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Deficits in executive function (EF) are linked to with development of posttraumatic stress disorder (PTSD) symptoms and exacerbation of such symptoms over time, new research suggests.

“To our knowledge, this study is the first to show that executive-function deficits maintain PTSD symptoms following trauma exposure,” investigators noted in research presented at the Anxiety and Depression Association of America (ADAA) Anxiety & Depression conference.

Dr. Joseph R. Bardeen, Department of Psychological Sciences, Auburn University, Alabama
Courtesy Auburn University
Dr. Joseph R. Bardeen

The results are important in “developing precision medicine–based approaches for alleviating [posttraumatic stress] symptoms, and improving well-established PTSD treatments for those with relative deficits in executive function,” study investigator Joseph R. Bardeen, PhD, associate professor at Auburn (Ala.) University, told meeting attendees.

The findings were published in the Journal of Anxiety Disorders.
 

Cognitive impairment

In earlier research, deficits in EF were associated with an increased vulnerability for PTSD symptoms. However, less is known about the role of these deficits, which can impair higher-level cognitive ability, in sustaining PTSD symptoms.

To investigate, the authors conducted a longitudinal study that included 98 participants aged 18-65 years who had been identified via phone screening as experiencing clinically significant PTSD symptoms.

Participants completed self-report measures for PTSD symptoms, as well as measures for EF deficits at baseline and 6-month (n = 92) and 12-month (n = 91) follow-up sessions.

A path analysis showed a significant relationship between baseline PTSD symptoms and EF deficits at 6 months (P < .001). Baseline PTSD symptoms were associated with 12-month PTSD symptoms (P < .04).

EF deficits at 6 months were also associated with 12-month PTSD symptoms (P = .02).

Importantly, no associations were observed between baseline or 6-month PTSD symptoms and EF deficits at 12 months. However, EF deficits at 6 months drove the relationship between PTSD symptoms at baseline and at 1 year (indirect effect = .061).

“What this suggests is that executive-function deficits are a mechanism that maintains patients’ symptoms over the course of 1 year,” Dr. Bardeen said.

“And you don’t see the reverse,” he added. “You don’t see that PTSD symptoms at [6 months] mediate the relationship between [baseline] and 6 month executive-function deficits.”
 

Surprising finding

The findings suggest deficits in executive functioning have a stronger role in maintaining PTSD symptoms than these symptoms have in maintaining EF deficits, Dr. Bardeen told this news organization.

“I had originally hypothesized a bidirectional relationship in which PTSD symptoms influenced future executive-function deficits and executive-function deficits influenced future PTSD symptoms,” he said.

“So, it was a surprise that, when accounting for both variables in the same model, executive-function deficits predicted future PTSD symptoms, but PTSD symptoms did not significantly predict future EF deficits,” he added.

Dr. Bardeen noted this suggests that EF deficits “may be a particularly important maintenance factor.”  

In addition, he recommended the use of neuropsychological assessments prior to treatment to identify individuals with EF deficits and distinguish those deficits from PTSD symptoms.

“There is certainly overlap between executive-function deficits and PTSD symptoms,” Dr. Bardeen said. “For example, several of the symptoms of PTSD, such as concentration difficulties, may be indicators of executive-function deficits.”

He noted assessments such as the Delis Kaplan Executive Function System, and Clinician Administered PTSD Scale for DSM-5, when used as part of a larger assessment battery, can help differentiate between the EF deficits and PTSD.

“This would take several hours to administer, but in cases in which serious cognitive impairment is suspected, a comprehensive assessment is the way to go,” Dr. Bardeen said.

The standard approaches of prolonged exposure therapy and cognitive processing therapy can be effective in patients without EF deficits, while some modifications may benefit those with these deficits, he added.

“For example, it’s important to provide a more directive and structured environment in which the practitioner repeats key points frequently, uses concrete language, simplifies worksheets, and provides written summaries and reminder cards,” he said.
 

 

 

Further findings

In additional research presented at the meeting, Elsa Mattson, a PhD student from Case Western Reserve University, Cleveland, and colleagues reported findings further distinguishing the role of EF in PTSD.

In that study of 149 patients with chronic PTSD, those with low performing working memory, but not high working memory, had higher pre- as well as posttreatment PTSD symptom severity and depressive symptoms.

“Clinicians should consider that impairments in executive function may play a role in reduced treatment response, potentially impairing a client’s ability to learn new information in treatment,” the investigators wrote.

“Understanding how executive function processes change over the course of treatment, particularly in relation to processing the trauma memories, is an important next step,” they added.

The first study was supported by a grant from the National Institute of Mental Health. The investigators have disclosed no relevant financial relationships.

