Geriatrics

Alzheimer’s disease is recognized as the most common cause of dementia, and many in the laity use the two terms almost interchangeably. However, there is increasing recognition that dementia in old age is a complex disorder, with mixed neuropathologies being the norm rather than the exception (Ann Neurol. 2018 Jan;83[1]:74-83).

Alzheimer’s disease (AD) and cerebrovascular pathologies are the most common, but another pathology is receiving increasing attention in relation to cognitive disorders in very old individuals – that related to the transactive response DNA binding protein of 43 kDa (TDP-43). This protein is expressed in most human tissues, including the brain, is localized mostly in nuclei, and binds to RNA and DNA as well as numerous proteins, with the role of regulating gene expression.

It has been known for nearly 2 decades that TDP-43 can become abnormally phosphorylated and translocated to the cytoplasm to produce a proteinopathy that forms the basis of a significant proportion of frontotemporal dementia (FTD) and the majority of amyotrophic lateral sclerosis. More recently, it has also been reported to be common in the brains of older people (over age 80 years) and associated with a cognitive disorder characterized by an amnestic picture that mimics AD. Since the protein deposition is predominantly in the limbic regions (amygdala, hippocampus, insula), it has been termed “‘limbic-predominant, age-related TDP-43 encephalopathy”, or LATE.

A recently convened international working group has published consensus criteria for LATE and provided guidelines for its staging. Community-based autopsy studies suggest that 20%-50% of people aged over 80 years have the neuropathologic change associated with LATE. The clinical presentation resembles amnestic dementia syndrome, much like AD. Both LATE and AD pathologies often occur in the same individual, but the relative predominance of one or the other varies greatly between individuals. The genetic risks of LATE overlap with those for FTD and AD, and other risk factors may also be shared with AD, which remains an area for further investigation. There are at present no specific biomarkers of LATE. It is associated with hippocampal sclerosis in some cases, which may be visible on MRI, but hippocampal sclerosis itself is not specific to TDP-43 pathology.

The LATE consensus working group report ^{(Brain. 2019 Apr 30. d}oi: 10.1093/brain/awz099⁾ underlines several gaps in our understanding of LATE and calls for systematic study of the causes of dementia – which may be nearly as common as AD in the very old. The report should be read widely and should remind us of the diverse pathologies that contribute to cognitive disorders, alone and in combination with one another.

Dr. Sachdev is Scientia Professor of Neuropsychiatry and codirector of the Center for Healthy Brain Aging at the University of New South Wales, Sydney; and clinical director of the Neuropsychiatric Institute at the Prince of Wales Hospital, also in Sydney. His major areas of research are drug-induced movement disorders, brain imaging, cognitive aging and dementia. Dr. Sachdev also served on the Neurocognitive Disorders Work Group of the DSM-5.

Alzheimer’s disease is recognized as the most common cause of dementia, and many in the laity use the two terms almost interchangeably. However, there is increasing recognition that dementia in old age is a complex disorder, with mixed neuropathologies being the norm rather than the exception (Ann Neurol. 2018 Jan;83[1]:74-83).

Alzheimer’s disease (AD) and cerebrovascular pathologies are the most common, but another pathology is receiving increasing attention in relation to cognitive disorders in very old individuals – that related to the transactive response DNA binding protein of 43 kDa (TDP-43). This protein is expressed in most human tissues, including the brain, is localized mostly in nuclei, and binds to RNA and DNA as well as numerous proteins, with the role of regulating gene expression.

It has been known for nearly 2 decades that TDP-43 can become abnormally phosphorylated and translocated to the cytoplasm to produce a proteinopathy that forms the basis of a significant proportion of frontotemporal dementia (FTD) and the majority of amyotrophic lateral sclerosis. More recently, it has also been reported to be common in the brains of older people (over age 80 years) and associated with a cognitive disorder characterized by an amnestic picture that mimics AD. Since the protein deposition is predominantly in the limbic regions (amygdala, hippocampus, insula), it has been termed “‘limbic-predominant, age-related TDP-43 encephalopathy”, or LATE.

A recently convened international working group has published consensus criteria for LATE and provided guidelines for its staging. Community-based autopsy studies suggest that 20%-50% of people aged over 80 years have the neuropathologic change associated with LATE. The clinical presentation resembles amnestic dementia syndrome, much like AD. Both LATE and AD pathologies often occur in the same individual, but the relative predominance of one or the other varies greatly between individuals. The genetic risks of LATE overlap with those for FTD and AD, and other risk factors may also be shared with AD, which remains an area for further investigation. There are at present no specific biomarkers of LATE. It is associated with hippocampal sclerosis in some cases, which may be visible on MRI, but hippocampal sclerosis itself is not specific to TDP-43 pathology.

The LATE consensus working group report ^{(Brain. 2019 Apr 30. d}oi: 10.1093/brain/awz099⁾ underlines several gaps in our understanding of LATE and calls for systematic study of the causes of dementia – which may be nearly as common as AD in the very old. The report should be read widely and should remind us of the diverse pathologies that contribute to cognitive disorders, alone and in combination with one another.

Dr. Sachdev is Scientia Professor of Neuropsychiatry and codirector of the Center for Healthy Brain Aging at the University of New South Wales, Sydney; and clinical director of the Neuropsychiatric Institute at the Prince of Wales Hospital, also in Sydney. His major areas of research are drug-induced movement disorders, brain imaging, cognitive aging and dementia. Dr. Sachdev also served on the Neurocognitive Disorders Work Group of the DSM-5.

Alzheimer’s disease is recognized as the most common cause of dementia, and many in the laity use the two terms almost interchangeably. However, there is increasing recognition that dementia in old age is a complex disorder, with mixed neuropathologies being the norm rather than the exception (Ann Neurol. 2018 Jan;83[1]:74-83).

Alzheimer’s disease (AD) and cerebrovascular pathologies are the most common, but another pathology is receiving increasing attention in relation to cognitive disorders in very old individuals – that related to the transactive response DNA binding protein of 43 kDa (TDP-43). This protein is expressed in most human tissues, including the brain, is localized mostly in nuclei, and binds to RNA and DNA as well as numerous proteins, with the role of regulating gene expression.

It has been known for nearly 2 decades that TDP-43 can become abnormally phosphorylated and translocated to the cytoplasm to produce a proteinopathy that forms the basis of a significant proportion of frontotemporal dementia (FTD) and the majority of amyotrophic lateral sclerosis. More recently, it has also been reported to be common in the brains of older people (over age 80 years) and associated with a cognitive disorder characterized by an amnestic picture that mimics AD. Since the protein deposition is predominantly in the limbic regions (amygdala, hippocampus, insula), it has been termed “‘limbic-predominant, age-related TDP-43 encephalopathy”, or LATE.

A recently convened international working group has published consensus criteria for LATE and provided guidelines for its staging. Community-based autopsy studies suggest that 20%-50% of people aged over 80 years have the neuropathologic change associated with LATE. The clinical presentation resembles amnestic dementia syndrome, much like AD. Both LATE and AD pathologies often occur in the same individual, but the relative predominance of one or the other varies greatly between individuals. The genetic risks of LATE overlap with those for FTD and AD, and other risk factors may also be shared with AD, which remains an area for further investigation. There are at present no specific biomarkers of LATE. It is associated with hippocampal sclerosis in some cases, which may be visible on MRI, but hippocampal sclerosis itself is not specific to TDP-43 pathology.

The LATE consensus working group report ^{(Brain. 2019 Apr 30. d}oi: 10.1093/brain/awz099⁾ underlines several gaps in our understanding of LATE and calls for systematic study of the causes of dementia – which may be nearly as common as AD in the very old. The report should be read widely and should remind us of the diverse pathologies that contribute to cognitive disorders, alone and in combination with one another.

Dr. Sachdev is Scientia Professor of Neuropsychiatry and codirector of the Center for Healthy Brain Aging at the University of New South Wales, Sydney; and clinical director of the Neuropsychiatric Institute at the Prince of Wales Hospital, also in Sydney. His major areas of research are drug-induced movement disorders, brain imaging, cognitive aging and dementia. Dr. Sachdev also served on the Neurocognitive Disorders Work Group of the DSM-5.

