September 18, 2026 by Haley Hansen, PT, DPT
Steve Kerschke: All right, it’s nine o’clock, so we should get started. Those of you who are frequent flyers of our webinars, welcome back. If you’re new to QLI and our webinars, welcome. We got Dr. Jeff Snell, a regular with us today. So welcome back, Jeff.
Jeff Snell: Feels good to be back.
Steve Kerschke: Glad to have you. We’ll do the normal just housekeeping. So Jeff, if you can kind of advance the slide here. Quick rundown of QLI, if you’re unfamiliar, we’re based in Omaha, Nebraska. We’re really known for our post-acute rehab program and more so being known for our outpatient and innovative telerehab program. In both cases, we work with individuals with traumatic brain injury, spinal cord injury, chronic pain, limb loss, and stroke. So pretty specialized in what we do and certainly have a lot of great people. And you can see our campus there on the right, fortunate to work at a beautiful facility. As for today, just use the Q&A. If you have questions along the way, between Jeff and I, we’ll be monitoring that. We’re a little light on personnel today, so we’re missing Laura and Don, so we’ll do the best to cover for them, but we’ll answer the Q&A as we go or there’ll definitely be time at the end.
As for your CEUs, just ask that you stay the majority of the presentation. We know that sometimes you have to drop off all good. There will be one poll question at the end. That one poll question will pop up. Just answer that. That is part one of what we asked in order to get your CEUs. And then once you click leave webinar, you should get prompted to fill out a job form. Once you submit that job form, you should automatically get emailed your CEU certificate as well as the slides for this presentation. So those will be all in one document. We do have some issues typically on your end in terms of firewalls and things like that. If you have any issues, just reach out to me. I’ll get you set up with whatever you need. So with that, Jeff, you’re going to be talking about aging today.
Excited to hear what you
Jeff Snell: Got. Yeah, something I have a lot of personal experience with as well, aging. There is a question, are the slides available for downloading or for printing at this point?
Steve Kerschke: Yep. So once you hit submit, you’ll get those emailed and you should be able to download and print those. So
Jeff Snell: Good
Steve Kerschke: To go there.
Jeff Snell: So after the presentation is over, they’ll be available.
Steve Kerschke: Okay,
Jeff Snell: Sounds good.
Steve Kerschke: Alrighty.
Jeff Snell: Then in that case, I will jump right into it. So our primary topic today, again, thank you for joining. Great to see a crowd online today with us. I was trying to see what is the total attendees?
Steve Kerschke: Looks like we got 242.
Jeff Snell: 242. Excellent. That’s fantastic. So welcome everybody, and thank you for joining us. Our topic today is going to be aging after TBI, and I emphasize the word after because it’s a very different topic than aging and TBI. We know there’s an increased risk associated with aging and then experiencing a TBI from a variety of etiologies. As a matter of fact, the older you get, the more likely you are to have a TBI according to the data, but we’re going to be focusing on what is the impact on the aging process when one has previously experienced a TBI? How is the trajectory of aging potentially changed or altered by having experienced a TBI? Now, as we age, our cognitive and physical abilities change, but what impact does that TBI have on the typical aging process? What are the increased risks that we are more exposed to as we age with a history of having had a TBI?
And knowing those risks, how can we best prepare? How can we treat and foster healthy aging after TBI? I have had a couple of people ask if the data similarly apply to the more broad diagnosis of acquired brain injury. And I have to say that the vast majority of research that’s been conducted on the subject is specific to traumatic brain injury. Now that being said, I did uncover an editorial article from a couple of years ago, 2024, that states that there is evidence over recent years that acquired brain injury, non-traumatic in nature, is associated with a similar accelerated brain aging, although the author noted that there are very few studies focused on acquired brain injury as opposed to traumatic brain injury, and that more studies are needed to examine the underlying mechanisms by which these changes may occur. So accordingly, aging after brain injury, traumatic brain injury will be the data supported research underlying today’s presentation.
Now, the relationship between aging and TBI is complicated, and as is suggested by highlighting of the word after in the title of this presentation, changing that word can result in a very different set of information. With regard to aging and TBI, we know that there’s an increased risk associated with aging and then experiencing a TBI from a variety of etiologies. The risk of experiencing a TBI goes up dramatically as we age with significantly higher risk for individuals over 65 years of age and those individuals 75 and above having the highest rates of and mortality from traumatic brain injury. And those are primarily due to falls. You see in the graph here the admission rate for individuals that are hospitalized after a head injury. It is the blue line for all folks for all injuries, and the admission rate of trauma on the red line is that for moderate to severe head injury.
So as we get older, medical practice dictates, I mean, if you go to the hospital with a fall and you’re on a blood thinner, you are almost certainly going to get a CT scan and you’re more likely to have a bleed on the surface of the brain just because of the normal atrophy that occurs over time and those bridging veins being more vulnerable to ripping and tearing from a fall. So falls tend to be disproportionately for an elderly population, one of the reasons that people are hospitalized and subsequently diagnosed with a brain injury. So what we’re going to focus on today, what’s the impact of the aging process when you previously had a TBI and how is the trajectory of aging potentially changed or altered by having experienced a TBI? If I was asked to summarize the impact that having a moderate to severe brain injury has on the human body, not just brain function, but all aspects of physiological functioning, I would have to say the evidence supports an accelerated aging process.