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

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Deficits in executive function (EF) are linked to with development of posttraumatic stress disorder (PTSD) symptoms and exacerbation of such symptoms over time, new research suggests.

“To our knowledge, this study is the first to show that executive-function deficits maintain PTSD symptoms following trauma exposure,” investigators noted in research presented at the Anxiety and Depression Association of America (ADAA) Anxiety & Depression conference.

Dr. Joseph R. Bardeen, Department of Psychological Sciences, Auburn University, Alabama
Courtesy Auburn University
Dr. Joseph R. Bardeen

The results are important in “developing precision medicine–based approaches for alleviating [posttraumatic stress] symptoms, and improving well-established PTSD treatments for those with relative deficits in executive function,” study investigator Joseph R. Bardeen, PhD, associate professor at Auburn (Ala.) University, told meeting attendees.

The findings were published in the Journal of Anxiety Disorders.
 

Cognitive impairment

In earlier research, deficits in EF were associated with an increased vulnerability for PTSD symptoms. However, less is known about the role of these deficits, which can impair higher-level cognitive ability, in sustaining PTSD symptoms.

To investigate, the authors conducted a longitudinal study that included 98 participants aged 18-65 years who had been identified via phone screening as experiencing clinically significant PTSD symptoms.

Participants completed self-report measures for PTSD symptoms, as well as measures for EF deficits at baseline and 6-month (n = 92) and 12-month (n = 91) follow-up sessions.

A path analysis showed a significant relationship between baseline PTSD symptoms and EF deficits at 6 months (P < .001). Baseline PTSD symptoms were associated with 12-month PTSD symptoms (P < .04).

EF deficits at 6 months were also associated with 12-month PTSD symptoms (P = .02).

Importantly, no associations were observed between baseline or 6-month PTSD symptoms and EF deficits at 12 months. However, EF deficits at 6 months drove the relationship between PTSD symptoms at baseline and at 1 year (indirect effect = .061).

“What this suggests is that executive-function deficits are a mechanism that maintains patients’ symptoms over the course of 1 year,” Dr. Bardeen said.

“And you don’t see the reverse,” he added. “You don’t see that PTSD symptoms at [6 months] mediate the relationship between [baseline] and 6 month executive-function deficits.”
 

Surprising finding

The findings suggest deficits in executive functioning have a stronger role in maintaining PTSD symptoms than these symptoms have in maintaining EF deficits, Dr. Bardeen told this news organization.

“I had originally hypothesized a bidirectional relationship in which PTSD symptoms influenced future executive-function deficits and executive-function deficits influenced future PTSD symptoms,” he said.

“So, it was a surprise that, when accounting for both variables in the same model, executive-function deficits predicted future PTSD symptoms, but PTSD symptoms did not significantly predict future EF deficits,” he added.

Dr. Bardeen noted this suggests that EF deficits “may be a particularly important maintenance factor.”  

In addition, he recommended the use of neuropsychological assessments prior to treatment to identify individuals with EF deficits and distinguish those deficits from PTSD symptoms.

“There is certainly overlap between executive-function deficits and PTSD symptoms,” Dr. Bardeen said. “For example, several of the symptoms of PTSD, such as concentration difficulties, may be indicators of executive-function deficits.”

He noted assessments such as the Delis Kaplan Executive Function System, and Clinician Administered PTSD Scale for DSM-5, when used as part of a larger assessment battery, can help differentiate between the EF deficits and PTSD.

“This would take several hours to administer, but in cases in which serious cognitive impairment is suspected, a comprehensive assessment is the way to go,” Dr. Bardeen said.

The standard approaches of prolonged exposure therapy and cognitive processing therapy can be effective in patients without EF deficits, while some modifications may benefit those with these deficits, he added.

“For example, it’s important to provide a more directive and structured environment in which the practitioner repeats key points frequently, uses concrete language, simplifies worksheets, and provides written summaries and reminder cards,” he said.
 

 

 

Further findings

In additional research presented at the meeting, Elsa Mattson, a PhD student from Case Western Reserve University, Cleveland, and colleagues reported findings further distinguishing the role of EF in PTSD.

In that study of 149 patients with chronic PTSD, those with low performing working memory, but not high working memory, had higher pre- as well as posttreatment PTSD symptom severity and depressive symptoms.

“Clinicians should consider that impairments in executive function may play a role in reduced treatment response, potentially impairing a client’s ability to learn new information in treatment,” the investigators wrote.

“Understanding how executive function processes change over the course of treatment, particularly in relation to processing the trauma memories, is an important next step,” they added.

The first study was supported by a grant from the National Institute of Mental Health. The investigators have disclosed no relevant financial relationships.

