September 21, 2026 by Haley Hansen, PT, DPT
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. We are excited to welcome Dr. Jeff Snell again. Jeff is a regular presenter with us, so Jeff, thanks for volunteering. And to our listeners, a little bit of a forecast. Jeff has volunteered for six webinars this year, so it made our job easy in terms of finding quality presenters. And then also I’m excited for the content that between Jeff and myself and the rest of our clinical teams, we were able to come up with. So looking forward to that. But as it sits today, we’re going to be talking about sleep. And if you just signed on, you missed some terrific dad jokes, and we’ll try to keep those to a minimum the rest of the presentation. But we will tell you a little bit about QLI before we get started.
So those of you familiar with QLI, welcome back and glad to see some familiar names. But if you’re not familiar with QLI, we are based in Omaha, Nebraska. We are primarily known for our post-acute rehabilitation program, but we’ve also slowly developed an outpatient telerehab program. So think of it as an outpatient virtual clinic. In either case, we focus on traumatic brain injury, spinal cord injury, chronic pain, limb loss, and stroke. So those are our main areas of expertise. And Jeff is going to be talking about how sleep interacts primarily with brain injury today. We also know that your CEUs are important, so we just ask that you stay for the majority of the presentation. You will answer one poll question. It’s towards the end. Jeff has already timestamped it, so we’ll see how close he is. So it’ll be about 10 minutes to 10. And so if you feel like you missed it, you didn’t miss it till the very end.
Also, the way you get your CEUs is once you click leave webinar, it should automatically take you to fill out a job form. And once you hit submit, that gives us feedback and then automatically triggers an email back to you with your CEUs and the slides all in one file. So you should get that as well. Just a reminder, please use the Q&A between Don, myself, and Laura. We will be monitoring that. We’ll have Jeff answer them as it works throughout the presentation, but there should be some time at the end to hit questions. So with that, Dr. Snell, over to you.
Jeff Snell: Thank you very much, Steve. Yeah, I’ll try to keep the dad jokes to a minimum as well. And we should be, as you said, hitting the poll question around 9:52 to 9:55 if I timed it out correctly. Depends on how much I run down rabbit holes and tell other stories. So we’re going to start with an overview of sleep. That’s what we’re covering today. What is sleep? Seems like such a simple question, but like most things that involve the brain, it’s got complex answers. And you ask five people, you’ll get seven different answers. Although there’s a tremendous amount of information known about sleep, what we don’t know is what we have yet to discover and what we have yet to learn about it. Steve, you mentioned we got six new presentations coming up this year. I love that because I learn so much every time I put one of these together.
So we’ll be talking about sleep, what it is, what the function or functions that it serves and why the process and function of sleep is so vulnerable to various types of neurological insults. The result of disruption of sleep can influence recovery after brain injury. And we will talk about why that is sometimes profoundly the case, particularly with more serious injuries. We’ll review the underlying mechanisms of potential disruptions specific to our TBI population, and then we’ll transition to reviewing treatment options that have been shown to be effective for individuals who experience a disruption of sleep after brain injury. Some of the points we’re going to cover regarding the treatment of sleep disruption are common to sleep in general, so the healthy habits and environmental factors associated with such treatment can also benefit everyone. So in addition to information that can be helpful to working with our rehab clients and patients, there are recommendations in here that can benefit all of us as well.
All right, so what is sleep? Again, seems like an extremely simple question because we all sleep, but the function of sleep is an area of study where there continues to be advances in understanding and knowledge. Sleep is essential for all mammals, but it’s also a highly vulnerable state that increases the chance of being targeted by predators. Being at the top of the food chain, we have a little bit better way of dealing with that with structures and things that keep us a little bit more safe while we’re asleep. But the fact that all mammals sleep suggests that despite the huge risk, sleep is of critical biological importance. Now, one purpose of sleep has been hypothesized to be equivalent to recharging a battery. We need that time of inactivity to store up energy depleted by our waking activity. From the standpoint of our brain, the amount of power consumption of our brain only decreases by about 25% as we sleep, and that suggests that it’s not just energy conservation or recharging our battery that drives sleep.
There’s extensive research that has existed for decades showing that our brain has periods of activity during sleep that is associated with memory consolidation, the transfer of memory into long-term storage, and also processes that are involved in learning and emotional regulation. Over the last decade, we’ve also seen that the sleep state is a time of dramatically increased activity in the glymphatic system, our brain’s waste removal process and that the glymphatic system is suppressed when we are alert and awake. So while we’re asleep, particularly deep sleep, our brain is cleaning house, a process that decreases dramatically when we’re awake. So the primary functions of sleep as we currently understand it are to, within the brain, organize and store new information, memory consolidation in particular. Sleep is associated with neural reorganization. A lot of neuroplasticity occurs as we sleep. Sleep involves emotional processing and waste clearance. Within the body, sleep is associated with the release of proteins and hormones related to tissue repair and restoration of energy, strengthening of the immune system, strengthening of metabolic health.
And again, from the standpoint of emotional health, sleep is important in mood regulation, resilience and stress reduction. Now, when we sleep, our brain cycles through several different stages of sleep, and this can get kind of confusing because those stages get defined differently when you look at different sources. You’ll sometimes see sleep described as five different stages as in the graphic on your screen here, four stages or even three stages. And often that reflects breaking out the fine details of sleep that can be differentiated by brainwave activities common to a given stage or by combining similar stages into a single stage. So in the graphic you see here, the stages of sleep are broken out into five distinct phases with stage one reflecting the initial process of entering sleep. That is when you lie down and get sleepy and start to drift off. Our muscles relax a little bit.
