TBD Meeting (3473-16)

SAN FRANCISCO – Prodromal anxiety and depression are common in Parkinson’s disease and may develop years earlier than conventionally thought, according to data presented at the 2016 congress of the International Psychogeriatric Association.

“In some cases, the psychiatric prodrome can appear 25 or more years earlier than the onset of motor symptoms,” said Andrea Seritan, MD, a geriatric psychiatrist at the University of California, San Francisco. Psychiatrists need to keep this fact in mind when treating patients with anxiety or depression, and refer them to a neurologist if they notice or are informed of motor symptoms, she emphasized.

Amy Karon/Frontline Medical News

Patients with Parkinson’s disease often have developed anxiety or depression before the onset of motor symptoms. Historically, this psychiatric prodrome was thought to begin anywhere from 5 to 10 years before motor symptoms, “depending on which expert you ask,” Dr. Seritan said. But after observing that some of her Parkinson’s patients reported decades-long histories of anxiety or depression, she and her colleagues reviewed medical charts for 39 patients aged 50 years or more with confirmed Parkinson’s disease who were referred for psychiatric evaluation at the UCSF Movement Disorder and Neuromodulation Center in 2015 or 2016. A total of 28 patients (72%) were men, mean age at referral was 65 years (standard deviation, 7.6 years), and the patients had been diagnosed with Parkinson’s disease an average of 12 years previously (standard deviation, 6.7 years).

At referral, a total of 34 (87%) patients met DSM-5 criteria for major depressive disorder, dysthymia, or an unspecified depressive disorder, while 68% met DSM-5 criteria for generalized anxiety disorder, panic disorder, social anxiety disorder, other anxiety disorders, Dr. Seritan said. About two-thirds of patients had comorbid depression and anxiety. Other DSM-5 diagnoses included impulse control disorders (15% of patients), substance abuse disorders (13%), and mild (21%) or major (13%) neurocognitive disorders.

Exactly 50% of patients had depression preceding their Parkinson’s disease diagnosis, while 43% of patients had prodromal anxiety, Dr. Seritan and her colleagues determined. The average age of onset of psychiatric symptoms was in the 30s, but this ranged from childhood or adolescence into the 60s. Mean ages of Parkinson’s diagnosis were much later – 58 years for patients whose primary prodrome was anxiety and 56 years for patients whose primary prodrome was depression, with a standard deviation of 9.8 years for each group.

The findings suggest that a decades-long prodrome of anxiety or depression is common in Parkinson’s disease, Dr. Seritan concluded. Psychiatrists should be alert to the possibility of Parkinson’s disease in patients with depression or anxiety, because individuals with movement disorders can be very susceptible to the side effects of antidepressants and antipsychotics, she emphasized.

Dr. Seritan reported no funding sources and had no conflicts of interest.

SAN FRANCISCO – Prodromal anxiety and depression are common in Parkinson’s disease and may develop years earlier than conventionally thought, according to data presented at the 2016 congress of the International Psychogeriatric Association.

“In some cases, the psychiatric prodrome can appear 25 or more years earlier than the onset of motor symptoms,” said Andrea Seritan, MD, a geriatric psychiatrist at the University of California, San Francisco. Psychiatrists need to keep this fact in mind when treating patients with anxiety or depression, and refer them to a neurologist if they notice or are informed of motor symptoms, she emphasized.

Amy Karon/Frontline Medical News

Patients with Parkinson’s disease often have developed anxiety or depression before the onset of motor symptoms. Historically, this psychiatric prodrome was thought to begin anywhere from 5 to 10 years before motor symptoms, “depending on which expert you ask,” Dr. Seritan said. But after observing that some of her Parkinson’s patients reported decades-long histories of anxiety or depression, she and her colleagues reviewed medical charts for 39 patients aged 50 years or more with confirmed Parkinson’s disease who were referred for psychiatric evaluation at the UCSF Movement Disorder and Neuromodulation Center in 2015 or 2016. A total of 28 patients (72%) were men, mean age at referral was 65 years (standard deviation, 7.6 years), and the patients had been diagnosed with Parkinson’s disease an average of 12 years previously (standard deviation, 6.7 years).

At referral, a total of 34 (87%) patients met DSM-5 criteria for major depressive disorder, dysthymia, or an unspecified depressive disorder, while 68% met DSM-5 criteria for generalized anxiety disorder, panic disorder, social anxiety disorder, other anxiety disorders, Dr. Seritan said. About two-thirds of patients had comorbid depression and anxiety. Other DSM-5 diagnoses included impulse control disorders (15% of patients), substance abuse disorders (13%), and mild (21%) or major (13%) neurocognitive disorders.

Exactly 50% of patients had depression preceding their Parkinson’s disease diagnosis, while 43% of patients had prodromal anxiety, Dr. Seritan and her colleagues determined. The average age of onset of psychiatric symptoms was in the 30s, but this ranged from childhood or adolescence into the 60s. Mean ages of Parkinson’s diagnosis were much later – 58 years for patients whose primary prodrome was anxiety and 56 years for patients whose primary prodrome was depression, with a standard deviation of 9.8 years for each group.

The findings suggest that a decades-long prodrome of anxiety or depression is common in Parkinson’s disease, Dr. Seritan concluded. Psychiatrists should be alert to the possibility of Parkinson’s disease in patients with depression or anxiety, because individuals with movement disorders can be very susceptible to the side effects of antidepressants and antipsychotics, she emphasized.

Dr. Seritan reported no funding sources and had no conflicts of interest.

SAN FRANCISCO – Prodromal anxiety and depression are common in Parkinson’s disease and may develop years earlier than conventionally thought, according to data presented at the 2016 congress of the International Psychogeriatric Association.

“In some cases, the psychiatric prodrome can appear 25 or more years earlier than the onset of motor symptoms,” said Andrea Seritan, MD, a geriatric psychiatrist at the University of California, San Francisco. Psychiatrists need to keep this fact in mind when treating patients with anxiety or depression, and refer them to a neurologist if they notice or are informed of motor symptoms, she emphasized.

Amy Karon/Frontline Medical News

Patients with Parkinson’s disease often have developed anxiety or depression before the onset of motor symptoms. Historically, this psychiatric prodrome was thought to begin anywhere from 5 to 10 years before motor symptoms, “depending on which expert you ask,” Dr. Seritan said. But after observing that some of her Parkinson’s patients reported decades-long histories of anxiety or depression, she and her colleagues reviewed medical charts for 39 patients aged 50 years or more with confirmed Parkinson’s disease who were referred for psychiatric evaluation at the UCSF Movement Disorder and Neuromodulation Center in 2015 or 2016. A total of 28 patients (72%) were men, mean age at referral was 65 years (standard deviation, 7.6 years), and the patients had been diagnosed with Parkinson’s disease an average of 12 years previously (standard deviation, 6.7 years).

At referral, a total of 34 (87%) patients met DSM-5 criteria for major depressive disorder, dysthymia, or an unspecified depressive disorder, while 68% met DSM-5 criteria for generalized anxiety disorder, panic disorder, social anxiety disorder, other anxiety disorders, Dr. Seritan said. About two-thirds of patients had comorbid depression and anxiety. Other DSM-5 diagnoses included impulse control disorders (15% of patients), substance abuse disorders (13%), and mild (21%) or major (13%) neurocognitive disorders.

Exactly 50% of patients had depression preceding their Parkinson’s disease diagnosis, while 43% of patients had prodromal anxiety, Dr. Seritan and her colleagues determined. The average age of onset of psychiatric symptoms was in the 30s, but this ranged from childhood or adolescence into the 60s. Mean ages of Parkinson’s diagnosis were much later – 58 years for patients whose primary prodrome was anxiety and 56 years for patients whose primary prodrome was depression, with a standard deviation of 9.8 years for each group.

The findings suggest that a decades-long prodrome of anxiety or depression is common in Parkinson’s disease, Dr. Seritan concluded. Psychiatrists should be alert to the possibility of Parkinson’s disease in patients with depression or anxiety, because individuals with movement disorders can be very susceptible to the side effects of antidepressants and antipsychotics, she emphasized.

Dr. Seritan reported no funding sources and had no conflicts of interest.

SAN FRANCISCO – Autism spectrum disorders often are missed in older adults, even though they cause substantial morbidity; identifying these disorders enables clinicians to teach more effective caregiving strategies and adjust medications, which can substantially reduce distress for all concerned, according to Shabbir Amanullah, MD.

About 1% of adults have an autism spectrum disorder (ASD), and so will about 700,000 U.S. seniors by 2030, said Dr. Amanullah, a geriatric psychiatrist at Woodstock General Hospital in Ontario. Like their younger peers, older patients with ASD show persistent social deficit and rigid thinking, adhere to inflexible routines, and may have perseverative interests. Many also are high-functioning retired professionals with children, belying stereotypes of autism as a severely disabling disorder of childhood, Dr. Amanullah said. These factors can complicate diagnosis of ASD, especially when patients or family members cannot or will not provide a detailed childhood and psychiatric history.

Undetected ASD is especially burdensome in institutional settings, where patients struggle to adjust and “become angry, even violent,” Dr. Amanullah said at the 2016 congress of the International Psychogeriatric Association.

He noted the case of a 72-year-old nursing home resident referred to him for persistently hostile behavior; she “had never really settled in,” slept poorly, and constantly complained about the staff, food, and other residents, whom she “smacked on the bum with her cane.” She also had complained about the facility to local officials, triggering investigations of minor issues. Staff avoided her whenever possible, her children were estranged, and she failed to improve despite therapy with several psychotropic medications.

This is a classic case of autism spectrum disorder, said Dr. Amanullah, also an adjunct professor  Dalhousie University, Halifax, N.S., and at the University of Western Ontario. The patient acted out most in high-stimulus environments such as the crowded nursing home cafeteria, and interpreted promises to help her “in a minute” literally, becoming enraged when staff arrived 5 minutes later instead. When questioned, she reported having always been “disliked” and without friends. But instead of ruminating over past wrongs as patients with paranoia tend to do, she became uncomfortable and looked down when describing having been bullied as a child.

All these clues had gone unrecognized, according to Dr. Amanullah. “Nobody gave importance to the real reason this patient was complaining. Staff were distracted by the fact that she’d been employed and had children, and did not recognize that someone with ASD can meet this description,” he said.

But staff members often did know children with autism, and so their frustration often turned to compassion after they were educated about her diagnosis and connected it with her behaviors, he said. The patient, for her part, stopped complaining as much about the food after she was allowed to avoid the dining room during busy times and eat in her room if she wished. She also became less recalcitrant after staff began reviewing her schedule with her each morning. If she avoided her most severe behaviors, a staff person also sat with her to keep her company at the end of the day.

Such changes can make a tremendous difference in and outside of institutional settings, but patients with ASD often also need treatment for concurrent Axis I disorders, Dr. Amanullah said. This patient met that description, and Dr. Amanullah increased her antidepressant dose while tapering her off an antipsychotic. He said 20 mg citalopram once daily works well but can manifest as inappropriate jokes rather than physical behaviors. "Autistic individuals vary in their expression of sexuality and may make odd remarks that can be misconstrued," he said in an interview. "But generally, they don't act out." All this underscores the need for clinicians to “consider the power of bias” in their thinking, he said. “We have to be willing to change the way we see things, and even more importantly, recognize what the problem was to begin with.”

Dr. Amanullah disclosed no funding sources or relevant financial conflicts.

SAN FRANCISCO – Autism spectrum disorders often are missed in older adults, even though they cause substantial morbidity; identifying these disorders enables clinicians to teach more effective caregiving strategies and adjust medications, which can substantially reduce distress for all concerned, according to Shabbir Amanullah, MD.

About 1% of adults have an autism spectrum disorder (ASD), and so will about 700,000 U.S. seniors by 2030, said Dr. Amanullah, a geriatric psychiatrist at Woodstock General Hospital in Ontario. Like their younger peers, older patients with ASD show persistent social deficit and rigid thinking, adhere to inflexible routines, and may have perseverative interests. Many also are high-functioning retired professionals with children, belying stereotypes of autism as a severely disabling disorder of childhood, Dr. Amanullah said. These factors can complicate diagnosis of ASD, especially when patients or family members cannot or will not provide a detailed childhood and psychiatric history.