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

Deficits in executive function (EF) are linked to with development of posttraumatic stress disorder (PTSD) symptoms and exacerbation of such symptoms over time, new research suggests.

“To our knowledge, this study is the first to show that executive-function deficits maintain PTSD symptoms following trauma exposure,” investigators noted in research presented at the Anxiety and Depression Association of America (ADAA) Anxiety & Depression conference.

Dr. Joseph R. Bardeen, Department of Psychological Sciences, Auburn University, Alabama
Courtesy Auburn University
Dr. Joseph R. Bardeen

The results are important in “developing precision medicine–based approaches for alleviating [posttraumatic stress] symptoms, and improving well-established PTSD treatments for those with relative deficits in executive function,” study investigator Joseph R. Bardeen, PhD, associate professor at Auburn (Ala.) University, told meeting attendees.

The findings were published in the Journal of Anxiety Disorders.
 

Cognitive impairment

In earlier research, deficits in EF were associated with an increased vulnerability for PTSD symptoms. However, less is known about the role of these deficits, which can impair higher-level cognitive ability, in sustaining PTSD symptoms.

To investigate, the authors conducted a longitudinal study that included 98 participants aged 18-65 years who had been identified via phone screening as experiencing clinically significant PTSD symptoms.

Participants completed self-report measures for PTSD symptoms, as well as measures for EF deficits at baseline and 6-month (n = 92) and 12-month (n = 91) follow-up sessions.

A path analysis showed a significant relationship between baseline PTSD symptoms and EF deficits at 6 months (P < .001). Baseline PTSD symptoms were associated with 12-month PTSD symptoms (P < .04).

EF deficits at 6 months were also associated with 12-month PTSD symptoms (P = .02).

Importantly, no associations were observed between baseline or 6-month PTSD symptoms and EF deficits at 12 months. However, EF deficits at 6 months drove the relationship between PTSD symptoms at baseline and at 1 year (indirect effect = .061).

“What this suggests is that executive-function deficits are a mechanism that maintains patients’ symptoms over the course of 1 year,” Dr. Bardeen said.

“And you don’t see the reverse,” he added. “You don’t see that PTSD symptoms at [6 months] mediate the relationship between [baseline] and 6 month executive-function deficits.”
 

Surprising finding

The findings suggest deficits in executive functioning have a stronger role in maintaining PTSD symptoms than these symptoms have in maintaining EF deficits, Dr. Bardeen told this news organization.

“I had originally hypothesized a bidirectional relationship in which PTSD symptoms influenced future executive-function deficits and executive-function deficits influenced future PTSD symptoms,” he said.

“So, it was a surprise that, when accounting for both variables in the same model, executive-function deficits predicted future PTSD symptoms, but PTSD symptoms did not significantly predict future EF deficits,” he added.

Dr. Bardeen noted this suggests that EF deficits “may be a particularly important maintenance factor.”  

In addition, he recommended the use of neuropsychological assessments prior to treatment to identify individuals with EF deficits and distinguish those deficits from PTSD symptoms.

“There is certainly overlap between executive-function deficits and PTSD symptoms,” Dr. Bardeen said. “For example, several of the symptoms of PTSD, such as concentration difficulties, may be indicators of executive-function deficits.”

He noted assessments such as the Delis Kaplan Executive Function System, and Clinician Administered PTSD Scale for DSM-5, when used as part of a larger assessment battery, can help differentiate between the EF deficits and PTSD.

“This would take several hours to administer, but in cases in which serious cognitive impairment is suspected, a comprehensive assessment is the way to go,” Dr. Bardeen said.

The standard approaches of prolonged exposure therapy and cognitive processing therapy can be effective in patients without EF deficits, while some modifications may benefit those with these deficits, he added.

“For example, it’s important to provide a more directive and structured environment in which the practitioner repeats key points frequently, uses concrete language, simplifies worksheets, and provides written summaries and reminder cards,” he said.
 

 

 

Further findings

In additional research presented at the meeting, Elsa Mattson, a PhD student from Case Western Reserve University, Cleveland, and colleagues reported findings further distinguishing the role of EF in PTSD.

In that study of 149 patients with chronic PTSD, those with low performing working memory, but not high working memory, had higher pre- as well as posttreatment PTSD symptom severity and depressive symptoms.

“Clinicians should consider that impairments in executive function may play a role in reduced treatment response, potentially impairing a client’s ability to learn new information in treatment,” the investigators wrote.

“Understanding how executive function processes change over the course of treatment, particularly in relation to processing the trauma memories, is an important next step,” they added.

The first study was supported by a grant from the National Institute of Mental Health. The investigators have disclosed no relevant financial relationships.

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

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