Trauma

A power outage, like the 1977 blackout in New York City, can lead to an increase in violent crime. However, complete darkness can also have an upside, as it can encourage intimacy and subsequently boost birth rates. The Christmas season, sometimes called the festival of love, appears to stimulate human interactions. Yet this, also, has its downsides, as recently reported by Dr. Nikolaos Pyrgidis and other urologists at Ludwig Maximilian University of Munich in Germany. The less cheerful aspect of the holiday season is penile fractures.

The team found that the Christmas period, in particular, is that bit more risky for this injury after they evaluated data from about 3400 men (average age 42) treated for penile fractures between 2005 and 2021. The data was provided by Germany’s Federal Bureau of Statistics.

Out of the 3400 penile fractures that were reported during this period, 40 (1.2%) occurred over 51 Christmas days (from 24th to 26th December each year). The daily incidence rate of penile fractures during the Christmas period was 0.78, with an incidence rate ratio (IRR) of 1.43. The authors note that, if every day were like Christmas, there would have been a 43% increase in penile fractures in Germany since 2005. Interestingly, only 28 (0.82%) penile fractures were reported during the New Year (from 31 December to 2 January in the period between 2005 and 2021), with an IRR of 0.98.

More generally, most patients with penile fractures were admitted to the hospital over the weekend (n=1322; IRR 1.58). Notably, Sunday saw the most admissions due to this injury, followed by Saturday. This suggests that men engaging in sexual activities on Saturday night bear the highest risk of penile fractures, followed by those active on Friday nights.

Penile fractures also increased in the summer months (n=929; IRR 1.11). But the COVID-19 pandemic (n=385; IRR 1.06) and the lockdowns (n=93; IRR 1.95%) did not impact the frequency of this injury.

Rare, Painful, and an Emergency

Penile fractures are a rare urological emergency. The tunica albuginea of one or both corpora cavernosa must tear to be considered problematic, as another team of authors reported in a recent publication. Involvement of the urethra and corpus spongiosum is also possible.

Injuries often occur during an erection because it makes the tunica albuginea stiffer and thinner than when the penis is flaccid. Patients report hearing a snap when the penis is forced into an angle during sexual activity. This was reportedly the case with German singer-song writer Dieter Bohlen, whose ex-girlfriend Nadja Abd El Farrag is said to have written in her book “Ungelogen”, or “Honestly”, that there was a sudden snap during an intimate moment one December night (Christmas?), after which she called the fire brigade in her distress.

Multiple Causes Possible

Other factors contributing to penile fractures include rolling over in bed onto an erect penis, forced bending to achieve detumescence, and blunt external traumas like kicks.

Some penile fractures can be caused by patients “kneading and ripping” their erect penis to quickly reduce swelling. In an Iranian study, 269 out of 352 patients (76%) who underwent this process, known as “ taqaandan” in Iran, suffered a penile fracture.

Penile fractures can also occur in children, as evidenced by the case history of a 7-year-old boy described a few years ago in the journal Urology where the cause was a fall onto the penis.

Immediate Action Required

The treatment of choice for a fresh penile fracture is surgical repair of the tunica albuginea defect and, if necessary, the urethra. Timely surgical intervention yields significantly better long-term outcomes than conservative therapy regarding late complications such as erectile dysfunction and penile curvature. It also reduces the rate of early complications, such as severe corporal infections. Conservative therapy should be reserved for patients who explicitly refuse surgical intervention after thorough consultation.

This article was translated from Univadis Germany using ChatGPT followed by human editing.

A version of this article appeared on Medscape.com.

A power outage, like the 1977 blackout in New York City, can lead to an increase in violent crime. However, complete darkness can also have an upside, as it can encourage intimacy and subsequently boost birth rates. The Christmas season, sometimes called the festival of love, appears to stimulate human interactions. Yet this, also, has its downsides, as recently reported by Dr. Nikolaos Pyrgidis and other urologists at Ludwig Maximilian University of Munich in Germany. The less cheerful aspect of the holiday season is penile fractures.

The team found that the Christmas period, in particular, is that bit more risky for this injury after they evaluated data from about 3400 men (average age 42) treated for penile fractures between 2005 and 2021. The data was provided by Germany’s Federal Bureau of Statistics.

Out of the 3400 penile fractures that were reported during this period, 40 (1.2%) occurred over 51 Christmas days (from 24th to 26th December each year). The daily incidence rate of penile fractures during the Christmas period was 0.78, with an incidence rate ratio (IRR) of 1.43. The authors note that, if every day were like Christmas, there would have been a 43% increase in penile fractures in Germany since 2005. Interestingly, only 28 (0.82%) penile fractures were reported during the New Year (from 31 December to 2 January in the period between 2005 and 2021), with an IRR of 0.98.

More generally, most patients with penile fractures were admitted to the hospital over the weekend (n=1322; IRR 1.58). Notably, Sunday saw the most admissions due to this injury, followed by Saturday. This suggests that men engaging in sexual activities on Saturday night bear the highest risk of penile fractures, followed by those active on Friday nights.

Penile fractures also increased in the summer months (n=929; IRR 1.11). But the COVID-19 pandemic (n=385; IRR 1.06) and the lockdowns (n=93; IRR 1.95%) did not impact the frequency of this injury.

Rare, Painful, and an Emergency

Penile fractures are a rare urological emergency. The tunica albuginea of one or both corpora cavernosa must tear to be considered problematic, as another team of authors reported in a recent publication. Involvement of the urethra and corpus spongiosum is also possible.

Injuries often occur during an erection because it makes the tunica albuginea stiffer and thinner than when the penis is flaccid. Patients report hearing a snap when the penis is forced into an angle during sexual activity. This was reportedly the case with German singer-song writer Dieter Bohlen, whose ex-girlfriend Nadja Abd El Farrag is said to have written in her book “Ungelogen”, or “Honestly”, that there was a sudden snap during an intimate moment one December night (Christmas?), after which she called the fire brigade in her distress.

Multiple Causes Possible

Other factors contributing to penile fractures include rolling over in bed onto an erect penis, forced bending to achieve detumescence, and blunt external traumas like kicks.

Some penile fractures can be caused by patients “kneading and ripping” their erect penis to quickly reduce swelling. In an Iranian study, 269 out of 352 patients (76%) who underwent this process, known as “ taqaandan” in Iran, suffered a penile fracture.

Penile fractures can also occur in children, as evidenced by the case history of a 7-year-old boy described a few years ago in the journal Urology where the cause was a fall onto the penis.

Immediate Action Required

The treatment of choice for a fresh penile fracture is surgical repair of the tunica albuginea defect and, if necessary, the urethra. Timely surgical intervention yields significantly better long-term outcomes than conservative therapy regarding late complications such as erectile dysfunction and penile curvature. It also reduces the rate of early complications, such as severe corporal infections. Conservative therapy should be reserved for patients who explicitly refuse surgical intervention after thorough consultation.

This article was translated from Univadis Germany using ChatGPT followed by human editing.

A version of this article appeared on Medscape.com.

A power outage, like the 1977 blackout in New York City, can lead to an increase in violent crime. However, complete darkness can also have an upside, as it can encourage intimacy and subsequently boost birth rates. The Christmas season, sometimes called the festival of love, appears to stimulate human interactions. Yet this, also, has its downsides, as recently reported by Dr. Nikolaos Pyrgidis and other urologists at Ludwig Maximilian University of Munich in Germany. The less cheerful aspect of the holiday season is penile fractures.

The team found that the Christmas period, in particular, is that bit more risky for this injury after they evaluated data from about 3400 men (average age 42) treated for penile fractures between 2005 and 2021. The data was provided by Germany’s Federal Bureau of Statistics.

Out of the 3400 penile fractures that were reported during this period, 40 (1.2%) occurred over 51 Christmas days (from 24th to 26th December each year). The daily incidence rate of penile fractures during the Christmas period was 0.78, with an incidence rate ratio (IRR) of 1.43. The authors note that, if every day were like Christmas, there would have been a 43% increase in penile fractures in Germany since 2005. Interestingly, only 28 (0.82%) penile fractures were reported during the New Year (from 31 December to 2 January in the period between 2005 and 2021), with an IRR of 0.98.

More generally, most patients with penile fractures were admitted to the hospital over the weekend (n=1322; IRR 1.58). Notably, Sunday saw the most admissions due to this injury, followed by Saturday. This suggests that men engaging in sexual activities on Saturday night bear the highest risk of penile fractures, followed by those active on Friday nights.

Penile fractures also increased in the summer months (n=929; IRR 1.11). But the COVID-19 pandemic (n=385; IRR 1.06) and the lockdowns (n=93; IRR 1.95%) did not impact the frequency of this injury.

Rare, Painful, and an Emergency

Penile fractures are a rare urological emergency. The tunica albuginea of one or both corpora cavernosa must tear to be considered problematic, as another team of authors reported in a recent publication. Involvement of the urethra and corpus spongiosum is also possible.

Injuries often occur during an erection because it makes the tunica albuginea stiffer and thinner than when the penis is flaccid. Patients report hearing a snap when the penis is forced into an angle during sexual activity. This was reportedly the case with German singer-song writer Dieter Bohlen, whose ex-girlfriend Nadja Abd El Farrag is said to have written in her book “Ungelogen”, or “Honestly”, that there was a sudden snap during an intimate moment one December night (Christmas?), after which she called the fire brigade in her distress.

Multiple Causes Possible

Other factors contributing to penile fractures include rolling over in bed onto an erect penis, forced bending to achieve detumescence, and blunt external traumas like kicks.

Some penile fractures can be caused by patients “kneading and ripping” their erect penis to quickly reduce swelling. In an Iranian study, 269 out of 352 patients (76%) who underwent this process, known as “ taqaandan” in Iran, suffered a penile fracture.

Penile fractures can also occur in children, as evidenced by the case history of a 7-year-old boy described a few years ago in the journal Urology where the cause was a fall onto the penis.

Immediate Action Required

The treatment of choice for a fresh penile fracture is surgical repair of the tunica albuginea defect and, if necessary, the urethra. Timely surgical intervention yields significantly better long-term outcomes than conservative therapy regarding late complications such as erectile dysfunction and penile curvature. It also reduces the rate of early complications, such as severe corporal infections. Conservative therapy should be reserved for patients who explicitly refuse surgical intervention after thorough consultation.

This article was translated from Univadis Germany using ChatGPT followed by human editing.

A version of this article appeared on Medscape.com.

Early childhood trauma alters brain function in adults, according to new research.

In a meta-analysis of 83 functional magnetic resonance imaging (fMRI) studies that included more than 5000 patients, exposure to adversity was associated with higher amygdala reactivity and lower prefrontal cortical reactivity across a range of task domains. 

The altered responses were only observed in studies including adult participants and were clearest in participants who had been exposed to severe threat and trauma. Children and adolescents did not show significant adversity-related differences in brain function.

“By integrating the results from 83 previous brain imaging studies, we were able to provide what is arguably the clearest evidence to date that adults who have been exposed to early life trauma have different brain responses to psychological challenges,” senior author Marco Leyton, PhD, professor of psychiatry and director of the Temperament Adversity Biology Lab at McGill University in Montreal, Quebec, Canada, said in a press release. “This includes exaggerated responses in a region that processes emotionally intense information (the amygdala) and reduced responses in a region that helps people regulate emotions and associated behaviors (the frontal cortex).”

The findings were published in JAMA Network Open.
 

Changes in Reactivity 

“One big issue we have in psychology, and especially in neuroscience, is that single-study results are often not reproducible,” lead author Niki Hosseini-Kamkar, PhD, neuroimaging research associate at Atlas Institute for Veterans and Families at Royal Ottawa Hospital, said in an interview.

“It was very important to me to use a meta-analysis to get an overall picture of what brain regions are consistently reported across all these different studies. That is what we did here,” she added. Dr. Hosseini-Kamkar conducted this analysis while she was a postdoctoral research fellow at McGill University in Montreal.

She and her group examined adversity exposure and brain function in the following four domains of task-based fMRI: emotion processing, memory processing, inhibitory control, and reward processing. Their study included 5242 participants. The researchers used multilevel kernel density analyses (MKDA) to analyze the data more accurately. 

Adversity exposure was associated with higher amygdala reactivity (P < .001) and lower prefrontal cortical reactivity (P < .001), compared with controls with no adversity exposure.

Threat types of adversity were associated with greater blood-oxygen-level-dependent (BOLD) responses in the superior temporal gyrus and lower prefrontal cortex activity in participants exposed to threat, compared with controls. 

Analysis of studies of inhibitory control tasks found greater activity in the claustrum, anterior cingulate cortex, and insula in the adversity-exposed participants, compared with controls.

In addition, studies that administered emotion processing tasks showed greater amygdala reactivity and lower prefrontal cortex (superior frontal gyrus) reactivity in the adversity exposure group, compared with controls.

“The main takeaway is that there’s an exaggerated activity in the amygdala, and diminished prefrontal cortex activity, and together, this might point to a mechanism for how a history of adversity diminishes the ability to cope with later stressors and can therefore heighten susceptibility to mental illness,” said Dr. Hosseini-Kamkar.
 

‘Important Next Step’ 

“Overall, the meta-analysis by Dr. Hosseini-Kamkar and colleagues represents an important next step in understanding associations of adversity exposure with brain function while highlighting the importance of considering the role of development,” wrote Dylan G. Gee, PhD, associate professor of psychology at Yale University in New Haven, Connecticut, and Alexis Brieant, PhD, assistant professor of research or creative works at the University of Vermont in Burlington, in an accompanying commentary. 

They also applauded the authors for their use of MKDA. They noted that the technique “allows inferences about the consistency and specificity of brain activation across studies and is thought to be more robust to small sample sizes than activation likelihood estimation (ALE) meta-analysis.” 

Dr. Gee and Dr. Brieant also observed that a recent ALE meta-analysis failed to find a link between adversity and brain function. “Although it is important to note that the file drawer problem — by which researchers are less likely to publish null results — presents challenges to the inferences that can be drawn in the current work, the current study may provide complementary information to prior ALE meta-analyses.” 
 

Epigenetic Changes? 

Commenting on the findings for this article, Victor Fornari, MD, director of child and adolescent psychiatry at Northwell Health in Glen Oaks, New York, said, “Historically, when someone went through a traumatic event, they were told to just get over it, because somehow trauma doesn’t have a lasting impact on the brain.” Dr. Fornari was not involved in the research.

“We have certainly learned so much more over the past decade about early adversity and that it does have a profound impact on the brain and probably even epigenetic changes in our genes,” Dr. Fornari said.

“This is a very important avenue of investigation. People are really trying to understand if there are biological markers that we can actually measure in the brain that will offer us a window to better understand the consequence of adversity, as well as possible avenues of treatment.” 

No funding source for this study was reported. Dr. Leyton, Dr. Hosseini-Kamkar, and Dr. Fornari report no relevant financial relationships. Gee reports receiving grants from the National Science Foundation and National Institutes of Health outside the submitted work. Dr. Brieant reports receiving grants from the National Institute of Mental Health outside the submitted work. 