We can easily be awakened in this stage. Stage two involves the physical processes that reflect transition to a legitimate sleep state that dominates most of the sleep phases. It’s a slowing of our rate of breathing and our heart rate. Stage three is a transition from that lighter sleep into a deeper sleep. When monitoring sleep via EEG recordings, this is a stage where slow delta waves tend to dominate, and then that deep sleep stage is reflected by stages four where you are maintaining that deep sleep for some period of time. Stage five is REM or rapid eye movement, and that reflects a time of increased neuronal activity when we experience dreaming. You typically will go through these stages in about 90 minutes and then you repeat that cycle throughout the night of sleep. Now here’s a simpler categorization of sleep stages that involves light sleep, deep sleep, and REM sleep.
Now in this representation, stage one of falling asleep and stage two of light sleep get combined into a general light sleep categorization. Stage three is that deep sleep. Now again, during deep sleep, functions like breathing and heart rate are very slow when your muscles are relaxed. It can be very difficult to wake up from that or for someone externally to wake you up out of that deep sleep. And if you do get jolted awake out of that, you tend to be very groggy and foggy. And again, it’s during that deep sleep that our glymphatic system is most active. Neuronal activity is dialed way down and interstitial space is enlarged, a space between the cells within our brain, and that allows cerebral spinal fluid to more easily flow through that space to clear waste products. Now you can see that the last stage of sleep here, REM sleep or rapid eye movement sleep as it’s called, it’s during REM sleep that we experience dreaming that’s called rapid eye movement because that’s characterized by rapid movements of your eyes back and forth beneath your closed eyelids.
During this stage of sleep, neural activity in our brain resembles that that is measured during wakefulness. Your brain shows a lot of activity. Now our skeletal muscles are temporarily paralyzed during this stage of sleep. It prevents us from thrashing around in the bed and physically acting out our dreamed movements. While deep sleep is important in the house cleaning aspects of brain function, REM sleep has been shown to be important in memory consolidation, emotional regulation, and overall brain development. Now this graphic also represents a circular or repetitive nature of our nightly experience of sleep. As I mentioned, a night’s sleep consists of four or five typically of these sleep cycles each taken somewhere between 90 and 120 minutes. The deep sleep stage tends to be more lengthy in the first few cycles of sleep, and as the night progresses, you have more REM sleep that becomes more predominant.
I’ve actually got a Oura ring that tells me all the different stages of sleep that I have during the night, and I see that on the graphic as well. Deep sleep tends to be within the first couple of cycles of sleep and not present at all in the last few stages.
Steve Kerschke: Jeff, should we understand it as REM sleep is deeper sleep than the deep sleep or is it not necessarily like a continuum? It’s just what happens
Jeff Snell: During that time how to continue. Completely different things going on. Different brainwave waves are active during that time. Physiologically, it is different as well. So yeah, deep sleep is distinct in that, as I previously mentioned, you can see in the graphic here, it plays a critical role in the functioning of the glymphatic system. Our brain’s waste removal. Now this process, like everything in the brain, is energy dependent and during deep sleep, energy is used to increase the volume of cerebral spinal fluid within the parenchyma or within the meat of the brain. This process is best accomplished and most efficient and effective at its job during periods of decreased neuronal activity. So like your question, Steve, REM sleep, there’s a lot more activity neuronal communication going on within our brain and less space between the cells as well. So as they are active, that would make it difficult to have the same degree of extracellular porosity, that flow of fluid within the interstitial space.
So the overall amount of energy in the brain, again, is reduced only by about 25%, but during deep sleep, neuronal activity is dialed way down and much more energy is being used by the cleaning crew. The glymphatic system is basically clearing our waste products while we sleep. Now, as I said, sleep is often profoundly disrupted by TBI, particularly in more severe injuries and restoration of sleep after an injury is one of the many clinical concerns encountered in treatment.
Now, reduced glymphatic clearance of waste products has been proposed as a mechanism by which impaired sleep is not just associated with, but actually contributes to poor TBI recovery. In other words, having toxic byproducts of cellular breakdown lingering in the brain for longer than would be the case if the cleaning system was working optimally may contribute to further secondary injury to brain tissue or a lengthened recovery cycle. So that makes the restoration of regular sleep cycles even more important after an injury. So this time is critical for moving damaged cellular and waste products out of the brain and promoting healthy healing. I would also note that prior studies specific to the glymphatic system indicate that this system which operates at its best when we sleep, doesn’t seem to care whether that sleep is natural or chemically induced. It goes to work either way. So restoring a regular sleep pattern is important and that’s likely to include medications designed to treat that.
Now, the brain’s unique structure and physiology makes it highly vulnerable to force, to injury associated with TBI, much more so than most other structures or organs within the body. Within the brain, there are multiple key structures that are associated with sleep-wake state, so it makes sense that damage to any of these components of the brain has the capability to alter our sleep-wake processes. There are, for example, specific arousal systems located in the brainstem, the posterior and lateral hypothalamus and the basal forebrain. They use a variety of neurotransmitters and neuropeptides in these area of the brain have roles in our waking condition, behavior, sensory processing, and autonomic control. These arousal systems direct cortical activity indirectly through projections to and through the thalamus, the lateral hypothalamus and the basal forebrain, as well as direct projections into the cortex. Now, although these pathways mediate our arousal and awareness, they’re also critical in the process of sleep.
