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Concussion effects may linger on MRI 1 year after athletes resume play
Among athletes with concussion, the effects of the injury on brain physiology may persist when they return to play and 1 year later.
MRI measures from 24 athletes with concussion significantly differed from those of controls at various time points and changed over time, according to a study published in Neurology. “Different aspects of brain physiology have different patterns of long-term recovery,” the researchers wrote.
While guidelines for safe return to play mainly rely on the resolution of symptoms, “the findings in this study indicate that more research is needed ... to better understand optimal recovery time from a biological standpoint,” wrote first author Nathan W. Churchill, PhD, a researcher at St. Michael’s Hospital in Toronto, and colleagues.
The study provides “evidence of incomplete or ongoing recovery” when athletes return to play, which could entail “a potential risk for long-term sequelae, given the evidence of worse outcomes if a second concussion occurs before recovery is complete,” according to the investigators. In addition,
To examine whether concussion-related brain changes dissipate by 1 year after athletes receive medical clearance to return to play, Dr. Churchill and colleagues analyzed MRI data from 24 college athletes with concussion and 122 control athletes without concussion.
Athletes with concussion were scanned within 1 week of the injury, at return to play a median of 27 days after the concussion, and 1 year after return to play. Control athletes were scanned before the start of the season. Participants’ sports included volleyball, hockey, soccer, football, rugby, basketball, lacrosse, and water polo. The participants had a mean age of about 20 years, and about half were women.
Athletes with concussion had elevated mean diffusivity within 1 week of injury, at return to play, and 1 year later, compared with controls. In athletes with concussion, cerebral blood flow was elevated soon after concussion, normal at return to play, and decreased 1 year later, relative to controls. Global functional connectivity increased and white matter fractional anisotropy decreased near the time of injury and at return to play, but these measures did not significantly differ from those of controls at 1 year.
The study did not capture MRI changes between return to play and 1 year later. In addition, MRI changes might be influenced by a lack of training before resuming play, as well as by exertion and subconcussive impacts after returning to play, the authors noted.
The Canadian Institutes of Health Research, the Canadian Institute for Military and Veterans Health Research, and Siemens Healthineers Canada supported the study. Siemens makes the MRI equipment used in the study. Dr. Churchill and colleagues had no relevant disclosures.
SOURCE: Churchill NW et al. Neurology. 2019 Oct 16. doi: 10.1212/WNL.0000000000008523.
Among athletes with concussion, the effects of the injury on brain physiology may persist when they return to play and 1 year later.
MRI measures from 24 athletes with concussion significantly differed from those of controls at various time points and changed over time, according to a study published in Neurology. “Different aspects of brain physiology have different patterns of long-term recovery,” the researchers wrote.
While guidelines for safe return to play mainly rely on the resolution of symptoms, “the findings in this study indicate that more research is needed ... to better understand optimal recovery time from a biological standpoint,” wrote first author Nathan W. Churchill, PhD, a researcher at St. Michael’s Hospital in Toronto, and colleagues.
The study provides “evidence of incomplete or ongoing recovery” when athletes return to play, which could entail “a potential risk for long-term sequelae, given the evidence of worse outcomes if a second concussion occurs before recovery is complete,” according to the investigators. In addition,
To examine whether concussion-related brain changes dissipate by 1 year after athletes receive medical clearance to return to play, Dr. Churchill and colleagues analyzed MRI data from 24 college athletes with concussion and 122 control athletes without concussion.
Athletes with concussion were scanned within 1 week of the injury, at return to play a median of 27 days after the concussion, and 1 year after return to play. Control athletes were scanned before the start of the season. Participants’ sports included volleyball, hockey, soccer, football, rugby, basketball, lacrosse, and water polo. The participants had a mean age of about 20 years, and about half were women.
Athletes with concussion had elevated mean diffusivity within 1 week of injury, at return to play, and 1 year later, compared with controls. In athletes with concussion, cerebral blood flow was elevated soon after concussion, normal at return to play, and decreased 1 year later, relative to controls. Global functional connectivity increased and white matter fractional anisotropy decreased near the time of injury and at return to play, but these measures did not significantly differ from those of controls at 1 year.
The study did not capture MRI changes between return to play and 1 year later. In addition, MRI changes might be influenced by a lack of training before resuming play, as well as by exertion and subconcussive impacts after returning to play, the authors noted.
The Canadian Institutes of Health Research, the Canadian Institute for Military and Veterans Health Research, and Siemens Healthineers Canada supported the study. Siemens makes the MRI equipment used in the study. Dr. Churchill and colleagues had no relevant disclosures.
SOURCE: Churchill NW et al. Neurology. 2019 Oct 16. doi: 10.1212/WNL.0000000000008523.
Among athletes with concussion, the effects of the injury on brain physiology may persist when they return to play and 1 year later.
MRI measures from 24 athletes with concussion significantly differed from those of controls at various time points and changed over time, according to a study published in Neurology. “Different aspects of brain physiology have different patterns of long-term recovery,” the researchers wrote.