As we age, all of us experience brain volume loss, that’s known as atrophy, a shrinking of brain volume. This process typically begins in our 30s and 40s with a relative steady decline of around 0.2 to 0.4% annually, year by year. This atrophy becomes more pronounced and more progressive. It accelerates over the age of 60, increasing to 0.5% of volume or more per year. This occurs in typical and healthy individuals, but it’s more pronounced in those individuals who are diagnosed with some neurodegenerative condition such as dementia or in those individuals who have sustained a traumatic brain injury. One of the striking findings of research involves physiological evidence of changes within the brain that can result in premature atrophy, that is a reduction of the physical volume of brain tissue at a younger than typical chronological age. So studies that have done this have looked at predictive modeling of brain age scores within MRI data, looking at complicated mild, looking at moderate and severe traumatic brain injury, all are associated with a higher predicted age difference.
In such studies, a predictive algorithm estimates age on the basis of specific MRI findings, and those individuals who had moderate to severe or even complicated mild brain injuries demonstrated a greater difference or discrepancy between their actual chronological age and their predicted brain age. Having a TBI, moderate to severe or even complicated mild injury produces an increase in biological brain age as compared to chronological age, averaging across several studies, similar findings indicated around a five-year discrepancy between actual and predicted age for moderate to severe TBI, and a one to three year discrepancy for complicated mild TBI. Now, in the same study, findings showed that a higher predicted age difference widened with a longer time since injury with men showing more advanced brain age than women. This study concluded that changes in brain structure after TBI are dynamic with an initial period of change followed by a relative stability in brain morphometry that is basically from a radiological perspective, the brain’s shape, size, and form, but eventually leading to further changes in the decades after a single TBI event.
That curve of increasing difference between chronological and observed brain age began to increase at about seven years post-injury and continued to widen thereafter. So that initial period of change followed by relative stability is consistent to what we’re pretty much all familiar with in terms of traumatic brain injury. There is an acute phase of recovery following a neurological insult followed by some degree of plateau of medical status and functional abilities. We often refer to that as reaching maximum medical improvement. But what research has demonstrated is that the changes to the brain resultant from that injury, individuals experience an accelerated process of aging over time, and that acceleration continues to increase with time as well.
Even in mild cases of TBI, studies have shown steeper rates of regional gray matter annual volume loss in healthy than in healthy controls. For mild TBI, this finding was observed in approximately 80% of the cases studied. This finding is interpreted as reflecting “older than expected” regional brain ages in those subjects who had experienced even a mild traumatic brain injury. Those regional changes are typically more focused in frontal and hippocampal brain volume. Now, several studies have reported associations between TBI with loss of consciousness and Alzheimer’s disease. The Institute of Medicine concluded a moderate to severe brain injury was an Alzheimer’s disease risk factor. There is an association between TBI with loss of consciousness and accumulation of neurofibrillary tangleds, which is an Alzheimer’s disease risk that is associated with Alzheimer’s disease. In prior studies, similar associations have been observed with Parkinson’s disease as well, Parkinsonism, and Lewy body disease, as well as other neuropathic changes.
So regardless of the classification of the type of dementia, there is an increase in incidents noted following moderate to severe TBI with a stronger association noted when loss of consciousness was present as a result of the injury. We have to acknowledge that TBI is not a heterogeneous diagnosis. It is an umbrella that covers everything from a mild concussion with which you might have complete resolution in a matter of minutes or hours to life-ending injury and everything in between. So there are a host of possible effects that can result from a brain injury that may or may not be present in a given case and also exist on a spectrum of severity. These are all things that potentially can change as a result of a brain injury.
Now, these comparisons we’re going to be talking about take into account the changes in various aspects of functioning that are considered typical as we age. According to data from the CDC, approximately 93% of adults age 65 or older have at least one chronic condition with aging associated with increased risks for a number of different conditions. The cognitive declines associated with dementia are a point of overlap, and the risk of dementia increases substantially with age beyond just mental lapses and forgetfulness that most people attribute to aging. Our bodies change as we age and our motor strength and our reflexes decline. Hearing and vision in particular are issues that are common with age. Depression is not considered a “normal effect of aging,” but often stems from life changes that result in loss of independence and loneliness or changes associated with chronic illness. There are behavioral and personality changes that are associated with various forms of dementia that impact frontal brain functioning that is not related to TBI.
According to the National Council on Aging, the five most common chronic health conditions associated with typical aging include elevated blood pressure, elevated cholesterol, arthritis, obesity, and diabetes. Now, given that some of the changes associated with typical aging are also overlapping and associated with brain injury, you can see it can be difficult without a clear history to differentiate the etiology of these presentations purely on the basis of reported symptoms. But what studies have found is that there’s a greater acceleration of decline in all of these various aspects of functioning after TBI relative to a non – TBI population, declines that occur earlier and are more pronounced in an aging population of individuals who have previously sustained a TBI.