They’re the gatekeepers of that sleep-wake balance. So inhibiting the arousal centers is a necessary part of sleep. So the primary sleep-related structures within the brain mirror those that are necessary to produce wakefulness, and they have to be dialed down in order to allow the sleep state. If either the structural components necessary to achieve that inhibition or the neurotransmitters necessary to initiate and maintain the sleep state are disrupted by the injury, then the result is an inability to establish and maintain a typical sleep-wake cycle. Now, despite there being a great deal of knowledge in the literature regarding the brain structural components that are associated with sleep, the underlying. Well, jumped ahead there.
The underlying neurophysiological changes that drive post – TBI sleep disruption is not really well understood. The statement that was actually made within the conclusions of a very recent, actually 2005 publication summarizing TBI-related sleep disruption said that that’s just the case. Research shows that most individuals who experience a mild TBI don’t exhibit any abnormal imagery findings, and even in the majority of severe TBI cases, radiological investigation does not reveal obvious structural abnormalities contributing to sleep-wake disruption. This all kind of, I think, goes back to the fact that brain injury as a diagnosis is not a homogeneous construct. It covers such a heterogeneous condition and the complexity of interplay between neuronal circuitry that is such a simple answer as what is causing the disruption really can’t be wrapped up in a single answer. That being the case, however, the gross anatomy of sleep-wake-related architecture appears to lie within the brainstem and the midbrain structures.
And of course, these can be compromised by the forces involved in a TBI. In particular, the hypothalamus is highly vulnerable to damage secondary to its location directly below the thalamus, from which it gets its name, and very near the sharp edges of the sphenoid bone. When the brain is subjected to lateral forces, this subjects hypothalamic tissue to mechanical impact and shearing forces.
In addition to that, the tissue of the hypothalamus is in a vulnerable location and the blood vessels that supply that area with fresh oxygenated blood, those blood vessels are long and relatively fragile, which makes them susceptible to the same forces of impact and shearing. If that occurs and those vasculature is disrupted, there’s the possibility of ischemia within the hypothalamus if those blood vessels are compromised. In a brain injury, the hypothalamus is also vulnerable to changes in a cranial pressure, which can result from swelling after the injury. It’s vulnerable to global hypoxia where respiratory status is compromised, and ongoing inflammation is a secondary process after injury. So the bottom line is that research indicates that around 30% of all TBIs lead to neuroendocrine dysfunction involving the hypothalamic and pituitary axis. Now, the hypothalamus is critical structure identified as a primary regulator of hormonal and neurotransmitter production and release.
So metabolic disruption can certainly be directly related to the structural alterations associated with the components of the brain that regulate that metabolic functioning. When such disruption occurs, if these hormones or neurotransmitters or neuropeptides that are associated with sleep are disrupted, then those metabolic disruptions can manifest as sleep disruptions. Melatonin is a key hormone that promotes drowsiness at night as opposed to cortisol, which is the wake up hormone that peaks in the morning. As we’ll talk about in a bit, one of the pharmacological interventions associated with attempting to reestablish regular sleep routines is administration of melatonin. Serotonin, which is the pictured molecule there in the graphic, that’s involved in many neural networks, one of which is sleep and specifically regulation of sleep. Growth hormone is primarily released during sleep stages. Glutamate, the next one listed there, it has a very complicated relationship with sleep. It’s actually an excitatory neurotransmitter and a promoter of alertness and wakefulness.
So glutamate needs to be dialed down in order to achieve and maintain deeper stages of sleep. But this also speaks to your question earlier, Steve, glutamate levels rise during REM sleep, so there’s an increase of that excitatory neurotransmitter associated with the process of dreaming and of waking up. And then you see something listed there, orexin, orexin A and orexin B, which is also called hypocretin A or B, are most often just listed as ORX. This is a neuropeptide system, two different neuropeptides within the brain that was initially identified only around 1999. This neuropeptide acts as a master regulator of wakefulness, arousal, and energy balance. It’s produced in the lateral hypothalamus, and it’s a key component of sleep, wakefulness, energy homeostasis, reward, addiction, and stress response. So it’s tied to a lot of those midbrain functions. Thyroid hormones that are essential for metabolism can also disrupt sleep when imbalances occurred.
And then lastly on that list, leptin and ghrelin are hormones that control appetite. Now, these can be affected by sleep loss, and that kind of reinforces that circular path of hormonal disruption, which can result in sleep disruption, which can then result in hormonal disruption. So all of these hormones play a role in a circular cycle associated with sleep, and in that particular case with appetite and sleep. Now we’re going to transition to talking about different patterns or types of sleep disruption after TBI. Most of these are common to other conditions and environmental influences as well, and most of them are things that we might have experienced at one time or another. Excessive daytime sleepiness reflects an irrepressible need for sleep during normal awake periods, and falling asleep involuntarily are at inappropriate times during the day. My grandfather, who is a dairy farmer and also worked as a welder on a night shift, used to have substantial daytime sleepiness when he was on trips with us.
Remember one time he opened his passenger side door and then paused to let my grandmother and mother get out of the side door on the van. And as we started to walk into the restaurant, we turned around and looked, and John Glenn was sitting there asleep in the few seconds that it took for them to get out of the car. And that was driven by an overwhelming need for sleep, a sleep debt, that heightened sleep pressure, a physiological need for sleep that can be secondary to that excessive sleep debt or increased physiological sleep such as what we see after a brain injury. After TBI, individuals typically need more sleep. Part of that has to do with the cleaning process that is much more needed after a brain injury, as well as potentially some primary disruptions of those structures and neurotransmitters that we just talked about.