Undetected ASD is especially burdensome in institutional settings, where patients struggle to adjust and “become angry, even violent,” Dr. Amanullah said at the 2016 congress of the International Psychogeriatric Association.

He noted the case of a 72-year-old nursing home resident referred to him for persistently hostile behavior; she “had never really settled in,” slept poorly, and constantly complained about the staff, food, and other residents, whom she “smacked on the bum with her cane.” She also had complained about the facility to local officials, triggering investigations of minor issues. Staff avoided her whenever possible, her children were estranged, and she failed to improve despite therapy with several psychotropic medications.

This is a classic case of autism spectrum disorder, said Dr. Amanullah, also an adjunct professor  Dalhousie University, Halifax, N.S., and at the University of Western Ontario. The patient acted out most in high-stimulus environments such as the crowded nursing home cafeteria, and interpreted promises to help her “in a minute” literally, becoming enraged when staff arrived 5 minutes later instead. When questioned, she reported having always been “disliked” and without friends. But instead of ruminating over past wrongs as patients with paranoia tend to do, she became uncomfortable and looked down when describing having been bullied as a child.

All these clues had gone unrecognized, according to Dr. Amanullah. “Nobody gave importance to the real reason this patient was complaining. Staff were distracted by the fact that she’d been employed and had children, and did not recognize that someone with ASD can meet this description,” he said.

But staff members often did know children with autism, and so their frustration often turned to compassion after they were educated about her diagnosis and connected it with her behaviors, he said. The patient, for her part, stopped complaining as much about the food after she was allowed to avoid the dining room during busy times and eat in her room if she wished. She also became less recalcitrant after staff began reviewing her schedule with her each morning. If she avoided her most severe behaviors, a staff person also sat with her to keep her company at the end of the day.

Such changes can make a tremendous difference in and outside of institutional settings, but patients with ASD often also need treatment for concurrent Axis I disorders, Dr. Amanullah said. This patient met that description, and Dr. Amanullah increased her antidepressant dose while tapering her off an antipsychotic. He said 20 mg citalopram once daily works well but can manifest as inappropriate jokes rather than physical behaviors. "Autistic individuals vary in their expression of sexuality and may make odd remarks that can be misconstrued," he said in an interview. "But generally, they don't act out." All this underscores the need for clinicians to “consider the power of bias” in their thinking, he said. “We have to be willing to change the way we see things, and even more importantly, recognize what the problem was to begin with.”

Dr. Amanullah disclosed no funding sources or relevant financial conflicts.

SAN FRANCISCO – Autism spectrum disorders often are missed in older adults, even though they cause substantial morbidity; identifying these disorders enables clinicians to teach more effective caregiving strategies and adjust medications, which can substantially reduce distress for all concerned, according to Shabbir Amanullah, MD.

About 1% of adults have an autism spectrum disorder (ASD), and so will about 700,000 U.S. seniors by 2030, said Dr. Amanullah, a geriatric psychiatrist at Woodstock General Hospital in Ontario. Like their younger peers, older patients with ASD show persistent social deficit and rigid thinking, adhere to inflexible routines, and may have perseverative interests. Many also are high-functioning retired professionals with children, belying stereotypes of autism as a severely disabling disorder of childhood, Dr. Amanullah said. These factors can complicate diagnosis of ASD, especially when patients or family members cannot or will not provide a detailed childhood and psychiatric history.

Undetected ASD is especially burdensome in institutional settings, where patients struggle to adjust and “become angry, even violent,” Dr. Amanullah said at the 2016 congress of the International Psychogeriatric Association.

He noted the case of a 72-year-old nursing home resident referred to him for persistently hostile behavior; she “had never really settled in,” slept poorly, and constantly complained about the staff, food, and other residents, whom she “smacked on the bum with her cane.” She also had complained about the facility to local officials, triggering investigations of minor issues. Staff avoided her whenever possible, her children were estranged, and she failed to improve despite therapy with several psychotropic medications.

This is a classic case of autism spectrum disorder, said Dr. Amanullah, also an adjunct professor  Dalhousie University, Halifax, N.S., and at the University of Western Ontario. The patient acted out most in high-stimulus environments such as the crowded nursing home cafeteria, and interpreted promises to help her “in a minute” literally, becoming enraged when staff arrived 5 minutes later instead. When questioned, she reported having always been “disliked” and without friends. But instead of ruminating over past wrongs as patients with paranoia tend to do, she became uncomfortable and looked down when describing having been bullied as a child.

All these clues had gone unrecognized, according to Dr. Amanullah. “Nobody gave importance to the real reason this patient was complaining. Staff were distracted by the fact that she’d been employed and had children, and did not recognize that someone with ASD can meet this description,” he said.

But staff members often did know children with autism, and so their frustration often turned to compassion after they were educated about her diagnosis and connected it with her behaviors, he said. The patient, for her part, stopped complaining as much about the food after she was allowed to avoid the dining room during busy times and eat in her room if she wished. She also became less recalcitrant after staff began reviewing her schedule with her each morning. If she avoided her most severe behaviors, a staff person also sat with her to keep her company at the end of the day.

Such changes can make a tremendous difference in and outside of institutional settings, but patients with ASD often also need treatment for concurrent Axis I disorders, Dr. Amanullah said. This patient met that description, and Dr. Amanullah increased her antidepressant dose while tapering her off an antipsychotic. He said 20 mg citalopram once daily works well but can manifest as inappropriate jokes rather than physical behaviors. "Autistic individuals vary in their expression of sexuality and may make odd remarks that can be misconstrued," he said in an interview. "But generally, they don't act out." All this underscores the need for clinicians to “consider the power of bias” in their thinking, he said. “We have to be willing to change the way we see things, and even more importantly, recognize what the problem was to begin with.”

Dr. Amanullah disclosed no funding sources or relevant financial conflicts.

SAN FRANCISCO – Depression and psychosis were strongly correlated in Parkinson’s disease, while the presence of clinical anxiety upped the odds of psychosis by a statistically significant 8%, in a cross-sectional study presented at the 2016 congress of the International Psychogeriatric Association.

Felicia C. Goldstein, PhD, professor of neurology at Emory University, Atlanta, compared 48 patients with Parkinson’s disease and psychosis with 96 nonpsychotic controls who also had Parkinson’s disease. The groups were similar in terms of age, age of disease onset, educational level, Montreal Cognitive Assessment score (MoCA), and Unified Parkinson’s Disease Rating Scale (UPDRS) score, although patients with psychosis had about a 1.5-year longer mean duration of Parkinson’s disease than did controls (8.8 years vs. 7.3 years; P = .06).

Amy Karon/Frontline Medical News

Patients with psychosis were significantly more likely than controls to meet DSM-5 and Beck Depression Inventory II criteria for depression, with odds ratios of 8.0 (95% confidence interval, 2.5-25.6; P = .001) and 1.1 (1.02-1.1; P = .01), respectively. Patients with psychosis also were significantly more likely to have a positive result on the Beck Anxiety Inventory (OR, 1.1; 95% CI, 1.01-1.15; P = .01), and met DSM-5 criteria for anxiety more often than did controls (OR, 3.0; 95% CI, 0.9-9.5), although the latter correlation did not reach statistical significance (P = .07).

“The association between psychosis and anxiety has not been previously reported,” Dr. Goldstein noted. The findings underscore the link between psychosis and mood disorders in Parkinson’s disease and the need to treat these comorbidities, she said.

Neuropsychiatric symptoms in Parkinson’s disease also merit close monitoring and treatment, because they correlate with greater disability, faster progression of motor symptoms, and increased mortality, Adriana P. Hermida, MD, said in a separate oral presentation at the congress. In particular, depression is “the elephant in the room when it comes to Parkinson’s disease,” she said. “It is there, it is underrecognized, and it is undertreated.” Suicidal ideation is common, and patients should be treated even if they do not meet all criteria for a depressive disorder, added Dr. Hermida of the department of psychiatry and behavioral sciences at Emory.

Amy Karon/Frontline Medical News

For depression in Parkinson’s disease, Dr. Hermida said she typically starts with a selective serotonin reuptake inhibitor, most often escitalopram or sertraline. If the patient has a partial response, she adds another antidepressant, but if there is no response, she switches antidepressants. Second-line options for add-ons and switches include mirtazapine, which improves sleep and appetite and may improve tremor; venlafaxine extended release, which can raise blood pressure and may benefit hypotensive patients; and bupropion extended release, which is best for patients who need more activation, do not have substantial concerns with anxiety, and have REM sleep behavior disorder, she said. She said she also will consider dopamine agonists such as pramipexole, but they can increase the risk of psychosis, impulse control disorders, and dopamine dysregulation syndrome. She also noted that electroconvulsive therapy can rapidly improve both depression and motor symptoms, and should not be reserved for last-resort cases. Parkinson’s medications should be held the day of ECT, and cognition should be monitored afterward, she said.

Approximately 30% of Parkinson’s patients meet DSM-5 criteria for an anxiety disorder, and more than half have significant symptoms of anxiety, Dr. Hermida continued. Anxiety, like other signs and symptoms of Parkinson’s disease, can fluctuate throughout the day and tends to occur most frequently during “off” periods. No randomized controlled trials have examined anxiolytics in Parkinson’s disease patients, but studies of mindfulness-based cognitive therapy have yielded good results, she noted. Benzodiazepines “should be used sparingly, if at all,” as they increase the risk of confusion, gait abnormalities, and falls.

Psychosis should be treated if symptoms are ego-dystonic, she said. She said she uses first-line clozapine, which is more effective for delusions than quetiapine and has fewer adverse motor effects. She said she has not yet used pimavanserin (Nuplazid), a selective 5-HT_2A inverse agonist that in April 2016 became the first drug approved by the Food and Drug Administration for treating hallucinations and delusions in Parkinson’s disease. The pivotal trial lasted 6 weeks and included 199 patients; those who received pimavanserin had a median 5.8-point drop on the Scale to Access Psychosis in Parkinson’s Disease (SAPS-PD), compared with 2.7 for placebo (P = .001), Dr. Hermida noted. Patients did not experience sedation or motor impairment, which are common adverse effects of other antipsychotics in this population.

Dr. Goldstein and Dr. Hermida reported no funding sources or conflicts of interest.

SAN FRANCISCO – Depression and psychosis were strongly correlated in Parkinson’s disease, while the presence of clinical anxiety upped the odds of psychosis by a statistically significant 8%, in a cross-sectional study presented at the 2016 congress of the International Psychogeriatric Association.

Felicia C. Goldstein, PhD, professor of neurology at Emory University, Atlanta, compared 48 patients with Parkinson’s disease and psychosis with 96 nonpsychotic controls who also had Parkinson’s disease. The groups were similar in terms of age, age of disease onset, educational level, Montreal Cognitive Assessment score (MoCA), and Unified Parkinson’s Disease Rating Scale (UPDRS) score, although patients with psychosis had about a 1.5-year longer mean duration of Parkinson’s disease than did controls (8.8 years vs. 7.3 years; P = .06).

Amy Karon/Frontline Medical News

Patients with psychosis were significantly more likely than controls to meet DSM-5 and Beck Depression Inventory II criteria for depression, with odds ratios of 8.0 (95% confidence interval, 2.5-25.6; P = .001) and 1.1 (1.02-1.1; P = .01), respectively. Patients with psychosis also were significantly more likely to have a positive result on the Beck Anxiety Inventory (OR, 1.1; 95% CI, 1.01-1.15; P = .01), and met DSM-5 criteria for anxiety more often than did controls (OR, 3.0; 95% CI, 0.9-9.5), although the latter correlation did not reach statistical significance (P = .07).

“The association between psychosis and anxiety has not been previously reported,” Dr. Goldstein noted. The findings underscore the link between psychosis and mood disorders in Parkinson’s disease and the need to treat these comorbidities, she said.

Neuropsychiatric symptoms in Parkinson’s disease also merit close monitoring and treatment, because they correlate with greater disability, faster progression of motor symptoms, and increased mortality, Adriana P. Hermida, MD, said in a separate oral presentation at the congress. In particular, depression is “the elephant in the room when it comes to Parkinson’s disease,” she said. “It is there, it is underrecognized, and it is undertreated.” Suicidal ideation is common, and patients should be treated even if they do not meet all criteria for a depressive disorder, added Dr. Hermida of the department of psychiatry and behavioral sciences at Emory.