Underlying the changes observed after an individual experiences TBI are the alterations of brain’s functioning. The residual impact of having experienced a TBI reflects the changes to the neural structures and neural networks that are critical to those functions. Physical structural damage in a TBI is the immediate mechanical damage resulting from impact, from acceleration, from deceleration, from blast waves, things that deform brain tissue, and particularly vulnerable are the delicate transitions of gray matter and white matter boundaries within the brain. The brain vasculature is also vulnerable to structural damage and more severe injuries with damaged vasculature resulting in hematomas either on the surface of the brain as well as secondary processes involved in hemorrhagic neurological insults. When blood is present within the interstitial space of the brain, within the space between the cells of the brain, this can create toxicity, release of excitatory neurotransmitters or hormones, and potentially the breakdown of damaged tissue within the brain.
One relatively common issue associated with more severe injury is something called diffuse axonal injury or widespread damage to the insula, the white matter that makes up the primary super highways of communication throughout the brain. Diffuse axonal injury often shown within medical records is DAI and then graded on the basis of how widespread it is, diffuse axonal injury one, two, or three, three being the most widespread and involving the brain stem as well. Diffuse axonal injury is a potential consequence of the mechanical forces combined with the physical vulnerabilities of having jello-like brain tissue. It is easily damaged as a result of force, particularly the amount of mechanical force involved in severe injuries. Now, secondary processes can include neuroinflammation with cellular damage to the brain resulting in the release of damage-associated molecules which activate the brain’s immune response. This initial inflammatory response is typically focused on clearing debris and facilitating repair, but chronic neuroinflammation has the potential to produce further neuronal damage.
This cycle of ongoing neuroinflammation is believed to be a contributor to the ongoing neurodegeneration that is observed after a severe injury. Now, there are research findings that are brought to light the association between the increased risk of neurodegenerative disorders, including frontotemporal dementia and Lewy body dementia after TBI. Moderate to severe TBI is associated with significantly faster beta amyloid accumulation in men and in postmenopausal women. There’s some apparent hormonally regulated neuroprotective factors in pre-menopausal women, so that changes after that point. If there is reduced waste clearance within the brain, there is a risk of an increased rate of amyloid buildup. These protein aberrant protein chains build up within the brain, and this is likely one of the drivers of that increased risk of various types of neurodegenerative conditions. Vascular dementia occurs in typical aging in around one to 4% of individuals over 65. Now, vascular dementia is a neurodegenerative condition that results from blocked or reduced blood flow within the brain, and it can be sudden as in the case of a stroke or very gradual and insidious as in the combined effect of numerous microvascular ruptures.
When you combine factors such as age, diabetes, and alcohol abuse with hypertension, you almost are going to be guaranteed some degree of that insidious white matter change, which is microvascular strokes, lacunar strokes widespread throughout the brain. So again, when it comes to disruption of the vasculature, it can either be major as in the case of a stroke or ongoing and buildup of that over time that occur as a result of those microvascular ruptures. The upshot of all of that is the risk of vascular dementia after TBI is over a five-fold increase. So it goes from one to 4% to five to 20% when it comes to those individuals who experience vascular dementia secondary after a brain injury. That’s actually closer to a six-fold increase within some of the more recent data. Now, after a moderate to severe TBI, potential effects include cognitive effects, difficulty understanding and thinking clearly, trouble communicating, learning skills, problems with attention and concentration, difficulty remembering new information, or a general slowing of information processing.
Now, when we talk about memory, memory and brain injury are two constructs that both are so broad as to almost be useless as a single word or construct. To say somebody has a brain injury doesn’t give you very much information, and when you ask somebody how is their memory, they tend to respond as if memory is a unitary construct and it is not. We have so many different kinds of memory. We have verbal memory, visual memory, auditory memory, olfactory memory, immediate memory, short-term memory, long-term memory. Memory is a complex process within the brain, and it’s dependent upon key structures that are some common to all forms of memory such as the hippocampus, but also communication pathways that are specific to the type or the format even of the information. Likely because memory is such a complicated process, memory is easily disrupted by injury or by neurodegenerative processes.
Memory and particularly the restoration of memory functioning is one of the key metrics that we look at to utilize quantifying the severity of a brain injury. What is the length of time after an injury that a patient demonstrates the ability to accurately attend to, store, and retrieve new information? The longer that period of time that disruption of memory functioning is noted, well, that is associated with a more severe injury. The sooner that starts to come back, that resolution of post-traumatic amnesia, the quicker that comes back, the less we consider the severity of the injury. Now, likewise, processing speed, how quickly and efficiently we’re able to take in, process, understand, and respond to information is something that can be disrupted as a result of traumatic brain injury. If there’s widespread disruption of the communication pathways, as is often the case in more severe neurological insults, then it makes sense that information’s not going to be moving as quickly and efficiently as it was prior to those networks being disrupted.
As a neuropsychologist, measures that reflect processing speed are one of the many metrics that I’m looking at in assessing functional abilities after injury. As compared with other individuals of a given age and education level, where does your score fall on a task that requires quick processing or quick response on a timed completion, whether that be a simple or a complex task? Executive functioning, again, is another very, very, very broad umbrella term that incorporates things that are considered higher order brain functions, and they mostly reflect frontal lobe neural circuitry in concert with cerebellar regulation and automaticity. Again, there are functions that are diametrically opposed to each other that fall under executive function. So when somebody says, well, they’ve got executive functioning impairments or compromise, you have to ask the follow-up question of, okay, which ones? Because there are a bunch of different ones that fall within that bucket.