BIRMINGHAM, ENGLAND – Being diagnosed with rheumatoid arthritis at age 75 years or older made it less likely that patients would receive intensive therapy than their younger counterparts, but that did not mean that they were treated any less favorably overall, according to findings derived from the Early RA Network cohort.

“The claim that the elderly are treated less aggressively isn’t completely true throughout the whole treat-to-target strategy,” said Simone Howard of King’s College London at the British Society for Rheumatology annual conference. While older patients were less likely to receive intensive treatment up to 2 years after their diagnosis, there was a shorter delay between the onset of symptoms and the first outpatient visit to a rheumatology clinic.

When compared against patients who were younger than 65 years, those aged 65-74 years and 75 years and older were 11% (P = .02) and 15% (P = .02) more likely to have their first outpatient visit within 10 months.

Furthermore, no significant differences were seen between any age groups in the time to first initiation of a conventional synthetic disease-modifying antirheumatic drug (csDMARD), which averaged nearly 3 months after symptoms appeared.

Ms. Howard, who has previously worked at the European Medicines Agency, noted that, during her time at the EMA, “there was a real push to incorporate the elderly into the regulatory framework more. In parallel, there were also reports of the elderly being treated less aggressively. So the question was, where was that coming from?”

Similar therapeutic approaches are advocated for older and younger RA patients, and to look for any disparities, Ms. Howard and associates turned to the Early RA Network (ERAN) to “investigate potential treatment bias against the elderly.”

ERAN is a hospital-based inception cohort of 1,236 patients with early RA who were recruited across 23 centers in the United Kingdom and Ireland between 2002 and 2014.

Of 1,131 patients used in the analyses, 9.7% (n = 110) were 75 years or older, 21.5% (n = 243) were aged 65-74 years, and 68.8% (n = 778) were 65 years or younger. The majority (67.7%) of patients were female.

Patients aged 75 years and older were more likely to present with comorbidities than the youngest group, and they had higher health assessment questionnaire scores at baseline. However, they were no more likely to have high disease activity at the first visit, which was defined as a disease activity score in 28 joints of more than 5, and the older patients were 27% less likely to be seropositive (P = .004).

“It’s when we come to pharmacological aspects of care that we are seeing treatment biases,” Ms. Howard noted. Patients over 75 years were significantly more likely than the youngest age group to be treated with glucocorticoids or csDMARD monotherapy at 1 year, and 23% more likely to be on less aggressive therapy (P equal to or less than .0001). Aggressive therapy was defined as the use of a combination of csDMARDs or the use of biologic drugs.

At 2 years, the oldest patients were 46% more likely than those under 65 years to be on less-intensive therapies (P equal to or less than .0001), with those aged 65-74 years 19% more likely to be on glucocorticoid or csDMARD therapy (P = .005).

Factors such as patient choice and tolerance were not considered in the analyses and could be important, Ms. Howard conceded in response to a question after her presentation.

Another point raised was that perhaps the prescribing of aggressive therapy would rationally be different in someone diagnosed with RA at age 85 versus 65 because the duration of time that would be likely to be lived with accumulating joint damage would be shorter at the older age and that would be balanced against the other effects of the therapy. So, there may be important reasons in shared decision making that influenced the treatment choices other than the age of patients.

Ms. Howard agreed, noting that this demonstrated the need to be careful around the language used for defining what constituted aggressive or intensive therapy.

She and her coauthors reported no conflicts of interest.

SOURCE: Howard S et al. Rheumatology. 2019;58(suppl 3), Abstract 011.

BIRMINGHAM, ENGLAND – Being diagnosed with rheumatoid arthritis at age 75 years or older made it less likely that patients would receive intensive therapy than their younger counterparts, but that did not mean that they were treated any less favorably overall, according to findings derived from the Early RA Network cohort.

“The claim that the elderly are treated less aggressively isn’t completely true throughout the whole treat-to-target strategy,” said Simone Howard of King’s College London at the British Society for Rheumatology annual conference. While older patients were less likely to receive intensive treatment up to 2 years after their diagnosis, there was a shorter delay between the onset of symptoms and the first outpatient visit to a rheumatology clinic.

When compared against patients who were younger than 65 years, those aged 65-74 years and 75 years and older were 11% (P = .02) and 15% (P = .02) more likely to have their first outpatient visit within 10 months.

Furthermore, no significant differences were seen between any age groups in the time to first initiation of a conventional synthetic disease-modifying antirheumatic drug (csDMARD), which averaged nearly 3 months after symptoms appeared.

Ms. Howard, who has previously worked at the European Medicines Agency, noted that, during her time at the EMA, “there was a real push to incorporate the elderly into the regulatory framework more. In parallel, there were also reports of the elderly being treated less aggressively. So the question was, where was that coming from?”

Similar therapeutic approaches are advocated for older and younger RA patients, and to look for any disparities, Ms. Howard and associates turned to the Early RA Network (ERAN) to “investigate potential treatment bias against the elderly.”

ERAN is a hospital-based inception cohort of 1,236 patients with early RA who were recruited across 23 centers in the United Kingdom and Ireland between 2002 and 2014.

Of 1,131 patients used in the analyses, 9.7% (n = 110) were 75 years or older, 21.5% (n = 243) were aged 65-74 years, and 68.8% (n = 778) were 65 years or younger. The majority (67.7%) of patients were female.

Patients aged 75 years and older were more likely to present with comorbidities than the youngest group, and they had higher health assessment questionnaire scores at baseline. However, they were no more likely to have high disease activity at the first visit, which was defined as a disease activity score in 28 joints of more than 5, and the older patients were 27% less likely to be seropositive (P = .004).

“It’s when we come to pharmacological aspects of care that we are seeing treatment biases,” Ms. Howard noted. Patients over 75 years were significantly more likely than the youngest age group to be treated with glucocorticoids or csDMARD monotherapy at 1 year, and 23% more likely to be on less aggressive therapy (P equal to or less than .0001). Aggressive therapy was defined as the use of a combination of csDMARDs or the use of biologic drugs.

At 2 years, the oldest patients were 46% more likely than those under 65 years to be on less-intensive therapies (P equal to or less than .0001), with those aged 65-74 years 19% more likely to be on glucocorticoid or csDMARD therapy (P = .005).

Factors such as patient choice and tolerance were not considered in the analyses and could be important, Ms. Howard conceded in response to a question after her presentation.

Another point raised was that perhaps the prescribing of aggressive therapy would rationally be different in someone diagnosed with RA at age 85 versus 65 because the duration of time that would be likely to be lived with accumulating joint damage would be shorter at the older age and that would be balanced against the other effects of the therapy. So, there may be important reasons in shared decision making that influenced the treatment choices other than the age of patients.

Ms. Howard agreed, noting that this demonstrated the need to be careful around the language used for defining what constituted aggressive or intensive therapy.

She and her coauthors reported no conflicts of interest.

SOURCE: Howard S et al. Rheumatology. 2019;58(suppl 3), Abstract 011.

BIRMINGHAM, ENGLAND – Being diagnosed with rheumatoid arthritis at age 75 years or older made it less likely that patients would receive intensive therapy than their younger counterparts, but that did not mean that they were treated any less favorably overall, according to findings derived from the Early RA Network cohort.

“The claim that the elderly are treated less aggressively isn’t completely true throughout the whole treat-to-target strategy,” said Simone Howard of King’s College London at the British Society for Rheumatology annual conference. While older patients were less likely to receive intensive treatment up to 2 years after their diagnosis, there was a shorter delay between the onset of symptoms and the first outpatient visit to a rheumatology clinic.

When compared against patients who were younger than 65 years, those aged 65-74 years and 75 years and older were 11% (P = .02) and 15% (P = .02) more likely to have their first outpatient visit within 10 months.

