the brain include the mammillary bodies, hippocampus, and medial temporal lobe, which are involved with memory, as well as the substantia nigra, which is involved with movement.
There is no treatment available for CTE once it has developed. As is usually the case, prevention is the best medicine.
The need for a safe culture in sports and the rest of life is becoming increasingly emphasized.
It's important to encourage athletes to report when they are suffering from the effects of a head injury and to follow guidelines for returning to play after such an injury.
Moreover, coaches should teach their players the correct techniques for personal protection, and they need to make an effort to limit full contact during practices and drills. Neck strengthening exercises should also be incorporated into practices to help minimize head injury, especially in younger players.
Referees also play a role in preventing head injuries and the subsequent development of CTE. They need to uphold all the rules of the game in order to create as safe of a playing environment as possible.
Wearing protective equipment—like an appropriately padded helmet and mouthguard—can protect against traumatic head injuries.
That said, these protective measures should not give players a false sense of security. Engaging in reckless and/or violent play is never warranted. In other words, it’s good to play hard, but it’s even more important to play safe.
Although the process begins focally, it gradually spreads to involve widespread regions of the brain including the frontal and temporal lobes, medial temporal lobe, diencephalon, and brainstem. TDP-43 abnormalities are found in most CTE cases; in advanced CTE, TDP-43 pathology is severe and widespread.