Planning, organizing, impulse control, initiation, inhibition, emotional regulation, these are all frontal executive functions. Another big one, particularly when it comes to more severe brain injury, is self-awareness and insight, awareness of one’s own deficits and ability to therefore potentially compensate for them. You can’t compensate for something that you’re not aware of. These are considered within the realm of executive functioning, and they’re heavily dependent upon neural circuits within the bilateral frontal lobes as well as the right parietal region of the brain. So damage to the frontal lobes can impair that particular executive functioning as well. That might very well be why when you have someone who needs drop-in support but otherwise is living independently, might tell the person who shows up to be that helper, “Don’t need you. I’m fine. Thanks.” So individuals who are significantly compromised after brain injury often do not have that level of self-awareness of areas in which they are different, kind of a failure to update their registry of what their capacities are, something that we naturally do over time with those gradual changes when we do have awareness, but can be compromised by a brain injury.
Now, there’s some degree of decline in these cognitive abilities that are associated with typical aging, but what studies have found is that this decline is heightened or accelerated in a population of individuals who have experienced a traumatic brain injury. That decline is more noticeable and occurs at an earlier age relative to a cohort of individuals who have not experienced a TBI. Like all the aspects of accelerated aging that we’re talking about, this undoubtedly reflects a lowered plateau of functional ability post TBI relative to that individual’s prior abilities. But the accelerated decline over time relative to their age is what we’re talking about today with that accelerated aging process. Now, along with accelerated aging comes more significant declines in physical activity with accompanying deconditioning and reduced independence in daily activities, declines that are associated with vestibular and musculoskeletal systems and a heightened risk of falls. Older adults have a higher risk of falls secondary to changes in reaction time, in strength, vestibular changes, but when you add in the residual symptoms from a TBI or the aspect of accelerated aging, falls become more of a risk for a subsequent injury at an earlier age.
Then there are the physical issues associated with normal aging that are related to changes in a variety of issues. We have a change in our immune system as we age. We have a less robust immune response. We have increased risk of cardiovascular diseases, metabolic diseases such as diabetes and obesity, and musculoskeletal diseases such as osteoporosis and osteoarthritis and others. Many of these diseases and disorders are associated with our level of physical activity and anything that changes our physical capabilities and/or our physiological functioning can be a direct consequence of TBI and put us at greater risk of those diseases. If you’re unable to return to work, for example, as a result of an injury or unable to return to your normal routines, I live on a farm, I do a lot of work around here, and that keeps me physically active and healthy. If I were to have an injury that changed my physical abilities where I could no longer engage in that level of physical activity, it would have an impact on my physiological functioning.
It would have an accelerated impact on my aging as well. The activity demands of your regular life and work routines keep you healthy. If those routines are no longer in place, then one consequence is a level of deconditioning that makes us further vulnerable to physiological decline.
In a study looking at health-related comorbidities associated with aging and TBI, one of the major findings was that compared with a non – TBI cohort of similarly aged individuals, that there was a significantly higher comorbidity burden, primarily driven by elevated rates of mental health disorders. This was particularly true for depression and anxiety symptoms of the TBI participants in that particular study. Emotional or mood issues can include reacting with heightened emotional response, increased nervousness and anxiety, feeling more angry, irritable, aggressive even, or a very common change of increased incidents of sadness and depression. These are all issues that can be a direct consequence of TBI and dramatically impact an individual’s life satisfaction and engagement. Behavioral challenges can include troubled self-regulating behavioral response, what we would call personality changes, particularly frontal executive dysfunction that results in greater impulsivity, less filtering of those automatic reactions that We may have to a given situation.
Although this tends to be much more of an issue in the immediate acute phase of recovery, that agitation and restlessness that often accompanies the earliest stages of cognitive recovery, in cases of more severe injury or specific focal aspects of damage to frontal neural networks associated with inhibition or self-awareness, you can have chronic residual effects of decreased frontal executive functioning present to varying degrees across the lifespan. That has an impact. In cases where there remains significant frontal executive impairment, and again, particularly when it comes to dysregulation of emotional or behavioral actions, this baseline of disinhibition can make assessment, diagnosis, and treatment of frontal dementia-like presentations difficult to quantify. This brings up the point that when conducting an assessment in which dementia is suspected or a differential diagnosis of dementia is the goal, it is important to gather accurate history regarding the potential of a presence of a prior brain injury, particularly traumatic brain injury.
And if present, the degree to which that individual’s abilities were impacted by that injury. In other words, what was the highest post injury baseline of functional, emotional, and behavioral regulation that was achieved? Because that really muddies the water when you are looking at the disinhibition that might be associated with different types of dementia as well.
Steve, not seeing any questions so far. I’m just going to keep on rolling until somebody asks me. Okay?
Steve Kerschke: Go on, Jeff. You’re doing great. Or you
Jeff Snell: Can jump in too. Yeah, feel free.
The accelerated aging of the brain after TBI that we’ve talked about is manifested as accelerated declines and it impacts participation and engagement, the ability to meet our life or work demands, or even just our hobbies or activities. These are things that can impact a lot of different aspects of our life. Motor changes and physical limitations. They’re common in aging and progressive loss of strength declines in balance, musculoskeletal deterioration. I mean, these can present as primary symptoms of brain injury and their presence at an earlier age than would be typical without a brain injury brings the functional limitations that would otherwise not be encountered until a later age. It’s effectively an accelerated physical functional decline, which includes reduced participation challenges and health conditions that would typically be reflected in a more aged population. I do see a couple of questions popping up. I’m going to see if I can put on my mind and put on my glasses.
