Death Of Former NHL Player Steve Montador Promotes Discussions Of Concussions

Steve Montador became the fifth former NHL player to be diagnosed with chronic traumatic encephalopathy (CTE) posthumously. Montador passed away on February 15, 2015; he was only thirty-five years old. During his NHL career, Montador played for the Calgary Flames, Florida Panthers, Anaheim Ducks, Boston Bruins, Buffalo Sabres, and Chicago Blackhawks.

Montador, a player who suffered numerous concussions during his NHL career, actually offered to donate his brain prior to his death in an effort to further research. His brain was examined at the Krembil Neuroscience Centre at Toronto Western Hospital.

Before Montador’s death, four other former NHL players suffered the same fate–Reggie Flemming (73), Bob Probert (45), Rick Martin (59), and Derek Boogaard (28). Not only has this neurodegenerative disease been associated with hockey, but also with football, boxing, rugby, and soccer.

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Forensic pathologist Bennet Omalu discovered CTE while performing an autopsy on legendary Pittsburgh Steeler Mike Webster. Omalu thoroughly inspected Webster’s brain–even though it was believed he died from a heart attack–since he was informed of Webster’s puzzling and erratic behavior after his football career.

Initially he thought Webster could have been suffering from dementia pugilistica, which is often found in boxers, based on Webster’s mental deterioration. But when Omalu extracted his brain, it oddly appeared normal. CT and MRI scans of his brain were routine as well. With permission from his supervisors and Webster’s family, Omalu strayed from the protocol to investigate Webster’s brain.

While utilizing cutting boards, knives, a microscope, and new specialized stained slides prepared by a lab at the University of Pittsburgh, Omalu found accumulations of tau proteins in Webster’s brain. Tau proteins are also associated with Alzheimer’s disease, just located in different parts of the brain (hence the similarities in dementia symptoms, though it is unknown if every case of CTE presents that symptom). In those who have developed CTE, tau proteins kill brain cells that are responsible for a person’s mood, emotions, and executive functions. Through a microscope, tau proteins appear as red and brown splotches. This is how Omalu discovered chronic traumatic encephalopathy.

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CTE is caused by hard blows to the head, thus the association of the neurodegenerative disease with concussions. Subconcussive blows, hits that do not necessarily register as traumatic brain injuries (TBIs) or cause symptoms, also contribute to the development of CTE. According to researchers at Boston University, “the brain degeneration is associated with memory loss, confusion, impaired judgement, impulse control problems, aggression, depression, and, eventually, progressive dementia.”

Thus far, CTE has only been diagnosed conclusively via autopsies by examining cross-sections of brain tissue stained with AT8 (an amino acid) under a microscope. The neurodegenerative disease is indistinguishable from other brain conditions through current imaging technologies. Even when a person is clearly cognitively dysfunctional due to a traumatic brain injury, existing technology cannot identify structural damage to the brain. Regardless of being resolved of symptoms, abnormalities may permanently persist in the brain; those abnormalities can include tau proteins accruing in brain cells, or CTE.

While the focus of some researchers has been studying the brains of deceased players to expand their knowledge of CTE, others are intently searching to find a detection method for CTE in living players. Brain-imaging technology is currently used to identify mild traumatic brain injuries. Some of these technologies could be used in the future to image tau and amyloid proteins, finally allows diagnosis of CTE in living beings.

Magnetic resonance imaging (MRI) could be one method of identifying CTE. MRI tests utilize a magnetic field to create detailed images of the brain. Over time, there has been improvements in expanding the capabilities of MRIs. The following are more specialized models of the MRI, ones that may eventually be able to detect CTE:

• Susceptibility weighted imaging (SWI) “is used to detect microhemorrhages, the intact structure of the venous system, and oxygen saturation following neurotrauma.” Through SWI, blood-brain barrier disruptions can be identified and mapped, as well as perivascular tau deposition. It is believed that iron deposition also are involved in CTE symptoms manifesting the brain. SWI can localize concentrations of paramagnetic iron as well as areas of iron translocation.