In measuring or documenting excessive daytime sleepiness, things like sleep latency, how long does it take to fall asleep, and other observable or self-report instruments are used. My own experience with that sleepiness had to do with keeping a regular schedule in school when I was back in graduate school and working in the lab all the time. I volunteered for a sleep study, and so they hooked me up with earbuds and EEG and covered my eyes and all that. And to start the study that night, I had to lie in a completely dark, quiet room and stay awake for five minutes while they get a baseline of me being awake before they could record my sleep measures. Through the earbuds, I kept hearing, “Jeff, wake up. Jeff, wake up,” because I could not stay awake for the five minutes because I was fairly sleep-deprived. I think graduate students tend to be so for the most part.
New parents as well with all those disruptions during the night tend to be sleep-deprived.
Steve Kerschke: Jeff, what’s the impact of age? You talked about your grandpa, and how is that similar or different to TBI, and where does that fit in with maybe some of the excessive daytime sleepiness and things like that that we see?
Jeff Snell: Well, I think one of the broad things that’s known about sleep as we age is that we tend to sleep less as we age. Younger people tend to have more lengthy sleep, and as we age, we cycle through those sleep cycles a little bit faster, and we also don’t necessarily have as many of those sleep cycles in the night. Part of it also has to do with the demands of your lifestyle as well. If you’re used to developing a routine of getting up at a certain time every day and going to bed every night, which is actually optimal, that can also result in an earlier awakening. Of course, there’s just the general stereotype of as we get older, we tend to wake up earlier in the morning. Sometimes that’s driven by having things to do, got chores around the farm that we got to take care of, so we get up with the sun and go to bed with the sun, but having less sleep is somewhat common as we age.
If you’re measuring or documenting excessive daytime sleeping is things like sleep latency, how long does it take to fall asleep, and other observable or self-report instruments are used. There’s the multiple sleep latency test and the Upworth Sleepiness Scale, but those two instruments don’t necessarily correlate highly. Therefore, it appears that they may be measuring slightly different constructs. With the multiple sleep latency tests, you assess how quickly a subject falls asleep and enters REM sleep by scheduling four to five daytime naps and utilizing polysomnography. In other words, you’re using brainwave measurements and measuring the average latency of less than eight minutes averaged across those four to five trials reflects positive excessive daytime sleepiness. So when you are in a position where you are comfortable and falling asleep in less than eight minutes routinely would reflect that kind of excessive daytime sleepiness. The Epworth Sleepiness Scale is a simple eight question self-report tool that just asks how likely are you to fall asleep in common situations like reading, watching TV, or sitting in a meeting?
It’s on a zero to three point scale for each question, and that gives you a score of anywhere between zero and 24. If you score greater than 10, it suggests excessive daytime sleepiness.
Plisomnia is a term that refers to an increased need for sleep, or at least two hours longer per 24-hour period following traumatic brain injury. Now, this includes the presence or absence of excessive daytime sleepiness. So basically it’s just more sleep than typical. So again, for individuals on average following a TBI, they will require about two hours longer of sleep per day. Now, this term is often used interchangeably with hypersomnia, which is an increased need for sleep over a 24-hour period, or what we just referred to, the excessive daytime sleepiness. Prior research in this area reported an average of around three and a half hours in some studies of increased sleep following TBI compared with a pre-injury baseline, and that’s according to actigraphy recordings. The graph on this slide would be reflective of such a three and a half hour increase in sleep, even within the normal variations of daily sleep.
Patients in the chronic stage of a moderate to severe TBI tended to go to bed earlier, spend more time in bed, and had more daytime naps compared with a neurotypical healthy control. So this increased need for sleep is an ongoing issue, particularly after more severe TBI. A more common sleep disruption, which we are all susceptible is insomnia. I’d venture to guess that every one of us has had experience with occasional poor sleep, either trouble falling asleep, waking up in the middle of the night with difficulty getting back to sleep, tossing and turning, not getting restful sleep, or waking up too early and not being able to go back to sleep. Those instances are generally associated with situational factors or illness. Now, we tend to call that insomnia, but the technical definition of insomnia involves experiencing those symptoms at least three times a week for at least three months with significant personal distress and daytime functional impairments.
So insomnia can get in the way of your daily activities, make you feel sleepy during the day. It can interfere with attention and memory as well. Most of us experience that once in a while, but not necessarily to that degree. A diagnosis of insomnia is considered a significant health concern that’s associated with a host of significant outcomes, negative outcomes, many of which are reflected in poor physical or emotional health, hypertension, cardiovascular disease, diabetes, depression, anxiety, and increased risk of accidents and suicide are all associated with a medical diagnosis of insomnia.
Now, circadian rhythms have to do with our normal and typical rhythm of our body clock over the course of the day, depending on the schedule that we keep, and I’ve seen it defined as our core molecular clock mechanism within the brain.
The brain structure most associated with circadian rhythm is the suprachismatic nucleus, which is a tiny cluster of nerve cells, again, in the hypothalamus that acts as the body’s master clock. It synchronizes our daily cycles with light and dark cues from our eyes. For the majority of us, the circadian rhythm probably means sleeping at night and being active during the daylight hours. Now, that schedule can be altered or adjusted in response to conscious or intentional change like working the night shift or traveling across different time zones. Laura was just talking about a trip to Europe that she’s got coming up, and undoubtedly she will experience some degree of alteration of her circadian rhythm in In both directions. We call that jet lag, right? So it can also be due to unintended physiological disruptions like pain. If you’ve ever had a toothache, it’s really hard to sleep.