Speaking of aging, there we go. Are there any studies that quantify the percentage of post TBI individuals who experience disinhibition agitation behaviors? Yes, those are found typically within the TBI model systems. I would say that is probably the most accurate large end study where they have at this point tens of thousands of individuals that have been through similar treatment and assessment and follow-up. So I’d highly recommend that. I’ve got a referral to that actually toward the end of this presentation. And then another one just mentioning here, I’m viewing this from a patient’s family member, not a case manager at the moment and absorbing this differently. Yes, that very much is the case if you are a family member that you have seen this through a loved one. Are in some of our cases, and mine in particular as well because I turned 65 last year, falling into that aging population as well.
And thinking back on the two times that I had a loss of consciousness associated with a concussion in my youth, one of which I reported and one of which I kept quiet because I didn’t want my mom to make me stop riding my motorcycle. So yeah, these are all things that hit close to home.
Chronic health conditions associated with TBI would include neurodegeneration, greater susceptibility to dementia, to Alzheimer’s, to Parkinson’s, to other neurodegenerative diagnoses. We know that there’s an increased risk of epilepsy, of seizures following traumatic brain injury. And when present, this increased the risks of other aspects of physical injury. Also associated with traumatic brain injury is a risk of cardiovascular disease. Actual having had a traumatic brain injury puts you at greater risk for hypertension, for coronary artery disease, for stroke and for diabetes. These can be primary in relationship to the regulatory aspects of the brain affecting these physical manifestations. In other words, the hypothalamic pituitary axis often is injured in a traumatic brain injury just because of its vulnerability of where it is within the brain. And that changes our hormonal regulation. So that can result in some of these issues as well. They can also be secondary issues related to changes in activity level.
The more inactive we are, the more vulnerable we are to some of the cardiovascular issues as well. Seeing a note here, someone says, “I am seeing a common practice of obtaining eyebox tests, V-G-N-E-E-G, for TBI. How useful and accurate are these results?” The eyebox test is not something that I am familiar with and would actually have to look up to be able to answer your question. But I just attended a couple of weeks ago several sessions on looking at blood biomarkers, and that is something that we’re actually going to be doing a presentation on I think about four months down the road. There is a lot of new information coming out on the accuracy of different biomarkers that can quantify severity of injury.
And here’s a question that says, “This may be a little too left field, but how do you feel like we’ll be seeing similar symptoms from the aging metal/rock concert attendee community?” That one is left field. I’ll give you credit for that one. I would totally be talking out of the side of my mouth on this one because I don’t have any empirical data to go on, but I would have to see whether or not there is any indication within the literature that attending rock concerts could potentially have any impact on long-term chronic brain function. I don’t know. I’m assuming that you’re probably talking more about the head banging aspect of heavy metal, but yeah, I mean that certainly can be repetitive subclinical from the standpoint of impact on the surface of the brain. All right, I’m going to go back to gear here. And now as we’ve previously talked about, there are limiting aspects of cognitive changes and increased risk of various dementia presentations that are associated with traumatic brain injury.
In one 2024 published study, despite the inherent heterogeneity in various brain injury related research investigations, TBI was noted across multiple studies to significantly increase the risk of dementia, as we’ve talked about, with a stronger association found in cases of moderate to severe injury and as we’ve mentioned, when associated with loss of consciousness. There are several factors that have been identified as associated with poor aging outcomes after traumatic brain injury, including a higher risk of mortality. Chronic health complications and functional declines contribute to decreased participation and decreased engagement. These include comorbid conditions, hypertension, diabetes, preexisting comorbidities that complicate cognitive or physical functioning after injury. Although it’s somewhat circular in terms of causality, all of the impacts of TBI on an individual’s functional abilities have the potential to result in poorer outcomes. Immobility is associated with poor aging in the general population and there’s an increased risk of immobility or decreased physical capacities after traumatic brain injury.
There’s an increased risk of seizure disorder. I’ve mentioned that earlier after traumatic brain injury. And as mentioned, if a seizure disorder is present, there’s an increased risk of unintended physical injury. This factor is also associated with an increased risk for subsequent brain injury. We know that there is a greater risk of brain injury if you have had a prior brain injury, and part of that has to do with those increased risks of falls, which as we age tend to be the most common etiology of brain injury. Physical and mental health comorbidities were associated with poorer outcomes in the TBI population in the study that showed bidirectional association between physical, cognitive, and emotional health concerns on the one hand and reduced independence, the need for in-home support or skilled nursing facility placement that reflect that accelerated frailty on the other hand. Now, ultimately, the process of accelerated aging and the heightened risk of various issues associated with a reduced lifespan expectancy.