Furthermore, no significant differences were seen between any age groups in the time to first initiation of a conventional synthetic disease-modifying antirheumatic drug (csDMARD), which averaged nearly 3 months after symptoms appeared.

Ms. Howard, who has previously worked at the European Medicines Agency, noted that, during her time at the EMA, “there was a real push to incorporate the elderly into the regulatory framework more. In parallel, there were also reports of the elderly being treated less aggressively. So the question was, where was that coming from?”

Similar therapeutic approaches are advocated for older and younger RA patients, and to look for any disparities, Ms. Howard and associates turned to the Early RA Network (ERAN) to “investigate potential treatment bias against the elderly.”

ERAN is a hospital-based inception cohort of 1,236 patients with early RA who were recruited across 23 centers in the United Kingdom and Ireland between 2002 and 2014.

Of 1,131 patients used in the analyses, 9.7% (n = 110) were 75 years or older, 21.5% (n = 243) were aged 65-74 years, and 68.8% (n = 778) were 65 years or younger. The majority (67.7%) of patients were female.

Patients aged 75 years and older were more likely to present with comorbidities than the youngest group, and they had higher health assessment questionnaire scores at baseline. However, they were no more likely to have high disease activity at the first visit, which was defined as a disease activity score in 28 joints of more than 5, and the older patients were 27% less likely to be seropositive (P = .004).

“It’s when we come to pharmacological aspects of care that we are seeing treatment biases,” Ms. Howard noted. Patients over 75 years were significantly more likely than the youngest age group to be treated with glucocorticoids or csDMARD monotherapy at 1 year, and 23% more likely to be on less aggressive therapy (P equal to or less than .0001). Aggressive therapy was defined as the use of a combination of csDMARDs or the use of biologic drugs.

At 2 years, the oldest patients were 46% more likely than those under 65 years to be on less-intensive therapies (P equal to or less than .0001), with those aged 65-74 years 19% more likely to be on glucocorticoid or csDMARD therapy (P = .005).

Factors such as patient choice and tolerance were not considered in the analyses and could be important, Ms. Howard conceded in response to a question after her presentation.

Another point raised was that perhaps the prescribing of aggressive therapy would rationally be different in someone diagnosed with RA at age 85 versus 65 because the duration of time that would be likely to be lived with accumulating joint damage would be shorter at the older age and that would be balanced against the other effects of the therapy. So, there may be important reasons in shared decision making that influenced the treatment choices other than the age of patients.

Ms. Howard agreed, noting that this demonstrated the need to be careful around the language used for defining what constituted aggressive or intensive therapy.

She and her coauthors reported no conflicts of interest.

SOURCE: Howard S et al. Rheumatology. 2019;58(suppl 3), Abstract 011.

WASHINGTON – More lonely elderly patients suffered from health symptoms and received very aggressive end of life care than nonlonely elderly patients, according to a study presented at the annual meeting of the Society of General Internal Medicine.

“Loneliness and social isolation are very common problems, especially in older Americans, and inflict about 30%-40% of older Americans. But while we know that this may have implications for their quality [of] life and may actually lead to premature death, we know very little about the end of life experience,” said Nauzley Abedini, MD, MSc, a hospitalist in internal medicine at the University of Michigan, Ann Arbor.

The study sought to determine the association between loneliness and end of life experience as measured by symptom burden, intensity of care, and advance care planning in adults. The pooled cohort study used data from the Health and Retirement Study (HRS) to analyze older Americans (aged 50 years or more) who died between 2004 and 2014. Investigators conducted postmortem “exit interviews” with the next of kin after each participant’s death. There were 2,896 participants included in the survey. Of these participants, 34% (942) were lonely; the remaining 1,954 of elderly adults were classified as nonlonely.

Loneliness was defined using the three-item Revised University of California, Los Angeles, Loneliness Scale score from a decedent’s last HRS interview prior to death. These items included feeling left out, feeling isolated, and lacking companionship. Investigators used this data to create a loneliness variable on previously established cutpoints for “lonely” and “nonlonely” participants. The data was used from the most recent survey prior to death.

Results showed more lonely older adults suffered from health symptoms in the last year of life, compared with nonlonely older adults (69.1% vs. 59.5%; odds ratio, 1.52; 95% confidence interval, 1.30-1.78). These symptoms included being troubled by pain, having difficulty breathing, experiencing severe fatigue, and having periodic confusion.

Patients with loneliness associated with intensity of health care at the end of life were more likely to die in a nursing home than at home, compared with nonlonely adults (OR, 1.68; 95% CI, 1.25-2.27). The lonely patients also were more likely to use life support during their last 2 years of life (OR, 1.41; 95% CI, 1.16-1.70).

“For clinicians, we need to identify end of life as an additional vulnerable time for people who are lonely. Currently, most of our interventions in terms of screening for loneliness are in the outpatient setting, but I would argue that working in hospitals, hospices, nursing homes, and community organizations, where these folks are living and dying, would be useful places to screen for this,” Dr. Abedini said.

The authors had no disclosures.

WASHINGTON – More lonely elderly patients suffered from health symptoms and received very aggressive end of life care than nonlonely elderly patients, according to a study presented at the annual meeting of the Society of General Internal Medicine.

“Loneliness and social isolation are very common problems, especially in older Americans, and inflict about 30%-40% of older Americans. But while we know that this may have implications for their quality [of] life and may actually lead to premature death, we know very little about the end of life experience,” said Nauzley Abedini, MD, MSc, a hospitalist in internal medicine at the University of Michigan, Ann Arbor.

The study sought to determine the association between loneliness and end of life experience as measured by symptom burden, intensity of care, and advance care planning in adults. The pooled cohort study used data from the Health and Retirement Study (HRS) to analyze older Americans (aged 50 years or more) who died between 2004 and 2014. Investigators conducted postmortem “exit interviews” with the next of kin after each participant’s death. There were 2,896 participants included in the survey. Of these participants, 34% (942) were lonely; the remaining 1,954 of elderly adults were classified as nonlonely.

Loneliness was defined using the three-item Revised University of California, Los Angeles, Loneliness Scale score from a decedent’s last HRS interview prior to death. These items included feeling left out, feeling isolated, and lacking companionship. Investigators used this data to create a loneliness variable on previously established cutpoints for “lonely” and “nonlonely” participants. The data was used from the most recent survey prior to death.

Results showed more lonely older adults suffered from health symptoms in the last year of life, compared with nonlonely older adults (69.1% vs. 59.5%; odds ratio, 1.52; 95% confidence interval, 1.30-1.78). These symptoms included being troubled by pain, having difficulty breathing, experiencing severe fatigue, and having periodic confusion.

Patients with loneliness associated with intensity of health care at the end of life were more likely to die in a nursing home than at home, compared with nonlonely adults (OR, 1.68; 95% CI, 1.25-2.27). The lonely patients also were more likely to use life support during their last 2 years of life (OR, 1.41; 95% CI, 1.16-1.70).

“For clinicians, we need to identify end of life as an additional vulnerable time for people who are lonely. Currently, most of our interventions in terms of screening for loneliness are in the outpatient setting, but I would argue that working in hospitals, hospices, nursing homes, and community organizations, where these folks are living and dying, would be useful places to screen for this,” Dr. Abedini said.

The authors had no disclosures.

WASHINGTON – More lonely elderly patients suffered from health symptoms and received very aggressive end of life care than nonlonely elderly patients, according to a study presented at the annual meeting of the Society of General Internal Medicine.

“Loneliness and social isolation are very common problems, especially in older Americans, and inflict about 30%-40% of older Americans. But while we know that this may have implications for their quality [of] life and may actually lead to premature death, we know very little about the end of life experience,” said Nauzley Abedini, MD, MSc, a hospitalist in internal medicine at the University of Michigan, Ann Arbor.

The study sought to determine the association between loneliness and end of life experience as measured by symptom burden, intensity of care, and advance care planning in adults. The pooled cohort study used data from the Health and Retirement Study (HRS) to analyze older Americans (aged 50 years or more) who died between 2004 and 2014. Investigators conducted postmortem “exit interviews” with the next of kin after each participant’s death. There were 2,896 participants included in the survey. Of these participants, 34% (942) were lonely; the remaining 1,954 of elderly adults were classified as nonlonely.