A version of this article appeared on Medscape.com.

Early childhood trauma alters brain function in adults, according to new research.

In a meta-analysis of 83 functional magnetic resonance imaging (fMRI) studies that included more than 5000 patients, exposure to adversity was associated with higher amygdala reactivity and lower prefrontal cortical reactivity across a range of task domains. 

The altered responses were only observed in studies including adult participants and were clearest in participants who had been exposed to severe threat and trauma. Children and adolescents did not show significant adversity-related differences in brain function.

“By integrating the results from 83 previous brain imaging studies, we were able to provide what is arguably the clearest evidence to date that adults who have been exposed to early life trauma have different brain responses to psychological challenges,” senior author Marco Leyton, PhD, professor of psychiatry and director of the Temperament Adversity Biology Lab at McGill University in Montreal, Quebec, Canada, said in a press release. “This includes exaggerated responses in a region that processes emotionally intense information (the amygdala) and reduced responses in a region that helps people regulate emotions and associated behaviors (the frontal cortex).”

The findings were published in JAMA Network Open.
 

Changes in Reactivity 

“One big issue we have in psychology, and especially in neuroscience, is that single-study results are often not reproducible,” lead author Niki Hosseini-Kamkar, PhD, neuroimaging research associate at Atlas Institute for Veterans and Families at Royal Ottawa Hospital, said in an interview.

“It was very important to me to use a meta-analysis to get an overall picture of what brain regions are consistently reported across all these different studies. That is what we did here,” she added. Dr. Hosseini-Kamkar conducted this analysis while she was a postdoctoral research fellow at McGill University in Montreal.

She and her group examined adversity exposure and brain function in the following four domains of task-based fMRI: emotion processing, memory processing, inhibitory control, and reward processing. Their study included 5242 participants. The researchers used multilevel kernel density analyses (MKDA) to analyze the data more accurately. 

Adversity exposure was associated with higher amygdala reactivity (P < .001) and lower prefrontal cortical reactivity (P < .001), compared with controls with no adversity exposure.

Threat types of adversity were associated with greater blood-oxygen-level-dependent (BOLD) responses in the superior temporal gyrus and lower prefrontal cortex activity in participants exposed to threat, compared with controls. 

Analysis of studies of inhibitory control tasks found greater activity in the claustrum, anterior cingulate cortex, and insula in the adversity-exposed participants, compared with controls.

In addition, studies that administered emotion processing tasks showed greater amygdala reactivity and lower prefrontal cortex (superior frontal gyrus) reactivity in the adversity exposure group, compared with controls.

“The main takeaway is that there’s an exaggerated activity in the amygdala, and diminished prefrontal cortex activity, and together, this might point to a mechanism for how a history of adversity diminishes the ability to cope with later stressors and can therefore heighten susceptibility to mental illness,” said Dr. Hosseini-Kamkar.
 

‘Important Next Step’ 

“Overall, the meta-analysis by Dr. Hosseini-Kamkar and colleagues represents an important next step in understanding associations of adversity exposure with brain function while highlighting the importance of considering the role of development,” wrote Dylan G. Gee, PhD, associate professor of psychology at Yale University in New Haven, Connecticut, and Alexis Brieant, PhD, assistant professor of research or creative works at the University of Vermont in Burlington, in an accompanying commentary. 

They also applauded the authors for their use of MKDA. They noted that the technique “allows inferences about the consistency and specificity of brain activation across studies and is thought to be more robust to small sample sizes than activation likelihood estimation (ALE) meta-analysis.” 

Dr. Gee and Dr. Brieant also observed that a recent ALE meta-analysis failed to find a link between adversity and brain function. “Although it is important to note that the file drawer problem — by which researchers are less likely to publish null results — presents challenges to the inferences that can be drawn in the current work, the current study may provide complementary information to prior ALE meta-analyses.” 
 

Epigenetic Changes? 

Commenting on the findings for this article, Victor Fornari, MD, director of child and adolescent psychiatry at Northwell Health in Glen Oaks, New York, said, “Historically, when someone went through a traumatic event, they were told to just get over it, because somehow trauma doesn’t have a lasting impact on the brain.” Dr. Fornari was not involved in the research.

“We have certainly learned so much more over the past decade about early adversity and that it does have a profound impact on the brain and probably even epigenetic changes in our genes,” Dr. Fornari said.

“This is a very important avenue of investigation. People are really trying to understand if there are biological markers that we can actually measure in the brain that will offer us a window to better understand the consequence of adversity, as well as possible avenues of treatment.” 

No funding source for this study was reported. Dr. Leyton, Dr. Hosseini-Kamkar, and Dr. Fornari report no relevant financial relationships. Gee reports receiving grants from the National Science Foundation and National Institutes of Health outside the submitted work. Dr. Brieant reports receiving grants from the National Institute of Mental Health outside the submitted work. 

A version of this article appeared on Medscape.com.

Early childhood trauma alters brain function in adults, according to new research.

In a meta-analysis of 83 functional magnetic resonance imaging (fMRI) studies that included more than 5000 patients, exposure to adversity was associated with higher amygdala reactivity and lower prefrontal cortical reactivity across a range of task domains. 

The altered responses were only observed in studies including adult participants and were clearest in participants who had been exposed to severe threat and trauma. Children and adolescents did not show significant adversity-related differences in brain function.

“By integrating the results from 83 previous brain imaging studies, we were able to provide what is arguably the clearest evidence to date that adults who have been exposed to early life trauma have different brain responses to psychological challenges,” senior author Marco Leyton, PhD, professor of psychiatry and director of the Temperament Adversity Biology Lab at McGill University in Montreal, Quebec, Canada, said in a press release. “This includes exaggerated responses in a region that processes emotionally intense information (the amygdala) and reduced responses in a region that helps people regulate emotions and associated behaviors (the frontal cortex).”

The findings were published in JAMA Network Open.
 

Changes in Reactivity 

“One big issue we have in psychology, and especially in neuroscience, is that single-study results are often not reproducible,” lead author Niki Hosseini-Kamkar, PhD, neuroimaging research associate at Atlas Institute for Veterans and Families at Royal Ottawa Hospital, said in an interview.

“It was very important to me to use a meta-analysis to get an overall picture of what brain regions are consistently reported across all these different studies. That is what we did here,” she added. Dr. Hosseini-Kamkar conducted this analysis while she was a postdoctoral research fellow at McGill University in Montreal.

She and her group examined adversity exposure and brain function in the following four domains of task-based fMRI: emotion processing, memory processing, inhibitory control, and reward processing. Their study included 5242 participants. The researchers used multilevel kernel density analyses (MKDA) to analyze the data more accurately. 

Adversity exposure was associated with higher amygdala reactivity (P < .001) and lower prefrontal cortical reactivity (P < .001), compared with controls with no adversity exposure.

Threat types of adversity were associated with greater blood-oxygen-level-dependent (BOLD) responses in the superior temporal gyrus and lower prefrontal cortex activity in participants exposed to threat, compared with controls. 

Analysis of studies of inhibitory control tasks found greater activity in the claustrum, anterior cingulate cortex, and insula in the adversity-exposed participants, compared with controls.

In addition, studies that administered emotion processing tasks showed greater amygdala reactivity and lower prefrontal cortex (superior frontal gyrus) reactivity in the adversity exposure group, compared with controls.

“The main takeaway is that there’s an exaggerated activity in the amygdala, and diminished prefrontal cortex activity, and together, this might point to a mechanism for how a history of adversity diminishes the ability to cope with later stressors and can therefore heighten susceptibility to mental illness,” said Dr. Hosseini-Kamkar.
 

‘Important Next Step’ 

“Overall, the meta-analysis by Dr. Hosseini-Kamkar and colleagues represents an important next step in understanding associations of adversity exposure with brain function while highlighting the importance of considering the role of development,” wrote Dylan G. Gee, PhD, associate professor of psychology at Yale University in New Haven, Connecticut, and Alexis Brieant, PhD, assistant professor of research or creative works at the University of Vermont in Burlington, in an accompanying commentary. 

They also applauded the authors for their use of MKDA. They noted that the technique “allows inferences about the consistency and specificity of brain activation across studies and is thought to be more robust to small sample sizes than activation likelihood estimation (ALE) meta-analysis.” 

Dr. Gee and Dr. Brieant also observed that a recent ALE meta-analysis failed to find a link between adversity and brain function. “Although it is important to note that the file drawer problem — by which researchers are less likely to publish null results — presents challenges to the inferences that can be drawn in the current work, the current study may provide complementary information to prior ALE meta-analyses.” 
 

Epigenetic Changes? 

Commenting on the findings for this article, Victor Fornari, MD, director of child and adolescent psychiatry at Northwell Health in Glen Oaks, New York, said, “Historically, when someone went through a traumatic event, they were told to just get over it, because somehow trauma doesn’t have a lasting impact on the brain.” Dr. Fornari was not involved in the research.

“We have certainly learned so much more over the past decade about early adversity and that it does have a profound impact on the brain and probably even epigenetic changes in our genes,” Dr. Fornari said.

“This is a very important avenue of investigation. People are really trying to understand if there are biological markers that we can actually measure in the brain that will offer us a window to better understand the consequence of adversity, as well as possible avenues of treatment.” 

No funding source for this study was reported. Dr. Leyton, Dr. Hosseini-Kamkar, and Dr. Fornari report no relevant financial relationships. Gee reports receiving grants from the National Science Foundation and National Institutes of Health outside the submitted work. Dr. Brieant reports receiving grants from the National Institute of Mental Health outside the submitted work. 

A version of this article appeared on Medscape.com.

An experimental therapy that uses deep brain stimulation (DBS) to deliver precise electrical pulses to an area deep inside the brain restored executive function in patients with moderate to severe traumatic brain injury (msTBI) and chronic sequelae.

Participants in this first-in-humans trial experienced brain injuries between 3-18 years before the study that left them with persistent neuropsychological impairment and a range of functional disabilities.

This is the first time a DBS device has been implanted in the central thalamus in humans, an area of the brain measuring only a few millimeters wide that helps regulate consciousness.

Placing the electrodes required a novel surgical technique developed by the investigators that included virtual models of each participant’s brain, microelectrode recording, and neuroimaging to identify neuronal circuits affected by the TBI.

After 3 months of 12-hour daily DBS treatments, participants’ performance on cognitive tests improved by an average of 32% from baseline. Participants were able to read books, watch TV shows, play video games, complete schoolwork, and felt significantly less fatigued during the day.

Although the small trial only included five patients, the work is already being hailed by other experts as significant.“We were looking for partial restoration of executive attention and expected [the treatment] would have an effect, but I wouldn’t have anticipated the effect size we saw,” co-lead investigator Nicholas Schiff, MD, professor of neuroscience at Weill Cornell Medical College, New York City, said in an interview.

The findings were published online Dec. 4 in Nature Medicine.

“No Trivial Feat”

An estimated 5.3 million children and adults are living with a permanent TBI-related disability in the US today. There currently is no effective therapy for impaired attention, executive function, working memory or information-processing speed caused by the initial injury.

Previous research suggests that a loss of activity in key brain circuits in the thalamus may be associated with a loss of cognitive function.

The investigators recruited six adults (four men and two women) between the ages of 22 and 60 years with a history of msTBI and chronic neuropsychological impairment and functional disability. One participant was later withdrawn from the trial for protocol noncompliance.

Participants completed a range of questionnaires and tests to establish baseline cognitive, psychological, and quality-of-life status.

To restore lost executive functioning in the brain, investigators had to target not only the central lateral nucleus, but also the neuronal network connected to the region that reaches other parts of the brain.

“To do both of those things we had to develop a whole toolset in order to model both the target and trajectory, which had to be right to make it work properly,” co-lead investigator Jaimie Henderson, MD, professor of neurosurgery at Stanford University College of Medicine, Stanford, California, said in an interview. “That gave us a pretty narrow window in which to work and getting an electrode accurately to this target is not a trivial feat.”

“A Moving Target”

Each participant’s brain physiology was slightly different, meaning the path that worked for one individual might not work for another. The surgery was further complicated by shifting in the brain that occurred as individual electrodes were placed.

“It was a literal moving target,” Dr. Henderson said.

In the beginning, investigators used microelectrode recording to “listen” to individual neurons to see which ones weren’t firing correctly.

When that method failed to offer the precise information needed for electrode placement, the investigators switched to neuroimaging, which allowed them to complete the surgery more quickly and accurately.

Participants remained in the hospital 1-2 days after surgery. They returned for postoperative imaging 30 days after surgery and were randomly assigned to different schedules for a 14-day titration period to optimize DBS stimulation.

The primary outcome was a 10% improvement on part B of the trail-making test, a neuropsychological test that measures executive functioning.

After 90 days of 12-hour daily DBS treatments, participants’ scores increased 15%–52% (average 32%) from baseline. Participants also reported an average of 33% decline in fatigue, one of the most common side effects of msTBI, and an average 80% improvement in attention.

The main safety risk during the 3- to-4-hour procedure is bleeding, which didn’t affect any of the participants in this study. One participant developed a surgical site infection, but all other side effects were mild.

After the 90-day treatment period, the study plan called for patients to be randomly assigned to a blinded withdrawal of treatment, with the DBS turned off for 21 days. Two of the patients declined to be randomized. DBS was turned off in one participant while the other two continued as normal.

After 3 weeks, the patient whose DBS was turned off showed a 34% decline on cognitive tests. The device was reactivated after the study and that participant has since reported improvements.

The DBS devices continue to function in all participants. Although their performance is not being measured as part of the study, anecdotal reports indicate sustained improvement in executive functioning.

“The brain injury causes this global down-regulation of brain function and what we think that this is doing is turning that back up again,” Dr. Henderson said. “At a very simplistic level, what we’re trying to do is turn the lights back up after the dimmer switch is switched down from the injury.”

New Hope

TBI patients are usually treated aggressively during the first year, when significant improvements are most likely, but there are few therapeutic options beyond that time, said neurologist Javier Cardenas, MD, who commented on the findings for this article.

“Many providers throw their hands up after a year in terms of intervention and then we’re always looking at potential declines over time,” said Dr. Cardenas, director of the Concussion and Brain Injury Center at the Rockefeller Neuroscience Institution, West Virginia University, Morgantown. “Most people plateau and don’t decline but we’re always worried about a secondary decline in traumatic brain injury.”Surgery is usually only employed immediately following the brain injury. The notion of surgery as a therapeutic option years after the initial assault on the brain is novel, said Jimmy Yang, MD, assistant professor of neurologic surgery at Ohio State University College of Medicine, Columbus, who commented on the findings for this article.

“While deep brain stimulation surgery in clinical practice is specifically tailored to each patient we treat, this study goes a step further by integrating research tools that have not yet made it to the clinical realm,” Dr. Yang said. “As a result, while these methods are not commonly used in clinical care, the overall strategy highlights how research advances are linked to clinical advances.”