Amy Karon/Frontline Medical News

For depression in Parkinson’s disease, Dr. Hermida said she typically starts with a selective serotonin reuptake inhibitor, most often escitalopram or sertraline. If the patient has a partial response, she adds another antidepressant, but if there is no response, she switches antidepressants. Second-line options for add-ons and switches include mirtazapine, which improves sleep and appetite and may improve tremor; venlafaxine extended release, which can raise blood pressure and may benefit hypotensive patients; and bupropion extended release, which is best for patients who need more activation, do not have substantial concerns with anxiety, and have REM sleep behavior disorder, she said. She said she also will consider dopamine agonists such as pramipexole, but they can increase the risk of psychosis, impulse control disorders, and dopamine dysregulation syndrome. She also noted that electroconvulsive therapy can rapidly improve both depression and motor symptoms, and should not be reserved for last-resort cases. Parkinson’s medications should be held the day of ECT, and cognition should be monitored afterward, she said.

Approximately 30% of Parkinson’s patients meet DSM-5 criteria for an anxiety disorder, and more than half have significant symptoms of anxiety, Dr. Hermida continued. Anxiety, like other signs and symptoms of Parkinson’s disease, can fluctuate throughout the day and tends to occur most frequently during “off” periods. No randomized controlled trials have examined anxiolytics in Parkinson’s disease patients, but studies of mindfulness-based cognitive therapy have yielded good results, she noted. Benzodiazepines “should be used sparingly, if at all,” as they increase the risk of confusion, gait abnormalities, and falls.

Psychosis should be treated if symptoms are ego-dystonic, she said. She said she uses first-line clozapine, which is more effective for delusions than quetiapine and has fewer adverse motor effects. She said she has not yet used pimavanserin (Nuplazid), a selective 5-HT_2A inverse agonist that in April 2016 became the first drug approved by the Food and Drug Administration for treating hallucinations and delusions in Parkinson’s disease. The pivotal trial lasted 6 weeks and included 199 patients; those who received pimavanserin had a median 5.8-point drop on the Scale to Access Psychosis in Parkinson’s Disease (SAPS-PD), compared with 2.7 for placebo (P = .001), Dr. Hermida noted. Patients did not experience sedation or motor impairment, which are common adverse effects of other antipsychotics in this population.

Dr. Goldstein and Dr. Hermida reported no funding sources or conflicts of interest.

SAN FRANCISCO – Depression and psychosis were strongly correlated in Parkinson’s disease, while the presence of clinical anxiety upped the odds of psychosis by a statistically significant 8%, in a cross-sectional study presented at the 2016 congress of the International Psychogeriatric Association.

Felicia C. Goldstein, PhD, professor of neurology at Emory University, Atlanta, compared 48 patients with Parkinson’s disease and psychosis with 96 nonpsychotic controls who also had Parkinson’s disease. The groups were similar in terms of age, age of disease onset, educational level, Montreal Cognitive Assessment score (MoCA), and Unified Parkinson’s Disease Rating Scale (UPDRS) score, although patients with psychosis had about a 1.5-year longer mean duration of Parkinson’s disease than did controls (8.8 years vs. 7.3 years; P = .06).

Amy Karon/Frontline Medical News

Patients with psychosis were significantly more likely than controls to meet DSM-5 and Beck Depression Inventory II criteria for depression, with odds ratios of 8.0 (95% confidence interval, 2.5-25.6; P = .001) and 1.1 (1.02-1.1; P = .01), respectively. Patients with psychosis also were significantly more likely to have a positive result on the Beck Anxiety Inventory (OR, 1.1; 95% CI, 1.01-1.15; P = .01), and met DSM-5 criteria for anxiety more often than did controls (OR, 3.0; 95% CI, 0.9-9.5), although the latter correlation did not reach statistical significance (P = .07).

“The association between psychosis and anxiety has not been previously reported,” Dr. Goldstein noted. The findings underscore the link between psychosis and mood disorders in Parkinson’s disease and the need to treat these comorbidities, she said.

Neuropsychiatric symptoms in Parkinson’s disease also merit close monitoring and treatment, because they correlate with greater disability, faster progression of motor symptoms, and increased mortality, Adriana P. Hermida, MD, said in a separate oral presentation at the congress. In particular, depression is “the elephant in the room when it comes to Parkinson’s disease,” she said. “It is there, it is underrecognized, and it is undertreated.” Suicidal ideation is common, and patients should be treated even if they do not meet all criteria for a depressive disorder, added Dr. Hermida of the department of psychiatry and behavioral sciences at Emory.

Amy Karon/Frontline Medical News

For depression in Parkinson’s disease, Dr. Hermida said she typically starts with a selective serotonin reuptake inhibitor, most often escitalopram or sertraline. If the patient has a partial response, she adds another antidepressant, but if there is no response, she switches antidepressants. Second-line options for add-ons and switches include mirtazapine, which improves sleep and appetite and may improve tremor; venlafaxine extended release, which can raise blood pressure and may benefit hypotensive patients; and bupropion extended release, which is best for patients who need more activation, do not have substantial concerns with anxiety, and have REM sleep behavior disorder, she said. She said she also will consider dopamine agonists such as pramipexole, but they can increase the risk of psychosis, impulse control disorders, and dopamine dysregulation syndrome. She also noted that electroconvulsive therapy can rapidly improve both depression and motor symptoms, and should not be reserved for last-resort cases. Parkinson’s medications should be held the day of ECT, and cognition should be monitored afterward, she said.

Approximately 30% of Parkinson’s patients meet DSM-5 criteria for an anxiety disorder, and more than half have significant symptoms of anxiety, Dr. Hermida continued. Anxiety, like other signs and symptoms of Parkinson’s disease, can fluctuate throughout the day and tends to occur most frequently during “off” periods. No randomized controlled trials have examined anxiolytics in Parkinson’s disease patients, but studies of mindfulness-based cognitive therapy have yielded good results, she noted. Benzodiazepines “should be used sparingly, if at all,” as they increase the risk of confusion, gait abnormalities, and falls.

Psychosis should be treated if symptoms are ego-dystonic, she said. She said she uses first-line clozapine, which is more effective for delusions than quetiapine and has fewer adverse motor effects. She said she has not yet used pimavanserin (Nuplazid), a selective 5-HT_2A inverse agonist that in April 2016 became the first drug approved by the Food and Drug Administration for treating hallucinations and delusions in Parkinson’s disease. The pivotal trial lasted 6 weeks and included 199 patients; those who received pimavanserin had a median 5.8-point drop on the Scale to Access Psychosis in Parkinson’s Disease (SAPS-PD), compared with 2.7 for placebo (P = .001), Dr. Hermida noted. Patients did not experience sedation or motor impairment, which are common adverse effects of other antipsychotics in this population.

Dr. Goldstein and Dr. Hermida reported no funding sources or conflicts of interest.

SAN FRANCISCO – An absence of guidelines on cannabis in older adults makes it difficult for clinicians to advise seniors, particularly those who use it for medical reasons, Adrienne Withall, PhD, said at the 2016 congress of the International Psychogeriatric Association.

“We don’t really know the impacts of cannabis use on older people. They may be positive or negative, depending on what it’s being used for,” said Dr. Withall of the University of New South Wales in Sydney.

Questions about how cannabis affects older people are growing as the boomer generation ages and cannabis becomes easier to legally obtain.

“Our picture of the cannabis user as a young adult or teen is inaccurate,” Dr. Withall said. “Many reports show that adults aged 50 and up are using cannabis for pain management or other therapeutic reasons, although we suspect they are also using it for recreation.” In the United States, regular use of cannabis rose by 455% among 55- to 64-year-olds between 2002 and 2014, according to data from the U.S. National Survey on Drug Use and Health. In Australia, studies of middle-aged and older chronic pain patients, including those without cancer, suggest that about 15% have used cannabis for pain, Dr. Withall said.

Older patients may ask if cannabis causes cognitive deficits. “Anecdotally, the answer is yes. There is certainly evidence in younger cohorts that cannabis affects cognition, although this remains fiercely debated,” Dr. Withall said. She cited a 25-year longitudinal cohort study of persistent cannabis users in which habitual cannabis use during adolescence led to significant cognitive impairment in executive function, information processing speed, and other cognitive domains in adulthood. Importantly, those deficits did not fully reverse after users stopped. In contrast, users who started as adults developed milder cognitive deficits and greater restoration of cognitive function after cessation. In another study that is currently under review, 42% of cannabis-using older adults had significant cognitive impairment (scores of less than 88 on the ACE-R [Addenbrooke’s Cognitive Examination-Revised]), Dr. Withall said.

These users did have comorbid substance abuse, depression, and other potential confounders, but nonetheless, more frequent cannabis use approached statistical significance as a negative predictor of ACE-R scores, she added.

The effects of various cannabis products depend on their ratio of cannabidiol (CBD) and tetrahydrocannabinol (THC), Dr. Withall emphasized. “There is increasing preclinical evidence that the endocannabinoid system regulates neurodegenerative processes common to various dementias, including excess glutamate, glial activation, oxidative stress, and neuroinflammation,” she said. Some studies suggest a neuroprotective role for CBD, while in safety studies, THC was well tolerated in patients with dementia but did not improve cognition. In another 4-week, uncontrolled, open-label trial of 10 patients with Alzheimer’s disease, adding medical cannabis oil to regular care was associated with significant decreases in delusions, agitation or aggression, irritability, apathy, sleep, and caregiver distress, Dr. Withall said (J Alzheimers Dis. 2016;51[1]15-9).

So what to tell patients who ask about cannabis or are habitual users?

“At the moment, we are trying to encourage people to minimize use of cannabis, but we don’t have enough information,” she concluded. “Even though we suspect it is having a detrimental effect on patients, it may be that certain groups are showing benefits. There is just not enough to hang a hat on yet.”

Dr. Withall disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – An absence of guidelines on cannabis in older adults makes it difficult for clinicians to advise seniors, particularly those who use it for medical reasons, Adrienne Withall, PhD, said at the 2016 congress of the International Psychogeriatric Association.

“We don’t really know the impacts of cannabis use on older people. They may be positive or negative, depending on what it’s being used for,” said Dr. Withall of the University of New South Wales in Sydney.

Questions about how cannabis affects older people are growing as the boomer generation ages and cannabis becomes easier to legally obtain.

“Our picture of the cannabis user as a young adult or teen is inaccurate,” Dr. Withall said. “Many reports show that adults aged 50 and up are using cannabis for pain management or other therapeutic reasons, although we suspect they are also using it for recreation.” In the United States, regular use of cannabis rose by 455% among 55- to 64-year-olds between 2002 and 2014, according to data from the U.S. National Survey on Drug Use and Health. In Australia, studies of middle-aged and older chronic pain patients, including those without cancer, suggest that about 15% have used cannabis for pain, Dr. Withall said.

Older patients may ask if cannabis causes cognitive deficits. “Anecdotally, the answer is yes. There is certainly evidence in younger cohorts that cannabis affects cognition, although this remains fiercely debated,” Dr. Withall said. She cited a 25-year longitudinal cohort study of persistent cannabis users in which habitual cannabis use during adolescence led to significant cognitive impairment in executive function, information processing speed, and other cognitive domains in adulthood. Importantly, those deficits did not fully reverse after users stopped. In contrast, users who started as adults developed milder cognitive deficits and greater restoration of cognitive function after cessation. In another study that is currently under review, 42% of cannabis-using older adults had significant cognitive impairment (scores of less than 88 on the ACE-R [Addenbrooke’s Cognitive Examination-Revised]), Dr. Withall said.

These users did have comorbid substance abuse, depression, and other potential confounders, but nonetheless, more frequent cannabis use approached statistical significance as a negative predictor of ACE-R scores, she added.

The effects of various cannabis products depend on their ratio of cannabidiol (CBD) and tetrahydrocannabinol (THC), Dr. Withall emphasized. “There is increasing preclinical evidence that the endocannabinoid system regulates neurodegenerative processes common to various dementias, including excess glutamate, glial activation, oxidative stress, and neuroinflammation,” she said. Some studies suggest a neuroprotective role for CBD, while in safety studies, THC was well tolerated in patients with dementia but did not improve cognition. In another 4-week, uncontrolled, open-label trial of 10 patients with Alzheimer’s disease, adding medical cannabis oil to regular care was associated with significant decreases in delusions, agitation or aggression, irritability, apathy, sleep, and caregiver distress, Dr. Withall said (J Alzheimers Dis. 2016;51[1]15-9).