Loneliness was defined using the three-item Revised University of California, Los Angeles, Loneliness Scale score from a decedent’s last HRS interview prior to death. These items included feeling left out, feeling isolated, and lacking companionship. Investigators used this data to create a loneliness variable on previously established cutpoints for “lonely” and “nonlonely” participants. The data was used from the most recent survey prior to death.

Results showed more lonely older adults suffered from health symptoms in the last year of life, compared with nonlonely older adults (69.1% vs. 59.5%; odds ratio, 1.52; 95% confidence interval, 1.30-1.78). These symptoms included being troubled by pain, having difficulty breathing, experiencing severe fatigue, and having periodic confusion.

Patients with loneliness associated with intensity of health care at the end of life were more likely to die in a nursing home than at home, compared with nonlonely adults (OR, 1.68; 95% CI, 1.25-2.27). The lonely patients also were more likely to use life support during their last 2 years of life (OR, 1.41; 95% CI, 1.16-1.70).

“For clinicians, we need to identify end of life as an additional vulnerable time for people who are lonely. Currently, most of our interventions in terms of screening for loneliness are in the outpatient setting, but I would argue that working in hospitals, hospices, nursing homes, and community organizations, where these folks are living and dying, would be useful places to screen for this,” Dr. Abedini said.

The authors had no disclosures.

The Food and Drug Administration will now require that certain medications prescribed for insomnia carry a boxed warning because of associated complex sleep behaviors.

cpalmer@mdedge.com

The Food and Drug Administration will now require that certain medications prescribed for insomnia carry a boxed warning because of associated complex sleep behaviors.

cpalmer@mdedge.com

The Food and Drug Administration will now require that certain medications prescribed for insomnia carry a boxed warning because of associated complex sleep behaviors.

cpalmer@mdedge.com

A recent letter, “Hypoglycemia in the elderly: Watch for atypical symptoms” (J Fam Pract. 2019;68:116) provided an incomplete list of the letter’s authors. The list should have read: Jan Brož, MD, Jana Urbanová, MD, PhD, Prague, Czech Republic; Brian M. Frier, MD, BSc, Edinburgh, United Kingdom.

A recent letter, “Hypoglycemia in the elderly: Watch for atypical symptoms” (J Fam Pract. 2019;68:116) provided an incomplete list of the letter’s authors. The list should have read: Jan Brož, MD, Jana Urbanová, MD, PhD, Prague, Czech Republic; Brian M. Frier, MD, BSc, Edinburgh, United Kingdom.

A recent letter, “Hypoglycemia in the elderly: Watch for atypical symptoms” (J Fam Pract. 2019;68:116) provided an incomplete list of the letter’s authors. The list should have read: Jan Brož, MD, Jana Urbanová, MD, PhD, Prague, Czech Republic; Brian M. Frier, MD, BSc, Edinburgh, United Kingdom.

An international group of experts has proposed a new name, staging criteria, and recommendations for a recently recognized brain disorder that mimics Alzheimer’s disease and is marked by a proteinopathy caused by malformed transactive response DNA-binding protein of 43 kDa (TDP-43).

The term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in an effort to raise awareness and kick-start research into this “pathway to dementia,” the experts wrote in a report appearing in Brain.

“As there is currently no universally agreed-upon terminology or staging system for common age-related TDP-43 proteinopathy, this condition is understudied and not well recognized, even among investigators in the field of dementia research,” wrote the authors of the report, led by Peter T. Nelson, MD, PhD, of the University of Kentucky, Lexington.

LATE neuropathologic changes, associated with a progressive amnesia syndrome that mimics Alzheimer’s, are seen in more than 20% of individuals past the age of 80 years, according to large, community-based autopsy series. It coexists with Alzheimer’s disease in many patients, lowering the threshold for developing dementia, authors said.

The term LATE is designed to encompass several other terms related to TDP-43 pathology, including hippocampal sclerosis and cerebral age-related TDP-43 with sclerosis, Dr. Nelson and coauthors noted in their report.

The TDP-43 protein is encoded by the TARDBP gene and provides several functions related to the regulation of gene expression, the authors wrote.

Misfolded TDP-43 was known to play a causative role in amyotrophic lateral sclerosis and frontotemporal lobar degeneration, the authors noted, and then was also identified in the brains of older individuals with hippocampal sclerosis or Alzheimer’s disease neuropathologic changes.

The authors proposed a three-stage classification system for LATE neuropathologic change based on TDP-43 immunohistochemistry performed during routine autopsy evaluation of the amygdala, hippocampus, and middle frontal gyrus.

The amygdala is an area affected early in the course of the disease (Stage 1), whereas involvement of the hippocampus represents a more intermediate stage (Stage 2), and the middle frontal gyrus is more affected in advanced stages of the disease (Stage 3), according to the schema.

Five genes have been identified with risk alleles for LATE neuropathologic changes, authors said. Of note, several groups have found that the apolipoprotein E epsilon 4 (APOE4) allele, known to be a risk factor for Alzheimer’s disease neuropathologic changes and Lewy body disease, is also linked to increased risk of TDP-43 proteinopathy.

There are no established biomarkers specific to TDP-43 proteinopathy yet, which hampers development of clinical trials designed to test interventions to treat or prevent LATE, Dr. Nelson and colleagues said in their report.

LATE could also obscure the effects of potentially disease-modifying agents being tested in Alzheimer’s disease clinical trials, which can complicate the interpretation of study results, they added.

“Until there are biomarkers for LATE, clinical trials should be powered to account for TDP-43 proteinopathy,” they wrote.

Dr. Nelson and coauthors of the report in Brain reported no competing interests.

SOURCE: Nelson PT, et al. Brain. 2019 Apr 30. doi: 10.1093/brain/awz099

An international group of experts has proposed a new name, staging criteria, and recommendations for a recently recognized brain disorder that mimics Alzheimer’s disease and is marked by a proteinopathy caused by malformed transactive response DNA-binding protein of 43 kDa (TDP-43).

The term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in an effort to raise awareness and kick-start research into this “pathway to dementia,” the experts wrote in a report appearing in Brain.

“As there is currently no universally agreed-upon terminology or staging system for common age-related TDP-43 proteinopathy, this condition is understudied and not well recognized, even among investigators in the field of dementia research,” wrote the authors of the report, led by Peter T. Nelson, MD, PhD, of the University of Kentucky, Lexington.

LATE neuropathologic changes, associated with a progressive amnesia syndrome that mimics Alzheimer’s, are seen in more than 20% of individuals past the age of 80 years, according to large, community-based autopsy series. It coexists with Alzheimer’s disease in many patients, lowering the threshold for developing dementia, authors said.

The term LATE is designed to encompass several other terms related to TDP-43 pathology, including hippocampal sclerosis and cerebral age-related TDP-43 with sclerosis, Dr. Nelson and coauthors noted in their report.

The TDP-43 protein is encoded by the TARDBP gene and provides several functions related to the regulation of gene expression, the authors wrote.

Misfolded TDP-43 was known to play a causative role in amyotrophic lateral sclerosis and frontotemporal lobar degeneration, the authors noted, and then was also identified in the brains of older individuals with hippocampal sclerosis or Alzheimer’s disease neuropathologic changes.

The authors proposed a three-stage classification system for LATE neuropathologic change based on TDP-43 immunohistochemistry performed during routine autopsy evaluation of the amygdala, hippocampus, and middle frontal gyrus.

The amygdala is an area affected early in the course of the disease (Stage 1), whereas involvement of the hippocampus represents a more intermediate stage (Stage 2), and the middle frontal gyrus is more affected in advanced stages of the disease (Stage 3), according to the schema.