Investigators are working to secure funding for a larger phase 2 trial.

“With millions of people affected by traumatic brain injury but without effective therapies, this study brings hope that options are on the horizon to help these patients,” Dr. Yang said.

The study was supported by funding from the National Institute of Health BRAIN Initiative and a grant from the Translational Science Center at Weill Cornell Medical College. Surgical implants were provided by Medtronic. Dr. Henderson and Dr. Schiff are listed as inventors on several patent applications for the experimental DBS therapy described in the study. Dr. Cardenas and Dr. Yang report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

An experimental therapy that uses deep brain stimulation (DBS) to deliver precise electrical pulses to an area deep inside the brain restored executive function in patients with moderate to severe traumatic brain injury (msTBI) and chronic sequelae.

Participants in this first-in-humans trial experienced brain injuries between 3-18 years before the study that left them with persistent neuropsychological impairment and a range of functional disabilities.

This is the first time a DBS device has been implanted in the central thalamus in humans, an area of the brain measuring only a few millimeters wide that helps regulate consciousness.

Placing the electrodes required a novel surgical technique developed by the investigators that included virtual models of each participant’s brain, microelectrode recording, and neuroimaging to identify neuronal circuits affected by the TBI.

After 3 months of 12-hour daily DBS treatments, participants’ performance on cognitive tests improved by an average of 32% from baseline. Participants were able to read books, watch TV shows, play video games, complete schoolwork, and felt significantly less fatigued during the day.

Although the small trial only included five patients, the work is already being hailed by other experts as significant.“We were looking for partial restoration of executive attention and expected [the treatment] would have an effect, but I wouldn’t have anticipated the effect size we saw,” co-lead investigator Nicholas Schiff, MD, professor of neuroscience at Weill Cornell Medical College, New York City, said in an interview.

The findings were published online Dec. 4 in Nature Medicine.

“No Trivial Feat”

An estimated 5.3 million children and adults are living with a permanent TBI-related disability in the US today. There currently is no effective therapy for impaired attention, executive function, working memory or information-processing speed caused by the initial injury.

Previous research suggests that a loss of activity in key brain circuits in the thalamus may be associated with a loss of cognitive function.

The investigators recruited six adults (four men and two women) between the ages of 22 and 60 years with a history of msTBI and chronic neuropsychological impairment and functional disability. One participant was later withdrawn from the trial for protocol noncompliance.

Participants completed a range of questionnaires and tests to establish baseline cognitive, psychological, and quality-of-life status.

To restore lost executive functioning in the brain, investigators had to target not only the central lateral nucleus, but also the neuronal network connected to the region that reaches other parts of the brain.

“To do both of those things we had to develop a whole toolset in order to model both the target and trajectory, which had to be right to make it work properly,” co-lead investigator Jaimie Henderson, MD, professor of neurosurgery at Stanford University College of Medicine, Stanford, California, said in an interview. “That gave us a pretty narrow window in which to work and getting an electrode accurately to this target is not a trivial feat.”

“A Moving Target”

Each participant’s brain physiology was slightly different, meaning the path that worked for one individual might not work for another. The surgery was further complicated by shifting in the brain that occurred as individual electrodes were placed.

“It was a literal moving target,” Dr. Henderson said.

In the beginning, investigators used microelectrode recording to “listen” to individual neurons to see which ones weren’t firing correctly.

When that method failed to offer the precise information needed for electrode placement, the investigators switched to neuroimaging, which allowed them to complete the surgery more quickly and accurately.

Participants remained in the hospital 1-2 days after surgery. They returned for postoperative imaging 30 days after surgery and were randomly assigned to different schedules for a 14-day titration period to optimize DBS stimulation.

The primary outcome was a 10% improvement on part B of the trail-making test, a neuropsychological test that measures executive functioning.

After 90 days of 12-hour daily DBS treatments, participants’ scores increased 15%–52% (average 32%) from baseline. Participants also reported an average of 33% decline in fatigue, one of the most common side effects of msTBI, and an average 80% improvement in attention.

The main safety risk during the 3- to-4-hour procedure is bleeding, which didn’t affect any of the participants in this study. One participant developed a surgical site infection, but all other side effects were mild.

After the 90-day treatment period, the study plan called for patients to be randomly assigned to a blinded withdrawal of treatment, with the DBS turned off for 21 days. Two of the patients declined to be randomized. DBS was turned off in one participant while the other two continued as normal.

After 3 weeks, the patient whose DBS was turned off showed a 34% decline on cognitive tests. The device was reactivated after the study and that participant has since reported improvements.

The DBS devices continue to function in all participants. Although their performance is not being measured as part of the study, anecdotal reports indicate sustained improvement in executive functioning.

“The brain injury causes this global down-regulation of brain function and what we think that this is doing is turning that back up again,” Dr. Henderson said. “At a very simplistic level, what we’re trying to do is turn the lights back up after the dimmer switch is switched down from the injury.”

New Hope

TBI patients are usually treated aggressively during the first year, when significant improvements are most likely, but there are few therapeutic options beyond that time, said neurologist Javier Cardenas, MD, who commented on the findings for this article.

“Many providers throw their hands up after a year in terms of intervention and then we’re always looking at potential declines over time,” said Dr. Cardenas, director of the Concussion and Brain Injury Center at the Rockefeller Neuroscience Institution, West Virginia University, Morgantown. “Most people plateau and don’t decline but we’re always worried about a secondary decline in traumatic brain injury.”Surgery is usually only employed immediately following the brain injury. The notion of surgery as a therapeutic option years after the initial assault on the brain is novel, said Jimmy Yang, MD, assistant professor of neurologic surgery at Ohio State University College of Medicine, Columbus, who commented on the findings for this article.

“While deep brain stimulation surgery in clinical practice is specifically tailored to each patient we treat, this study goes a step further by integrating research tools that have not yet made it to the clinical realm,” Dr. Yang said. “As a result, while these methods are not commonly used in clinical care, the overall strategy highlights how research advances are linked to clinical advances.”

Investigators are working to secure funding for a larger phase 2 trial.

“With millions of people affected by traumatic brain injury but without effective therapies, this study brings hope that options are on the horizon to help these patients,” Dr. Yang said.

The study was supported by funding from the National Institute of Health BRAIN Initiative and a grant from the Translational Science Center at Weill Cornell Medical College. Surgical implants were provided by Medtronic. Dr. Henderson and Dr. Schiff are listed as inventors on several patent applications for the experimental DBS therapy described in the study. Dr. Cardenas and Dr. Yang report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

An experimental therapy that uses deep brain stimulation (DBS) to deliver precise electrical pulses to an area deep inside the brain restored executive function in patients with moderate to severe traumatic brain injury (msTBI) and chronic sequelae.

Participants in this first-in-humans trial experienced brain injuries between 3-18 years before the study that left them with persistent neuropsychological impairment and a range of functional disabilities.

This is the first time a DBS device has been implanted in the central thalamus in humans, an area of the brain measuring only a few millimeters wide that helps regulate consciousness.

Placing the electrodes required a novel surgical technique developed by the investigators that included virtual models of each participant’s brain, microelectrode recording, and neuroimaging to identify neuronal circuits affected by the TBI.

After 3 months of 12-hour daily DBS treatments, participants’ performance on cognitive tests improved by an average of 32% from baseline. Participants were able to read books, watch TV shows, play video games, complete schoolwork, and felt significantly less fatigued during the day.

Although the small trial only included five patients, the work is already being hailed by other experts as significant.“We were looking for partial restoration of executive attention and expected [the treatment] would have an effect, but I wouldn’t have anticipated the effect size we saw,” co-lead investigator Nicholas Schiff, MD, professor of neuroscience at Weill Cornell Medical College, New York City, said in an interview.

The findings were published online Dec. 4 in Nature Medicine.

“No Trivial Feat”

An estimated 5.3 million children and adults are living with a permanent TBI-related disability in the US today. There currently is no effective therapy for impaired attention, executive function, working memory or information-processing speed caused by the initial injury.

Previous research suggests that a loss of activity in key brain circuits in the thalamus may be associated with a loss of cognitive function.

The investigators recruited six adults (four men and two women) between the ages of 22 and 60 years with a history of msTBI and chronic neuropsychological impairment and functional disability. One participant was later withdrawn from the trial for protocol noncompliance.

Participants completed a range of questionnaires and tests to establish baseline cognitive, psychological, and quality-of-life status.

To restore lost executive functioning in the brain, investigators had to target not only the central lateral nucleus, but also the neuronal network connected to the region that reaches other parts of the brain.

“To do both of those things we had to develop a whole toolset in order to model both the target and trajectory, which had to be right to make it work properly,” co-lead investigator Jaimie Henderson, MD, professor of neurosurgery at Stanford University College of Medicine, Stanford, California, said in an interview. “That gave us a pretty narrow window in which to work and getting an electrode accurately to this target is not a trivial feat.”

“A Moving Target”

Each participant’s brain physiology was slightly different, meaning the path that worked for one individual might not work for another. The surgery was further complicated by shifting in the brain that occurred as individual electrodes were placed.

“It was a literal moving target,” Dr. Henderson said.

In the beginning, investigators used microelectrode recording to “listen” to individual neurons to see which ones weren’t firing correctly.

When that method failed to offer the precise information needed for electrode placement, the investigators switched to neuroimaging, which allowed them to complete the surgery more quickly and accurately.

Participants remained in the hospital 1-2 days after surgery. They returned for postoperative imaging 30 days after surgery and were randomly assigned to different schedules for a 14-day titration period to optimize DBS stimulation.

The primary outcome was a 10% improvement on part B of the trail-making test, a neuropsychological test that measures executive functioning.

After 90 days of 12-hour daily DBS treatments, participants’ scores increased 15%–52% (average 32%) from baseline. Participants also reported an average of 33% decline in fatigue, one of the most common side effects of msTBI, and an average 80% improvement in attention.

The main safety risk during the 3- to-4-hour procedure is bleeding, which didn’t affect any of the participants in this study. One participant developed a surgical site infection, but all other side effects were mild.

After the 90-day treatment period, the study plan called for patients to be randomly assigned to a blinded withdrawal of treatment, with the DBS turned off for 21 days. Two of the patients declined to be randomized. DBS was turned off in one participant while the other two continued as normal.

After 3 weeks, the patient whose DBS was turned off showed a 34% decline on cognitive tests. The device was reactivated after the study and that participant has since reported improvements.

The DBS devices continue to function in all participants. Although their performance is not being measured as part of the study, anecdotal reports indicate sustained improvement in executive functioning.

“The brain injury causes this global down-regulation of brain function and what we think that this is doing is turning that back up again,” Dr. Henderson said. “At a very simplistic level, what we’re trying to do is turn the lights back up after the dimmer switch is switched down from the injury.”

New Hope

TBI patients are usually treated aggressively during the first year, when significant improvements are most likely, but there are few therapeutic options beyond that time, said neurologist Javier Cardenas, MD, who commented on the findings for this article.

“Many providers throw their hands up after a year in terms of intervention and then we’re always looking at potential declines over time,” said Dr. Cardenas, director of the Concussion and Brain Injury Center at the Rockefeller Neuroscience Institution, West Virginia University, Morgantown. “Most people plateau and don’t decline but we’re always worried about a secondary decline in traumatic brain injury.”Surgery is usually only employed immediately following the brain injury. The notion of surgery as a therapeutic option years after the initial assault on the brain is novel, said Jimmy Yang, MD, assistant professor of neurologic surgery at Ohio State University College of Medicine, Columbus, who commented on the findings for this article.

“While deep brain stimulation surgery in clinical practice is specifically tailored to each patient we treat, this study goes a step further by integrating research tools that have not yet made it to the clinical realm,” Dr. Yang said. “As a result, while these methods are not commonly used in clinical care, the overall strategy highlights how research advances are linked to clinical advances.”

Investigators are working to secure funding for a larger phase 2 trial.

“With millions of people affected by traumatic brain injury but without effective therapies, this study brings hope that options are on the horizon to help these patients,” Dr. Yang said.

The study was supported by funding from the National Institute of Health BRAIN Initiative and a grant from the Translational Science Center at Weill Cornell Medical College. Surgical implants were provided by Medtronic. Dr. Henderson and Dr. Schiff are listed as inventors on several patent applications for the experimental DBS therapy described in the study. Dr. Cardenas and Dr. Yang report no relevant financial relationships.

A version of this article first appeared on Medscape.com .

TOPLINE:

The addition of early and empirical high-dose cryoprecipitate to usual care does not improve clinical outcomes in patients with trauma and bleeding who required activation of a major hemorrhage protocol (MHP).

METHODOLOGY:

• CRYOSTAT-2 was an interventional, randomized, open-label, parallel-group controlled, international, multicenter study.
• A total of 1,604 patients were enrolled from 25 major trauma centers in the United Kingdom (n = 1,555) and 1 in the United States (n = 49) between August 2017 and November 2021.
• A total of 805 patients were randomly assigned to receive the standard MHP (standard care), and 799 were randomly assigned to receive an additional three pools of cryoprecipitate.
• The primary outcome was all-cause mortality at 28 days.

TAKEAWAY:

• Addition of early cryoprecipitate versus standard care did not improve all-cause 28-day mortality in the intent-to-treat population (25.3% vs. 26.1%; P = .74).
• In patient subgroup with penetrating trauma, 28-day mortality was significantly higher in the cryoprecipitate group than in the standard care group (16.2% vs. 10.0%; odds ratio, 1.74; P = .006).
• Massive transfusion (RBC ≥ 10 U) was similar between the cryoprecipitate and standard care groups.

IN PRACTICE:

According to the authors, it is possible that certain patients may have benefited from cryoprecipitate, but they did not receive it promptly or in adequate doses to restore functional fibrinogen levels. Despite the study’s goal of early cryoprecipitate administration, the median time to the first transfusion exceeded 1 hour after the patient’s arrival, which highlights the logistical challenges of preparing and delivering a frozen blood component from a distant blood laboratory to the patient.

SOURCE:

The study, with first author Ross Davenport, PhD, of Queen Mary University of London and colleagues, was published in JAMA).

LIMITATIONS:

There was variability of timing of cryoprecipitate administration and an overlap with patients in the standard care group receiving the intervention as part of their usual MHP treatment.

DISCLOSURES:

The study was funded by the U.K. National Institute for Health and Care Research: Health Technology Assessment and Barts Charity, U.K.

A version of this article first appeared on Medscape.com.

TOPLINE:

The addition of early and empirical high-dose cryoprecipitate to usual care does not improve clinical outcomes in patients with trauma and bleeding who required activation of a major hemorrhage protocol (MHP).