So what to tell patients who ask about cannabis or are habitual users?

“At the moment, we are trying to encourage people to minimize use of cannabis, but we don’t have enough information,” she concluded. “Even though we suspect it is having a detrimental effect on patients, it may be that certain groups are showing benefits. There is just not enough to hang a hat on yet.”

Dr. Withall disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – An absence of guidelines on cannabis in older adults makes it difficult for clinicians to advise seniors, particularly those who use it for medical reasons, Adrienne Withall, PhD, said at the 2016 congress of the International Psychogeriatric Association.

“We don’t really know the impacts of cannabis use on older people. They may be positive or negative, depending on what it’s being used for,” said Dr. Withall of the University of New South Wales in Sydney.

Questions about how cannabis affects older people are growing as the boomer generation ages and cannabis becomes easier to legally obtain.

“Our picture of the cannabis user as a young adult or teen is inaccurate,” Dr. Withall said. “Many reports show that adults aged 50 and up are using cannabis for pain management or other therapeutic reasons, although we suspect they are also using it for recreation.” In the United States, regular use of cannabis rose by 455% among 55- to 64-year-olds between 2002 and 2014, according to data from the U.S. National Survey on Drug Use and Health. In Australia, studies of middle-aged and older chronic pain patients, including those without cancer, suggest that about 15% have used cannabis for pain, Dr. Withall said.

Older patients may ask if cannabis causes cognitive deficits. “Anecdotally, the answer is yes. There is certainly evidence in younger cohorts that cannabis affects cognition, although this remains fiercely debated,” Dr. Withall said. She cited a 25-year longitudinal cohort study of persistent cannabis users in which habitual cannabis use during adolescence led to significant cognitive impairment in executive function, information processing speed, and other cognitive domains in adulthood. Importantly, those deficits did not fully reverse after users stopped. In contrast, users who started as adults developed milder cognitive deficits and greater restoration of cognitive function after cessation. In another study that is currently under review, 42% of cannabis-using older adults had significant cognitive impairment (scores of less than 88 on the ACE-R [Addenbrooke’s Cognitive Examination-Revised]), Dr. Withall said.

These users did have comorbid substance abuse, depression, and other potential confounders, but nonetheless, more frequent cannabis use approached statistical significance as a negative predictor of ACE-R scores, she added.

The effects of various cannabis products depend on their ratio of cannabidiol (CBD) and tetrahydrocannabinol (THC), Dr. Withall emphasized. “There is increasing preclinical evidence that the endocannabinoid system regulates neurodegenerative processes common to various dementias, including excess glutamate, glial activation, oxidative stress, and neuroinflammation,” she said. Some studies suggest a neuroprotective role for CBD, while in safety studies, THC was well tolerated in patients with dementia but did not improve cognition. In another 4-week, uncontrolled, open-label trial of 10 patients with Alzheimer’s disease, adding medical cannabis oil to regular care was associated with significant decreases in delusions, agitation or aggression, irritability, apathy, sleep, and caregiver distress, Dr. Withall said (J Alzheimers Dis. 2016;51[1]15-9).

So what to tell patients who ask about cannabis or are habitual users?

“At the moment, we are trying to encourage people to minimize use of cannabis, but we don’t have enough information,” she concluded. “Even though we suspect it is having a detrimental effect on patients, it may be that certain groups are showing benefits. There is just not enough to hang a hat on yet.”

Dr. Withall disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – Patients with unchecked inflammation, depression, and slow gait make up a “depressed frail phenotype at grave risk of death,” Patrick J. Brown, PhD, said at the 2016 congress of the International Psychogeriatric Association..

“There are multiple pathways into this phenotypic cycle. Depression and slow gait share a bidirectional relationship, and inflammation may indirectly lead to depression because of its impact on mobility,” said Dr. Brown, a clinical psychologist in the department of psychiatry at Columbia University, New York. Clinicians should consider aggressive interventions for older patients with depression and frailty, recognizing that exercise and dietary changes may be “much more relevant” than switching or augmenting antidepressants and other psychotropic medications, which can be especially risky for seniors, he said.

Models of psychiatric illness, particularly depression, come from studies of younger adults “and have failed us in geriatric medicine,” Dr. Brown emphasized. About 3%-7% of adults above age 65 years meet criteria for major depressive disorder, and another 15% have “significant but subthreshold” depressive symptoms, but less than half of depressed seniors have responded to antidepressants in controlled trials. High rates of treatment failure in late-life depression suggest that it has diverse etiologies that have to be identified and targeted to improve outcomes, Dr. Brown said. Frailty, characterized by slowed gait, weak grip, and decreased physical activity and energy, resembles and often co-occurs with late-life depression, giving rise to the concept of a “depressed-frail” phenotype at potentially greater risk of imminent death, he added.

To test that idea, Dr. Brown and his associates analyzed 10-year longitudinal data for 3,075 white and African American adults aged 68-80 years who were free from significant disabilities or functional limitations at baseline. These participants were from the Dynamics of Health, Aging, and Body Composition study, which annually measured body composition, gait, grip strength, comorbidities, and other clinical data. Using a method called latent class analysis, the researchers examined trajectories of depression (defined as a score of at least 10 on the Center for Epidemiologic Studies Depression Scale, slow gait (walking speed less than 1.02 meters per second), and inflammation (serum interleukin-6 [IL-6] levels above 3.24 pg/mL) over time. They also used multivariable regression to understand how each of those features correlated with mortality.

The latent class analysis showed that 22% of participants had either rising or consistently high probabilities of inflammation, slow gait, and depression. Slow gait was associated with inflammation (r = 0.40; P less than .001) and depression (r = 0.49; P less than .001). Inflammation was independently associated with mortality (P less than .001), while slow gait was linked to mortality only in participants with depression that worsened over time (P less than .01). Among the 247 patients with a high level of inflammation and slow gait with increasing or a consistently high level of depression, the 10-year mortality was 85%, the highest of any group of patients in the study, Dr. Brown said.

The study also confirmed the overlap between depression and frailty. Depression and inflammation each independently predicted slow gait, with odds ratios of 1.37 (95% confidence interval, 1.17-1.60) and 1.22 (1.05-1.41), respectively. Slow gait also was a significant predictor of depression (OR, 1.27; 1.08-1.50), even after the investigators accounted for age, sex, body mass index, comorbidities, use of anti-inflammatories, and scores on the Modified Mini-Mental State Examination.

These and other recent findings highlight frailty as a physical manifestation of greater biologic aging, Dr. Brown said. Accordingly, researchers are studying whether combatting age-related deterioration can improve outcomes in late-life depression. Specific protocols under study include anaerobic exercise to reverse mitochondrial dysfunction, anti-inflammatories targeting acute phase proteins (C-reactive protein) and cytokines (IL-6 and tumor necrosis factor–alpha), and treatments that augment dopaminergic neurotransmission, he said.

The National Institutes of Health provided funding. Dr. Brown had no relevant financial disclosures.

SAN FRANCISCO – Patients with unchecked inflammation, depression, and slow gait make up a “depressed frail phenotype at grave risk of death,” Patrick J. Brown, PhD, said at the 2016 congress of the International Psychogeriatric Association..

“There are multiple pathways into this phenotypic cycle. Depression and slow gait share a bidirectional relationship, and inflammation may indirectly lead to depression because of its impact on mobility,” said Dr. Brown, a clinical psychologist in the department of psychiatry at Columbia University, New York. Clinicians should consider aggressive interventions for older patients with depression and frailty, recognizing that exercise and dietary changes may be “much more relevant” than switching or augmenting antidepressants and other psychotropic medications, which can be especially risky for seniors, he said.

Models of psychiatric illness, particularly depression, come from studies of younger adults “and have failed us in geriatric medicine,” Dr. Brown emphasized. About 3%-7% of adults above age 65 years meet criteria for major depressive disorder, and another 15% have “significant but subthreshold” depressive symptoms, but less than half of depressed seniors have responded to antidepressants in controlled trials. High rates of treatment failure in late-life depression suggest that it has diverse etiologies that have to be identified and targeted to improve outcomes, Dr. Brown said. Frailty, characterized by slowed gait, weak grip, and decreased physical activity and energy, resembles and often co-occurs with late-life depression, giving rise to the concept of a “depressed-frail” phenotype at potentially greater risk of imminent death, he added.

To test that idea, Dr. Brown and his associates analyzed 10-year longitudinal data for 3,075 white and African American adults aged 68-80 years who were free from significant disabilities or functional limitations at baseline. These participants were from the Dynamics of Health, Aging, and Body Composition study, which annually measured body composition, gait, grip strength, comorbidities, and other clinical data. Using a method called latent class analysis, the researchers examined trajectories of depression (defined as a score of at least 10 on the Center for Epidemiologic Studies Depression Scale, slow gait (walking speed less than 1.02 meters per second), and inflammation (serum interleukin-6 [IL-6] levels above 3.24 pg/mL) over time. They also used multivariable regression to understand how each of those features correlated with mortality.

The latent class analysis showed that 22% of participants had either rising or consistently high probabilities of inflammation, slow gait, and depression. Slow gait was associated with inflammation (r = 0.40; P less than .001) and depression (r = 0.49; P less than .001). Inflammation was independently associated with mortality (P less than .001), while slow gait was linked to mortality only in participants with depression that worsened over time (P less than .01). Among the 247 patients with a high level of inflammation and slow gait with increasing or a consistently high level of depression, the 10-year mortality was 85%, the highest of any group of patients in the study, Dr. Brown said.

The study also confirmed the overlap between depression and frailty. Depression and inflammation each independently predicted slow gait, with odds ratios of 1.37 (95% confidence interval, 1.17-1.60) and 1.22 (1.05-1.41), respectively. Slow gait also was a significant predictor of depression (OR, 1.27; 1.08-1.50), even after the investigators accounted for age, sex, body mass index, comorbidities, use of anti-inflammatories, and scores on the Modified Mini-Mental State Examination.

These and other recent findings highlight frailty as a physical manifestation of greater biologic aging, Dr. Brown said. Accordingly, researchers are studying whether combatting age-related deterioration can improve outcomes in late-life depression. Specific protocols under study include anaerobic exercise to reverse mitochondrial dysfunction, anti-inflammatories targeting acute phase proteins (C-reactive protein) and cytokines (IL-6 and tumor necrosis factor–alpha), and treatments that augment dopaminergic neurotransmission, he said.

The National Institutes of Health provided funding. Dr. Brown had no relevant financial disclosures.

SAN FRANCISCO – Patients with unchecked inflammation, depression, and slow gait make up a “depressed frail phenotype at grave risk of death,” Patrick J. Brown, PhD, said at the 2016 congress of the International Psychogeriatric Association..

“There are multiple pathways into this phenotypic cycle. Depression and slow gait share a bidirectional relationship, and inflammation may indirectly lead to depression because of its impact on mobility,” said Dr. Brown, a clinical psychologist in the department of psychiatry at Columbia University, New York. Clinicians should consider aggressive interventions for older patients with depression and frailty, recognizing that exercise and dietary changes may be “much more relevant” than switching or augmenting antidepressants and other psychotropic medications, which can be especially risky for seniors, he said.

Models of psychiatric illness, particularly depression, come from studies of younger adults “and have failed us in geriatric medicine,” Dr. Brown emphasized. About 3%-7% of adults above age 65 years meet criteria for major depressive disorder, and another 15% have “significant but subthreshold” depressive symptoms, but less than half of depressed seniors have responded to antidepressants in controlled trials. High rates of treatment failure in late-life depression suggest that it has diverse etiologies that have to be identified and targeted to improve outcomes, Dr. Brown said. Frailty, characterized by slowed gait, weak grip, and decreased physical activity and energy, resembles and often co-occurs with late-life depression, giving rise to the concept of a “depressed-frail” phenotype at potentially greater risk of imminent death, he added.