Five genes have been identified with risk alleles for LATE neuropathologic changes, authors said. Of note, several groups have found that the apolipoprotein E epsilon 4 (APOE4) allele, known to be a risk factor for Alzheimer’s disease neuropathologic changes and Lewy body disease, is also linked to increased risk of TDP-43 proteinopathy.

There are no established biomarkers specific to TDP-43 proteinopathy yet, which hampers development of clinical trials designed to test interventions to treat or prevent LATE, Dr. Nelson and colleagues said in their report.

LATE could also obscure the effects of potentially disease-modifying agents being tested in Alzheimer’s disease clinical trials, which can complicate the interpretation of study results, they added.

“Until there are biomarkers for LATE, clinical trials should be powered to account for TDP-43 proteinopathy,” they wrote.

Dr. Nelson and coauthors of the report in Brain reported no competing interests.

SOURCE: Nelson PT, et al. Brain. 2019 Apr 30. doi: 10.1093/brain/awz099

An international group of experts has proposed a new name, staging criteria, and recommendations for a recently recognized brain disorder that mimics Alzheimer’s disease and is marked by a proteinopathy caused by malformed transactive response DNA-binding protein of 43 kDa (TDP-43).

The term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in an effort to raise awareness and kick-start research into this “pathway to dementia,” the experts wrote in a report appearing in Brain.

“As there is currently no universally agreed-upon terminology or staging system for common age-related TDP-43 proteinopathy, this condition is understudied and not well recognized, even among investigators in the field of dementia research,” wrote the authors of the report, led by Peter T. Nelson, MD, PhD, of the University of Kentucky, Lexington.

LATE neuropathologic changes, associated with a progressive amnesia syndrome that mimics Alzheimer’s, are seen in more than 20% of individuals past the age of 80 years, according to large, community-based autopsy series. It coexists with Alzheimer’s disease in many patients, lowering the threshold for developing dementia, authors said.

The term LATE is designed to encompass several other terms related to TDP-43 pathology, including hippocampal sclerosis and cerebral age-related TDP-43 with sclerosis, Dr. Nelson and coauthors noted in their report.

The TDP-43 protein is encoded by the TARDBP gene and provides several functions related to the regulation of gene expression, the authors wrote.

Misfolded TDP-43 was known to play a causative role in amyotrophic lateral sclerosis and frontotemporal lobar degeneration, the authors noted, and then was also identified in the brains of older individuals with hippocampal sclerosis or Alzheimer’s disease neuropathologic changes.

The authors proposed a three-stage classification system for LATE neuropathologic change based on TDP-43 immunohistochemistry performed during routine autopsy evaluation of the amygdala, hippocampus, and middle frontal gyrus.

The amygdala is an area affected early in the course of the disease (Stage 1), whereas involvement of the hippocampus represents a more intermediate stage (Stage 2), and the middle frontal gyrus is more affected in advanced stages of the disease (Stage 3), according to the schema.

Five genes have been identified with risk alleles for LATE neuropathologic changes, authors said. Of note, several groups have found that the apolipoprotein E epsilon 4 (APOE4) allele, known to be a risk factor for Alzheimer’s disease neuropathologic changes and Lewy body disease, is also linked to increased risk of TDP-43 proteinopathy.

There are no established biomarkers specific to TDP-43 proteinopathy yet, which hampers development of clinical trials designed to test interventions to treat or prevent LATE, Dr. Nelson and colleagues said in their report.

LATE could also obscure the effects of potentially disease-modifying agents being tested in Alzheimer’s disease clinical trials, which can complicate the interpretation of study results, they added.

“Until there are biomarkers for LATE, clinical trials should be powered to account for TDP-43 proteinopathy,” they wrote.

Dr. Nelson and coauthors of the report in Brain reported no competing interests.

SOURCE: Nelson PT, et al. Brain. 2019 Apr 30. doi: 10.1093/brain/awz099

Being diagnosed with an elevated amyloid-beta biomarker that indicates greater risk of Alzheimer’s disease did not lead to increased consideration of physician-assisted death (PAD), according to an analysis of patients interviewed during clinical trials on cognitive decline.

“Our findings suggest that learning one’s amyloid imaging result does not change baseline attitudes regarding the acceptability of PAD,” wrote Emily A. Largent, PhD, of the department of medical ethics and health policy at the University of Pennsylvania, Philadelphia, and coauthors. The study was published as a research letter in JAMA Neurology.

Participants were recruited from two ongoing clinical trials, one of which included patients with elevated amyloid-beta (n = 50), whereas the other did not (n = 30). All participants completed an interview 4-12 weeks after receiving their biomarker results; 47 and 30 participants, respectively, also completed a follow-up interview at 12 months.

When asked whether they had considered PAD, nearly two-thirds of interviewees with the Alzheimer’s disease biomarker stated that they neither had nor would. Roughly one in five from that group said they would pursue PAD if they began to suffer from cognitive impairment or became a burden on others. Interviewees who did not have elevated amyloid beta, when asked whether a reversed result would have led to PAD or suicide, showed interest in roughly similar proportion to their at-risk counterparts.

The coauthors acknowledged the limitations of their study, including not asking about other end-of-life preferences or perceived quality of life for people with dementia. They also noted that, although their sample mirrors the populations of the two studies they drew from, “its homogeneity limits generalizability.” As such, they stressed that “further research is indicated to better understand end-of-life care preferences among people at increased risk for dementia.”

The study was supported by grants from the Alzheimer’s Association and the National Institute on Aging. One author reported receiving grants from those two organizations during the study; another reported receiving grants from Lilly and Novartis. No other conflicts of interest were reported.

SOURCE: Largent EA et al. JAMA Neurol. 2019 Apr 29. doi: 10.1001/jamaneurol.2019.0797.

Being diagnosed with an elevated amyloid-beta biomarker that indicates greater risk of Alzheimer’s disease did not lead to increased consideration of physician-assisted death (PAD), according to an analysis of patients interviewed during clinical trials on cognitive decline.

“Our findings suggest that learning one’s amyloid imaging result does not change baseline attitudes regarding the acceptability of PAD,” wrote Emily A. Largent, PhD, of the department of medical ethics and health policy at the University of Pennsylvania, Philadelphia, and coauthors. The study was published as a research letter in JAMA Neurology.

Participants were recruited from two ongoing clinical trials, one of which included patients with elevated amyloid-beta (n = 50), whereas the other did not (n = 30). All participants completed an interview 4-12 weeks after receiving their biomarker results; 47 and 30 participants, respectively, also completed a follow-up interview at 12 months.

When asked whether they had considered PAD, nearly two-thirds of interviewees with the Alzheimer’s disease biomarker stated that they neither had nor would. Roughly one in five from that group said they would pursue PAD if they began to suffer from cognitive impairment or became a burden on others. Interviewees who did not have elevated amyloid beta, when asked whether a reversed result would have led to PAD or suicide, showed interest in roughly similar proportion to their at-risk counterparts.

The coauthors acknowledged the limitations of their study, including not asking about other end-of-life preferences or perceived quality of life for people with dementia. They also noted that, although their sample mirrors the populations of the two studies they drew from, “its homogeneity limits generalizability.” As such, they stressed that “further research is indicated to better understand end-of-life care preferences among people at increased risk for dementia.”

The study was supported by grants from the Alzheimer’s Association and the National Institute on Aging. One author reported receiving grants from those two organizations during the study; another reported receiving grants from Lilly and Novartis. No other conflicts of interest were reported.

SOURCE: Largent EA et al. JAMA Neurol. 2019 Apr 29. doi: 10.1001/jamaneurol.2019.0797.

Being diagnosed with an elevated amyloid-beta biomarker that indicates greater risk of Alzheimer’s disease did not lead to increased consideration of physician-assisted death (PAD), according to an analysis of patients interviewed during clinical trials on cognitive decline.

“Our findings suggest that learning one’s amyloid imaging result does not change baseline attitudes regarding the acceptability of PAD,” wrote Emily A. Largent, PhD, of the department of medical ethics and health policy at the University of Pennsylvania, Philadelphia, and coauthors. The study was published as a research letter in JAMA Neurology.