METHODOLOGY:

• CRYOSTAT-2 was an interventional, randomized, open-label, parallel-group controlled, international, multicenter study.
• A total of 1,604 patients were enrolled from 25 major trauma centers in the United Kingdom (n = 1,555) and 1 in the United States (n = 49) between August 2017 and November 2021.
• A total of 805 patients were randomly assigned to receive the standard MHP (standard care), and 799 were randomly assigned to receive an additional three pools of cryoprecipitate.
• The primary outcome was all-cause mortality at 28 days.

TAKEAWAY:

• Addition of early cryoprecipitate versus standard care did not improve all-cause 28-day mortality in the intent-to-treat population (25.3% vs. 26.1%; P = .74).
• In patient subgroup with penetrating trauma, 28-day mortality was significantly higher in the cryoprecipitate group than in the standard care group (16.2% vs. 10.0%; odds ratio, 1.74; P = .006).
• Massive transfusion (RBC ≥ 10 U) was similar between the cryoprecipitate and standard care groups.

IN PRACTICE:

According to the authors, it is possible that certain patients may have benefited from cryoprecipitate, but they did not receive it promptly or in adequate doses to restore functional fibrinogen levels. Despite the study’s goal of early cryoprecipitate administration, the median time to the first transfusion exceeded 1 hour after the patient’s arrival, which highlights the logistical challenges of preparing and delivering a frozen blood component from a distant blood laboratory to the patient.

SOURCE:

The study, with first author Ross Davenport, PhD, of Queen Mary University of London and colleagues, was published in JAMA).

LIMITATIONS:

There was variability of timing of cryoprecipitate administration and an overlap with patients in the standard care group receiving the intervention as part of their usual MHP treatment.

DISCLOSURES:

The study was funded by the U.K. National Institute for Health and Care Research: Health Technology Assessment and Barts Charity, U.K.

A version of this article first appeared on Medscape.com.

TOPLINE:

The addition of early and empirical high-dose cryoprecipitate to usual care does not improve clinical outcomes in patients with trauma and bleeding who required activation of a major hemorrhage protocol (MHP).

METHODOLOGY:

• CRYOSTAT-2 was an interventional, randomized, open-label, parallel-group controlled, international, multicenter study.
• A total of 1,604 patients were enrolled from 25 major trauma centers in the United Kingdom (n = 1,555) and 1 in the United States (n = 49) between August 2017 and November 2021.
• A total of 805 patients were randomly assigned to receive the standard MHP (standard care), and 799 were randomly assigned to receive an additional three pools of cryoprecipitate.
• The primary outcome was all-cause mortality at 28 days.

TAKEAWAY:

• Addition of early cryoprecipitate versus standard care did not improve all-cause 28-day mortality in the intent-to-treat population (25.3% vs. 26.1%; P = .74).
• In patient subgroup with penetrating trauma, 28-day mortality was significantly higher in the cryoprecipitate group than in the standard care group (16.2% vs. 10.0%; odds ratio, 1.74; P = .006).
• Massive transfusion (RBC ≥ 10 U) was similar between the cryoprecipitate and standard care groups.

IN PRACTICE:

According to the authors, it is possible that certain patients may have benefited from cryoprecipitate, but they did not receive it promptly or in adequate doses to restore functional fibrinogen levels. Despite the study’s goal of early cryoprecipitate administration, the median time to the first transfusion exceeded 1 hour after the patient’s arrival, which highlights the logistical challenges of preparing and delivering a frozen blood component from a distant blood laboratory to the patient.

SOURCE:

The study, with first author Ross Davenport, PhD, of Queen Mary University of London and colleagues, was published in JAMA).

LIMITATIONS:

There was variability of timing of cryoprecipitate administration and an overlap with patients in the standard care group receiving the intervention as part of their usual MHP treatment.

DISCLOSURES:

The study was funded by the U.K. National Institute for Health and Care Research: Health Technology Assessment and Barts Charity, U.K.

A version of this article first appeared on Medscape.com.

A recent review by Hadanny and colleagues recommends hyperbaric oxygen therapy (HBOT) for acute moderate to severe traumatic brain injury (TBI) and selected patients with prolonged postconcussive syndrome.

This article piqued my curiosity because I trained in HBOT more than 20 years ago. As a passionate scuba diver, my motivation was to master treatment for air embolism and decompression illness. Thankfully, these diving accidents are rare. However, I used HBOT for nonhealing wounds, and its efficacy was sometimes remarkable.
 

Paradoxical results with oxygen therapy

Although it may seem self-evident that “more oxygen is better” for medical illness, this is not necessarily true. I recently interviewed Ola Didrik Saugstad, MD, who demonstrated that the traditional practice of resuscitating newborns with 100% oxygen was more toxic than resuscitation with air (which contains 21% oxygen). His counterintuitive discovery led to a lifesaving change in the international newborn resuscitation guidelines.

The Food and Drug Administration has approved HBOT for a wide variety of conditions, but some practitioners enthusiastically promote it for off-label indications. These include antiaging, autism, multiple sclerosis, and the aforementioned TBI.

More than 50 years ago, HBOT was proposed for stroke, another disorder where the brain has been deprived of oxygen. Despite obvious logic, clinical trials have been unconvincing. The FDA has not approved HBOT for stroke.
 

HBOT in practice

During HBOT, the patient breathes 100% oxygen while the whole body is pressurized within a hyperbaric chamber. The chamber’s construction allows pressures above normal sea level of 1.0 atmosphere absolute (ATA). For example, The U.S. Navy Treatment Table for decompression sickness recommends 100% oxygen at 2.8 ATA. Chambers may hold one or more patients at a time.

The frequency of therapy varies but often consists of 20-60 sessions lasting 90-120 minutes. For off-label use like TBI, patients usually pay out of pocket. Given the multiple treatments, costs can add up.
 

Inconsistent evidence and sham controls

The unwieldy 33-page evidence review by Hadanny and colleagues cites multiple studies supporting HBOT for TBI. However, many, if not all, suffer from methodological flaws. These include vague inclusion criteria, lack of a control group, small patient numbers, treatment at different times since injury, poorly defined or varying HBOT protocols, varying outcome measures, and superficial results analysis.

A sham or control arm is essential for HBOT research trials, given the potential placebo effect of placing a human being inside a large, high-tech, sealed tube for an hour or more. In some sham-controlled studies, which consisted of low-pressure oxygen (that is, 1.3 ATA as sham vs. 2.4 ATA as treatment), all groups experienced symptom improvement. The review authors argue that the low-dose HBOT sham arms were biologically active and that the improvements seen mean that both high- and low-dose HBOT is therapeutic. The alternative explanation is that the placebo effect accounted for improvement in both groups.

The late Michael Bennett, a world authority on hyperbaric and underwater medicine, doubted that conventional HBOT sham controls could genuinely have a therapeutic effect, and I agree. The upcoming HOT-POCS trial (discussed below) should answer the question more definitively.
 

Mechanisms of action and safety

Mechanisms of benefit for HBOT include increased oxygen availability and angiogenesis. Animal research suggests that it may reduce secondary cell death from TBI, through stabilization of the blood-brain barrier and inflammation reduction.

HBOT is generally safe and well tolerated. A retrospective analysis of 1.5 million outpatient hyperbaric treatments revealed that less than 1% were associated with adverse events. The most common were ear and sinus barotrauma. Because HBOT uses increased air pressure, patients must equalize their ears and sinuses. Those who cannot because of altered consciousness, anatomical defects, or congestion must undergo myringotomy or terminate therapy. Claustrophobia was the second most common adverse effect. Convulsions and tension pneumocephalus were rare.

Perhaps the most concerning risk of HBOT for patients with TBI is the potential waste of human and financial resources.
 

Desperate physicians and patients

As a neurologist who regularly treats patients with TBI, I share the review authors’ frustration regarding the limited efficacy of available treatments. However, the suboptimal efficacy of currently available therapy is insufficient justification to recommend HBOT.

With respect to chronic TBI, it is difficult to imagine how HBOT could reverse brain injury that has been present for months or years. No other therapy exists that reliably encourages neuronal regeneration or prevents the development of posttraumatic epilepsy.

Frank Conidi, MD, a board-certified sports neurologist and headache specialist, shared his thoughts via email. He agrees that HBOT may have a role in TBI, but after reviewing Hadanny and colleagues’ paper, he concluded that there is insufficient evidence for the use of HBOT in all forms of TBI. He would like to see large multicenter, well-designed studies with standardized pressures and duration and a standard definition of the various types of head injury.
 

Ongoing research

There are at least five ongoing trials on HBOT for TBI or postconcussive syndrome, including the well-designed placebo-controlled HOT-POCS study. The latter has a novel placebo gas system that addresses Hadanny and colleagues’ contention that even low-dose HBOT might be effective.

The placebo arm in HOT-POCS mimics the HBO environment but provides only 0.21 ATA of oxygen, the same as room air. The active arm provides 100% oxygen at 2.0 ATA. If patients in both arms improve, the benefit will be caused by a placebo response, not HBOT.
 

Conflict of interest

Another concern with the review is that all three authors are affiliated with Aviv Scientific. This company has an exclusive partnership with the world’s largest hyperbaric medicine and research facility, the Sagol Center at Shamir Medical Center in Be’er Ya’akov, Israel.

This conflict of interest does not a priori invalidate their conclusions. However, official HBOT guidelines from a leading organization like the Undersea and Hyperbaric Medicine Society or the American Academy of Neurology would be preferable.
 

Conclusion

There is an urgent unmet need for more effective treatments for postconcussive syndrome and chronic TBI. Despite tantalizing theoretical mechanisms as to why HBOT might promote brain healing after trauma, its efficacy remains unproven.

The review authors’ recommendations for HBOT seem premature. They are arguably a disservice to the many desperate patients and their families who will be tempted to expend valuable resources of time and money for an appealing but unproven therapy. Appropriately designed placebo-controlled studies such as HOT-POCS will help separate fact from wishful thinking.

Dr. Wilner is associate professor of neurology at University of Tennessee Health Science Center, Memphis. He reported a conflict of interest with Accordant Health Services.

A version of this article first appeared on Medscape.com.

A recent review by Hadanny and colleagues recommends hyperbaric oxygen therapy (HBOT) for acute moderate to severe traumatic brain injury (TBI) and selected patients with prolonged postconcussive syndrome.

This article piqued my curiosity because I trained in HBOT more than 20 years ago. As a passionate scuba diver, my motivation was to master treatment for air embolism and decompression illness. Thankfully, these diving accidents are rare. However, I used HBOT for nonhealing wounds, and its efficacy was sometimes remarkable.
 

Paradoxical results with oxygen therapy

Although it may seem self-evident that “more oxygen is better” for medical illness, this is not necessarily true. I recently interviewed Ola Didrik Saugstad, MD, who demonstrated that the traditional practice of resuscitating newborns with 100% oxygen was more toxic than resuscitation with air (which contains 21% oxygen). His counterintuitive discovery led to a lifesaving change in the international newborn resuscitation guidelines.

The Food and Drug Administration has approved HBOT for a wide variety of conditions, but some practitioners enthusiastically promote it for off-label indications. These include antiaging, autism, multiple sclerosis, and the aforementioned TBI.

More than 50 years ago, HBOT was proposed for stroke, another disorder where the brain has been deprived of oxygen. Despite obvious logic, clinical trials have been unconvincing. The FDA has not approved HBOT for stroke.
 

HBOT in practice

During HBOT, the patient breathes 100% oxygen while the whole body is pressurized within a hyperbaric chamber. The chamber’s construction allows pressures above normal sea level of 1.0 atmosphere absolute (ATA). For example, The U.S. Navy Treatment Table for decompression sickness recommends 100% oxygen at 2.8 ATA. Chambers may hold one or more patients at a time.

The frequency of therapy varies but often consists of 20-60 sessions lasting 90-120 minutes. For off-label use like TBI, patients usually pay out of pocket. Given the multiple treatments, costs can add up.
 

Inconsistent evidence and sham controls

The unwieldy 33-page evidence review by Hadanny and colleagues cites multiple studies supporting HBOT for TBI. However, many, if not all, suffer from methodological flaws. These include vague inclusion criteria, lack of a control group, small patient numbers, treatment at different times since injury, poorly defined or varying HBOT protocols, varying outcome measures, and superficial results analysis.

A sham or control arm is essential for HBOT research trials, given the potential placebo effect of placing a human being inside a large, high-tech, sealed tube for an hour or more. In some sham-controlled studies, which consisted of low-pressure oxygen (that is, 1.3 ATA as sham vs. 2.4 ATA as treatment), all groups experienced symptom improvement. The review authors argue that the low-dose HBOT sham arms were biologically active and that the improvements seen mean that both high- and low-dose HBOT is therapeutic. The alternative explanation is that the placebo effect accounted for improvement in both groups.

The late Michael Bennett, a world authority on hyperbaric and underwater medicine, doubted that conventional HBOT sham controls could genuinely have a therapeutic effect, and I agree. The upcoming HOT-POCS trial (discussed below) should answer the question more definitively.
 

Mechanisms of action and safety

Mechanisms of benefit for HBOT include increased oxygen availability and angiogenesis. Animal research suggests that it may reduce secondary cell death from TBI, through stabilization of the blood-brain barrier and inflammation reduction.

HBOT is generally safe and well tolerated. A retrospective analysis of 1.5 million outpatient hyperbaric treatments revealed that less than 1% were associated with adverse events. The most common were ear and sinus barotrauma. Because HBOT uses increased air pressure, patients must equalize their ears and sinuses. Those who cannot because of altered consciousness, anatomical defects, or congestion must undergo myringotomy or terminate therapy. Claustrophobia was the second most common adverse effect. Convulsions and tension pneumocephalus were rare.

Perhaps the most concerning risk of HBOT for patients with TBI is the potential waste of human and financial resources.
 

Desperate physicians and patients

As a neurologist who regularly treats patients with TBI, I share the review authors’ frustration regarding the limited efficacy of available treatments. However, the suboptimal efficacy of currently available therapy is insufficient justification to recommend HBOT.

With respect to chronic TBI, it is difficult to imagine how HBOT could reverse brain injury that has been present for months or years. No other therapy exists that reliably encourages neuronal regeneration or prevents the development of posttraumatic epilepsy.

Frank Conidi, MD, a board-certified sports neurologist and headache specialist, shared his thoughts via email. He agrees that HBOT may have a role in TBI, but after reviewing Hadanny and colleagues’ paper, he concluded that there is insufficient evidence for the use of HBOT in all forms of TBI. He would like to see large multicenter, well-designed studies with standardized pressures and duration and a standard definition of the various types of head injury.
 

Ongoing research

There are at least five ongoing trials on HBOT for TBI or postconcussive syndrome, including the well-designed placebo-controlled HOT-POCS study. The latter has a novel placebo gas system that addresses Hadanny and colleagues’ contention that even low-dose HBOT might be effective.

The placebo arm in HOT-POCS mimics the HBO environment but provides only 0.21 ATA of oxygen, the same as room air. The active arm provides 100% oxygen at 2.0 ATA. If patients in both arms improve, the benefit will be caused by a placebo response, not HBOT.
 