Life expectancy after a severe traumatic brain injury is reduced by an average of seven to nine years compared with the general population. Now, this statistic undoubtedly disproportionately is impacted by the fact that the first six months post-injury carries the highest risk of mortality, but that overall average is reduced. Moderate traumatic brain injury can reduce life expectancy by an average of four to nine years compared with the general population with a similar heightened risk of mortality in the first six months post-injury. Interestingly enough though, patients with a mild traumatic brain injury typically have a life expectancy that is nearly identical to the general population with studies showing a minimal reduction of only about six months, so a six-month reduction in overall average life expectancy for mild injury. So knowing all of these risks, what should we do? Well, first, clinicians should consider long-term cognitive screening and management for individuals who have a history of TBI, particularly those with moderate to severe injuries.
Because the base of evidence regarding the increased incidence in earlier onset of dementia for those aging with a history of TBI, ongoing monitoring through regular follow-up assessments has been recommended in order to make any necessary adjustments to maintain effectiveness of treatment strategies. Within these follow-ups, identifying any new or worsening symptoms is an important component. As with just about any presenting symptoms, early identification and intervention is recommended to optimize outcomes. As treatments develop that are able to slow neurodegenerative conditions, as these emerge and are refined, appropriate initiation and management of those treatments will be necessary based on the factors in any given case. I see a few questions popping up. Let me look at them. How is traumatic different than other brain injuries? In order for a brain injury to be classified as traumatic, it has to be as a result of force. In other words, mechanical forces cause damage to the brain.
This is different than an anoxic brain injury, which might be because of a cardiac infarction that stops your heart and are near drowning or strangulation. Those are anoxic or hypoxic injuries. The most frequent anoxic brain injuries occur as a result of anesthesia accidents in surgical procedures. So that is a non-traumatic. Also, infection is non-traumatic, toxic exposure is non-traumatic, and a stroke is not considered a traumatic brain injury, although it can be secondary to the result of traumatic injury. Loss of consciousness has been referred to several times. Does it matter if loss was due to medically induced comatose state? Loss of consciousness as a result of trauma is what we’re talking about in this particular instance. If it is a medically induced coma or medically induced loss of consciousness, no, that is not the same and does not carry with it the same risks. Would this accelerated risk of dementia and Parkinson’s also apply to survivors of ruptured brain aneurysms that are now healthy and active?
Again, the more recent data has suggested that that is possible, but we simply don’t have the empirical evidence of research studies out there to definitively say yes to answer that question. One would assume so if the conditions are similar to those encountered after a traumatic injury in terms of physical damage to the brain or the cytotoxicity of glutamate that causes further damage. But again, without that evidence out there, I can’t really say that that is the case.
All right, so considerations for monitoring. A comprehensive assessment of functional abilities is recommended for mobility, for communication, for mental health, and for social interactions so that appropriate emerging needs can be identified and appropriate interventions or supports can be put in place. Again, we know that individuals after a traumatic brain injury have these increased risks. We need to be monitoring for them specifically and more frequently than is typical. Now, part of the issue is as we get older, we tend to not go to the doctor necessarily as often. At least it’s a little bit harder to get men to go to the doctor, which is probably, can’t say it’s causative, but definitely associated with a shorter lifespan. And I mean health for all aspects of our body, including our eyes and our hearing and our teeth, which for some reason I do not understand, insurance does not consider to be part of our body.
We have to have separate insurance for some of those things. Don’t get me started.
Support for caregivers is recommended to be part of this routine monitoring as well, making sure that families are well supported and to help them deal with the demands and provide a higher quality of care. Beyond just the patient and the family long-term management of aging after TBI often involves collaboration with community-based services to bring in appropriate support resources that are needed. This can include medical support such as in-home services, general social services, case management, community-based recreational and socialization opportunities. We want to provide what all of us want as we age, a comprehensive support network that allows us to maximize our independence and have a sense of purpose and meaning at whatever stage of life we are in. Successful aging involves monitoring and treating a variety of different factors for all of us, but there are these specific risks to which a history of TBI exposes us so the relative emphasis may be altered depending on the effects imparted by that prior injury.
You see in the periphery of this graphic, the outside of the circle of factors that are supportive of healthy aging, specific aspects that are related to each of the major domains, socioeconomic demographics that bring more resources to the table, income, occupational level, education, and unfortunately whether or not a person has health insurance.
Again, don’t get me started. Socioeconomic demographics can play a role and are considered in the new taxonomy of brain injury as moderating factors that need to be taken into account, which can have predictive and prognostic value. We need to look at the psychological factors that we can focus on to improve our outlook, improve our physical and mental health, and healthy physical supports, nutrition and lifestyle that can allow us to age healthily. The goal in each of these areas is to improve and maintain good cognitive physical health and to remain engaged and active in living. Many of the recommendations for healthy aging after TBI mirror those for healthy aging in general. Regular physical activity. This goes back to what I’ve said many times before as a practicing psychologist. Somebody asked me, what can I do to improve my cognitive functioning? What can I do to improve my mood?
The answer is the same for either one. Get up, get active, get out, move, get out in the sunshine. To the degree to which you’re physically capable of doing so, engage in some form of physical activity and exercise on a daily basis. Our brains and our bodies are not separate and they’re not independent organisms, and you have to keep your body healthy to keep your brain healthy. Regular exercise is essential. These chronic conditions that we tend to have as we age, we could all do a better job of healthy aging or have those issues that we need to keep a close eye on as we age. A sedentary lifestyle is associated with one of the greatest risks as we age. It contributes to a variety of health issues including obesity, heart disease, hypertension, elevated cholesterol, and a host of other issues. Keep moving. Another recommendation is to avoid those things that place us at greater risk for physical injury or physiological compromise.