To test that idea, Dr. Brown and his associates analyzed 10-year longitudinal data for 3,075 white and African American adults aged 68-80 years who were free from significant disabilities or functional limitations at baseline. These participants were from the Dynamics of Health, Aging, and Body Composition study, which annually measured body composition, gait, grip strength, comorbidities, and other clinical data. Using a method called latent class analysis, the researchers examined trajectories of depression (defined as a score of at least 10 on the Center for Epidemiologic Studies Depression Scale, slow gait (walking speed less than 1.02 meters per second), and inflammation (serum interleukin-6 [IL-6] levels above 3.24 pg/mL) over time. They also used multivariable regression to understand how each of those features correlated with mortality.

The latent class analysis showed that 22% of participants had either rising or consistently high probabilities of inflammation, slow gait, and depression. Slow gait was associated with inflammation (r = 0.40; P less than .001) and depression (r = 0.49; P less than .001). Inflammation was independently associated with mortality (P less than .001), while slow gait was linked to mortality only in participants with depression that worsened over time (P less than .01). Among the 247 patients with a high level of inflammation and slow gait with increasing or a consistently high level of depression, the 10-year mortality was 85%, the highest of any group of patients in the study, Dr. Brown said.

The study also confirmed the overlap between depression and frailty. Depression and inflammation each independently predicted slow gait, with odds ratios of 1.37 (95% confidence interval, 1.17-1.60) and 1.22 (1.05-1.41), respectively. Slow gait also was a significant predictor of depression (OR, 1.27; 1.08-1.50), even after the investigators accounted for age, sex, body mass index, comorbidities, use of anti-inflammatories, and scores on the Modified Mini-Mental State Examination.

These and other recent findings highlight frailty as a physical manifestation of greater biologic aging, Dr. Brown said. Accordingly, researchers are studying whether combatting age-related deterioration can improve outcomes in late-life depression. Specific protocols under study include anaerobic exercise to reverse mitochondrial dysfunction, anti-inflammatories targeting acute phase proteins (C-reactive protein) and cytokines (IL-6 and tumor necrosis factor–alpha), and treatments that augment dopaminergic neurotransmission, he said.

The National Institutes of Health provided funding. Dr. Brown had no relevant financial disclosures.

SAN FRANCISCO – Metabolic dysregulation and particularly abdominal obesity lead to failure to remit in late-life depression, according to a multicenter, prospective cohort study.

The finding highlights the need for comprehensive interventions for comorbid late-life depression and metabolic syndrome, Radboud M. Marijnissen, MD, said during an oral presentation at the 2016 congress of the International Psychogeriatric Association..

Late-life depression is notoriously refractory to antidepressant monotherapy, he said. Metabolic syndrome becomes more common with age and is reciprocally related to depression, but few studies have examined links between these two conditions, said Dr. Marijnissen of the department of old age psychiatry at the Pro Persona Medical Center in Wolfheze, the Netherlands. Therefore, he and his associates examined Inventory of Depressive Symptomatology (IDS) scores and metabolic data from 285 patients aged 60 years and older who met DSM-IV criteria for depressive disorders. The patients were participants in the observational, prospective multicenter Netherlands study of depression in older persons (NESDO), which assessed patients every 6 months for 2 years. The researchers defined metabolic syndrome based on National Cholesterol Education Program (NCEP-ATP III) criteria, which include measures for central obesity, hypertension, and elevated blood levels of glucose, triglycerides, and high-density lipoprotein cholesterol, Dr. Marijnissen said. In his study, most patients were receiving regular mental health care, including antidepressants and psychotherapy.

At 2 years, patients were significantly less likely to have achieved complete remission from depression when they had components of metabolic syndrome than otherwise (42% vs. 58%; P = .01). Furthermore, each additional component of metabolic syndrome increased the odds of failure to remit by 27% (odds ratio, 1.27; 95% confidence interval, 1.03-1.58; P = .028), even after the investigators controlled for multiple potential confounders, including age, sex, marital status, tobacco and alcohol use, level of education, physical activity, comorbidities, the presence of cognitive impairment, and the use of psychotropic and anti-inflammatory drugs.

Interestingly, specific components of metabolic syndrome seemed to exert different effects on the likelihood of remission, Dr. Marijnissen said. Increased waist circumference and HDL cholesterol each independently predicted failure to achieve remission, with odds ratios of 1.96 (95% CI, 1.15-3.32; P = .013) and 2.35 (1.21-4.53; P = .011), respectively. In contrast, elevated triglycerides predicted remission failure, but the link did not reach statistical significance, and hypertension and elevated fasting blood glucose levels showed no trend in either direction.

Further analyses of scores on the three subscales of the IDS again linked abdominal obesity, as well as elevated fasting blood glucose, with persistent somatic features of depression (P = .046 and .02, respectively). In contrast, neither the total number of metabolic syndrome components nor the presence or absence of any individual component predicted persistently elevated scores on the mood or motivation subscales of the IDS (P greater than .4 for each association). In addition, neither metabolic syndrome nor its individual components predicted depression severity.

These findings suggest that metabolic dysregulation leads to remission failure with persistent somatic symptoms in late-life depression, and that central obesity drives this relationship, Dr. Marijnissen concluded. “Metabolic depression calls for specific interventions,” he added. “People who are suffering from this subtype of depression may benefit from vascular disease management, healthy nutrition, and programs that emphasize exercise, including resistance training to help turn white fat into brown fat, which lowers metabolic risk as well as depressive symptoms.”

Dr. Marijnissen reported no funding sources or conflicts of interest.

SAN FRANCISCO – Metabolic dysregulation and particularly abdominal obesity lead to failure to remit in late-life depression, according to a multicenter, prospective cohort study.

The finding highlights the need for comprehensive interventions for comorbid late-life depression and metabolic syndrome, Radboud M. Marijnissen, MD, said during an oral presentation at the 2016 congress of the International Psychogeriatric Association..

Late-life depression is notoriously refractory to antidepressant monotherapy, he said. Metabolic syndrome becomes more common with age and is reciprocally related to depression, but few studies have examined links between these two conditions, said Dr. Marijnissen of the department of old age psychiatry at the Pro Persona Medical Center in Wolfheze, the Netherlands. Therefore, he and his associates examined Inventory of Depressive Symptomatology (IDS) scores and metabolic data from 285 patients aged 60 years and older who met DSM-IV criteria for depressive disorders. The patients were participants in the observational, prospective multicenter Netherlands study of depression in older persons (NESDO), which assessed patients every 6 months for 2 years. The researchers defined metabolic syndrome based on National Cholesterol Education Program (NCEP-ATP III) criteria, which include measures for central obesity, hypertension, and elevated blood levels of glucose, triglycerides, and high-density lipoprotein cholesterol, Dr. Marijnissen said. In his study, most patients were receiving regular mental health care, including antidepressants and psychotherapy.

At 2 years, patients were significantly less likely to have achieved complete remission from depression when they had components of metabolic syndrome than otherwise (42% vs. 58%; P = .01). Furthermore, each additional component of metabolic syndrome increased the odds of failure to remit by 27% (odds ratio, 1.27; 95% confidence interval, 1.03-1.58; P = .028), even after the investigators controlled for multiple potential confounders, including age, sex, marital status, tobacco and alcohol use, level of education, physical activity, comorbidities, the presence of cognitive impairment, and the use of psychotropic and anti-inflammatory drugs.

Interestingly, specific components of metabolic syndrome seemed to exert different effects on the likelihood of remission, Dr. Marijnissen said. Increased waist circumference and HDL cholesterol each independently predicted failure to achieve remission, with odds ratios of 1.96 (95% CI, 1.15-3.32; P = .013) and 2.35 (1.21-4.53; P = .011), respectively. In contrast, elevated triglycerides predicted remission failure, but the link did not reach statistical significance, and hypertension and elevated fasting blood glucose levels showed no trend in either direction.

Further analyses of scores on the three subscales of the IDS again linked abdominal obesity, as well as elevated fasting blood glucose, with persistent somatic features of depression (P = .046 and .02, respectively). In contrast, neither the total number of metabolic syndrome components nor the presence or absence of any individual component predicted persistently elevated scores on the mood or motivation subscales of the IDS (P greater than .4 for each association). In addition, neither metabolic syndrome nor its individual components predicted depression severity.

These findings suggest that metabolic dysregulation leads to remission failure with persistent somatic symptoms in late-life depression, and that central obesity drives this relationship, Dr. Marijnissen concluded. “Metabolic depression calls for specific interventions,” he added. “People who are suffering from this subtype of depression may benefit from vascular disease management, healthy nutrition, and programs that emphasize exercise, including resistance training to help turn white fat into brown fat, which lowers metabolic risk as well as depressive symptoms.”

Dr. Marijnissen reported no funding sources or conflicts of interest.

SAN FRANCISCO – Metabolic dysregulation and particularly abdominal obesity lead to failure to remit in late-life depression, according to a multicenter, prospective cohort study.

The finding highlights the need for comprehensive interventions for comorbid late-life depression and metabolic syndrome, Radboud M. Marijnissen, MD, said during an oral presentation at the 2016 congress of the International Psychogeriatric Association..

Late-life depression is notoriously refractory to antidepressant monotherapy, he said. Metabolic syndrome becomes more common with age and is reciprocally related to depression, but few studies have examined links between these two conditions, said Dr. Marijnissen of the department of old age psychiatry at the Pro Persona Medical Center in Wolfheze, the Netherlands. Therefore, he and his associates examined Inventory of Depressive Symptomatology (IDS) scores and metabolic data from 285 patients aged 60 years and older who met DSM-IV criteria for depressive disorders. The patients were participants in the observational, prospective multicenter Netherlands study of depression in older persons (NESDO), which assessed patients every 6 months for 2 years. The researchers defined metabolic syndrome based on National Cholesterol Education Program (NCEP-ATP III) criteria, which include measures for central obesity, hypertension, and elevated blood levels of glucose, triglycerides, and high-density lipoprotein cholesterol, Dr. Marijnissen said. In his study, most patients were receiving regular mental health care, including antidepressants and psychotherapy.

At 2 years, patients were significantly less likely to have achieved complete remission from depression when they had components of metabolic syndrome than otherwise (42% vs. 58%; P = .01). Furthermore, each additional component of metabolic syndrome increased the odds of failure to remit by 27% (odds ratio, 1.27; 95% confidence interval, 1.03-1.58; P = .028), even after the investigators controlled for multiple potential confounders, including age, sex, marital status, tobacco and alcohol use, level of education, physical activity, comorbidities, the presence of cognitive impairment, and the use of psychotropic and anti-inflammatory drugs.

Interestingly, specific components of metabolic syndrome seemed to exert different effects on the likelihood of remission, Dr. Marijnissen said. Increased waist circumference and HDL cholesterol each independently predicted failure to achieve remission, with odds ratios of 1.96 (95% CI, 1.15-3.32; P = .013) and 2.35 (1.21-4.53; P = .011), respectively. In contrast, elevated triglycerides predicted remission failure, but the link did not reach statistical significance, and hypertension and elevated fasting blood glucose levels showed no trend in either direction.

Further analyses of scores on the three subscales of the IDS again linked abdominal obesity, as well as elevated fasting blood glucose, with persistent somatic features of depression (P = .046 and .02, respectively). In contrast, neither the total number of metabolic syndrome components nor the presence or absence of any individual component predicted persistently elevated scores on the mood or motivation subscales of the IDS (P greater than .4 for each association). In addition, neither metabolic syndrome nor its individual components predicted depression severity.

These findings suggest that metabolic dysregulation leads to remission failure with persistent somatic symptoms in late-life depression, and that central obesity drives this relationship, Dr. Marijnissen concluded. “Metabolic depression calls for specific interventions,” he added. “People who are suffering from this subtype of depression may benefit from vascular disease management, healthy nutrition, and programs that emphasize exercise, including resistance training to help turn white fat into brown fat, which lowers metabolic risk as well as depressive symptoms.”

Dr. Marijnissen reported no funding sources or conflicts of interest.

SAN FRANCISCO – Among patients with mild cognitive impairment, those with extrapyramidal signs were about six times more likely to develop non-Alzheimer’s forms of dementia than those without baseline extrapyramidal signs, according to a prospective multicenter analysis.