Illness or our topic today, TBI. TBI can result in imbalances of those hormones and neurotransmitters that we covered a few slides back, and those imbalances are secondary to structural alterations within the neural networks involved in sleep. Like many autonomic function regulations, the hypothalamus plays a role in sleep regulation, which as we reviewed is vulnerable to the mechanical forces in a TBI. Now, just as an aside, circadian rhythms are not to be confused with circadian rhythm, which is what you get if you leave out the first R when you spell circadian. Sorry, Steve, I was just entertaining myself when I was You just couldn’t help it. I could not help myself.
If you want to see this band, they only come out every 14 to 17 years. All right, back to the show. Yeah. Okay. Circadian rhythm sleep disturbance can easily be overlooked after TBI, particularly after milder injuries. And in one prior study, for example, the individuals that had mild TBI that were seeking treatment for insomnia, 42% of those individuals actually had circadian rhythm sleep disturbance. Now, this is an important discrimination to make because the treatment approaches differ depending on the diagnosis. The most commonly associated circadian rhythm sleep disturbance are the delayed sleep phase syndrome and irregular sleep wake pattern. Now, the first one, delayed sleep phase syndrome is a chronic circadian rhythm disorder where your internal clock is delayed, causing you to fall asleep and awaken on a schedule that is much later or delayed from typical times. So you see within the graph, the targeted typical circadian rhythm for someone who needs to be awake during the day versus a delayed circadian rhythm means that you’re showing the same pattern, it’s simply delayed by several hours.
Now, this differs from the intentional adjustment of sleep to an atypical pattern that accommodates shift work. Delayed sleep phase syndrome is associated with otherwise typical schedule of work and life demands, and the symptoms associated result in you having to start your day before you’re really ready to get up, results in daytime sleepiness, poor concentration, which can in turn cause problems in school or work. I think the schedule’s most typically associated with teens who have the opportunity to establish later hours of sleep initiation and termination during the summer when school demands don’t dictate their schedule. It results in some difficulty reacclimating at the end of summer when a more standard schedule is necessary. Now, this disruption of sleep tends to be more associated with habits than injuries, but it is treatable with some of the same treatment modalities and practices that we’ll be talking about later.
Irregular sleep-wake rhythm disorder on the other hand is where an individual lacks a regular sleep-wake pattern resulting in multiple short naps and wakefulness throughout the day and night. In what you see here, this is a sleep log and the black bar would be when you mark in, you would fill in those hours of when you sleep. Typically, you want to see that as a kind of a solid block across that week. If you’re getting up at the same time in the morning, going to bed at the same time at night and sleeping well throughout the night, you don’t have all of these breaks, stops and starts. This pattern is relatively common in cases of severe brain injury, but it’s otherwise relatively rare condition. It is characterized by a lack of defined sleep schedule in multiple sleep-wake periods, usually three plus sleep periods in a 24-hour time span.
This presentation is more associated with the acute phase after TBI.
After a TBI, we use restoration of memory function as one of the landmarks of a cognitive indicator of recovery. So in other words, emergence from post-traumatic amnesia or post-traumatic confusional state is a marker that we use for this person is getting better, they are improving, they are recovering after injury. Well, the restoration of a normal sleep-wake pattern after TBI is one of the basic physiological functional indicators of recovery. At what point after injury did the normalization of sleep patterns begin to emerge? Now, we’ve already covered the importance of deep restorative sleep in clearing waste products in the brain and a potential bidirectional connection between slower recovery and compromised lymphatic functioning. So after injury, we want to reestablish a normal or typical sleep-wake pattern because sleep is such an important basic function and it also contributes to a number of other neurological functions and abilities. That’s what makes it important to address this in terms of treatment after injury.
So what is the effect of these common sleep disruptions on the process of rehabilitation after injury? And keep in mind again that disruption of sleep-wake pattern often results in multiple periods of sleep versus wake throughout the day and throughout the night. Now, given the role that sleep plays in memory consolidation, there is an extended process of memory functioning, memory recovery that would be anticipated, and that has been shown in research. If you compromise someone’s ability to sleep to the point that they are not experiencing or experiencing less REM sleep, there is less memory consolidation involved there. So the upshot of that being poor carryover of information. Fatigue is a factor that is related to sleep disruption and is a factor to consider in scheduling. For example, from a neuropsychological perspective at QLI, we almost exclusively schedule our neuropsych assessments in the mornings and we limit the length of time of those assessments so that the energy and attention demands don’t exceed the limitations that fatigue places on the individual’s ability to participate in that assessment process.
Sleep plays a role in emotional and behavioral regulation, therefore disruption of sleep can result in agitation, aggression, depression, or extension of those factors as well. The role of sleep in neuroplasticity means that there’s reduced restoration and reorganization, again, lengthening the neurological healing process and the functional limitations imposed by that increased need for sleep and interruptions of daytime sleepiness, all of those interfere with the normal routines and return to independence. From a rehab perspective, that includes the inconsistencies of availability to engage in the therapy process or reduced participation in those therapies attended. So all of those are the upshot of experiencing significant sleep-wake disruption or excessive daytime sleepiness that are a consequence of that brain injury.
So what you’re going to do is going to depend on the type and severity of the sleep disorder. That gives you an idea of what to target. You’ll notice that in the graphic to the right here, there are a variety of sleep disorders listed that we didn’t talk about, but that also have the potential to be involved after TBI. The ones that we did cover are among the most prevalent are the ones that are most closely associated with the neurological disruption of the brain injury itself. But because we’re working with individuals who may have had some other issues such as sleep apnea prior to injury, those issues also have to be considered and treated appropriately. The primary two prongs of sleep disorder treatment within post – TBI population can largely be broken down into pharmacological and non-pharmacological interventions.
