What Happened to Junior Seau?

Seau had chronic traumatic encephalopathy (CTE).

Junior Seau
Photographer/Getty Images

In early August 2015, Junior Seau, the legendary linebacker who played 20 seasons in the NFL, was inducted into the Hall of Fame. Seau's induction is bittersweet for fans everywhere who fondly remember his passionate play on the gridiron. Seau was famous for head-first, no-guts-no-glory tackles which propelled him to a Super Bowl victory and a score of Pro Bowl appearances. However, years of bodily sacrifice on the field caused Seau to experience brain damage called chronic traumatic encephalopathy (CTE), a degenerative disorder that impairs cognition and causes depression.

  This brain damage most definitely contributed to Seau's suicide in 2012 from a self-inflicted gunshot wound to the chest.

For years, CTE has been linked to boxers who routinely endure mild traumatic brain injury. In fact, CTE was originally called dementia pugilistica (think Muhammad Ali). More recently, this condition has been identified among football players and combat veterans exposed to repeated blasts. Even subconcussive blows or blows that don't result in a loss of consciousness can lead to CTE.

Like Alzheimer's disease and other tauopathies, CTE is characterized by neurofibrillary inclusions such as neurofibrillary tangles, glial tangles and neuropil threads composed of tau protein. However, unlike Alzheimer's disease, these neurofibrillary inclusions deposit in an irregular, uneven and more superficial fashion—on the temporal, frontal and insular cortices of the brain. Furthermore, in CTE, these tangles are typically denser than those found in Alzheimer's disease and are most dense at the depths of the cortical sulci.

(Sulci refer to grooves on the surface of the brain.) They are also perivascular, meaning that they surround blood vessels. Of note, in CTE, neurofibrillary inclusions can also been found in the basal ganglia, diencephalon, brainstem and subcortical white matter.

Experts think that neurofibrillary inclusions may result from diffuse axonal (nerve) injury set in motion by initial injury followed by subsequent repeated injury as happens in sports like boxing, rugby, professional wrestling, and football.

With CTE, axons shear and the permeability of their membranes is altered thus triggering tau protein formation. As more tau and neurofibrillary inclusions accumulate, symptoms of CTE worsen.

Although not as prevalent as in those with Alzheimer's disease, beta-amyloid deposits are found in about 45 percent of all people with CTE. Additionally as with Alzheimer's disease, CTE results in atrophy or shrinkage of portions of the brain. In CTE, the third and lateral ventricles are also enlarged, and the cavum septum pellucidum or fifth ventricle contains fenestrations or small holes. (The ventricles contain cerebrospinal fluid or CSF.)

Currently, there are no definitive clinical or pathological criteria for the diagnosis of CTE. Instead, athletes like Seau are usually diagnosed using biopsy after death. Nevertheless, based on history and symptoms, a diagnosis of CTE can often be inferred by clinicians. For example, it's estimated that nearly half of all professional boxers suffer from CTE. Eventually, clinicians and researchers hope to use a combination of neuropsychological tests, brain imaging, and biomarkers to definitively diagnosed this disease.

In a 2013 article published in Neurology Today, researchers suggest that CTE is divided into four pathological stages:

I) headaches and issues related to attention and concentration are common; stage 2) depression, explosivity and short-term memory impairment; stage 3) cognitive impairment and problems with executive functions, specifically planning, organization, multitasking and judgment; stage 4) full-blown dementia.

In most people, CTE seems to slowly progress with full-blown dementia evident late in life. In other words, many professional athletes, like Seau, present with worsening symptoms after retirement. Researchers speculate that Seau may have been in the second stage of illness.

It probably comes as no surprise that we're likely a long way off from discovering an effective treatment for CTE. Right now, researchers are focusing on diagnosis and prevention. Nevertheless, there are some drugs in development which show some promise.

Football is often compared to war. However, in modern warfare, soldiers rarely take direct blows delivered from other human beings as is the case with football. Currently, most war is fought from the sky with smart bombs, carpet bombs, missiles and so forth. If anything, the daily physical rigors and repercussions of football far outweigh those of war with athletes enduring not only chronic brain damage but also bone and muscle damage, too. Alas, Seau represents only one of countless athletes destroyed by sport.

Sources

Article titled "Chronic Traumatic Encephalopathy: A Potential Late Effect of Sport-Related Concussive and Subconcussive Head Trauma" by B Gavett and co-authors published in Clinical Sports Medicine in 2012.  Accessed July 30, 2015.

Ropper AH, Samuels MA, Klein JP. Chapter 35. Craniocerebral Trauma. In: Ropper AH, Samuels MA, Klein JP. eds. Adams & Victor's Principles of Neurology, 10e. New York, NY: McGraw-Hill; 2014. Accessed July 30, 2015.

Article titled "NIH: NFL's Junior Seau Had Chronic Traumatic Encephalopathy" by K Samson published in Neurology Today in 2013.  Accessed on 7/30/2015.

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