The study is among the first to examine the link between extrapyramidal signs and dementia other than Alzheimer’s disease, said Woojae Myung, MD, of Sungkyunkwan University School of Medicine in Seoul, South Korea, and his associates. “Our results suggest that careful assessment of extrapyramidal signs in patients with incident mild cognitive impairment (MCI) can yield important clinical information for prognosis,” the researchers wrote in a poster presented at the 2016 congress of the International Psychogeriatric Association.

©alexdans/Thinkstock

The study included 882 adults who were enrolled in the Clinical Research Center for Dementia of Korea (CREDOS) registry between 2006 and 2012. All participants met criteria for mild cognitive impairment based on the Korean version of the Mini-Mental State Examination (K-MMSE) and also underwent standardized neurologic examinations, magnetic resonance imaging, and the 15-item Geriatric Depression Scale (GDS-15) at baseline, Dr. Myung and his coinvestigators reported.

In all, 234 patients (26%) converted to dementia over a median follow-up time of 1.44 years (interquartile range, 1.02-2.24 years). Most (92%, or 216) patients who developed dementia had probable Alzheimer’s disease, while 9 had vascular dementia, 4 had Lewy body dementia, 3 had frontotemporal dementia, 1 had progressive supranuclear palsy, and 1 had dementia associated with normal pressure hydrocephalus.

Baseline extrapyramidal signs were the only significant factor associated with progression to non-Alzheimer’s forms of dementia (hazard ratio, 6.33; 95% confidence interval, 2.30-13.39; P less than .001) after controlling for age, gender, educational level, diabetes, hypertension, MRI evidence of matter hyperintensity, GDS-15 score, and level of cognitive impairment at baseline, the researchers reported. Furthermore, patients with baseline extrapyramidal signs were about 30% less likely to develop Alzheimer’s disease than were patients who did not have extrapyramidal signs at baseline.

Significant predictors of Alzheimer’s disease included older age, higher educational level, absence of hypertension, and a lower K-MMSE score, as well as the presence of amnestic mild cognitive impairment, the investigators noted.

They disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – Among patients with mild cognitive impairment, those with extrapyramidal signs were about six times more likely to develop non-Alzheimer’s forms of dementia than those without baseline extrapyramidal signs, according to a prospective multicenter analysis.

The study is among the first to examine the link between extrapyramidal signs and dementia other than Alzheimer’s disease, said Woojae Myung, MD, of Sungkyunkwan University School of Medicine in Seoul, South Korea, and his associates. “Our results suggest that careful assessment of extrapyramidal signs in patients with incident mild cognitive impairment (MCI) can yield important clinical information for prognosis,” the researchers wrote in a poster presented at the 2016 congress of the International Psychogeriatric Association.

©alexdans/Thinkstock

The study included 882 adults who were enrolled in the Clinical Research Center for Dementia of Korea (CREDOS) registry between 2006 and 2012. All participants met criteria for mild cognitive impairment based on the Korean version of the Mini-Mental State Examination (K-MMSE) and also underwent standardized neurologic examinations, magnetic resonance imaging, and the 15-item Geriatric Depression Scale (GDS-15) at baseline, Dr. Myung and his coinvestigators reported.

In all, 234 patients (26%) converted to dementia over a median follow-up time of 1.44 years (interquartile range, 1.02-2.24 years). Most (92%, or 216) patients who developed dementia had probable Alzheimer’s disease, while 9 had vascular dementia, 4 had Lewy body dementia, 3 had frontotemporal dementia, 1 had progressive supranuclear palsy, and 1 had dementia associated with normal pressure hydrocephalus.

Baseline extrapyramidal signs were the only significant factor associated with progression to non-Alzheimer’s forms of dementia (hazard ratio, 6.33; 95% confidence interval, 2.30-13.39; P less than .001) after controlling for age, gender, educational level, diabetes, hypertension, MRI evidence of matter hyperintensity, GDS-15 score, and level of cognitive impairment at baseline, the researchers reported. Furthermore, patients with baseline extrapyramidal signs were about 30% less likely to develop Alzheimer’s disease than were patients who did not have extrapyramidal signs at baseline.

Significant predictors of Alzheimer’s disease included older age, higher educational level, absence of hypertension, and a lower K-MMSE score, as well as the presence of amnestic mild cognitive impairment, the investigators noted.

They disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – Among patients with mild cognitive impairment, those with extrapyramidal signs were about six times more likely to develop non-Alzheimer’s forms of dementia than those without baseline extrapyramidal signs, according to a prospective multicenter analysis.

The study is among the first to examine the link between extrapyramidal signs and dementia other than Alzheimer’s disease, said Woojae Myung, MD, of Sungkyunkwan University School of Medicine in Seoul, South Korea, and his associates. “Our results suggest that careful assessment of extrapyramidal signs in patients with incident mild cognitive impairment (MCI) can yield important clinical information for prognosis,” the researchers wrote in a poster presented at the 2016 congress of the International Psychogeriatric Association.

©alexdans/Thinkstock

The study included 882 adults who were enrolled in the Clinical Research Center for Dementia of Korea (CREDOS) registry between 2006 and 2012. All participants met criteria for mild cognitive impairment based on the Korean version of the Mini-Mental State Examination (K-MMSE) and also underwent standardized neurologic examinations, magnetic resonance imaging, and the 15-item Geriatric Depression Scale (GDS-15) at baseline, Dr. Myung and his coinvestigators reported.

In all, 234 patients (26%) converted to dementia over a median follow-up time of 1.44 years (interquartile range, 1.02-2.24 years). Most (92%, or 216) patients who developed dementia had probable Alzheimer’s disease, while 9 had vascular dementia, 4 had Lewy body dementia, 3 had frontotemporal dementia, 1 had progressive supranuclear palsy, and 1 had dementia associated with normal pressure hydrocephalus.

Baseline extrapyramidal signs were the only significant factor associated with progression to non-Alzheimer’s forms of dementia (hazard ratio, 6.33; 95% confidence interval, 2.30-13.39; P less than .001) after controlling for age, gender, educational level, diabetes, hypertension, MRI evidence of matter hyperintensity, GDS-15 score, and level of cognitive impairment at baseline, the researchers reported. Furthermore, patients with baseline extrapyramidal signs were about 30% less likely to develop Alzheimer’s disease than were patients who did not have extrapyramidal signs at baseline.

Significant predictors of Alzheimer’s disease included older age, higher educational level, absence of hypertension, and a lower K-MMSE score, as well as the presence of amnestic mild cognitive impairment, the investigators noted.

They disclosed no funding sources or conflicts of interest.

SAN FRANCISCO – Whole body cryotherapy led to significant improvements in memory and significant but less durable reductions in depressive symptoms among older patients with mild cognitive impairment in a small, uncontrolled trial.

“We cannot call whole body cryotherapy a treatment yet, but we have some good preliminary results suggesting that this might be a natural method of treating memory impairment,” Joanna Rymaszewska, MD, PhD, of Wroclaw (Poland) Medical University said during an oral presentation at the at the 2016 congress of the International Psychogeriatric Association. Based on this and other work, whole body cryotherapy also might ease depression if patients were able to undergo regular long-term treatment, she said.

Very low temperatures have antioxidant and anti-inflammatory effects, which originally sparked the idea that cryotherapy might help prevent dementia, Dr. Rymaszewska said. To test that hypothesis, she and her colleagues exposed 21 patients with mild cognitive impairment (average baseline Montreal Cognitive Assessment (MoCA) score, 23.8; range, 20-26) to whole body cryotherapy for 2 minutes a day for 10 days, excluding weekends. Patients donned swimsuits, socks, gloves, and mouth covers to facilitate breathing and then walked in pairs around a chamber cooled to between –110° C and –160° C (–166° F to –256° F). “The temperature is so low that you actually cannot feel it,” Dr. Rymaszewska said. The group averaged 65 years of age, and two-thirds were women.

Immediately after the final cryotherapy session and 2 weeks later, patients had improved significantly (P less than .05) from baseline on two-word recall subscales of the DemTect, a psychometric screening tool; on the semantic and anterograde subscales of the 5-minute Test Your Memory (TYM) scale; and on the logical memory subscale of the Saint Louis University Mental Status (SLUMS) exam, Dr. Rymaszewska said.

Enzyme-linked immunoassays showed no significant changes in plasma levels of brain-derived neurotrophic factor or in the cytokines interleukin-6, IL-8, or IL-10 before and after cryotherapy, Dr. Rymaszewska said. But after treatment, patients produced significantly more brain-derived neurotrophic factor and significantly less IL-6 and IL-10 and in response to amyloid-beta, she added. “These preliminary results show a positive influence of whole body cryostimulation on mnestic processes in people with mild cognitive impairment, but the biological mechanisms need further investigation,” she concluded.

Patients also improved significantly on the short form,15-item Geriatric Depression Scale (GDS-15) immediately after finishing cryotherapy. However, the effect was less durable, having lost statistical significance 2 weeks later, Dr. Rymaszewska said. However, parallel studies of the effects of whole body cryotherapy on mood and depression are showing early positive results, she said.

Cryotherapy is so well known in Poland that it would not have been possible to blind a control group to a less-cold “placebo” intervention, Dr. Rymaszewska noted.

The Ministry of Science and Higher Education in Poland helped fund the research. Dr. Rymaszewska had no disclosures.

SAN FRANCISCO – Whole body cryotherapy led to significant improvements in memory and significant but less durable reductions in depressive symptoms among older patients with mild cognitive impairment in a small, uncontrolled trial.

“We cannot call whole body cryotherapy a treatment yet, but we have some good preliminary results suggesting that this might be a natural method of treating memory impairment,” Joanna Rymaszewska, MD, PhD, of Wroclaw (Poland) Medical University said during an oral presentation at the at the 2016 congress of the International Psychogeriatric Association. Based on this and other work, whole body cryotherapy also might ease depression if patients were able to undergo regular long-term treatment, she said.

Very low temperatures have antioxidant and anti-inflammatory effects, which originally sparked the idea that cryotherapy might help prevent dementia, Dr. Rymaszewska said. To test that hypothesis, she and her colleagues exposed 21 patients with mild cognitive impairment (average baseline Montreal Cognitive Assessment (MoCA) score, 23.8; range, 20-26) to whole body cryotherapy for 2 minutes a day for 10 days, excluding weekends. Patients donned swimsuits, socks, gloves, and mouth covers to facilitate breathing and then walked in pairs around a chamber cooled to between –110° C and –160° C (–166° F to –256° F). “The temperature is so low that you actually cannot feel it,” Dr. Rymaszewska said. The group averaged 65 years of age, and two-thirds were women.

Immediately after the final cryotherapy session and 2 weeks later, patients had improved significantly (P less than .05) from baseline on two-word recall subscales of the DemTect, a psychometric screening tool; on the semantic and anterograde subscales of the 5-minute Test Your Memory (TYM) scale; and on the logical memory subscale of the Saint Louis University Mental Status (SLUMS) exam, Dr. Rymaszewska said.

Enzyme-linked immunoassays showed no significant changes in plasma levels of brain-derived neurotrophic factor or in the cytokines interleukin-6, IL-8, or IL-10 before and after cryotherapy, Dr. Rymaszewska said. But after treatment, patients produced significantly more brain-derived neurotrophic factor and significantly less IL-6 and IL-10 and in response to amyloid-beta, she added. “These preliminary results show a positive influence of whole body cryostimulation on mnestic processes in people with mild cognitive impairment, but the biological mechanisms need further investigation,” she concluded.

Patients also improved significantly on the short form,15-item Geriatric Depression Scale (GDS-15) immediately after finishing cryotherapy. However, the effect was less durable, having lost statistical significance 2 weeks later, Dr. Rymaszewska said. However, parallel studies of the effects of whole body cryotherapy on mood and depression are showing early positive results, she said.

Cryotherapy is so well known in Poland that it would not have been possible to blind a control group to a less-cold “placebo” intervention, Dr. Rymaszewska noted.

The Ministry of Science and Higher Education in Poland helped fund the research. Dr. Rymaszewska had no disclosures.

SAN FRANCISCO – Whole body cryotherapy led to significant improvements in memory and significant but less durable reductions in depressive symptoms among older patients with mild cognitive impairment in a small, uncontrolled trial.