• Another specialized MRI is diffusion tensor imaging (DTI). In conjunction with DTI, SWI can reveal which areas of white matter are impaired by microhemorrhages. Thus far, DTI seems to be a useful technique for tracking structural correlations with repetitive brain injuries. Prior to routine clinical use of this test, DTI requires considerable technological improvements in both accuracy and precision.

• Magnetic resonance spectroscopy (MRS) measures brain chemistry linked with diffuse axonal injury (DAI) and neuronal injury. MRS can identify metabolite levels within the brain, which change after an injury. Metabolite levels can stay altered even after symptoms subside, evidencing the long-term degeneration that can occur from a TBI. Therefore, MRS tests are exemplary models for observing long-term effects of brain injuries and clarifying CTE pathophysiology.

Positron emission tomography (PET) scans inject low-level radioactive tracers into a vein and track the tracer through a scanner. Currently, researchers are engaged in developing PET markers to detect abnormalities in tau proteins that are associated with CTE.

The Semel Institute for Neuroscience and Human Behavior at UCLA recently injected five former NFL players with FDDNP, a radioactive compound that acts as a tracer that binds to tau proteins. In PET scans, these tracers showed varying densities. Low densities were represented by a blue glow, while high densities appeared red. All of the athletes in this study sustained between two and twenty documented concussions during their football careers. All of their PET scans red in the same regions of the brain where tau abnormalities were discovered in posthumous CTE diagnoses.

Although this was too small of a sample to definitively accept this method, further testing could establish this as a proven method to identify tau protein accumulations and abnormalities in the brains living athletes. Once tau abnormalities can be pinpointed, a level of prevalent abnormalities has to be established to determine when a player should suspend their athletic career.

Other PET scans that could potentially evolve to help diagnose CTE are event-related potentials (ERPs) and quantitative electroencephalography (EEGs). During these tests a mesh cap (with electrodes) is placed on a person’s head in order to record brain waves. EEGs may be able to assess neurophysiological changes and cognitive effects associated with TBIs, helping identify athletes who are predisposed to the development of CTE.

Single photon emission computerized tomography (SPECT) is employed to differentiate types of dementia. SPECT has not yet been utilized in CTE studies, so it is unknown whether CTE can be differentiated from other neurodegenerative diseases by this scan. CTE’s association with amyloid protein deposition could explain abnormal results on a SPECT.

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Regardless of the progress in CTE research, the National Hockey League has failed to acknowledge the influence of their game on deaths’ of these players. The NHL made a statement once it was discovered that Montador exhibited CTE last week:

“Our thoughts, condolences and prayers remain with Steve’s family and friends. However, we do not agree that the reports and allegations made today establish any link between Steve’s death and his N.H.L. career.”

Although CTE research is far from complete, it appears there is enough data to at least suggest a connection between an NHL career with chronic traumatic encephalopathy. But the NHL’s continuing insistence that CTE is not linked to hockey is not entirely unexpected––the NHL who conducted a study on concussions for seven years, waited an additional seven years to release any results, and ultimately dubbed the study inconclusive, stating that more information was needed to proceed. If the NHL were to publicly acknowledge the link between CTE and NHL careers, it would only be used as evidence against the league in the class action lawsuit it is currently defending regarding concussions. But it must be noted that their lack of acceptance of CTE does not mean the NHL is absolutely inept with respect to concussions––the NHL was the first professional sports league to mandate baseline and neuropsychological testing for concussions.

A career in the NHL often causes irreversible damage to the brains of players, but players accept the risks. Some players even conceal their concussion symptoms to continue playing. But these players deserve a certain level care and respect after dedicating an exceptional part of their lives to the league.

The NHL’s statement in response to Montador’s CTE diagnosis exemplifies how the league tries to relinquish themselves of the responsibility for these players who die as a result of the symptoms of CTE. As a result, the onus is placed upon the players to acknowledge CTE and the consequences of concussions sustained while playing hockey—regardless of the NHL’s stance.

Current Chicago Blackhawks forward Daniel Carcillo’s contribution to The Players’ Tribune started the conversation regarding the changes that need to be implemented to advocate for players who sustain concussion, and like Montador, ultimately deteriorate from CTE.