Now, I present this information with the caveat that I am not a physician. It is beyond my scope of practice as a neuropsychologist to prescribe or even recommend medications. With that in mind, I did seek out current information within the literature regarding medications that are typically utilized to help with sleep after an acquired brain injury and a couple that are not recommended. So I’m passing all this along as secondhand information. Now, melatonin, we mentioned earlier, it’s a naturally occurring neural hormone secreted within the brain at night and helps regulate circadian rhythms. In more severe cases of TBI, melatonin levels are often reduced. Of the medication interventions mentioned on this slide, melatonin is the only over-the-counter med that I have seen frequently used in medical practice. There are, of course, many other herbal and over-the-counter sleep aids, but I’m limiting this discussion to those that are most often used in inpatient medical acute rehab or post-hospital inpatient and outpatient services.
From the standpoint of non-over-the-counter medications, there is a listing there. The first one, Rymeltion, trade name Rozarm, it’s a melatonin agonist, so it is basically acting to activate those melatonin receptors within our brain that then have the effect of helping us get to sleep. Now, it acts as a CNS depressant, and it is reportedly effective in helping people get to sleep and stay asleep longer. The next three that you see there are all non-benzodiazepine GABA agonists. So in other words, they act against one of the excitatory neurotransmitters within our brain. They’re generally referred to as sedative hypnotic medications. Those trade names listed there in order, Ambien, Sonata and Lunesta. Now, typically avoided in TBI treatment for sleep are tricyclic antidepressants. They are sometimes used, but you have to keep in mind they’re anticholinergic effects, which have potential side effects of confusion and memory difficulties, which often are things that we are also targeting for treatment.
So it’s a balance there between the usefulness for sleep versus the potential negative effects. There are also physiological effects that need to be taken into account as well, dry mouth, blurred vision, urinary retention. So any of the host of TCAs have those potential side effects. The other that is typically avoided after brain injury are benzodiazepines, and those are avoided for similar reasons to the tricyclic antidepressants, cognitive effects that can include confusion. Those are medications like Xanax, Librium, Klonopin, things that you will sometimes see used, and there are times that it is appropriate to do that. If you can’t get, again, normal sleep-wake function back, there are a number of different pharmacological things that might be trialed in that case because that might be considered more important than the issues that are otherwise side effects.
Now, within the more recently identified role of the neuropeptide system of orexin A and orexin B, or just ORX as they’re called, there are some newer medications that are FDA approved to treat sleep disruption by blocking the wake promoting symptoms of orexin. So in other words, orexin is very much tied to the sleep-wake cycle in terms of activating waking up. So if you can suppress that, if you can dial down the action of ORX in the brain, that acts as a master regulator of wakefulness and arousers. So theoretically, you can get longer sleep in that case. Now, a physician would need to determine the appropriateness of the use of these meds in a TBI population, again, because some of the common side effects. For Belsomra, for example, side effects listed include confusion and memory problems. So like the TCAs and benzos that we just mentioned on the previous page, the side effects of a given medication might be contraindicated if cognitive disruption is also a focus of treatment or can lengthen the time of recovery for that particular function.
Now, if you’ll notice on this graphic as well, orexin plays a role in the sleep-wake cycle and arousal, but it’s also implicated in a lot of other things, particularly energy, homeostasis, blood pressure regulation, and sympathetic nervous activity. It’s implicated in addiction because of the midbrain structures involved, obesity, and then there’s also anti-tumor applications. So this thing actually, these neuropeptides actually cover a wide range of functions. As of 2025, these same orexin receptor antagonists are also in clinical trials to treat addiction as well as mood disorders due to their associated actions with the reward within the midbrain.
Now then, we’re going to shift to more non-pharmacological interventions. These can be used in concert with pharmacological interventions, and that combination of treatments can be very effective. Quite frankly, when it comes to emotional functioning and cognitive behavior therapy, it’s often considered part of that two-pronged approach of medication interventions as well as non-medication interventions. And in combination, those tend to show the best efficacy, the most empirical evidence for effectiveness within our populations. One formal intervention I want to mention here is CBTi, cognitive behavioral therapy for insomnia. This is a short-term evidence-based therapy designed to treat individuals with chronic insomnia to improve their sleep quality. CBTI involves focusing on sleep habits, getting rid of unhealthy sleep behaviors, and replacing them with more healthy and sleep supportive alternatives. And like the probably more familiar cognitive behavioral therapy without the eye on it, it involves challenging negative thoughts and beliefs about sleep in this case that may be contributing to that patient’s difficulty sleeping.
Changing the I won’t ever fall asleep thought to I will eventually fall asleep, or changing, I’m going to be so tired tomorrow, to I’ve been tired before and I will probably sleep better tomorrow because of it. It’s really learning not to catastrophize, which typically results in more negative rumination, and that then keeps you awake. It is altering your thought processes to change your expectations and anticipations and lower your anxiety. Stimulus control involves developing habits with sleep in terms of the bed, developing the habit that the bed is a place for sleeping, and avoiding things that keep you awake when you’re in bed, like being on your phone, like scrolling on the internet or watching movies or videos on TV or some streaming device. All the technology that we have now makes available things that just weren’t present previously, and the difficulty with breaking that habit of grabbing the phone when you wake up in the middle of the night can actually keep you awake longer.