Conflict of interest

Another concern with the review is that all three authors are affiliated with Aviv Scientific. This company has an exclusive partnership with the world’s largest hyperbaric medicine and research facility, the Sagol Center at Shamir Medical Center in Be’er Ya’akov, Israel.

This conflict of interest does not a priori invalidate their conclusions. However, official HBOT guidelines from a leading organization like the Undersea and Hyperbaric Medicine Society or the American Academy of Neurology would be preferable.
 

Conclusion

There is an urgent unmet need for more effective treatments for postconcussive syndrome and chronic TBI. Despite tantalizing theoretical mechanisms as to why HBOT might promote brain healing after trauma, its efficacy remains unproven.

The review authors’ recommendations for HBOT seem premature. They are arguably a disservice to the many desperate patients and their families who will be tempted to expend valuable resources of time and money for an appealing but unproven therapy. Appropriately designed placebo-controlled studies such as HOT-POCS will help separate fact from wishful thinking.

Dr. Wilner is associate professor of neurology at University of Tennessee Health Science Center, Memphis. He reported a conflict of interest with Accordant Health Services.

A version of this article first appeared on Medscape.com.

A recent review by Hadanny and colleagues recommends hyperbaric oxygen therapy (HBOT) for acute moderate to severe traumatic brain injury (TBI) and selected patients with prolonged postconcussive syndrome.

This article piqued my curiosity because I trained in HBOT more than 20 years ago. As a passionate scuba diver, my motivation was to master treatment for air embolism and decompression illness. Thankfully, these diving accidents are rare. However, I used HBOT for nonhealing wounds, and its efficacy was sometimes remarkable.
 

Paradoxical results with oxygen therapy

Although it may seem self-evident that “more oxygen is better” for medical illness, this is not necessarily true. I recently interviewed Ola Didrik Saugstad, MD, who demonstrated that the traditional practice of resuscitating newborns with 100% oxygen was more toxic than resuscitation with air (which contains 21% oxygen). His counterintuitive discovery led to a lifesaving change in the international newborn resuscitation guidelines.

The Food and Drug Administration has approved HBOT for a wide variety of conditions, but some practitioners enthusiastically promote it for off-label indications. These include antiaging, autism, multiple sclerosis, and the aforementioned TBI.

More than 50 years ago, HBOT was proposed for stroke, another disorder where the brain has been deprived of oxygen. Despite obvious logic, clinical trials have been unconvincing. The FDA has not approved HBOT for stroke.
 

HBOT in practice

During HBOT, the patient breathes 100% oxygen while the whole body is pressurized within a hyperbaric chamber. The chamber’s construction allows pressures above normal sea level of 1.0 atmosphere absolute (ATA). For example, The U.S. Navy Treatment Table for decompression sickness recommends 100% oxygen at 2.8 ATA. Chambers may hold one or more patients at a time.

The frequency of therapy varies but often consists of 20-60 sessions lasting 90-120 minutes. For off-label use like TBI, patients usually pay out of pocket. Given the multiple treatments, costs can add up.
 

Inconsistent evidence and sham controls

The unwieldy 33-page evidence review by Hadanny and colleagues cites multiple studies supporting HBOT for TBI. However, many, if not all, suffer from methodological flaws. These include vague inclusion criteria, lack of a control group, small patient numbers, treatment at different times since injury, poorly defined or varying HBOT protocols, varying outcome measures, and superficial results analysis.

A sham or control arm is essential for HBOT research trials, given the potential placebo effect of placing a human being inside a large, high-tech, sealed tube for an hour or more. In some sham-controlled studies, which consisted of low-pressure oxygen (that is, 1.3 ATA as sham vs. 2.4 ATA as treatment), all groups experienced symptom improvement. The review authors argue that the low-dose HBOT sham arms were biologically active and that the improvements seen mean that both high- and low-dose HBOT is therapeutic. The alternative explanation is that the placebo effect accounted for improvement in both groups.

The late Michael Bennett, a world authority on hyperbaric and underwater medicine, doubted that conventional HBOT sham controls could genuinely have a therapeutic effect, and I agree. The upcoming HOT-POCS trial (discussed below) should answer the question more definitively.
 

Mechanisms of action and safety

Mechanisms of benefit for HBOT include increased oxygen availability and angiogenesis. Animal research suggests that it may reduce secondary cell death from TBI, through stabilization of the blood-brain barrier and inflammation reduction.

HBOT is generally safe and well tolerated. A retrospective analysis of 1.5 million outpatient hyperbaric treatments revealed that less than 1% were associated with adverse events. The most common were ear and sinus barotrauma. Because HBOT uses increased air pressure, patients must equalize their ears and sinuses. Those who cannot because of altered consciousness, anatomical defects, or congestion must undergo myringotomy or terminate therapy. Claustrophobia was the second most common adverse effect. Convulsions and tension pneumocephalus were rare.

Perhaps the most concerning risk of HBOT for patients with TBI is the potential waste of human and financial resources.
 

Desperate physicians and patients

As a neurologist who regularly treats patients with TBI, I share the review authors’ frustration regarding the limited efficacy of available treatments. However, the suboptimal efficacy of currently available therapy is insufficient justification to recommend HBOT.

With respect to chronic TBI, it is difficult to imagine how HBOT could reverse brain injury that has been present for months or years. No other therapy exists that reliably encourages neuronal regeneration or prevents the development of posttraumatic epilepsy.

Frank Conidi, MD, a board-certified sports neurologist and headache specialist, shared his thoughts via email. He agrees that HBOT may have a role in TBI, but after reviewing Hadanny and colleagues’ paper, he concluded that there is insufficient evidence for the use of HBOT in all forms of TBI. He would like to see large multicenter, well-designed studies with standardized pressures and duration and a standard definition of the various types of head injury.
 

Ongoing research

There are at least five ongoing trials on HBOT for TBI or postconcussive syndrome, including the well-designed placebo-controlled HOT-POCS study. The latter has a novel placebo gas system that addresses Hadanny and colleagues’ contention that even low-dose HBOT might be effective.

The placebo arm in HOT-POCS mimics the HBO environment but provides only 0.21 ATA of oxygen, the same as room air. The active arm provides 100% oxygen at 2.0 ATA. If patients in both arms improve, the benefit will be caused by a placebo response, not HBOT.
 

Conflict of interest

Another concern with the review is that all three authors are affiliated with Aviv Scientific. This company has an exclusive partnership with the world’s largest hyperbaric medicine and research facility, the Sagol Center at Shamir Medical Center in Be’er Ya’akov, Israel.

This conflict of interest does not a priori invalidate their conclusions. However, official HBOT guidelines from a leading organization like the Undersea and Hyperbaric Medicine Society or the American Academy of Neurology would be preferable.
 

Conclusion

There is an urgent unmet need for more effective treatments for postconcussive syndrome and chronic TBI. Despite tantalizing theoretical mechanisms as to why HBOT might promote brain healing after trauma, its efficacy remains unproven.

The review authors’ recommendations for HBOT seem premature. They are arguably a disservice to the many desperate patients and their families who will be tempted to expend valuable resources of time and money for an appealing but unproven therapy. Appropriately designed placebo-controlled studies such as HOT-POCS will help separate fact from wishful thinking.

Dr. Wilner is associate professor of neurology at University of Tennessee Health Science Center, Memphis. He reported a conflict of interest with Accordant Health Services.

A version of this article first appeared on Medscape.com.

TOPLINE:

Ultrasonography may serve as an alternative to radiography for diagnosing pediatric forearm fractures, thus reducing the number of children undergoing radiography at initial emergency department presentation, as well as their waiting time in ED.

METHODOLOGY:

• After the World Health Organization reported a lack of access to any diagnostic imaging in approximately two-thirds of the world population in 2010, ultrasonography has gained popularity in low- and middle-income countries.
• The initial use of ultrasonography is in accordance with the principle of maintaining radiation levels as low as reasonably achievable.
• The BUCKLED trial was conducted, including 270 pediatric patients (age, 5-15 years) who presented to the ED with isolated, acute, clinically nondeformed distal forearm fractures.
• The participants were randomly assigned to receive initial point-of-care ultrasonography (n = 135) or radiography (n = 135) in the ED.
• The primary outcome was the physical function of the affected arm at 4 weeks evaluated using the Pediatric Upper Extremity Short Patient-Reported Outcomes Measurement Information System (PROMIS) tool.

TAKEAWAY:

• At 4 weeks, mean PROMIS scores were 36.4 and 36.3 points in ultrasonography and radiography groups, respectively (mean difference, 0.1 point; 95% confidence interval, − 1.3 to 1.4), indicating noninferiority of ultrasonography over radiography.
• Ultrasonography and radiography groups showed similar efficacy in terms of PROMIS scores at 1 week (MD, 0.7 points; 95% CI, − 1.4 to 2.8) and 8 weeks (MD, 0.1 points; 95% CI, − 0.5 to 0.7).
• Participants in the ultrasonography group had a shorter length of stay in the ED (median difference, 15 minutes; 95% CI, 1-29) and a shorter treatment time (median difference, 28 minutes; 95% CI, 17-40) than those in the radiography group.
• No important fractures were missed with ultrasonography, and no significant difference was observed in the frequency of adverse events or unplanned returns to the ED between the two groups.

IN PRACTICE:

Noting the benefit-risk profile of an ultrasound-first approach in an ED setting, the lead author, Peter J. Snelling, MB, BS, MPH&TM, from Menzies Health Institute Queensland, Gold Coast, Australia, said: “It is highly unlikely that any important fractures would be missed using the protocol that we trained clinicians. The risk is low and the benefit is moderate, such as reducing length of stay and increased level of patient satisfaction.”

He further added that, “with an ultrasound-first approach, clinicians can scan the patient at time of review and may even be able to discharge them immediately (two-thirds of instances in our NEJM trial). This places the patient at the center of care being provided.”
 

SOURCE: 

Authors from the BUCKLED Trial Group published their study in the New England Journal of Medicine.

LIMITATIONS:

PROMIS scores may have been affected by variations in subsequent therapeutic interventions rather than the initial diagnostic method. PROMIS tool was not validated in children younger than 5 years of age.

DISCLOSURES:

The study was funded by the Emergency Medicine Foundation and others. The authors have declared no relevant interests to disclose.

A version of this article first appeared on Medscape.com.

TOPLINE:

Ultrasonography may serve as an alternative to radiography for diagnosing pediatric forearm fractures, thus reducing the number of children undergoing radiography at initial emergency department presentation, as well as their waiting time in ED.

METHODOLOGY:

• After the World Health Organization reported a lack of access to any diagnostic imaging in approximately two-thirds of the world population in 2010, ultrasonography has gained popularity in low- and middle-income countries.
• The initial use of ultrasonography is in accordance with the principle of maintaining radiation levels as low as reasonably achievable.
• The BUCKLED trial was conducted, including 270 pediatric patients (age, 5-15 years) who presented to the ED with isolated, acute, clinically nondeformed distal forearm fractures.
• The participants were randomly assigned to receive initial point-of-care ultrasonography (n = 135) or radiography (n = 135) in the ED.
• The primary outcome was the physical function of the affected arm at 4 weeks evaluated using the Pediatric Upper Extremity Short Patient-Reported Outcomes Measurement Information System (PROMIS) tool.

TAKEAWAY:

• At 4 weeks, mean PROMIS scores were 36.4 and 36.3 points in ultrasonography and radiography groups, respectively (mean difference, 0.1 point; 95% confidence interval, − 1.3 to 1.4), indicating noninferiority of ultrasonography over radiography.
• Ultrasonography and radiography groups showed similar efficacy in terms of PROMIS scores at 1 week (MD, 0.7 points; 95% CI, − 1.4 to 2.8) and 8 weeks (MD, 0.1 points; 95% CI, − 0.5 to 0.7).
• Participants in the ultrasonography group had a shorter length of stay in the ED (median difference, 15 minutes; 95% CI, 1-29) and a shorter treatment time (median difference, 28 minutes; 95% CI, 17-40) than those in the radiography group.
• No important fractures were missed with ultrasonography, and no significant difference was observed in the frequency of adverse events or unplanned returns to the ED between the two groups.

IN PRACTICE:

Noting the benefit-risk profile of an ultrasound-first approach in an ED setting, the lead author, Peter J. Snelling, MB, BS, MPH&TM, from Menzies Health Institute Queensland, Gold Coast, Australia, said: “It is highly unlikely that any important fractures would be missed using the protocol that we trained clinicians. The risk is low and the benefit is moderate, such as reducing length of stay and increased level of patient satisfaction.”

He further added that, “with an ultrasound-first approach, clinicians can scan the patient at time of review and may even be able to discharge them immediately (two-thirds of instances in our NEJM trial). This places the patient at the center of care being provided.”
 

SOURCE: 

Authors from the BUCKLED Trial Group published their study in the New England Journal of Medicine.

LIMITATIONS:

PROMIS scores may have been affected by variations in subsequent therapeutic interventions rather than the initial diagnostic method. PROMIS tool was not validated in children younger than 5 years of age.

DISCLOSURES:

The study was funded by the Emergency Medicine Foundation and others. The authors have declared no relevant interests to disclose.

A version of this article first appeared on Medscape.com.

TOPLINE:

Ultrasonography may serve as an alternative to radiography for diagnosing pediatric forearm fractures, thus reducing the number of children undergoing radiography at initial emergency department presentation, as well as their waiting time in ED.

METHODOLOGY:

• After the World Health Organization reported a lack of access to any diagnostic imaging in approximately two-thirds of the world population in 2010, ultrasonography has gained popularity in low- and middle-income countries.
• The initial use of ultrasonography is in accordance with the principle of maintaining radiation levels as low as reasonably achievable.
• The BUCKLED trial was conducted, including 270 pediatric patients (age, 5-15 years) who presented to the ED with isolated, acute, clinically nondeformed distal forearm fractures.
• The participants were randomly assigned to receive initial point-of-care ultrasonography (n = 135) or radiography (n = 135) in the ED.
• The primary outcome was the physical function of the affected arm at 4 weeks evaluated using the Pediatric Upper Extremity Short Patient-Reported Outcomes Measurement Information System (PROMIS) tool.

TAKEAWAY:

• At 4 weeks, mean PROMIS scores were 36.4 and 36.3 points in ultrasonography and radiography groups, respectively (mean difference, 0.1 point; 95% confidence interval, − 1.3 to 1.4), indicating noninferiority of ultrasonography over radiography.
• Ultrasonography and radiography groups showed similar efficacy in terms of PROMIS scores at 1 week (MD, 0.7 points; 95% CI, − 1.4 to 2.8) and 8 weeks (MD, 0.1 points; 95% CI, − 0.5 to 0.7).
• Participants in the ultrasonography group had a shorter length of stay in the ED (median difference, 15 minutes; 95% CI, 1-29) and a shorter treatment time (median difference, 28 minutes; 95% CI, 17-40) than those in the radiography group.
• No important fractures were missed with ultrasonography, and no significant difference was observed in the frequency of adverse events or unplanned returns to the ED between the two groups.