Participants were recruited from two ongoing clinical trials, one of which included patients with elevated amyloid-beta (n = 50), whereas the other did not (n = 30). All participants completed an interview 4-12 weeks after receiving their biomarker results; 47 and 30 participants, respectively, also completed a follow-up interview at 12 months.

When asked whether they had considered PAD, nearly two-thirds of interviewees with the Alzheimer’s disease biomarker stated that they neither had nor would. Roughly one in five from that group said they would pursue PAD if they began to suffer from cognitive impairment or became a burden on others. Interviewees who did not have elevated amyloid beta, when asked whether a reversed result would have led to PAD or suicide, showed interest in roughly similar proportion to their at-risk counterparts.

The coauthors acknowledged the limitations of their study, including not asking about other end-of-life preferences or perceived quality of life for people with dementia. They also noted that, although their sample mirrors the populations of the two studies they drew from, “its homogeneity limits generalizability.” As such, they stressed that “further research is indicated to better understand end-of-life care preferences among people at increased risk for dementia.”

The study was supported by grants from the Alzheimer’s Association and the National Institute on Aging. One author reported receiving grants from those two organizations during the study; another reported receiving grants from Lilly and Novartis. No other conflicts of interest were reported.

SOURCE: Largent EA et al. JAMA Neurol. 2019 Apr 29. doi: 10.1001/jamaneurol.2019.0797.

Medical cannabis is safe, effective, and may reduce opioid use in elderly patients with chronic medical conditions, results of a recent retrospective chart review suggest. Treatment with medical cannabis improved pain, sleep, anxiety, and neuropathy in patients aged 75 years of age and older, and was associated with reduced use of opioids in about one-third of cases, according to authors of the study, which will be presented at the annual meeting of the American Academy of Neurology.

LPETTET/Getty Images

“Our findings are promising and can help fuel further research into medical marijuana as an additional option for this group of people who often have chronic conditions,” said lead investigator Laszlo Mechtler, MD, of Dent Neurologic Institute in Buffalo, N.Y., in a news release. However, additional randomized, placebo-controlled studies are needed to confirm results of this study, Dr. Mechtler added.

The chart review focused on 204 elderly patients who participated in New York State’s medical marijuana program and were followed in a neurologic outpatient setting. The cohort included 129 female and 75 male patients, ranging in age from 75 to 102 years, with a mean age of 81 years. The medical marijuana was taken by mouth as a liquid extract tincture, capsule, or in an electronic vaporizer.

With an average exposure time of 16.8 weeks, 69% of patients experienced symptomatic benefit, according to patient self-report. The most commonly reported benefit was relief of chronic pain in 49%, while improvements in sleep, neuropathy, and anxiety were reported in 18%, 15%, and 10%, respectively. Reductions in opioid pain medication were noted in about one-third of cases, they found.

While 34% of patients had adverse effects on medical marijuana, only 21% reported adverse effects after cannabinoid doses were adjusted, investigators said. Adverse effects led to discontinuation of medical cannabis in seven patients, or 3.4% of the overall cohort. Somnolence, disequilibrium, and gastrointestinal disturbance were the most common adverse effects, occurring in 13%, 7%, and 7% of patients, respectively. Euphoria was reported in 3% of patients.

Among patients who had no reported adverse effects, the most commonly used formulation was a balanced 1:1 tincture of tetrahydrocannabinol to cannabidiol, investigators said.

Further trials could explore optimal dosing of medical cannabis in elderly patients and shed more light on adverse effects such as somnolence and disequilibrium, according to Dr. Mechtler and colleagues.

The study was supported by the Dent Family Foundation.

SOURCE: Bargnes V et al. AAN 2019, Abstract P4.1-014.

Medical cannabis is safe, effective, and may reduce opioid use in elderly patients with chronic medical conditions, results of a recent retrospective chart review suggest. Treatment with medical cannabis improved pain, sleep, anxiety, and neuropathy in patients aged 75 years of age and older, and was associated with reduced use of opioids in about one-third of cases, according to authors of the study, which will be presented at the annual meeting of the American Academy of Neurology.

LPETTET/Getty Images

“Our findings are promising and can help fuel further research into medical marijuana as an additional option for this group of people who often have chronic conditions,” said lead investigator Laszlo Mechtler, MD, of Dent Neurologic Institute in Buffalo, N.Y., in a news release. However, additional randomized, placebo-controlled studies are needed to confirm results of this study, Dr. Mechtler added.

The chart review focused on 204 elderly patients who participated in New York State’s medical marijuana program and were followed in a neurologic outpatient setting. The cohort included 129 female and 75 male patients, ranging in age from 75 to 102 years, with a mean age of 81 years. The medical marijuana was taken by mouth as a liquid extract tincture, capsule, or in an electronic vaporizer.

With an average exposure time of 16.8 weeks, 69% of patients experienced symptomatic benefit, according to patient self-report. The most commonly reported benefit was relief of chronic pain in 49%, while improvements in sleep, neuropathy, and anxiety were reported in 18%, 15%, and 10%, respectively. Reductions in opioid pain medication were noted in about one-third of cases, they found.

While 34% of patients had adverse effects on medical marijuana, only 21% reported adverse effects after cannabinoid doses were adjusted, investigators said. Adverse effects led to discontinuation of medical cannabis in seven patients, or 3.4% of the overall cohort. Somnolence, disequilibrium, and gastrointestinal disturbance were the most common adverse effects, occurring in 13%, 7%, and 7% of patients, respectively. Euphoria was reported in 3% of patients.

Among patients who had no reported adverse effects, the most commonly used formulation was a balanced 1:1 tincture of tetrahydrocannabinol to cannabidiol, investigators said.

Further trials could explore optimal dosing of medical cannabis in elderly patients and shed more light on adverse effects such as somnolence and disequilibrium, according to Dr. Mechtler and colleagues.

The study was supported by the Dent Family Foundation.

SOURCE: Bargnes V et al. AAN 2019, Abstract P4.1-014.

Medical cannabis is safe, effective, and may reduce opioid use in elderly patients with chronic medical conditions, results of a recent retrospective chart review suggest. Treatment with medical cannabis improved pain, sleep, anxiety, and neuropathy in patients aged 75 years of age and older, and was associated with reduced use of opioids in about one-third of cases, according to authors of the study, which will be presented at the annual meeting of the American Academy of Neurology.

LPETTET/Getty Images

“Our findings are promising and can help fuel further research into medical marijuana as an additional option for this group of people who often have chronic conditions,” said lead investigator Laszlo Mechtler, MD, of Dent Neurologic Institute in Buffalo, N.Y., in a news release. However, additional randomized, placebo-controlled studies are needed to confirm results of this study, Dr. Mechtler added.

The chart review focused on 204 elderly patients who participated in New York State’s medical marijuana program and were followed in a neurologic outpatient setting. The cohort included 129 female and 75 male patients, ranging in age from 75 to 102 years, with a mean age of 81 years. The medical marijuana was taken by mouth as a liquid extract tincture, capsule, or in an electronic vaporizer.

With an average exposure time of 16.8 weeks, 69% of patients experienced symptomatic benefit, according to patient self-report. The most commonly reported benefit was relief of chronic pain in 49%, while improvements in sleep, neuropathy, and anxiety were reported in 18%, 15%, and 10%, respectively. Reductions in opioid pain medication were noted in about one-third of cases, they found.

While 34% of patients had adverse effects on medical marijuana, only 21% reported adverse effects after cannabinoid doses were adjusted, investigators said. Adverse effects led to discontinuation of medical cannabis in seven patients, or 3.4% of the overall cohort. Somnolence, disequilibrium, and gastrointestinal disturbance were the most common adverse effects, occurring in 13%, 7%, and 7% of patients, respectively. Euphoria was reported in 3% of patients.

Among patients who had no reported adverse effects, the most commonly used formulation was a balanced 1:1 tincture of tetrahydrocannabinol to cannabidiol, investigators said.