Smoking’s not the issue it used to be, but smoke and vaping is still around, probably not the most healthy thing one can do. Alcohol. Alcohol use is associated with unintended injury as well as many health problems. It is an avoidable risk multiplier. We’ve talked about the increased need for medical monitoring as we age, but avoiding or skipping doctor visits can put us at greater risk as we age as well. Keep up with your appointments, manage those aspects of physiological risk to which we are all exposed. If you’ve got hypertension, treat it. If you have hyperlipidemia, treat it. There are medications that control those things quite well. Given that hypertension is considered one of the highest risks associated with aging, antihypertensive medications are likely to be one of your front lines of defense against many of the cognitive declines that we’ve talked about. Diet, a diet designed to reduce oxidative stress and manage neuroinflammation such as Mediterranean or ketogenic diet.
These are among current recommendations within the literature. Basically, eat healthy. Also, as a psychologist, I recommend stress reduction exercises to reduce cardiovascular risks. In addition to medication, meditation, relaxation, even something as simple as breathing exercises that can lower your heart rate and lower your muscle tension or import it. Basically for any medical diagnosis for which a treatment exists, follow those recommendations. Keep up with those ongoing visits. Something that’s a callback to my last webinar, sleep. Make sure you’re getting good sleep hygiene practices, getting the amount and quality of sleep that you need. Deep sleep is when your brain’s cleaning crew goes to work, so practice those recommendations that are supportive of good quality sleep. Challenge yourself cognitively through learning new information or skills or engaging in reading or listening to podcasts. All the better if you can challenge yourself cognitively with others. Socialization, maintain social connections to find an environment where you can expand your social network, strike up a conversation with a stranger and learn something new.
Lastly, look at home safety modifications to decrease risks at home. Proactively make the home as fallproof as you can by removing trip hazards, increase lighting, install grab bars in the bathrooms. If you’re 65 and you’re considering moving to a new home, maybe don’t choose one that has different levels for every room in the house. A single level home reduces the risk of falls. You can’t fall down the stairs if you don’t have stairs.
Now, as I stated early on, research regarding accelerated aging after brain injury is primarily applicable to those having sustained a traumatic brain injury, but I believe that a lot of the recommendations for healthy living apply equally to the larger umbrella term of acquired brain injury, as well as those of us who have never experienced a brain injury. I really liked a quote that I saw recently, which was, “Do not regret getting older.
It is a privilege that is denied to many,” or one that my wife had told me one time, “We all get to be young. We don’t all get to be old.” Now, I’d like to recommend this resource as assembled by the Model Systems Knowledge Translation Center, which is a part of the TBI model systems. This is their let’s get the information out webpage. It’s a collection of resources for people living with TBI and for their supporters. There are fact sheets in PDF format as well as videos and slideshows on a variety of topics, and there are over 30 topics that are currently covered there. Steve, I’m going to turn it over to you and then I’ll real quickly get to a few questions that we have here.
Steve Kerschke: Yeah, thanks, Jeff. So there’s a couple questions sitting in there for you, and then I had a direct question that I’m going to send you in our direct chat, so take a look at that as well. In the meantime, I will launch the poll question. That should populate on y’all’s screen. Go ahead and fill that out. And then if that chat one doesn’t come through, Jeff, I can text you directly.
Jeff Snell: Oh man, it won’t let me vote, Steve. You got me locked out of the vote.
Steve Kerschke: I think you know the answer to this one.
Jeff Snell: Well, it’s an open book test. I mean –
Steve Kerschke: That’s fair.
Jeff Snell: Right? Yeah.
Steve Kerschke: I just sent you a text in case that chat didn’t come through on the other question that I had.
Jeff Snell: Okay. I’m looking at a few of them here. Are the use of Alzheimer’s meds such as Aricept or Namenda recommended? I would say anything that is medically recommended for treatment of a diagnosis, if one has that diagnosis, would be appropriate. With brain injury, you have to keep in mind that sometimes the neural networks that are involved are altered, are structurally may not be the same and may not respond to medication in the same way. But if a diagnosis of Alzheimer’s is given and those are medications that certainly are given for Alzheimer’s, then that would certainly be appropriate. It says, “I talked about smoking and alcohol use avoidable as known to cause medical concerns long-term. What about cannabis and the entire legalization in some states and how that affects cognition and long-term effects?” Colorado was one of the first states to legalize recreational use of marijuana, and as such, had a lot of research early on and ongoing with the chronic effects of marijuana use, one of those being a disruption of memory functioning that is not just acutely to while you’re using, but also can be a chronic post-use issue as well.
If you have a brain injury and you have memory problems, vaping, smoking marijuana, taking THC is likely to further compromise memory functioning, and it’s not something I would necessarily recommend, and there are other unintended injury issues associated with that as well. What is the risk of psychological disorders such as schizophrenia with a TBI? There is an increased risk of brain injury in individuals who have certain psychiatric diagnoses, particularly those that result in some degree of disinhibition. And again, unintended injury is the primary means of such injuries, car accidents, falls, such as that. So bipolar disorder, schizophrenia, any of those potentially can be an increased risk for head injury. I have patient 5.5 years status post TBI who used alcohol and marijuana both before and after injury. About three years out, they were diagnosed with encephalomalacia of the brain, which has recently progressed quite rapidly to dementia.