So it is learning to associate the bed with sleep. Teaching relaxation techniques such as deep breathing, progressive muscle relaxation, or guided imagery. The goal here is to practice these things in session so they can be used to relax the body and relax the mind when it’s time to wind down and fall asleep. A sleep diary is often part of this approach by documenting when and how you sleep, you might gain insight into things that you’re doing or not doing that can either help or hurt the quality of your sleep. And lastly, CBTi is tailored to the individual. It involves finding a balance between the demands and needs of a given individual’s lifestyle and their preferences for potential adaptations and approaches. So it is tailoring all of those possible different interventions to what that individual is likely to benefit from.
And beyond formal treatment, there are also broad general recommendations that promote healthy, regular routines that are supportive of good quality sleep. And some of the recommendations that are typically offered are noted here. Again, some of these sleep hygiene dos and don’ts are also part of CBTI. Now, this is not an exhaustive list of sleep hygiene recommendations, and quite frankly, to present that would be an entire lecture series on the topic of sleep hygiene. This is just a short abbreviated list. And again, these are things that are useful to keep in mind in treatment. They’re also useful to keep in mind for us if we are having sleep difficulty or have recently had some disruption of sleep. I had some pain from a fall that kept me asleep for probably about a week and a half with my worst night being about two hours of sleep because pain can significantly disrupt our sleep.
So getting back to my regular sleep routine was something that I was very eager to pursue. So some of the things that you can do to improve your sleep, number one is routines, routines and repetition. Go to bed and wake up the same time every day, including weekends. Now, that can be a little difficult for folks who just kind of want to, “Well, I don’t have to work today, so I’m going to sleep in.” In doing so, you are disrupting your own routine. So again, making and keeping to a routine that fits your lifestyle, avoiding substances that can disrupt sleep. That includes caffeine, alcohol, and nicotine, getting exercise and sunshine every day. This is one that can’t be overstated in terms of how beneficial this is. Anytime somebody asks me, “What can I do to improve my cognitive functioning? What can I do to improve my emotional functioning or what can I do to improve my physical functioning?” The answer is the same for all of the above.
Move, get out, get outside and exercise, take a walk every day, do some cardio. All of these things are supportive of our brain health, our body health, and all of the routines that are necessary to keep us moving and keep us healthy. So I think of all of the different rehab disciplines, I think PT probably has the strongest influence here from the standpoint of the one thing that if somebody comes to me and says, “What can I do to improve my cognitive health?” Go talk to your PT, get an exercise program in place, get out and move. Doesn’t have to be going to the gym and bulking up. It’s just a matter of keeping your body moving, getting some exercise, and getting some sunshine. Minimize daytime sleeping as recovery progresses for our patients. As they are improving over time, we want to get them back to our schedule of sleeping at night and staying awake during the daytime.
That is the schedule that most of us keep, and so minimizing that daytime sleepiness. It might be necessary early on, but as recovery progresses, you don’t want to develop that habit of routinely napping during the day if your lifestyle did not support that and that was not a part of your routine pre-injury. Avoid doing a lot of exercising or eating a big meal within a few hours of bedtime. You don’t necessarily want to go to bed right after eating a big meal because your body’s not ready to sleep at that point. Same thing from the standpoint of a lot of exercising right before bed because you’re physiologically getting your body more active, giving it lots more wake signals. It’s going to take a little bit longer to get to sleep following that. Create and maintain an environment that is conducive to sleep, quiet room, cool temperature if you sleep better in a room that is colder, if you need a warmer room to sleep better, whatever environment is most conducive to your sleep patterns.
And then as I mentioned before, do not lie in bed scrolling on your phone or tablets. You are activating your brain, you are thinking, you are feeding it stimulus. That’s going to have to then be shut down before you can go back to sleep. So don’t interrupt that sleeping process by doomscrolling on your phone at night. And for the last point on the list, the goal is to make the bed a place associated with sleeping. If you legitimately, genuinely cannot get to sleep lying in bed, it’s one of those tossing and turning nights, don’t associate that with the bed. Get up, do a relaxing activity, practice some of that progressive muscle relaxation or mental imagery to help you wind down again. And then as you feel sleepier, go ahead and lie down and get to bed. Steve, I said 10:53. It is 10:53.
Steve Kerschke: Spot on.
Jeff Snell: On you, dude.
Steve Kerschke: All right, I will launch the poll question. Jeff, there are a couple questions in the Q&A, so while I launch that, if you want to take a look at those and we can get those answered as well. So here comes the poll question. Please answer this.
Jeff Snell: Q&A. Yeah, I didn’t have my Q&A window open. There we go. How can you tell. Your poll question just covered it up. There we go. Sorry about that. How can you tell whether sleep apnea relates to TBI or not? The big one there is was this an issue previously? And sometimes that is just on the basis of prior descriptors. We do get folks that have previously had sleep apnea identified but didn’t tolerate a CPAP or BiPAP and therefore just didn’t use it. So you have to ask that question, “Have you ever been diagnosed with this previously?” The other would be just general physiological characteristics that would be associated with sleep apnea, which have to do with weight and physical activity tolerance. In some cases, you cannot truly discriminate that if there’s not been a diagnosis previously, but you can certainly suspect that that might be an issue previously.
Did you snore, for example, heavily prior to injury? So questions to ask of those who know the individual well. Now, of course, very few of us actually know how much we snore at night because we are asleep and therefore not consciously aware of what’s going on around us, but a spouse can generally accurately tell you that. Is there research regarding TBI sleep and the impact of the female cycle if someone without a TBI female needed more sleep compared in the luteal phase versus the follicular phase with a TBI as a female? I’m curious about that for additional consideration. Really good question. One that I do not know the in-depth necessary information to be able to answer it. I would suspect yes, there is a difference simply because our brain and our body are intricately linked. They are not separated as much as we like to talk about them as being different.