IN PRACTICE:

Noting the benefit-risk profile of an ultrasound-first approach in an ED setting, the lead author, Peter J. Snelling, MB, BS, MPH&TM, from Menzies Health Institute Queensland, Gold Coast, Australia, said: “It is highly unlikely that any important fractures would be missed using the protocol that we trained clinicians. The risk is low and the benefit is moderate, such as reducing length of stay and increased level of patient satisfaction.”

He further added that, “with an ultrasound-first approach, clinicians can scan the patient at time of review and may even be able to discharge them immediately (two-thirds of instances in our NEJM trial). This places the patient at the center of care being provided.”
 

SOURCE: 

Authors from the BUCKLED Trial Group published their study in the New England Journal of Medicine.

LIMITATIONS:

PROMIS scores may have been affected by variations in subsequent therapeutic interventions rather than the initial diagnostic method. PROMIS tool was not validated in children younger than 5 years of age.

DISCLOSURES:

The study was funded by the Emergency Medicine Foundation and others. The authors have declared no relevant interests to disclose.

A version of this article first appeared on Medscape.com.

Traumatic brain injury (TBI) that occurs in early adulthood is associated with cognitive decline in later life, results from a study of identical twins who served in World War II show.

The research, which included almost 9,000 individuals, showed that twins who had experienced a TBI were more likely to have lower cognitive function at age 70 versus their twin who did not experience a TBI, especially if they had lost consciousness or were older than age 24 at the time of injury. In addition, their cognitive decline occurred at a more rapid rate.

“We know that TBI increases the risk of developing Alzheimer’s disease and other dementias in later life, but we haven’t known about TBI’s effect on cognitive decline that does not quite meet the threshold for dementia,” study investigator Marianne Chanti-Ketterl, PhD, Duke University, Durham, N.C., said in an interview.

“We know that TBI increases the risk of dementia in later life, but we haven’t known if TBI affects cognitive function, causes cognitive decline that has not progressed to the point of severity with Alzheimer’s or dementia,” she added.

Being able to study the impact of TBI in monozygotic twins gives this study a unique strength, she noted.

“The important thing about this is that they are monozygotic twins, and we know they shared a lot of early life exposure, and almost 100% genetics,” Dr. Chanti-Ketterl said.

The study was published online in Neurology.

For the study, the investigators assessed 8,662 participants born between 1917 and 1927 who were part of the National Academy of Sciences National Research Council’s Twin Registry. The registry is composed of male veterans of World War II with a history of TBI, as reported by themselves or a caregiver.

The men were followed up for many years as part of the registry, but cognitive assessment only began in the 1990s. They were followed up at four different time points, at which time the Telephone Interview for Cognitive Status (TICS-m), an alternative to the Mini-Mental State Examination that must be given in person, was administered.

A total of 25% of participants had experienced concussion in their lifetime. Of this cohort, there were 589 pairs of monozygotic twins who were discordant (one twin had TBI and the other had not).

Among the monozygotic twin cohort, a history of any TBI and being older than age 24 at the time of TBI were associated with lower TICS-m scores.

A twin who experienced TBI after age 24 scored 0.59 points lower on the TICS-m at age 70 than his twin with no TBI, and cognitive function declined faster, by 0.05 points per year.
 

First study of its kind

Holly Elser, MD, PhD, MPH, an epidemiologist and resident physician in neurology at the University of Pennsylvania, Philadelphia, and coauthor of an accompanying editorial, said in an interview that the study’s twin design was a definite strength.

“There are lots of papers that have remarked on the apparent association between head injury and subsequent dementia or cognitive decline, but to my knowledge, this is one of the first, if not the first, to use a twin study design, which has the unique advantage of having better control over early life and genetic factors than would ever typically be possible in a dataset of unrelated adults,” said Dr. Elser.

She added that the study findings “strengthen our understanding of the relationship between TBI and later cognitive decline, so I think there is an etiologic value to the study.”

However, Dr. Elser noted that the composition of the study population may limit the extent to which the results apply to contemporary populations.

“This was a population of White male twins born between 1917 and 1927,” she noted. “However, does the experience of people who were in the military generalize to civilian populations? Are twins representative of the general population or are they unique in terms of their risk factors?”

It is always important to emphasize inclusivity in clinical research, and in dementia research in particular, Dr. Elser added.

“There are many examples of instances where racialized and otherwise economically marginalized groups have been excluded from analysis, which is problematic because there are already economically and socially marginalized groups who disproportionately bear the brunt of dementia.

“This is not a criticism of the authors’ work, that their data didn’t include a more diverse patient base, but I think it is an important reminder that we should always interpret study findings within the limitations of the data. It’s a reminder to be thoughtful about taking explicit steps to include more diverse groups in future research,” she said.

The study was funded by the National Institute on Aging/National Institutes of Health and the Department of Defense. Dr. Chanti-Ketterl and Dr. Elser have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Traumatic brain injury (TBI) that occurs in early adulthood is associated with cognitive decline in later life, results from a study of identical twins who served in World War II show.

The research, which included almost 9,000 individuals, showed that twins who had experienced a TBI were more likely to have lower cognitive function at age 70 versus their twin who did not experience a TBI, especially if they had lost consciousness or were older than age 24 at the time of injury. In addition, their cognitive decline occurred at a more rapid rate.

“We know that TBI increases the risk of developing Alzheimer’s disease and other dementias in later life, but we haven’t known about TBI’s effect on cognitive decline that does not quite meet the threshold for dementia,” study investigator Marianne Chanti-Ketterl, PhD, Duke University, Durham, N.C., said in an interview.

“We know that TBI increases the risk of dementia in later life, but we haven’t known if TBI affects cognitive function, causes cognitive decline that has not progressed to the point of severity with Alzheimer’s or dementia,” she added.

Being able to study the impact of TBI in monozygotic twins gives this study a unique strength, she noted.

“The important thing about this is that they are monozygotic twins, and we know they shared a lot of early life exposure, and almost 100% genetics,” Dr. Chanti-Ketterl said.

The study was published online in Neurology.

For the study, the investigators assessed 8,662 participants born between 1917 and 1927 who were part of the National Academy of Sciences National Research Council’s Twin Registry. The registry is composed of male veterans of World War II with a history of TBI, as reported by themselves or a caregiver.

The men were followed up for many years as part of the registry, but cognitive assessment only began in the 1990s. They were followed up at four different time points, at which time the Telephone Interview for Cognitive Status (TICS-m), an alternative to the Mini-Mental State Examination that must be given in person, was administered.

A total of 25% of participants had experienced concussion in their lifetime. Of this cohort, there were 589 pairs of monozygotic twins who were discordant (one twin had TBI and the other had not).

Among the monozygotic twin cohort, a history of any TBI and being older than age 24 at the time of TBI were associated with lower TICS-m scores.

A twin who experienced TBI after age 24 scored 0.59 points lower on the TICS-m at age 70 than his twin with no TBI, and cognitive function declined faster, by 0.05 points per year.
 

First study of its kind

Holly Elser, MD, PhD, MPH, an epidemiologist and resident physician in neurology at the University of Pennsylvania, Philadelphia, and coauthor of an accompanying editorial, said in an interview that the study’s twin design was a definite strength.

“There are lots of papers that have remarked on the apparent association between head injury and subsequent dementia or cognitive decline, but to my knowledge, this is one of the first, if not the first, to use a twin study design, which has the unique advantage of having better control over early life and genetic factors than would ever typically be possible in a dataset of unrelated adults,” said Dr. Elser.

She added that the study findings “strengthen our understanding of the relationship between TBI and later cognitive decline, so I think there is an etiologic value to the study.”

However, Dr. Elser noted that the composition of the study population may limit the extent to which the results apply to contemporary populations.

“This was a population of White male twins born between 1917 and 1927,” she noted. “However, does the experience of people who were in the military generalize to civilian populations? Are twins representative of the general population or are they unique in terms of their risk factors?”

It is always important to emphasize inclusivity in clinical research, and in dementia research in particular, Dr. Elser added.

“There are many examples of instances where racialized and otherwise economically marginalized groups have been excluded from analysis, which is problematic because there are already economically and socially marginalized groups who disproportionately bear the brunt of dementia.

“This is not a criticism of the authors’ work, that their data didn’t include a more diverse patient base, but I think it is an important reminder that we should always interpret study findings within the limitations of the data. It’s a reminder to be thoughtful about taking explicit steps to include more diverse groups in future research,” she said.

The study was funded by the National Institute on Aging/National Institutes of Health and the Department of Defense. Dr. Chanti-Ketterl and Dr. Elser have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Traumatic brain injury (TBI) that occurs in early adulthood is associated with cognitive decline in later life, results from a study of identical twins who served in World War II show.

The research, which included almost 9,000 individuals, showed that twins who had experienced a TBI were more likely to have lower cognitive function at age 70 versus their twin who did not experience a TBI, especially if they had lost consciousness or were older than age 24 at the time of injury. In addition, their cognitive decline occurred at a more rapid rate.

“We know that TBI increases the risk of developing Alzheimer’s disease and other dementias in later life, but we haven’t known about TBI’s effect on cognitive decline that does not quite meet the threshold for dementia,” study investigator Marianne Chanti-Ketterl, PhD, Duke University, Durham, N.C., said in an interview.

“We know that TBI increases the risk of dementia in later life, but we haven’t known if TBI affects cognitive function, causes cognitive decline that has not progressed to the point of severity with Alzheimer’s or dementia,” she added.

Being able to study the impact of TBI in monozygotic twins gives this study a unique strength, she noted.

“The important thing about this is that they are monozygotic twins, and we know they shared a lot of early life exposure, and almost 100% genetics,” Dr. Chanti-Ketterl said.

The study was published online in Neurology.

For the study, the investigators assessed 8,662 participants born between 1917 and 1927 who were part of the National Academy of Sciences National Research Council’s Twin Registry. The registry is composed of male veterans of World War II with a history of TBI, as reported by themselves or a caregiver.

The men were followed up for many years as part of the registry, but cognitive assessment only began in the 1990s. They were followed up at four different time points, at which time the Telephone Interview for Cognitive Status (TICS-m), an alternative to the Mini-Mental State Examination that must be given in person, was administered.

A total of 25% of participants had experienced concussion in their lifetime. Of this cohort, there were 589 pairs of monozygotic twins who were discordant (one twin had TBI and the other had not).

Among the monozygotic twin cohort, a history of any TBI and being older than age 24 at the time of TBI were associated with lower TICS-m scores.

A twin who experienced TBI after age 24 scored 0.59 points lower on the TICS-m at age 70 than his twin with no TBI, and cognitive function declined faster, by 0.05 points per year.
 

First study of its kind

Holly Elser, MD, PhD, MPH, an epidemiologist and resident physician in neurology at the University of Pennsylvania, Philadelphia, and coauthor of an accompanying editorial, said in an interview that the study’s twin design was a definite strength.

“There are lots of papers that have remarked on the apparent association between head injury and subsequent dementia or cognitive decline, but to my knowledge, this is one of the first, if not the first, to use a twin study design, which has the unique advantage of having better control over early life and genetic factors than would ever typically be possible in a dataset of unrelated adults,” said Dr. Elser.

She added that the study findings “strengthen our understanding of the relationship between TBI and later cognitive decline, so I think there is an etiologic value to the study.”

However, Dr. Elser noted that the composition of the study population may limit the extent to which the results apply to contemporary populations.

“This was a population of White male twins born between 1917 and 1927,” she noted. “However, does the experience of people who were in the military generalize to civilian populations? Are twins representative of the general population or are they unique in terms of their risk factors?”

It is always important to emphasize inclusivity in clinical research, and in dementia research in particular, Dr. Elser added.

“There are many examples of instances where racialized and otherwise economically marginalized groups have been excluded from analysis, which is problematic because there are already economically and socially marginalized groups who disproportionately bear the brunt of dementia.

“This is not a criticism of the authors’ work, that their data didn’t include a more diverse patient base, but I think it is an important reminder that we should always interpret study findings within the limitations of the data. It’s a reminder to be thoughtful about taking explicit steps to include more diverse groups in future research,” she said.

The study was funded by the National Institute on Aging/National Institutes of Health and the Department of Defense. Dr. Chanti-Ketterl and Dr. Elser have reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

A version of this article first appeared on Medscape.com.

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

A version of this article first appeared on Medscape.com.

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

A version of this article first appeared on Medscape.com.

Among military veterans who die by suicide, those who experience a traumatic brain injury (TBI) during service take their lives 21% sooner after deployment than those without a TBI history, a new study shows.

Investigators also found that increases in new mental health diagnoses are significantly higher in soldiers with a history of TBI – in some cases, strikingly higher. For example, cases of substance use disorder rose by 100% among veterans with TBI compared to just 14.5% in those with no brain injury.

Veterans Health Administration

“We had had pieces of these findings for a long time but to be able to lay out this longitudinal story over time is the part that’s new and important to really switch the focus to people’s whole lives and things that happen over time, both psychological and physical,” lead author Lisa Brenner, PhD, director of the Veterans Health Administration (VHA) Rocky Mountain Mental Illness Research Education and Clinical Center, Aurora, Colo., said in an interview.

“If we take that life-course view, it’s a very different way about thinking about conceptualizing exposures and conceptualizing risk and it’s a different way of thinking about treatment and prevention,” added Dr. Brenner, professor of physical medicine and rehabilitation, psychiatry, and neurology at the University of Colorado, Aurora. “I think that definitely applies to civilian populations.”

The findings were published online in JAMA Network Open.
 

Largest, longest study to date

Researchers have long suspected that TBI and a higher rate of new mental illness and a shorter time to suicide are all somehow linked. But this study examined all three components longitudinally, in what is thought to be the largest and longest study on the topic to date, including more than 860,000 people who were followed for up to a decade.

Investigators studied health data from the Substance Use and Psychological Injury Combat Study database on 860,892 U.S. Army soldiers who returned from deployment in Iraq or Afghanistan between 2008 and 2014 and were 18-24 years old at the end of that deployment. They then examined new mental health diagnoses and suicide trends over time.

Nearly 109,000 (12.6%) experienced a TBI during deployment, and 2,695 had died by suicide through the end of 2018.

New-onset diagnoses of anxiety, mood disorders, posttraumatic stress disorder, alcohol use, and substance use disorder (SUD) after deployment were all more common in soldiers who experienced PTSD while serving compared with those with no history of TBI.

There was a 67.7% increase in mood disorders in participants with TBI compared with a 37.5% increase in those without TBI. The increase in new cases of alcohol use disorder was also greater in the TBI group (a 31.9% increase vs. a 10.3% increase).

But the sharpest difference was the increase in substance use disorder among those with TBI, which rose 100% compared with a 14.5% increase in solders with no history of TBI.
 