Further trials could explore optimal dosing of medical cannabis in elderly patients and shed more light on adverse effects such as somnolence and disequilibrium, according to Dr. Mechtler and colleagues.

The study was supported by the Dent Family Foundation.

SOURCE: Bargnes V et al. AAN 2019, Abstract P4.1-014.

New guidelines on treating obstructive sleep apnea with positive airway pressure include recommendations for using positive airway pressure (PAP) versus no therapy, using either continuous PAP (CPAP) or automatic PAP (APAP) for ongoing treatment, and providing educational interventions to patients starting PAP. The complete guidelines, issued by the American Academy of Sleep Medicine, were published in the Journal of Clinical Sleep Medicine.

The guidelines were driven by improvements in PAP adherence and device technology, wrote lead author Susheel P. Patil, MD, of Johns Hopkins University, Baltimore, and his colleagues.

The guidelines begin with a pair of Good Practice Statements to ensure effective and appropriate management of obstructive sleep apnea (OSA) in adults. First, “Treatment of OSA with PAP therapy should be based on a diagnosis of OSA established using objective sleep apnea testing.” Second, “Adequate follow-up, including troubleshooting and monitoring of objective efficacy and usage data to ensure adequate treatment and adherence, should occur following PAP therapy initiation and during treatment of OSA.”

The nine recommendations, approved by the AASM board of directors, include four strong recommendations that clinicians should follow under most circumstances, and five conditional recommendations that are suggested but lack strong clinical support for their appropriateness for all patients in all circumstances.

The first of the strong recommendations, for using PAP versus no therapy to treat adults with OSA and excessive sleepiness, was based on a high level of evidence from a meta-analysis of 38 randomized, controlled trials and the conclusion that the benefits of PAP outweighed the harms.

The second strong recommendation for using either CPAP or APAP for ongoing treatment was based on data from 26 trials that showed no clinically significant difference between the two. The third strong recommendation that PAP therapy be initiated using either APAP at home or in-laboratory PAP titration in adults with OSA and no significant comorbidities was supported by a meta-analysis of 10 trials that showed no clinically significant difference between at-home and laboratory initiation, and that each option has its benefits. The authors noted that “the majority of well-informed adult patients with OSA and without significant comorbidities would prefer initiation of PAP using the most rapid, convenient, and cost-effective strategy.” This comment supports the fourth strong recommendation for providing educational interventions to patients starting PAP.

The conditional recommendations include using PAP versus no therapy for adults with OSA and impaired quality of life related to poor sleep, such as insomnia, snoring, morning headaches, and daytime fatigue. Other conditional recommendations include using PAP versus no therapy for adults with OSA and comorbid hypertension, choosing CPAP or APAP over bilateral PAP for routine treatment of OSA in adults, providing behavioral interventions or troubleshooting during patients’ initial use of PAP, and using telemonitoring-guided interventions to monitor patients during their initial use of PAP.

“The ultimate judgment regarding any specific care must be made by the treating clinician and the patient, taking into consideration the individual circumstances of the patient, available treatment options, and resources,” the authors noted.

“When implementing the recommendations, providers should consider additional strategies that will maximize the individual patient’s comfort and adherence such as nasal/intranasal over oronasal mask interface and heated humidification,” they added.

The guidelines were developed by a task force commissioned by the AASM that included board-certified sleep specialists and experts in PAP use, and will be reviewed and updated as new information surfaces, the authors wrote.

Dr. Patil reported no financial conflicts; several coauthors reported conflicts that were managed by their not voting on guidelines related to those conflicts.

SOURCE: Patil SP et al. J Clin Sleep Med. 2018 Feb 15;15(2):335-43.

New guidelines on treating obstructive sleep apnea with positive airway pressure include recommendations for using positive airway pressure (PAP) versus no therapy, using either continuous PAP (CPAP) or automatic PAP (APAP) for ongoing treatment, and providing educational interventions to patients starting PAP. The complete guidelines, issued by the American Academy of Sleep Medicine, were published in the Journal of Clinical Sleep Medicine.

The guidelines were driven by improvements in PAP adherence and device technology, wrote lead author Susheel P. Patil, MD, of Johns Hopkins University, Baltimore, and his colleagues.

The guidelines begin with a pair of Good Practice Statements to ensure effective and appropriate management of obstructive sleep apnea (OSA) in adults. First, “Treatment of OSA with PAP therapy should be based on a diagnosis of OSA established using objective sleep apnea testing.” Second, “Adequate follow-up, including troubleshooting and monitoring of objective efficacy and usage data to ensure adequate treatment and adherence, should occur following PAP therapy initiation and during treatment of OSA.”

The nine recommendations, approved by the AASM board of directors, include four strong recommendations that clinicians should follow under most circumstances, and five conditional recommendations that are suggested but lack strong clinical support for their appropriateness for all patients in all circumstances.

The first of the strong recommendations, for using PAP versus no therapy to treat adults with OSA and excessive sleepiness, was based on a high level of evidence from a meta-analysis of 38 randomized, controlled trials and the conclusion that the benefits of PAP outweighed the harms.

The second strong recommendation for using either CPAP or APAP for ongoing treatment was based on data from 26 trials that showed no clinically significant difference between the two. The third strong recommendation that PAP therapy be initiated using either APAP at home or in-laboratory PAP titration in adults with OSA and no significant comorbidities was supported by a meta-analysis of 10 trials that showed no clinically significant difference between at-home and laboratory initiation, and that each option has its benefits. The authors noted that “the majority of well-informed adult patients with OSA and without significant comorbidities would prefer initiation of PAP using the most rapid, convenient, and cost-effective strategy.” This comment supports the fourth strong recommendation for providing educational interventions to patients starting PAP.

The conditional recommendations include using PAP versus no therapy for adults with OSA and impaired quality of life related to poor sleep, such as insomnia, snoring, morning headaches, and daytime fatigue. Other conditional recommendations include using PAP versus no therapy for adults with OSA and comorbid hypertension, choosing CPAP or APAP over bilateral PAP for routine treatment of OSA in adults, providing behavioral interventions or troubleshooting during patients’ initial use of PAP, and using telemonitoring-guided interventions to monitor patients during their initial use of PAP.

“The ultimate judgment regarding any specific care must be made by the treating clinician and the patient, taking into consideration the individual circumstances of the patient, available treatment options, and resources,” the authors noted.

“When implementing the recommendations, providers should consider additional strategies that will maximize the individual patient’s comfort and adherence such as nasal/intranasal over oronasal mask interface and heated humidification,” they added.

The guidelines were developed by a task force commissioned by the AASM that included board-certified sleep specialists and experts in PAP use, and will be reviewed and updated as new information surfaces, the authors wrote.

Dr. Patil reported no financial conflicts; several coauthors reported conflicts that were managed by their not voting on guidelines related to those conflicts.

SOURCE: Patil SP et al. J Clin Sleep Med. 2018 Feb 15;15(2):335-43.

New guidelines on treating obstructive sleep apnea with positive airway pressure include recommendations for using positive airway pressure (PAP) versus no therapy, using either continuous PAP (CPAP) or automatic PAP (APAP) for ongoing treatment, and providing educational interventions to patients starting PAP. The complete guidelines, issued by the American Academy of Sleep Medicine, were published in the Journal of Clinical Sleep Medicine.

The guidelines were driven by improvements in PAP adherence and device technology, wrote lead author Susheel P. Patil, MD, of Johns Hopkins University, Baltimore, and his colleagues.

The guidelines begin with a pair of Good Practice Statements to ensure effective and appropriate management of obstructive sleep apnea (OSA) in adults. First, “Treatment of OSA with PAP therapy should be based on a diagnosis of OSA established using objective sleep apnea testing.” Second, “Adequate follow-up, including troubleshooting and monitoring of objective efficacy and usage data to ensure adequate treatment and adherence, should occur following PAP therapy initiation and during treatment of OSA.”

The nine recommendations, approved by the AASM board of directors, include four strong recommendations that clinicians should follow under most circumstances, and five conditional recommendations that are suggested but lack strong clinical support for their appropriateness for all patients in all circumstances.