Anything that is impacting you physiologically at a given moment is going to impact your brain’s function as well. Are you familiar with any of the research on non-sleep deep rest protocols? If so, well, my answer to the first question is no, I don’t have the in-depth information necessary to comment on that, so I’m not really able to tell you if it’s beneficial or not. It is something that, thanks to your question, I’m going to go look up, quite frankly. I learned a lot in putting this presentation together, but that is not one of the things that I learned. What is the best sleep position? That’s going to differ by person.
I’ve seen a little bit of research from the standpoint of lymphatic function that suggested that sleeping on your right side might be a little bit better than left, but I don’t know that there’s enough research to say that empirically that is supported. Sleeping on your side and on your shoulder in particular can sometimes cause shoulder pain, which can be disruptive of sleep. But for the individual, that is going to vary. And again, your position is going to change several times throughout the night, so whatever position you go to sleep in is not necessarily the position that you wake up in simply because that tossing and turning. Then lastly, disrupt. Oh, that’s the sleep pole back up there again. Oh, I was about to read that to you. A patient with preexisting bruxism, how does this impact or disrupt sleeping patterns? Again, physiologically, anything that has the potential to disrupt your body function, in this case, grinding your teeth when you are asleep, also has the potential to impact sleep.
Question: Do catecholamines have anything to do with sleep disturbances? I’m assuming it would depend on part of the brain that is injured. However, wouldn’t that complicate a normal sleep pattern? Yes. Anything that has to do with a disruption of sleep-wake hormones, sleep-wake neurotransmitters, which catecholamine is a neurotransmitter, are neuropeptides, any of these have the potential to disrupt. Question here, “What are your thoughts on using white noise to help fall asleep?” Again, that is something that can be highly recommended if you otherwise are used to that, if that is part of your routine. I have to have a fan running in my room or else I will not get to sleep. If I wake up in the middle of the night and realize that I don’t have the fan on, I got to get up and turn it on to go back to sleep. So that actually is something that if you’re used to it, you need it, and it can help mask other noises that might otherwise be disrupting to your sleep.
Question here, what about isolation tanks for someone with TBI? Since we can’t quite reach those wave states in a non-injured brain during sleep, could this be a treatment modality? I don’t know of any research that would support that, and quite frankly, reaching those particular brainwave states could be beyond the capacities of someone who has a neurological disruption of sleep-wake mechanisms and neurotransmitters. So again, my answer there is I don’t know. I can look into that further, but I don’t know of any research I’ve encountered that are using isolation tanks for sleep-related issues after brain injury. Great questions, so thank you so much for those. You gave me some avenues to investigate.
Steve Kerschke: Well, Jeff, thank you again. Great information. As always, I learned plenty with your presentations, and I’m certain our audience is going to have a ton of great feedback for you after the fact, as they always do.
Jeff Snell: Within the handouts, there are lots of references here. You’ll notice that most of these are within the last couple of years. Only a few of them are before 2020. And one in particular was on this slide here. It’s bolded. That’s actually a 2025 published book chapter on sleep and circadian rhythms after TBI. And if you have interlibrary loan connections, I would highly recommend this because it’s got a ton of information and a really good comprehensive overview. And if you have other questions that we didn’t answer, I’m going to pop up my information here. Feel free to call or email me directly.
Steve Kerschke: Perfect. Well, just a reminder, click the submit button on hopefully the link that pops up to fill out the feedback form. This will give you your CEUs and the slides, which also has Dr. Snell’s information in it and all of the information that you saw today. So that should be hopefully in your inbox. If you do that, if you have issues, contact Don or myself. We’ll get you taken care of. If you had issues with the poll question, contact Don or myself. We’ll get you taken care of. And since we are just a minute past 10 o’clock, Dr. Snell, thanks again and thank you to everyone who joined us today. Really appreciate you being a part of our webinar series. We will be back in February and I’m blanking, is it sexuality Don? I believe. Sexuality 2.0. All right. We got sexuality 2.0. Those of you who are with us for the first sexuality presentation, it was a pretty hot topic.
We’ve done our best to take it to the next level. I’m certain that the group presenting will have some nice dialogue, offer opportunities to have and dig in on some of those tougher questions and tougher situations. So we listened to you and hopefully you join us for that next month. Have a great rest of your day.
Jeff Snell: Thanks, Steve.
Steve Kerschke: Thanks, Jeff.
Jeff Snell: Enjoyed it.
Steve Kerschke: Appreciate you. Thank you, Jeff.
Jeff Snell: Hate that Laura wasn’t around for the
Steve Kerschke: That was good.
Jeff Snell: Circadian rhythms. I spent way too much time on that and enjoyed it way too much. It was
Steve Kerschke: A good slide. It was a good slide.
Jeff Snell: It was out of the presentation until yesterday. I was like, oh, okay, what the heck?
Steve Kerschke: Well timed. Delivery was good.
Jeff Snell: Need a break in the middle. Yep.
Steve Kerschke: That’s right. Perfect. All right, we’re going to wrap it up so we can get this uploaded.
Jeff Snell: Sounds good. Thanks guys.
Steve Kerschke: Bye.
Jeff Snell: Bye.
September 18, 2026 by Haley Hansen, PT, DPT
Video Transcription 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 […]