Sharp differences in time to suicide

Death by suicide was only slightly more common in those with TBI compared with those without (0.4% vs. 0.3%, respectively). But those with a brain injury committed suicide 21.3% sooner than did those without a head injury, after the researchers controlled for sex, age, race, ethnicity, and fiscal year of return from deployment.

Time to suicide was faster in those with a TBI and two or more new mental health diagnoses and fastest among those with TBI and a new SUD diagnosis, who took their own lives 62.8% faster than did those without a TBI.

The findings offer an important message to medical professionals in many different specialties, Dr. Brenner said.

“Folks in mental health probably have a lot of patients who have brain injury in their practice, and they don’t know it and that’s an important thing to know,” she said, adding that “neurologists should screen for depression and other mental health conditions and make sure those people have evidence-based treatments for those mental health conditions while they’re addressing the TBI-related symptoms.”
 

Applicable to civilians?

“The complex interplay between TBI, its potential effects on mental health, and risk of suicide remains a vexing focus of ongoing investigations and academic inquiry,” Ross Zafonte, DO, president of Spaulding Rehabilitation Hospital Network and professor and chair of physical medicine and rehabilitation at Harvard Medical School, Boston, and colleagues, wrote in an accompanying editorial.

The study builds on earlier work, they added, and praised the study’s longitudinal design and large cohort as key to the findings. The data on increased rates of new-onset substance use disorder, which was also associated with a faster time to suicide in the TBI group, were of particular interest.

“In this work, Brenner and colleagues identified substance use disorder as a key factor in faster time to suicide for active-duty service members with a history of TBI compared with those without TBI and theorized that a multiple stress or exposure burden may enhance risk,” they wrote. “This theory is reasonable and has been postulated among individuals with medical sequelae linked to TBI.”

However, the authors caution against applying these findings in military veterans to civilians.

“While this work is critical in the military population, caution should be given to avoid direct generalization to other populations, such as athletes, for whom the linkage to suicidal ideation is less understood,” they wrote.

The study was funded by National Institute of Mental Health and Office of the Director at National Institutes of Health. Dr. Brenner has received personal fees from Wolters Kluwer, Rand, American Psychological Association, and Oxford University Press and serves as a consultant to sports leagues via her university affiliation. Dr. Zafonte reported receiving royalties from Springer/Demos; serving as a member of the editorial boards of Journal of Neurotrauma and Frontiers in Neurology and scientific advisory boards of Myomo, Nanodiagnostics, Onecare.ai, and Kisbee; and evaluating patients in the MGH Brain and Body-TRUST Program, which is funded by the National Football League Players Association.
 

A version of this article first appeared on Medscape.com.

Among military veterans who die by suicide, those who experience a traumatic brain injury (TBI) during service take their lives 21% sooner after deployment than those without a TBI history, a new study shows.

Investigators also found that increases in new mental health diagnoses are significantly higher in soldiers with a history of TBI – in some cases, strikingly higher. For example, cases of substance use disorder rose by 100% among veterans with TBI compared to just 14.5% in those with no brain injury.

Veterans Health Administration

“We had had pieces of these findings for a long time but to be able to lay out this longitudinal story over time is the part that’s new and important to really switch the focus to people’s whole lives and things that happen over time, both psychological and physical,” lead author Lisa Brenner, PhD, director of the Veterans Health Administration (VHA) Rocky Mountain Mental Illness Research Education and Clinical Center, Aurora, Colo., said in an interview.

“If we take that life-course view, it’s a very different way about thinking about conceptualizing exposures and conceptualizing risk and it’s a different way of thinking about treatment and prevention,” added Dr. Brenner, professor of physical medicine and rehabilitation, psychiatry, and neurology at the University of Colorado, Aurora. “I think that definitely applies to civilian populations.”

The findings were published online in JAMA Network Open.
 

Largest, longest study to date

Researchers have long suspected that TBI and a higher rate of new mental illness and a shorter time to suicide are all somehow linked. But this study examined all three components longitudinally, in what is thought to be the largest and longest study on the topic to date, including more than 860,000 people who were followed for up to a decade.

Investigators studied health data from the Substance Use and Psychological Injury Combat Study database on 860,892 U.S. Army soldiers who returned from deployment in Iraq or Afghanistan between 2008 and 2014 and were 18-24 years old at the end of that deployment. They then examined new mental health diagnoses and suicide trends over time.

Nearly 109,000 (12.6%) experienced a TBI during deployment, and 2,695 had died by suicide through the end of 2018.

New-onset diagnoses of anxiety, mood disorders, posttraumatic stress disorder, alcohol use, and substance use disorder (SUD) after deployment were all more common in soldiers who experienced PTSD while serving compared with those with no history of TBI.

There was a 67.7% increase in mood disorders in participants with TBI compared with a 37.5% increase in those without TBI. The increase in new cases of alcohol use disorder was also greater in the TBI group (a 31.9% increase vs. a 10.3% increase).

But the sharpest difference was the increase in substance use disorder among those with TBI, which rose 100% compared with a 14.5% increase in solders with no history of TBI.
 

Sharp differences in time to suicide

Death by suicide was only slightly more common in those with TBI compared with those without (0.4% vs. 0.3%, respectively). But those with a brain injury committed suicide 21.3% sooner than did those without a head injury, after the researchers controlled for sex, age, race, ethnicity, and fiscal year of return from deployment.

Time to suicide was faster in those with a TBI and two or more new mental health diagnoses and fastest among those with TBI and a new SUD diagnosis, who took their own lives 62.8% faster than did those without a TBI.

The findings offer an important message to medical professionals in many different specialties, Dr. Brenner said.

“Folks in mental health probably have a lot of patients who have brain injury in their practice, and they don’t know it and that’s an important thing to know,” she said, adding that “neurologists should screen for depression and other mental health conditions and make sure those people have evidence-based treatments for those mental health conditions while they’re addressing the TBI-related symptoms.”
 

Applicable to civilians?

“The complex interplay between TBI, its potential effects on mental health, and risk of suicide remains a vexing focus of ongoing investigations and academic inquiry,” Ross Zafonte, DO, president of Spaulding Rehabilitation Hospital Network and professor and chair of physical medicine and rehabilitation at Harvard Medical School, Boston, and colleagues, wrote in an accompanying editorial.

The study builds on earlier work, they added, and praised the study’s longitudinal design and large cohort as key to the findings. The data on increased rates of new-onset substance use disorder, which was also associated with a faster time to suicide in the TBI group, were of particular interest.

“In this work, Brenner and colleagues identified substance use disorder as a key factor in faster time to suicide for active-duty service members with a history of TBI compared with those without TBI and theorized that a multiple stress or exposure burden may enhance risk,” they wrote. “This theory is reasonable and has been postulated among individuals with medical sequelae linked to TBI.”

However, the authors caution against applying these findings in military veterans to civilians.

“While this work is critical in the military population, caution should be given to avoid direct generalization to other populations, such as athletes, for whom the linkage to suicidal ideation is less understood,” they wrote.

The study was funded by National Institute of Mental Health and Office of the Director at National Institutes of Health. Dr. Brenner has received personal fees from Wolters Kluwer, Rand, American Psychological Association, and Oxford University Press and serves as a consultant to sports leagues via her university affiliation. Dr. Zafonte reported receiving royalties from Springer/Demos; serving as a member of the editorial boards of Journal of Neurotrauma and Frontiers in Neurology and scientific advisory boards of Myomo, Nanodiagnostics, Onecare.ai, and Kisbee; and evaluating patients in the MGH Brain and Body-TRUST Program, which is funded by the National Football League Players Association.
 

A version of this article first appeared on Medscape.com.

Among military veterans who die by suicide, those who experience a traumatic brain injury (TBI) during service take their lives 21% sooner after deployment than those without a TBI history, a new study shows.

Investigators also found that increases in new mental health diagnoses are significantly higher in soldiers with a history of TBI – in some cases, strikingly higher. For example, cases of substance use disorder rose by 100% among veterans with TBI compared to just 14.5% in those with no brain injury.

Veterans Health Administration

“We had had pieces of these findings for a long time but to be able to lay out this longitudinal story over time is the part that’s new and important to really switch the focus to people’s whole lives and things that happen over time, both psychological and physical,” lead author Lisa Brenner, PhD, director of the Veterans Health Administration (VHA) Rocky Mountain Mental Illness Research Education and Clinical Center, Aurora, Colo., said in an interview.

“If we take that life-course view, it’s a very different way about thinking about conceptualizing exposures and conceptualizing risk and it’s a different way of thinking about treatment and prevention,” added Dr. Brenner, professor of physical medicine and rehabilitation, psychiatry, and neurology at the University of Colorado, Aurora. “I think that definitely applies to civilian populations.”

The findings were published online in JAMA Network Open.
 

Largest, longest study to date

Researchers have long suspected that TBI and a higher rate of new mental illness and a shorter time to suicide are all somehow linked. But this study examined all three components longitudinally, in what is thought to be the largest and longest study on the topic to date, including more than 860,000 people who were followed for up to a decade.

Investigators studied health data from the Substance Use and Psychological Injury Combat Study database on 860,892 U.S. Army soldiers who returned from deployment in Iraq or Afghanistan between 2008 and 2014 and were 18-24 years old at the end of that deployment. They then examined new mental health diagnoses and suicide trends over time.

Nearly 109,000 (12.6%) experienced a TBI during deployment, and 2,695 had died by suicide through the end of 2018.

New-onset diagnoses of anxiety, mood disorders, posttraumatic stress disorder, alcohol use, and substance use disorder (SUD) after deployment were all more common in soldiers who experienced PTSD while serving compared with those with no history of TBI.

There was a 67.7% increase in mood disorders in participants with TBI compared with a 37.5% increase in those without TBI. The increase in new cases of alcohol use disorder was also greater in the TBI group (a 31.9% increase vs. a 10.3% increase).

But the sharpest difference was the increase in substance use disorder among those with TBI, which rose 100% compared with a 14.5% increase in solders with no history of TBI.
 

Sharp differences in time to suicide

Death by suicide was only slightly more common in those with TBI compared with those without (0.4% vs. 0.3%, respectively). But those with a brain injury committed suicide 21.3% sooner than did those without a head injury, after the researchers controlled for sex, age, race, ethnicity, and fiscal year of return from deployment.

Time to suicide was faster in those with a TBI and two or more new mental health diagnoses and fastest among those with TBI and a new SUD diagnosis, who took their own lives 62.8% faster than did those without a TBI.

The findings offer an important message to medical professionals in many different specialties, Dr. Brenner said.

“Folks in mental health probably have a lot of patients who have brain injury in their practice, and they don’t know it and that’s an important thing to know,” she said, adding that “neurologists should screen for depression and other mental health conditions and make sure those people have evidence-based treatments for those mental health conditions while they’re addressing the TBI-related symptoms.”
 

Applicable to civilians?

“The complex interplay between TBI, its potential effects on mental health, and risk of suicide remains a vexing focus of ongoing investigations and academic inquiry,” Ross Zafonte, DO, president of Spaulding Rehabilitation Hospital Network and professor and chair of physical medicine and rehabilitation at Harvard Medical School, Boston, and colleagues, wrote in an accompanying editorial.

The study builds on earlier work, they added, and praised the study’s longitudinal design and large cohort as key to the findings. The data on increased rates of new-onset substance use disorder, which was also associated with a faster time to suicide in the TBI group, were of particular interest.

“In this work, Brenner and colleagues identified substance use disorder as a key factor in faster time to suicide for active-duty service members with a history of TBI compared with those without TBI and theorized that a multiple stress or exposure burden may enhance risk,” they wrote. “This theory is reasonable and has been postulated among individuals with medical sequelae linked to TBI.”

However, the authors caution against applying these findings in military veterans to civilians.

“While this work is critical in the military population, caution should be given to avoid direct generalization to other populations, such as athletes, for whom the linkage to suicidal ideation is less understood,” they wrote.

The study was funded by National Institute of Mental Health and Office of the Director at National Institutes of Health. Dr. Brenner has received personal fees from Wolters Kluwer, Rand, American Psychological Association, and Oxford University Press and serves as a consultant to sports leagues via her university affiliation. Dr. Zafonte reported receiving royalties from Springer/Demos; serving as a member of the editorial boards of Journal of Neurotrauma and Frontiers in Neurology and scientific advisory boards of Myomo, Nanodiagnostics, Onecare.ai, and Kisbee; and evaluating patients in the MGH Brain and Body-TRUST Program, which is funded by the National Football League Players Association.
 

A version of this article first appeared on Medscape.com.

It seemed like a typical kind of day. I was out the door by 6:00 a.m., heading into work for a shift on I-35 West, my daily commute. It was still dark out. A little bit colder that morning, but nothing us Texans aren’t used to.

I was cruising down the tollway, which is separated from the main highway by a barrier. That stretch has a slight hill and turns to the left. You can’t see anything beyond the hill when you’re at the bottom.

As I made my way up, I spotted brake lights about 400 yards ahead. I eased on my brake, and next thing I knew, I was sliding.

I realized, I’m on black ice.

I was driving a 2011 Toyota FJ Cruiser and I had it all beefed up – lift tires, winch bumpers front and back. I had never had any sort of issue like that.

My ABS brakes kicked in. I slowed, but not fast enough. I saw a wall of crashed cars in front of me.

I was in the left-hand lane, so I turned my steering wheel into the center median. I could hear the whole side of my vehicle scraping against it. I managed to slow down enough to just tap the vehicle in front of me.

I looked in my passenger side-view mirror and saw headlights coming in the right lane. But this car couldn’t slow down. It crashed into the wreckage to my right.

That’s when it sunk in: There was going to be a car coming in my lane, and it might not be able to stop.

I looked in my rear-view mirror and saw headlights. Sparks flying off that center median.

I didn’t know at the time, but it was a fully loaded semi-truck traveling about 60 miles an hour.

I had a split second to think: This is it. This is how it ends. I closed my eyes.

It was the most violent impact I’ve ever experienced in my life.

I had no idea until afterward, but I had slammed into the vehicle in front of me and my SUV did a kind of 360° barrel roll over the median into the northbound lanes, landing wheels down on top of my sheared off roof rack.

Everything stopped. I opened my eyes. All my airbags had deployed. I gently tried moving my arms and legs, and they worked. I couldn’t move my left foot. It was wedged underneath the brake pedal. But I wasn’t in any pain, just very confused and disoriented. I knew I needed to get out of the vehicle.

My door was wedged shut, so I crawled out of the broken window, slipping on the black ice. I realized I had hit a Fort Worth police cruiser, now all smashed up. The driver couldn’t open his door. So, I helped him force it open, got him out of the vehicle, and checked on him. He was fine.

I had no idea how many vehicles and people were involved. I was in so much shock that the only thing I could do was immediately revert back to my training. I was the only first responder there. No ambulances on scene yet, no fire. So, I did what I know how to do – except without any tools. I tried to triage as many people as I could.