Is this encephalomalacia something that a TBI would cause? Yes, the answer to that before I finish that sentence. And then can it also cause that rapid progression? Yes, it does. Encephalomalacia is the medical term for a softening or decreased volume within a given area of the brain as a result of damage. In other words, some degree of volume loss in a region of the brain, for example, within the frontal lobes. Encephalomalacia is often noted following TBI because the fact that frontal lobes are most often the point of impact in traumatic brain injury. So encephalomalacia is when you look at an MRI for an individual who’s previously suffered a brain injury, and that includes anoxic injury where you have a loss of tissue throughout a region of the brain or globally within the brain, that different look on an MRI of that kind of less dense tissue is classified as encephalomalacia, and it is a long-term consequence and it is associated with that accelerated aging as well.
Can you clarify if head injuries can be stacked, get worse with each one that one has or has that information been disputed? Again, typically it depends on the severity of injury, but a brain injury that occurs prior to the resolution of symptoms of a first injury, that second impact syndrome is well documented and can be life-threatening. And it’s typically because of a vascular response, basically the loss of blood flow as a result of a vascular response to that second injury, which is the equivalent of a global acute anoxic injury to the brain or global occlusion, even though it’s the arteries clamping down themselves, the muscles within the arteries causing the blood flow to decrease radically.
Is there a length of time one has to be unconscious to be considered a traumatic brain injury? No, it does not. A concussion with no loss of consciousness is also technically a brain injury, and there is now an ACR definition out there on how that is diagnosed. It’s basically a series of steps that you go through. If you have a mechanically plausible cause of injury and observable clinical signs immediately after injury, that is full stop all you need to diagnose concussion. In other words, with no loss of consciousness on the football field, player gets hit hard, falls down to the ground, immediately gets up, but then kind of staggers a little bit on the way back to the sideline, you have now diagnosed that individual with a mild brain injury and they need to be taken aside and a further examination done. For an individual with chronic back pain, do you have evidence that would support the use of edible marijuana as being preferred to opioid medications for pain?
That is so far out my wheelhouse that I’m not even going to try to answer that one. I don’t have any empirical evidence one way or the other. I have what I would consider to be a common sense response, but I’m not going to answer that one using just my common sense because my wife tells me sometimes it is not as common or sensical as I might otherwise presume. We are at 11 o’clock my time, 10 o’clock yours, Steve.
Steve Kerschke: Sharing the results of the poll. Jeff, I might have missed it. Did you – 100%.
Jeff Snell: Steve, 100%.
Steve Kerschke: We did all right. I might have missed – Congratulations,
Jeff Snell: Folks.
Steve Kerschke: Did you answer The text message poll question.
Jeff Snell: Oh, let me see that one real quick. Patient and family history of Parkinson’s, should the severity of TBI be taken into account before relating Parkinson’s disease to the TBI versus relationship being a natural progression or familial history? What level of TBI severity would likely lean towards PD being related to TBI? It depends on when and when these occurred in time. Certainly if the Parkinson’s was diagnosed prior to the TBI, then that natural progression might be a little bit accelerated by the injury itself. If it might be more the case, the TBI occurred prior to the diagnosis of Parkinson’s. It likely should be taken into account just from the standpoint of potential causative, what was the person’s baseline of recovery after the TBI? In other words, what aspects that would overlap with Parkinson’s may have existed post TBI, but pre Parkinson’s diagnosis. That would be important to take into account, but the treatment likely would not be affected very much at all from what I’ve seen in the literature.
In other words, after TBI, if symptoms present that are consistent with almost any given physical diagnosis, you treat the diagnosis as you would in the absence of a TBI. Just keeping in mind that you might have to alter it in different ways depending on what chronic issues come up. And I see a statement there that says, “I didn’t see the poll question.” And I would say if you did not see that, then Steve, likely they need to contact you.
Steve Kerschke: Yep. Just contact me if you didn’t get the poll question. Same thing. If you have issues with the form upon exiting the webinar, reach out. And then final reminder, Jeff, if you want to advance to your contact information, I’m sure
Jeff Snell: Jeff – And all the references are in here as well. If you want to do a deep dive, there’s a lot of really recent and good information there to find. Feel free to call me or send me an email directly if you did not get the opportunity to get your question answered, and I will be glad to respond.
Steve Kerschke: And then upon exiting, the form should automatically populate within your webinar or your internet web browser. If you have issues with that, likely it’s a pop-up issue on your end or a firewall issue on your company’s end. Please let me know if that happens to be the issue. We’ll send it to you directly. We’ve also had some issues with not getting the follow through email, whatever it is, just let us know. We’ll get you taken care of. With that, Jeff, thanks again. As always, already getting really great feedback and the information certainly relevant and appreciated that’s pretty cutting edge too. So thank you everyone for joining us. We will be off next month, but back then month after that. So looking forward to seeing you then.
September 21, 2026 by Haley Hansen, PT, DPT
Video Transcription Steve Kerschke: It’s nine o’clock. We’ll go ahead and get started. Well, welcome back to our webinar series, and this is our first one of the new year. […]
