Overview of Chronic Traumatic Encephalopathy (CTE)

Encephalopathies are disorders that alter brain function. Chronic traumatic encephalopathy (CTE) is a form of brain degeneration caused by repeated trauma to the head. It causes symptoms similar to those of Alzheimer’s disease, such as memory loss and mood changes.

Most confirmed cases of CTE have been in athletes of contact sports, like American football and boxing, but it can develop in anybody with a history of repeated head trauma.

It can take years for CTE symptoms to appear, but they can drastically impact quality of life by causing physical and mental impairment. CTE does not currently have a cure, so treatment revolves around managing symptoms.

Read on to learn more about CTE, including causes, symptoms, and risk factors.

CTE is a progressive neurodegenerative condition caused by repeated blows to the head. It usually onsets gradually after years of head trauma. Researchers have estimated that 17 percent of people with repetitive concussions or mild traumatic brain injury go on to develop CTE.

The severity of CTE is associated with the severity and frequency of brain trauma. Some people with a history of head injuries never develop CTE, while some develop symptoms within months, according to Boston University.

The reason why CTE appears in some people but not others still isn’t well understood. It’s theorized that repeated head injuries can lead to the buildup of an irregular protein called tau that interferes with neuron function. Tau protein is also associated with Alzheimer’s disease.

Most cases of CTE have been in contact sport athletes, especially for American football and boxing, but it can develop in anybody who experiences repeated head injuries.

CTE is divided into four stages depending on the severity of brain damage:

• Stage I. The brain appears mostly typical with tau protein found in a small number of locations, often the lateral and frontal parts of the brain and near small blood vessels in the grooves of the brain.
• Stage II. Larger irregularities may be noted, like an enlargement of the passages in your brain that allows cerebrospinal fluid to pass through.
• Stage III. Noticeable brain mass loss appears with the shrinking of the frontal and temporal lobes.
• Stage IV. Dramatic reduction in brain weight to about 1,000 grams compared to the usual 1,300 to 1,400 grams.

In the 1920s, CTE was called punch drunk syndrome since boxers often developed neurological symptoms like tremors, speech problems, and confusion. Some boxers would develop these symptoms while still competing in their 20s or 30s.

CTE has been the most common name for this condition since the 1940s. Most confirmed cases of CTE have been in athletes competing in contact sports with a high risk of head injuries, like American football and boxing, according to 2016 research.

It’s still not clear how common CTE is among athletes and how much trauma is needed to cause it. It’s believed to be caused by repetitive concussions.

The only way to confirm a CTE diagnosis is by examining a person’s brain after they pass away. A researcher named Bennet Omalu published the first evidence of CTE in a National Football League (NFL) player after performing an autopsy on former Pittsburgh Steeler player Mike Webster.

In the largest case series of CTE in deceased football players, researchers found a CTE prevalence of 87 percent across all levels of play and a prevalence of 99 percent (110 out of 111) in ex-NFL players.

Symptoms vary between people, but according to the National Health Service, they’re similar to those of other degenerative brain conditions, like Alzheimer’s.

Symptoms tend to develop gradually after repeated blows or concussions. These symptoms may include:

• short-term memory loss
• headaches
• mood changes
• erratic behavior, including aggression, depression, and suicidal thinking
• increased confusion and disorientation
• problems sustaining attention
• brain fog
• slurred speech
• significant memory problems
• tremor
• slow movement
• difficulty eating or swallowing (this is rare)

Symptoms tend to worsen as the condition progresses. The following clinical classifications have been suggested:

Anybody who receives repeated blows to the head is at risk of developing CTE, but it’s most common in athletes playing contact sports, such as:

• boxing
• American football
• martial arts
• soccer
• rugby
• hockey
• lacrosse

Other people with an increased risk include:

• military veterans with a history of repetitive brain injury
• people with repeated head injuries from
  • self-injury
  • recurrent assault
  • poorly controlled epilepsy

It’s been speculated that certain genes may make some people more prone to developing CTE. According to 2021 research, the gene that has gained the most attention is the ApoE e4 allele, which might inhibit the growth of neurons after brain injury.

In a 2020 study, researchers found that the odds of having CTE at the time of death in American football players doubled with every 2.6 years played.

The best way to prevent CTE is to protect yourself from developing head injuries and follow your doctor’s instructions when rehabilitating from an injury. Specifically, you can:

• wear proper protective equipment during contact sports, like an approved helmet
• follow proper return to play protocol after a concussion
• make sure contact sports for you and your child are supervised by a trained professional
• seek medical attention if symptoms of an old head injury return
• wear a seatbelt when in a moving automobile

If you believe you may have CTE, it’s critical to contact a healthcare professional. They will likely refer you to a neurologist with a background in diagnosing CTE. Although there’s no test that can confirm a CTE diagnosis, a doctor may be able to help rule out other conditions that could be causing your symptoms.

It’s also important to contact a doctor any time you experience a head injury for a proper evaluation and treatment plan.

If you may have CTE, a doctor can help you create and adjust your treatment to best manage your symptoms.

Currently, CTE can only be diagnosed by observing brain tissue after a person has passed away. Both CTE and Alzheimer’s are associated with a shrinking of the brain and neurofibrillary tangles that contain the protein tau.

Your doctor may suspect CTE if you display typical symptoms and have a history of head injuries.

Researchers are continuing to investigate techniques for diagnosing CTE in living people, such as magnetic resonance imaging (MRI).

CTE doesn’t have a cure. Treatment resolves around supportive measures that may include:

• speech therapy
• behavioral therapy to deal with mood changes
• memory exercises
• pain management therapy
• medications, such as
  • selective serotonin reuptake inhibitors (SSRIs)
  • atypical antipsychotics
  • cholinesterase inhibitors

According to 2020 research, monoclonal antibody therapy, a type of immunotherapy, is a promising treatment for targeting tau proteins, but more research is needed.

People with traumatic brain injuries in early or midlife are 2 to 4 times more likely to develop dementia later in life. Ways to manage your symptoms include:

• If you have memory problems, write things down.
• Create a daily routine.
• Be aware that you may be prone to impulsive behaviors, such as illegal drug use and gambling. Avoid these activities as much as possible.
• Build a support system of people you can trust and talk with.
• Manage stress and anxiety as well as you can.
• Get plenty of rest.
• Exercise regularly.
• Maintain a balanced diet.

CTE is a progressive brain condition caused by repeated head injuries. Most confirmed cases have been in athletes in contact sports, but anybody who experiences repeated head injuries can develop it.

CTE can only be diagnosed after death, and treatment is limited to managing your symptoms. If you suspect that you have CTE, a doctor can help you develop a plan to maximize your quality of life.

Your doctor may recommend treatments like speech therapy, memory exercises, or behavioral therapy, depending on your specific symptoms.