I was helping people with lacerations, back and neck issues from the violent impacts. When you’re involved in a mass casualty incident like that, you have to assess which patients will be the most viable and need the most immediate attention. You have greens, yellows, reds, and then blacks – the deceased. Someone who doesn’t have a pulse and isn’t breathing, you can’t necessarily do CPR because you don’t have enough resources. You have to use your best judgment.

Meanwhile, the crashes kept coming. I found out later I was roughly vehicle No. 50 in the pileup; 83 more would follow. I heard them over and over – a crash and then screams from people in their vehicles. Each time a car hit, the entire pileup would move a couple of inches, getting more and more compacted. With that going on, I couldn’t go in there to pull people out. That scene was absolutely unsafe.

It felt like forever, but about 10 minutes later, an ambulance showed up, and I walked over to them. Because I was in my work uniform, they thought I was there on a call.

A couple fire crews came, and a firefighter yelled, “Hey, we need a backboard!” So, I grabbed a backboard from their unit and helped load up a patient. Then I heard somebody screaming, “This patient needs a stretcher!” A woman was having lumbar pain that seemed excruciating. I helped move her from the wreckage and carry her over to the stretcher. I started trying to get as many people as I could out of their cars.

Around this time, one of my supervisors showed up. He thought I was there working. But then he asked me, “Why is your face bleeding? Why do you have blood coming from your nose?” I pointed to my vehicle, and his jaw just dropped. He said, “Okay, you’re done. Go sit in my vehicle over there.”

He put a stop to my helping out, which was probably for the best. Because I actually had a concussion, a bone contusion in my foot, and a severely sprained ankle. The next day, I felt like I had gotten hit by a truck. (I had!) But when you have so much adrenaline pumping, you don’t feel pain or emotion. You don’t really feel anything.

While I was sitting in that vehicle, I called my mom to let her know I was okay. My parents were watching the news, and there was an aerial view of the accident. It was massive – a giant pile of metal stretching 200 or 300 yards. Six people had perished, more than 60 were hurt.

That night, our public information officer reached out to me about doing an interview with NBC. So, I told my story about what happened. Because of the concussion, a lot of it was a blur.

A day later, I got a call on my cell phone and someone said, “This is Tyler from Toyota. We saw the NBC interview. We wanted to let you know, don’t worry about getting a new vehicle. Just tell us what color 4Runner you want.”

My first thought was: Okay, this can’t be real. This doesn’t happen to people like me. But it turned out that it was, and they put me in a brand new vehicle.

Toyota started sending me to events like NASCAR races, putting me up in VIP suites. It was a cool experience. But it’s just surface stuff – it’s never going to erase what happened. The experience left a mark. It took me 6 months to a year to get rid of that feeling of the impact. Every time I tried to fall asleep, the whole scenario would replay in my head.

In EMS, we have a saying: “Every patient is practice for the next one.” That pileup – you can’t train for something like that. We all learned from it, so we can better prepare if anything like that happens again.

Since then, I’ve seen people die in motor vehicle collisions from a lot less than what happened to me. I’m not religious or spiritual, but I believe there must be a reason why I’m still here.

Now I see patients in traffic accidents who are very distraught even though they’re going to be okay. I tell them, “I’m sorry this happened to you. But remember, this is not the end. You are alive. And I’m going to do everything I can to make sure that doesn’t change while you’re with me.”
 

Trey McDaniel is a paramedic with MedStar Mobile Healthcare in Fort Worth, Tex.

A version of this article first appeared on Medscape.com.

It seemed like a typical kind of day. I was out the door by 6:00 a.m., heading into work for a shift on I-35 West, my daily commute. It was still dark out. A little bit colder that morning, but nothing us Texans aren’t used to.

I was cruising down the tollway, which is separated from the main highway by a barrier. That stretch has a slight hill and turns to the left. You can’t see anything beyond the hill when you’re at the bottom.

As I made my way up, I spotted brake lights about 400 yards ahead. I eased on my brake, and next thing I knew, I was sliding.

I realized, I’m on black ice.

I was driving a 2011 Toyota FJ Cruiser and I had it all beefed up – lift tires, winch bumpers front and back. I had never had any sort of issue like that.

My ABS brakes kicked in. I slowed, but not fast enough. I saw a wall of crashed cars in front of me.

I was in the left-hand lane, so I turned my steering wheel into the center median. I could hear the whole side of my vehicle scraping against it. I managed to slow down enough to just tap the vehicle in front of me.

I looked in my passenger side-view mirror and saw headlights coming in the right lane. But this car couldn’t slow down. It crashed into the wreckage to my right.

That’s when it sunk in: There was going to be a car coming in my lane, and it might not be able to stop.

I looked in my rear-view mirror and saw headlights. Sparks flying off that center median.

I didn’t know at the time, but it was a fully loaded semi-truck traveling about 60 miles an hour.

I had a split second to think: This is it. This is how it ends. I closed my eyes.

It was the most violent impact I’ve ever experienced in my life.

I had no idea until afterward, but I had slammed into the vehicle in front of me and my SUV did a kind of 360° barrel roll over the median into the northbound lanes, landing wheels down on top of my sheared off roof rack.

Everything stopped. I opened my eyes. All my airbags had deployed. I gently tried moving my arms and legs, and they worked. I couldn’t move my left foot. It was wedged underneath the brake pedal. But I wasn’t in any pain, just very confused and disoriented. I knew I needed to get out of the vehicle.

My door was wedged shut, so I crawled out of the broken window, slipping on the black ice. I realized I had hit a Fort Worth police cruiser, now all smashed up. The driver couldn’t open his door. So, I helped him force it open, got him out of the vehicle, and checked on him. He was fine.

I had no idea how many vehicles and people were involved. I was in so much shock that the only thing I could do was immediately revert back to my training. I was the only first responder there. No ambulances on scene yet, no fire. So, I did what I know how to do – except without any tools. I tried to triage as many people as I could.

I was helping people with lacerations, back and neck issues from the violent impacts. When you’re involved in a mass casualty incident like that, you have to assess which patients will be the most viable and need the most immediate attention. You have greens, yellows, reds, and then blacks – the deceased. Someone who doesn’t have a pulse and isn’t breathing, you can’t necessarily do CPR because you don’t have enough resources. You have to use your best judgment.

Meanwhile, the crashes kept coming. I found out later I was roughly vehicle No. 50 in the pileup; 83 more would follow. I heard them over and over – a crash and then screams from people in their vehicles. Each time a car hit, the entire pileup would move a couple of inches, getting more and more compacted. With that going on, I couldn’t go in there to pull people out. That scene was absolutely unsafe.

It felt like forever, but about 10 minutes later, an ambulance showed up, and I walked over to them. Because I was in my work uniform, they thought I was there on a call.

A couple fire crews came, and a firefighter yelled, “Hey, we need a backboard!” So, I grabbed a backboard from their unit and helped load up a patient. Then I heard somebody screaming, “This patient needs a stretcher!” A woman was having lumbar pain that seemed excruciating. I helped move her from the wreckage and carry her over to the stretcher. I started trying to get as many people as I could out of their cars.

Around this time, one of my supervisors showed up. He thought I was there working. But then he asked me, “Why is your face bleeding? Why do you have blood coming from your nose?” I pointed to my vehicle, and his jaw just dropped. He said, “Okay, you’re done. Go sit in my vehicle over there.”

He put a stop to my helping out, which was probably for the best. Because I actually had a concussion, a bone contusion in my foot, and a severely sprained ankle. The next day, I felt like I had gotten hit by a truck. (I had!) But when you have so much adrenaline pumping, you don’t feel pain or emotion. You don’t really feel anything.

While I was sitting in that vehicle, I called my mom to let her know I was okay. My parents were watching the news, and there was an aerial view of the accident. It was massive – a giant pile of metal stretching 200 or 300 yards. Six people had perished, more than 60 were hurt.

That night, our public information officer reached out to me about doing an interview with NBC. So, I told my story about what happened. Because of the concussion, a lot of it was a blur.

A day later, I got a call on my cell phone and someone said, “This is Tyler from Toyota. We saw the NBC interview. We wanted to let you know, don’t worry about getting a new vehicle. Just tell us what color 4Runner you want.”

My first thought was: Okay, this can’t be real. This doesn’t happen to people like me. But it turned out that it was, and they put me in a brand new vehicle.

Toyota started sending me to events like NASCAR races, putting me up in VIP suites. It was a cool experience. But it’s just surface stuff – it’s never going to erase what happened. The experience left a mark. It took me 6 months to a year to get rid of that feeling of the impact. Every time I tried to fall asleep, the whole scenario would replay in my head.

In EMS, we have a saying: “Every patient is practice for the next one.” That pileup – you can’t train for something like that. We all learned from it, so we can better prepare if anything like that happens again.

Since then, I’ve seen people die in motor vehicle collisions from a lot less than what happened to me. I’m not religious or spiritual, but I believe there must be a reason why I’m still here.

Now I see patients in traffic accidents who are very distraught even though they’re going to be okay. I tell them, “I’m sorry this happened to you. But remember, this is not the end. You are alive. And I’m going to do everything I can to make sure that doesn’t change while you’re with me.”
 

Trey McDaniel is a paramedic with MedStar Mobile Healthcare in Fort Worth, Tex.

A version of this article first appeared on Medscape.com.

It seemed like a typical kind of day. I was out the door by 6:00 a.m., heading into work for a shift on I-35 West, my daily commute. It was still dark out. A little bit colder that morning, but nothing us Texans aren’t used to.

I was cruising down the tollway, which is separated from the main highway by a barrier. That stretch has a slight hill and turns to the left. You can’t see anything beyond the hill when you’re at the bottom.

As I made my way up, I spotted brake lights about 400 yards ahead. I eased on my brake, and next thing I knew, I was sliding.

I realized, I’m on black ice.

I was driving a 2011 Toyota FJ Cruiser and I had it all beefed up – lift tires, winch bumpers front and back. I had never had any sort of issue like that.

My ABS brakes kicked in. I slowed, but not fast enough. I saw a wall of crashed cars in front of me.

I was in the left-hand lane, so I turned my steering wheel into the center median. I could hear the whole side of my vehicle scraping against it. I managed to slow down enough to just tap the vehicle in front of me.

I looked in my passenger side-view mirror and saw headlights coming in the right lane. But this car couldn’t slow down. It crashed into the wreckage to my right.

That’s when it sunk in: There was going to be a car coming in my lane, and it might not be able to stop.

I looked in my rear-view mirror and saw headlights. Sparks flying off that center median.

I didn’t know at the time, but it was a fully loaded semi-truck traveling about 60 miles an hour.

I had a split second to think: This is it. This is how it ends. I closed my eyes.

It was the most violent impact I’ve ever experienced in my life.

I had no idea until afterward, but I had slammed into the vehicle in front of me and my SUV did a kind of 360° barrel roll over the median into the northbound lanes, landing wheels down on top of my sheared off roof rack.

Everything stopped. I opened my eyes. All my airbags had deployed. I gently tried moving my arms and legs, and they worked. I couldn’t move my left foot. It was wedged underneath the brake pedal. But I wasn’t in any pain, just very confused and disoriented. I knew I needed to get out of the vehicle.

My door was wedged shut, so I crawled out of the broken window, slipping on the black ice. I realized I had hit a Fort Worth police cruiser, now all smashed up. The driver couldn’t open his door. So, I helped him force it open, got him out of the vehicle, and checked on him. He was fine.

I had no idea how many vehicles and people were involved. I was in so much shock that the only thing I could do was immediately revert back to my training. I was the only first responder there. No ambulances on scene yet, no fire. So, I did what I know how to do – except without any tools. I tried to triage as many people as I could.

I was helping people with lacerations, back and neck issues from the violent impacts. When you’re involved in a mass casualty incident like that, you have to assess which patients will be the most viable and need the most immediate attention. You have greens, yellows, reds, and then blacks – the deceased. Someone who doesn’t have a pulse and isn’t breathing, you can’t necessarily do CPR because you don’t have enough resources. You have to use your best judgment.

Meanwhile, the crashes kept coming. I found out later I was roughly vehicle No. 50 in the pileup; 83 more would follow. I heard them over and over – a crash and then screams from people in their vehicles. Each time a car hit, the entire pileup would move a couple of inches, getting more and more compacted. With that going on, I couldn’t go in there to pull people out. That scene was absolutely unsafe.

It felt like forever, but about 10 minutes later, an ambulance showed up, and I walked over to them. Because I was in my work uniform, they thought I was there on a call.

A couple fire crews came, and a firefighter yelled, “Hey, we need a backboard!” So, I grabbed a backboard from their unit and helped load up a patient. Then I heard somebody screaming, “This patient needs a stretcher!” A woman was having lumbar pain that seemed excruciating. I helped move her from the wreckage and carry her over to the stretcher. I started trying to get as many people as I could out of their cars.

Around this time, one of my supervisors showed up. He thought I was there working. But then he asked me, “Why is your face bleeding? Why do you have blood coming from your nose?” I pointed to my vehicle, and his jaw just dropped. He said, “Okay, you’re done. Go sit in my vehicle over there.”

He put a stop to my helping out, which was probably for the best. Because I actually had a concussion, a bone contusion in my foot, and a severely sprained ankle. The next day, I felt like I had gotten hit by a truck. (I had!) But when you have so much adrenaline pumping, you don’t feel pain or emotion. You don’t really feel anything.

While I was sitting in that vehicle, I called my mom to let her know I was okay. My parents were watching the news, and there was an aerial view of the accident. It was massive – a giant pile of metal stretching 200 or 300 yards. Six people had perished, more than 60 were hurt.

That night, our public information officer reached out to me about doing an interview with NBC. So, I told my story about what happened. Because of the concussion, a lot of it was a blur.

A day later, I got a call on my cell phone and someone said, “This is Tyler from Toyota. We saw the NBC interview. We wanted to let you know, don’t worry about getting a new vehicle. Just tell us what color 4Runner you want.”

My first thought was: Okay, this can’t be real. This doesn’t happen to people like me. But it turned out that it was, and they put me in a brand new vehicle.

Toyota started sending me to events like NASCAR races, putting me up in VIP suites. It was a cool experience. But it’s just surface stuff – it’s never going to erase what happened. The experience left a mark. It took me 6 months to a year to get rid of that feeling of the impact. Every time I tried to fall asleep, the whole scenario would replay in my head.

In EMS, we have a saying: “Every patient is practice for the next one.” That pileup – you can’t train for something like that. We all learned from it, so we can better prepare if anything like that happens again.

Since then, I’ve seen people die in motor vehicle collisions from a lot less than what happened to me. I’m not religious or spiritual, but I believe there must be a reason why I’m still here.

Now I see patients in traffic accidents who are very distraught even though they’re going to be okay. I tell them, “I’m sorry this happened to you. But remember, this is not the end. You are alive. And I’m going to do everything I can to make sure that doesn’t change while you’re with me.”
 

Trey McDaniel is a paramedic with MedStar Mobile Healthcare in Fort Worth, Tex.

A version of this article first appeared on Medscape.com.