The first of the strong recommendations, for using PAP versus no therapy to treat adults with OSA and excessive sleepiness, was based on a high level of evidence from a meta-analysis of 38 randomized, controlled trials and the conclusion that the benefits of PAP outweighed the harms.

The second strong recommendation for using either CPAP or APAP for ongoing treatment was based on data from 26 trials that showed no clinically significant difference between the two. The third strong recommendation that PAP therapy be initiated using either APAP at home or in-laboratory PAP titration in adults with OSA and no significant comorbidities was supported by a meta-analysis of 10 trials that showed no clinically significant difference between at-home and laboratory initiation, and that each option has its benefits. The authors noted that “the majority of well-informed adult patients with OSA and without significant comorbidities would prefer initiation of PAP using the most rapid, convenient, and cost-effective strategy.” This comment supports the fourth strong recommendation for providing educational interventions to patients starting PAP.

The conditional recommendations include using PAP versus no therapy for adults with OSA and impaired quality of life related to poor sleep, such as insomnia, snoring, morning headaches, and daytime fatigue. Other conditional recommendations include using PAP versus no therapy for adults with OSA and comorbid hypertension, choosing CPAP or APAP over bilateral PAP for routine treatment of OSA in adults, providing behavioral interventions or troubleshooting during patients’ initial use of PAP, and using telemonitoring-guided interventions to monitor patients during their initial use of PAP.

“The ultimate judgment regarding any specific care must be made by the treating clinician and the patient, taking into consideration the individual circumstances of the patient, available treatment options, and resources,” the authors noted.

“When implementing the recommendations, providers should consider additional strategies that will maximize the individual patient’s comfort and adherence such as nasal/intranasal over oronasal mask interface and heated humidification,” they added.

The guidelines were developed by a task force commissioned by the AASM that included board-certified sleep specialists and experts in PAP use, and will be reviewed and updated as new information surfaces, the authors wrote.

Dr. Patil reported no financial conflicts; several coauthors reported conflicts that were managed by their not voting on guidelines related to those conflicts.

SOURCE: Patil SP et al. J Clin Sleep Med. 2018 Feb 15;15(2):335-43.

NEW ORLEANS – Patients ask their doctors whether dietary manipulation can extend lifespan and promote healthy aging. Right now, basic scientists and clinicians from many disciplines are teaming up under the broad umbrella of the field of geroscience to try to answer these and other concerns relevant to an aging population.

“The idea here is that, instead of going after each disease one at a time, as we do ... [we] instead go after disease vulnerability – and this is something that is shared, as a function of age,” Rozalyn Anderson, PhD, said of this new discipline. The work touches on disparate diseases such as cancer, dementia, and diabetes, she pointed out during a video interview at the annual meeting of the Endocrine Society.

“I separate these things out into ‘front-end’ and ‘back-end,’ work,” said Dr. Anderson of the University of Wisconsin-Madison’s aging and caloric restriction program. She explained that the caloric restriction she researches is back-end work to support the rapidly evolving field of nutritional modulation of aging.

When the basic science builds the framework, physicians and scientists can turn to front-end research, looking at humans to see which dietary manipulations are effective – and which are achievable.

“Take a paradigm that works, and then try to understand how it works,” said Dr. Anderson. “So [for example], we have this paradigm, and it’s tremendously effective in rodents. It’s effective in flies, in worms, in yeast, in spiders, in dogs – and in nonhuman primates.” Then, she and her team try to pull out clues “about the biology of aging itself, and what creates disease vulnerability as a function of age,” she said.

“The most important thing of all is that we can modify aging. This is not a foregone conclusion – no one would have believed it. But even in a primate species, we can change how they age. And the way in which we change is through nutrition.”

Dr Anderson added that “the paradigm of caloric restriction is tremendously effective, but [in reality], people are not going to do it.” It’s simply not practical to ask individuals to restrict calories by 30% or more over a lifespan, so “things such as intermittent fasting and time-restricted feeding come [into play] because they are achievable paradigms in normal human subjects.”

Dr. Anderson reported no relevant conflicts of interest or disclosures.

koakes@mdedge.com

NEW ORLEANS – Patients ask their doctors whether dietary manipulation can extend lifespan and promote healthy aging. Right now, basic scientists and clinicians from many disciplines are teaming up under the broad umbrella of the field of geroscience to try to answer these and other concerns relevant to an aging population.

“The idea here is that, instead of going after each disease one at a time, as we do ... [we] instead go after disease vulnerability – and this is something that is shared, as a function of age,” Rozalyn Anderson, PhD, said of this new discipline. The work touches on disparate diseases such as cancer, dementia, and diabetes, she pointed out during a video interview at the annual meeting of the Endocrine Society.

“I separate these things out into ‘front-end’ and ‘back-end,’ work,” said Dr. Anderson of the University of Wisconsin-Madison’s aging and caloric restriction program. She explained that the caloric restriction she researches is back-end work to support the rapidly evolving field of nutritional modulation of aging.

When the basic science builds the framework, physicians and scientists can turn to front-end research, looking at humans to see which dietary manipulations are effective – and which are achievable.

“Take a paradigm that works, and then try to understand how it works,” said Dr. Anderson. “So [for example], we have this paradigm, and it’s tremendously effective in rodents. It’s effective in flies, in worms, in yeast, in spiders, in dogs – and in nonhuman primates.” Then, she and her team try to pull out clues “about the biology of aging itself, and what creates disease vulnerability as a function of age,” she said.

“The most important thing of all is that we can modify aging. This is not a foregone conclusion – no one would have believed it. But even in a primate species, we can change how they age. And the way in which we change is through nutrition.”

Dr Anderson added that “the paradigm of caloric restriction is tremendously effective, but [in reality], people are not going to do it.” It’s simply not practical to ask individuals to restrict calories by 30% or more over a lifespan, so “things such as intermittent fasting and time-restricted feeding come [into play] because they are achievable paradigms in normal human subjects.”

Dr. Anderson reported no relevant conflicts of interest or disclosures.

koakes@mdedge.com

NEW ORLEANS – Patients ask their doctors whether dietary manipulation can extend lifespan and promote healthy aging. Right now, basic scientists and clinicians from many disciplines are teaming up under the broad umbrella of the field of geroscience to try to answer these and other concerns relevant to an aging population.

“The idea here is that, instead of going after each disease one at a time, as we do ... [we] instead go after disease vulnerability – and this is something that is shared, as a function of age,” Rozalyn Anderson, PhD, said of this new discipline. The work touches on disparate diseases such as cancer, dementia, and diabetes, she pointed out during a video interview at the annual meeting of the Endocrine Society.

“I separate these things out into ‘front-end’ and ‘back-end,’ work,” said Dr. Anderson of the University of Wisconsin-Madison’s aging and caloric restriction program. She explained that the caloric restriction she researches is back-end work to support the rapidly evolving field of nutritional modulation of aging.

When the basic science builds the framework, physicians and scientists can turn to front-end research, looking at humans to see which dietary manipulations are effective – and which are achievable.

“Take a paradigm that works, and then try to understand how it works,” said Dr. Anderson. “So [for example], we have this paradigm, and it’s tremendously effective in rodents. It’s effective in flies, in worms, in yeast, in spiders, in dogs – and in nonhuman primates.” Then, she and her team try to pull out clues “about the biology of aging itself, and what creates disease vulnerability as a function of age,” she said.

“The most important thing of all is that we can modify aging. This is not a foregone conclusion – no one would have believed it. But even in a primate species, we can change how they age. And the way in which we change is through nutrition.”

Dr Anderson added that “the paradigm of caloric restriction is tremendously effective, but [in reality], people are not going to do it.” It’s simply not practical to ask individuals to restrict calories by 30% or more over a lifespan, so “things such as intermittent fasting and time-restricted feeding come [into play] because they are achievable paradigms in normal human subjects.”

Dr. Anderson reported no relevant conflicts of interest or disclosures.

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