“We cannot call whole body cryotherapy a treatment yet, but we have some good preliminary results suggesting that this might be a natural method of treating memory impairment,” Joanna Rymaszewska, MD, PhD, of Wroclaw (Poland) Medical University said during an oral presentation at the at the 2016 congress of the International Psychogeriatric Association. Based on this and other work, whole body cryotherapy also might ease depression if patients were able to undergo regular long-term treatment, she said.

Very low temperatures have antioxidant and anti-inflammatory effects, which originally sparked the idea that cryotherapy might help prevent dementia, Dr. Rymaszewska said. To test that hypothesis, she and her colleagues exposed 21 patients with mild cognitive impairment (average baseline Montreal Cognitive Assessment (MoCA) score, 23.8; range, 20-26) to whole body cryotherapy for 2 minutes a day for 10 days, excluding weekends. Patients donned swimsuits, socks, gloves, and mouth covers to facilitate breathing and then walked in pairs around a chamber cooled to between –110° C and –160° C (–166° F to –256° F). “The temperature is so low that you actually cannot feel it,” Dr. Rymaszewska said. The group averaged 65 years of age, and two-thirds were women.

Immediately after the final cryotherapy session and 2 weeks later, patients had improved significantly (P less than .05) from baseline on two-word recall subscales of the DemTect, a psychometric screening tool; on the semantic and anterograde subscales of the 5-minute Test Your Memory (TYM) scale; and on the logical memory subscale of the Saint Louis University Mental Status (SLUMS) exam, Dr. Rymaszewska said.

Enzyme-linked immunoassays showed no significant changes in plasma levels of brain-derived neurotrophic factor or in the cytokines interleukin-6, IL-8, or IL-10 before and after cryotherapy, Dr. Rymaszewska said. But after treatment, patients produced significantly more brain-derived neurotrophic factor and significantly less IL-6 and IL-10 and in response to amyloid-beta, she added. “These preliminary results show a positive influence of whole body cryostimulation on mnestic processes in people with mild cognitive impairment, but the biological mechanisms need further investigation,” she concluded.

Patients also improved significantly on the short form,15-item Geriatric Depression Scale (GDS-15) immediately after finishing cryotherapy. However, the effect was less durable, having lost statistical significance 2 weeks later, Dr. Rymaszewska said. However, parallel studies of the effects of whole body cryotherapy on mood and depression are showing early positive results, she said.

Cryotherapy is so well known in Poland that it would not have been possible to blind a control group to a less-cold “placebo” intervention, Dr. Rymaszewska noted.

The Ministry of Science and Higher Education in Poland helped fund the research. Dr. Rymaszewska had no disclosures.

SAN FRANCISCO – Unexpectedly, worry predicted better cognitive performance among older adults with mild symptoms of anxiety and depression, according to a cross-sectional, community-based study.

“This just flies in the face of everything that we know about worry in the adult literature,” said Sherry A. Beaudreau, PhD, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University. The findings suggest that older worriers might score lower on some cognitive measures if their worry declines through treatment, she said at the 2016 congress of the International Psychogeriatric Association.

COURTESY DR. BEAUDREAU

Old age often is marked by mild symptoms of anxiety and depression that do not meet criteria for a psychiatric diagnosis, but nonetheless predict poorer cognitive performance and mild dementia, Dr. Beaudreau said. Recent work has linked anxiety to decreased attentional control, and late life depression, to slow information processing, delayed verbal memory, and other cognitive deficits. Emerging evidence also suggests that worry leads to worse performance on tests of inhibitory ability and delayed memory, Dr. Beaudreau added.

To further test these relationships, she and her associates studied 119 older adults who were living in the San Francisco Bay area between 2010 and 2012. They averaged 74 years of age (range, 65-91 years), 92% were non-Hispanic white, and 56% were women.

Most of the cohort performed well on the Rey Auditory Verbal Learning test, which assesses word recall after a delay of 20-30 minutes, and also scored above average on condition 3 of the Delis-Kaplan Executive Function System, which is a color word assessment of inhibitory control, Dr. Beaudreau reported. Individuals also tended to score low on the Beck Anxiety Inventory and the Beck Depressive Inventory II, with average scores of 3.7 (range, 0-29) and 5.6 (0-41), respectively. The mean score on the Penn State Worry Questionnaire was 37.7, with a range of 16-76.

Regardless of whether their anxiety score was low or high, those who worried more had significantly better inhibitory control than those who worried less (P = .003), Dr. Beaudreau said. “So folks with high worry actually seemed to be doing better in terms of their inhibitory ability,” she added. “This is intriguing to me, because we assume that anxiety is affecting cognition, but worry seems to be doing something different.”

©gpointstudio/Thinkstock

High worry also predicted significantly better inhibitory control among individuals with both low and high depression scores (P = .03), she reported. For the word recall test, worry did not seem to affect performance in the absence of depression, but high worry predicted significantly better word recall among individuals with high depression scores (P = .009).

“These results suggest that psychiatric symptoms of anxiety and depression are modulated by worry severity, and it’s interesting that this finding was so consistent throughout the analyses,” Dr. Beaudreau said. Future studies should examine these relationships in groups of older psychiatric patients stratified by symptom severity rather than diagnosis, she added.

The work was supported by the Alzheimer’s Association and the Stanford/VA Alzheimer’s Center. Dr. Beaudreau had no relevant financial disclosures.

SAN FRANCISCO – Unexpectedly, worry predicted better cognitive performance among older adults with mild symptoms of anxiety and depression, according to a cross-sectional, community-based study.

“This just flies in the face of everything that we know about worry in the adult literature,” said Sherry A. Beaudreau, PhD, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University. The findings suggest that older worriers might score lower on some cognitive measures if their worry declines through treatment, she said at the 2016 congress of the International Psychogeriatric Association.

COURTESY DR. BEAUDREAU

Old age often is marked by mild symptoms of anxiety and depression that do not meet criteria for a psychiatric diagnosis, but nonetheless predict poorer cognitive performance and mild dementia, Dr. Beaudreau said. Recent work has linked anxiety to decreased attentional control, and late life depression, to slow information processing, delayed verbal memory, and other cognitive deficits. Emerging evidence also suggests that worry leads to worse performance on tests of inhibitory ability and delayed memory, Dr. Beaudreau added.

To further test these relationships, she and her associates studied 119 older adults who were living in the San Francisco Bay area between 2010 and 2012. They averaged 74 years of age (range, 65-91 years), 92% were non-Hispanic white, and 56% were women.

Most of the cohort performed well on the Rey Auditory Verbal Learning test, which assesses word recall after a delay of 20-30 minutes, and also scored above average on condition 3 of the Delis-Kaplan Executive Function System, which is a color word assessment of inhibitory control, Dr. Beaudreau reported. Individuals also tended to score low on the Beck Anxiety Inventory and the Beck Depressive Inventory II, with average scores of 3.7 (range, 0-29) and 5.6 (0-41), respectively. The mean score on the Penn State Worry Questionnaire was 37.7, with a range of 16-76.

Regardless of whether their anxiety score was low or high, those who worried more had significantly better inhibitory control than those who worried less (P = .003), Dr. Beaudreau said. “So folks with high worry actually seemed to be doing better in terms of their inhibitory ability,” she added. “This is intriguing to me, because we assume that anxiety is affecting cognition, but worry seems to be doing something different.”

©gpointstudio/Thinkstock

High worry also predicted significantly better inhibitory control among individuals with both low and high depression scores (P = .03), she reported. For the word recall test, worry did not seem to affect performance in the absence of depression, but high worry predicted significantly better word recall among individuals with high depression scores (P = .009).

“These results suggest that psychiatric symptoms of anxiety and depression are modulated by worry severity, and it’s interesting that this finding was so consistent throughout the analyses,” Dr. Beaudreau said. Future studies should examine these relationships in groups of older psychiatric patients stratified by symptom severity rather than diagnosis, she added.

The work was supported by the Alzheimer’s Association and the Stanford/VA Alzheimer’s Center. Dr. Beaudreau had no relevant financial disclosures.

SAN FRANCISCO – Unexpectedly, worry predicted better cognitive performance among older adults with mild symptoms of anxiety and depression, according to a cross-sectional, community-based study.

“This just flies in the face of everything that we know about worry in the adult literature,” said Sherry A. Beaudreau, PhD, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University. The findings suggest that older worriers might score lower on some cognitive measures if their worry declines through treatment, she said at the 2016 congress of the International Psychogeriatric Association.

COURTESY DR. BEAUDREAU

Old age often is marked by mild symptoms of anxiety and depression that do not meet criteria for a psychiatric diagnosis, but nonetheless predict poorer cognitive performance and mild dementia, Dr. Beaudreau said. Recent work has linked anxiety to decreased attentional control, and late life depression, to slow information processing, delayed verbal memory, and other cognitive deficits. Emerging evidence also suggests that worry leads to worse performance on tests of inhibitory ability and delayed memory, Dr. Beaudreau added.

To further test these relationships, she and her associates studied 119 older adults who were living in the San Francisco Bay area between 2010 and 2012. They averaged 74 years of age (range, 65-91 years), 92% were non-Hispanic white, and 56% were women.

Most of the cohort performed well on the Rey Auditory Verbal Learning test, which assesses word recall after a delay of 20-30 minutes, and also scored above average on condition 3 of the Delis-Kaplan Executive Function System, which is a color word assessment of inhibitory control, Dr. Beaudreau reported. Individuals also tended to score low on the Beck Anxiety Inventory and the Beck Depressive Inventory II, with average scores of 3.7 (range, 0-29) and 5.6 (0-41), respectively. The mean score on the Penn State Worry Questionnaire was 37.7, with a range of 16-76.

Regardless of whether their anxiety score was low or high, those who worried more had significantly better inhibitory control than those who worried less (P = .003), Dr. Beaudreau said. “So folks with high worry actually seemed to be doing better in terms of their inhibitory ability,” she added. “This is intriguing to me, because we assume that anxiety is affecting cognition, but worry seems to be doing something different.”

©gpointstudio/Thinkstock

High worry also predicted significantly better inhibitory control among individuals with both low and high depression scores (P = .03), she reported. For the word recall test, worry did not seem to affect performance in the absence of depression, but high worry predicted significantly better word recall among individuals with high depression scores (P = .009).

“These results suggest that psychiatric symptoms of anxiety and depression are modulated by worry severity, and it’s interesting that this finding was so consistent throughout the analyses,” Dr. Beaudreau said. Future studies should examine these relationships in groups of older psychiatric patients stratified by symptom severity rather than diagnosis, she added.

The work was supported by the Alzheimer’s Association and the Stanford/VA Alzheimer’s Center. Dr. Beaudreau had no relevant financial disclosures.

SAN FRANCISCO – The patient, a man in his early 50s, smiled as he sang about flatulence. He seemed alert, relaxed, and aware of his wife and the neurologist in the room. Only the length and subject matter of his composition signaled a problem.

Two years later, this same patient was completely nonverbal – a classic case of frontotemporal dementia, said Howard Rosen, MD, a neurologist affiliated with the University of California, San Francisco. He and other experts discussed the disease at the 18th Congress of the International Psychogeriatric Association.

Frontotemporal dementia affects about 15-22 of every 100,000 individuals, and an additional 3-4 will be diagnosed in the next year, according to past studies (Int Rev Psychiatry. 2013 Apr;25[2]:130-7). This and other forms of dementia are often preceded by nondegenerative psychiatric syndromes, such as depression or anxiety, Dr. Rosen noted. “It is often unclear whether patients actually have that psychiatric disorder or symptoms of the disorder that are actually frontotemporal dementia,” he said. “Depression is most common and likely represents a misdiagnosis.”

Frontotemporal dementia also is often misdiagnosed as Alzheimer’s but differs in that about three-quarters of cases begin in midlife. This heightens the need for timely diagnosis and specialized services to support patients and caregivers, who may still have children at home, Dr. Rosen said. Unfortunately, such services are often lacking, he added.

Clinicians who treat patients with frontotemporal dementia encounter several “canonical variants” of the disease, he continued. These include nonfluent and semantic variants of primary progressive aphasia and a third behavioral variant. The nonfluent variant is characterized by frequent grammatical errors (agrammatism), hesitation over individual words, and speech apraxia. In contrast, patients with the semantic variant cannot name common objects, such as a ball or a cup, and only vaguely understand their use. Finally, those with the behavioral variant show “bizarre socioemotional changes,” including disinhibition and antisocial behavior, loss of empathy, “exceedingly poor” judgment, overeating, apathy, and hoarding and other compulsive behaviors, Dr. Rosen said.

Behavioral variant frontotemporal dementia can be especially difficult for family members, other experts said. Jan Oyebode, MD, of the University of Bradford, England, and her colleagues prospectively interviewed seven families and five patients with this form of dementia every 6-9 months to observe how the “lived experience” of the disease changed over time. Family members described struggling to understand emergent and worsening irritability, and lack of empathy in their loved one. “We saw this during the family interviews,” Dr. Oyebode added. “For example, one day a [caregiver with cancer] came back from chemotherapy, and her husband [the patient] turned to her and said something like, ‘you’re late. I’m hungry,’ and did not ask how the chemotherapy had gone. She had tears in her eyes. We had a number of examples like that.”

Another patient with behavioral variant frontotemporal dementia began “going off” on his children, something he had not done before, Dr. Oyebode said. Intellectually, he understood that frontotemporal dementia was causing his behavior, but he struggled to control his rage and could not empathize with his children’s pain, she added. “If you live with behavioral variant frontotemporal dementia, you may be only partially aware of changes in our empathy,” she added. “Because you don’t appreciate the way you have changed, you are puzzled by others’ reactions to you. And because you don’t understand the changes in your own abilities, you tend to attribute them to external factors and blame or avoid others.”

But over time, four of the five patients acknowledged that their families had the most insight into their changing cognition and behavior, and some clearly tried to control their behaviors, Dr. Oyebode said. Nonetheless, it is important to understand that even when patients factually accept their diagnosis, they tend not to “live it from the inside,” she emphasized. “Because you [the patient] feel the same, you may be somewhat bewildered by the changes in your life. But because you do not ‘feel’ the changes, you are able to accept them, even though they are dramatic.”

Such acceptance comes more easily when patients receive calm, direct feedback from family members, she also reported. Family members, too, valued open communication as key to their own process. “For families, there needed to be a [transition] from awareness of the dementia, to empathic understanding, to developing coping processes,” she said. For example, family members learned to help patients plan ahead, step by step, for outings and deconstruct tasks by working them out on a whiteboard, she said.

Studies like this one are important because there is little research on presenile dementia, Dr. Rosen said. “When you’re dealing with young-onset dementia, behavioral variant frontotemporal dementia has to be very prominent in your mind” – particularly because it progresses faster than do the other variants and about twice as fast as does Alzheimer’s disease. It can be easier to understand the symptomatic complexities of frontotemporal dementia by mapping them to specific neuroanatomy, Dr. Rosen added. Imaging is central to diagnosis, and indeed, frontotemporal dementia is the only neurodegenerative disease for which Medicare has approved FDG-PET scans as a diagnostic measure.

“What really differentiates frontotemporal dementia [from other dementias] is involvement of the orbital and medial lobes,” Dr. Rosen emphasized. “Think of Phineas Gage – the rod went right through the part of the brain we’re talking about.”

SAN FRANCISCO – The patient, a man in his early 50s, smiled as he sang about flatulence. He seemed alert, relaxed, and aware of his wife and the neurologist in the room. Only the length and subject matter of his composition signaled a problem.

Two years later, this same patient was completely nonverbal – a classic case of frontotemporal dementia, said Howard Rosen, MD, a neurologist affiliated with the University of California, San Francisco. He and other experts discussed the disease at the 18th Congress of the International Psychogeriatric Association.

Frontotemporal dementia affects about 15-22 of every 100,000 individuals, and an additional 3-4 will be diagnosed in the next year, according to past studies (Int Rev Psychiatry. 2013 Apr;25[2]:130-7). This and other forms of dementia are often preceded by nondegenerative psychiatric syndromes, such as depression or anxiety, Dr. Rosen noted. “It is often unclear whether patients actually have that psychiatric disorder or symptoms of the disorder that are actually frontotemporal dementia,” he said. “Depression is most common and likely represents a misdiagnosis.”

Frontotemporal dementia also is often misdiagnosed as Alzheimer’s but differs in that about three-quarters of cases begin in midlife. This heightens the need for timely diagnosis and specialized services to support patients and caregivers, who may still have children at home, Dr. Rosen said. Unfortunately, such services are often lacking, he added.

Clinicians who treat patients with frontotemporal dementia encounter several “canonical variants” of the disease, he continued. These include nonfluent and semantic variants of primary progressive aphasia and a third behavioral variant. The nonfluent variant is characterized by frequent grammatical errors (agrammatism), hesitation over individual words, and speech apraxia. In contrast, patients with the semantic variant cannot name common objects, such as a ball or a cup, and only vaguely understand their use. Finally, those with the behavioral variant show “bizarre socioemotional changes,” including disinhibition and antisocial behavior, loss of empathy, “exceedingly poor” judgment, overeating, apathy, and hoarding and other compulsive behaviors, Dr. Rosen said.

Behavioral variant frontotemporal dementia can be especially difficult for family members, other experts said. Jan Oyebode, MD, of the University of Bradford, England, and her colleagues prospectively interviewed seven families and five patients with this form of dementia every 6-9 months to observe how the “lived experience” of the disease changed over time. Family members described struggling to understand emergent and worsening irritability, and lack of empathy in their loved one. “We saw this during the family interviews,” Dr. Oyebode added. “For example, one day a [caregiver with cancer] came back from chemotherapy, and her husband [the patient] turned to her and said something like, ‘you’re late. I’m hungry,’ and did not ask how the chemotherapy had gone. She had tears in her eyes. We had a number of examples like that.”

Another patient with behavioral variant frontotemporal dementia began “going off” on his children, something he had not done before, Dr. Oyebode said. Intellectually, he understood that frontotemporal dementia was causing his behavior, but he struggled to control his rage and could not empathize with his children’s pain, she added. “If you live with behavioral variant frontotemporal dementia, you may be only partially aware of changes in our empathy,” she added. “Because you don’t appreciate the way you have changed, you are puzzled by others’ reactions to you. And because you don’t understand the changes in your own abilities, you tend to attribute them to external factors and blame or avoid others.”

But over time, four of the five patients acknowledged that their families had the most insight into their changing cognition and behavior, and some clearly tried to control their behaviors, Dr. Oyebode said. Nonetheless, it is important to understand that even when patients factually accept their diagnosis, they tend not to “live it from the inside,” she emphasized. “Because you [the patient] feel the same, you may be somewhat bewildered by the changes in your life. But because you do not ‘feel’ the changes, you are able to accept them, even though they are dramatic.”

Such acceptance comes more easily when patients receive calm, direct feedback from family members, she also reported. Family members, too, valued open communication as key to their own process. “For families, there needed to be a [transition] from awareness of the dementia, to empathic understanding, to developing coping processes,” she said. For example, family members learned to help patients plan ahead, step by step, for outings and deconstruct tasks by working them out on a whiteboard, she said.

Studies like this one are important because there is little research on presenile dementia, Dr. Rosen said. “When you’re dealing with young-onset dementia, behavioral variant frontotemporal dementia has to be very prominent in your mind” – particularly because it progresses faster than do the other variants and about twice as fast as does Alzheimer’s disease. It can be easier to understand the symptomatic complexities of frontotemporal dementia by mapping them to specific neuroanatomy, Dr. Rosen added. Imaging is central to diagnosis, and indeed, frontotemporal dementia is the only neurodegenerative disease for which Medicare has approved FDG-PET scans as a diagnostic measure.

“What really differentiates frontotemporal dementia [from other dementias] is involvement of the orbital and medial lobes,” Dr. Rosen emphasized. “Think of Phineas Gage – the rod went right through the part of the brain we’re talking about.”

SAN FRANCISCO – The patient, a man in his early 50s, smiled as he sang about flatulence. He seemed alert, relaxed, and aware of his wife and the neurologist in the room. Only the length and subject matter of his composition signaled a problem.

Two years later, this same patient was completely nonverbal – a classic case of frontotemporal dementia, said Howard Rosen, MD, a neurologist affiliated with the University of California, San Francisco. He and other experts discussed the disease at the 18th Congress of the International Psychogeriatric Association.

Frontotemporal dementia affects about 15-22 of every 100,000 individuals, and an additional 3-4 will be diagnosed in the next year, according to past studies (Int Rev Psychiatry. 2013 Apr;25[2]:130-7). This and other forms of dementia are often preceded by nondegenerative psychiatric syndromes, such as depression or anxiety, Dr. Rosen noted. “It is often unclear whether patients actually have that psychiatric disorder or symptoms of the disorder that are actually frontotemporal dementia,” he said. “Depression is most common and likely represents a misdiagnosis.”

Frontotemporal dementia also is often misdiagnosed as Alzheimer’s but differs in that about three-quarters of cases begin in midlife. This heightens the need for timely diagnosis and specialized services to support patients and caregivers, who may still have children at home, Dr. Rosen said. Unfortunately, such services are often lacking, he added.

Clinicians who treat patients with frontotemporal dementia encounter several “canonical variants” of the disease, he continued. These include nonfluent and semantic variants of primary progressive aphasia and a third behavioral variant. The nonfluent variant is characterized by frequent grammatical errors (agrammatism), hesitation over individual words, and speech apraxia. In contrast, patients with the semantic variant cannot name common objects, such as a ball or a cup, and only vaguely understand their use. Finally, those with the behavioral variant show “bizarre socioemotional changes,” including disinhibition and antisocial behavior, loss of empathy, “exceedingly poor” judgment, overeating, apathy, and hoarding and other compulsive behaviors, Dr. Rosen said.

Behavioral variant frontotemporal dementia can be especially difficult for family members, other experts said. Jan Oyebode, MD, of the University of Bradford, England, and her colleagues prospectively interviewed seven families and five patients with this form of dementia every 6-9 months to observe how the “lived experience” of the disease changed over time. Family members described struggling to understand emergent and worsening irritability, and lack of empathy in their loved one. “We saw this during the family interviews,” Dr. Oyebode added. “For example, one day a [caregiver with cancer] came back from chemotherapy, and her husband [the patient] turned to her and said something like, ‘you’re late. I’m hungry,’ and did not ask how the chemotherapy had gone. She had tears in her eyes. We had a number of examples like that.”

Another patient with behavioral variant frontotemporal dementia began “going off” on his children, something he had not done before, Dr. Oyebode said. Intellectually, he understood that frontotemporal dementia was causing his behavior, but he struggled to control his rage and could not empathize with his children’s pain, she added. “If you live with behavioral variant frontotemporal dementia, you may be only partially aware of changes in our empathy,” she added. “Because you don’t appreciate the way you have changed, you are puzzled by others’ reactions to you. And because you don’t understand the changes in your own abilities, you tend to attribute them to external factors and blame or avoid others.”

But over time, four of the five patients acknowledged that their families had the most insight into their changing cognition and behavior, and some clearly tried to control their behaviors, Dr. Oyebode said. Nonetheless, it is important to understand that even when patients factually accept their diagnosis, they tend not to “live it from the inside,” she emphasized. “Because you [the patient] feel the same, you may be somewhat bewildered by the changes in your life. But because you do not ‘feel’ the changes, you are able to accept them, even though they are dramatic.”

Such acceptance comes more easily when patients receive calm, direct feedback from family members, she also reported. Family members, too, valued open communication as key to their own process. “For families, there needed to be a [transition] from awareness of the dementia, to empathic understanding, to developing coping processes,” she said. For example, family members learned to help patients plan ahead, step by step, for outings and deconstruct tasks by working them out on a whiteboard, she said.

Studies like this one are important because there is little research on presenile dementia, Dr. Rosen said. “When you’re dealing with young-onset dementia, behavioral variant frontotemporal dementia has to be very prominent in your mind” – particularly because it progresses faster than do the other variants and about twice as fast as does Alzheimer’s disease. It can be easier to understand the symptomatic complexities of frontotemporal dementia by mapping them to specific neuroanatomy, Dr. Rosen added. Imaging is central to diagnosis, and indeed, frontotemporal dementia is the only neurodegenerative disease for which Medicare has approved FDG-PET scans as a diagnostic measure.

“What really differentiates frontotemporal dementia [from other dementias] is involvement of the orbital and medial lobes,” Dr. Rosen emphasized. “Think of Phineas Gage – the rod went right through the part of the brain we’re talking about.”