While guidelines for safe return to play mainly rely on the resolution of symptoms, “the findings in this study indicate that more research is needed ... to better understand optimal recovery time from a biological standpoint,” wrote first author Nathan W. Churchill, PhD, a researcher at St. Michael’s Hospital in Toronto, and colleagues.
The study provides “evidence of incomplete or ongoing recovery” when athletes return to play, which could entail “a potential risk for long-term sequelae, given the evidence of worse outcomes if a second concussion occurs before recovery is complete,” according to the investigators. In addition,
To examine whether concussion-related brain changes dissipate by 1 year after athletes receive medical clearance to return to play, Dr. Churchill and colleagues analyzed MRI data from 24 college athletes with concussion and 122 control athletes without concussion.
Athletes with concussion were scanned within 1 week of the injury, at return to play a median of 27 days after the concussion, and 1 year after return to play. Control athletes were scanned before the start of the season. Participants’ sports included volleyball, hockey, soccer, football, rugby, basketball, lacrosse, and water polo. The participants had a mean age of about 20 years, and about half were women.
Athletes with concussion had elevated mean diffusivity within 1 week of injury, at return to play, and 1 year later, compared with controls. In athletes with concussion, cerebral blood flow was elevated soon after concussion, normal at return to play, and decreased 1 year later, relative to controls. Global functional connectivity increased and white matter fractional anisotropy decreased near the time of injury and at return to play, but these measures did not significantly differ from those of controls at 1 year.
The study did not capture MRI changes between return to play and 1 year later. In addition, MRI changes might be influenced by a lack of training before resuming play, as well as by exertion and subconcussive impacts after returning to play, the authors noted.
The Canadian Institutes of Health Research, the Canadian Institute for Military and Veterans Health Research, and Siemens Healthineers Canada supported the study. Siemens makes the MRI equipment used in the study. Dr. Churchill and colleagues had no relevant disclosures.
SOURCE: Churchill NW et al. Neurology. 2019 Oct 16. doi: 10.1212/WNL.0000000000008523.
FROM NEUROLOGY
Key clinical point: Among athletes with concussion, the effects of the injury on brain physiology may persist when they return to play and 1 year later.
Major finding: Athletes with concussion had elevated mean diffusivity within 1 week of injury, at return to play, and 1 year later, compared with controls. In athletes with concussion, cerebral blood flow was elevated soon after concussion, normal at return to play, and decreased 1 year later. Global functional connectivity increased and white matter fractional anisotropy decreased near the time of injury and at return to play, but these measures did not significantly differ from those of controls at 1 year.
Study details: An observational study of 24 college athletes with concussion.
Disclosures: The study was supported by the Canadian Institutes of Health Research, the Canadian Institute for Military and Veterans Health Research, and Siemens Healthineers Canada. Siemens makes the MRI equipment used in the study. The researchers had no relevant disclosures.
Source: Churchill NW et al. Neurology. 2019 Oct 16. doi: 10.1212/WNL.0000000000008523.
In utero Zika exposure can have delayed consequences
WASHINGTON – Evidence continues to mount that infants born to moms infected with Zika virus during pregnancy can have neurodevelopmental abnormalities as they age even if they showed no defects at birth, based on follow-up of 890 Colombian children tracked by epidemiologists from the U.S. Centers for Disease Control and Prevention.
Among the 890 neonates born to mothers apparently infected with Zika during pregnancy and followed for up to 2 years, 40 of the 852 (5%) without a detectable birth defect at delivery went on to show some type of neurodevelopmental sequelae during up to 24 months of age, Margaret Honein, PhD, said at an annual scientific meeting on infectious diseases.
In addition, among the children without birth defects at delivery who received follow-up examinations out to about 2 years, the incidence of “alerts” for possible neurodevelopmental issues was 15%-20% for each of the four domains studied (gross motor, fine motor, hearing and language, and personal and social functions), said Dr. Honein, an epidemiologist and chief of the birth defects branch of the CDC. In contrast, 17 of the 38 children (45%) followed who had identifiable birth defects at delivery also showed neurodevelopmental abnormalities when reexamined as long as 2 years after birth. These possible neurodevelopmental abnormalities, designated as alerts, were identified in comparison with a contemporaneous cohort of children born to uninfected mothers in the same regions of Colombia and assessed by the CDC researchers.
This cohort of children born to mothers who became infected with Zika virus during the 2016 Colombian epidemic will not undergo any planned, additional follow-up beyond the initial 2 years, Dr. Honein noted.
The findings she reported were consistent with observations from a much smaller cohort of 70 infants born to Colombian mothers infected with Zika virus while pregnant who had a normal head circumference and a normal clinical examination at delivery. When assessed once or twice 4-18 months after birth, these 70 infants showed an overall greater than one standard deviation (z-score) drop in their scores on the Warner Initial Developmental Evaluation of Adaptive and Functional Skills (WIDEA) metric by 12 months after birth and continuing out to 18 months, said Sarah B. Mulkey, MD, a fetal-neonatal neurologist at Children’s National Health System in Washington. These deficits were especially pronounced in the mobility and social cognition domains of the four-domain WIDEA metric. The social cognition domain is an important predictor of later problems with executive function and other neurologic disorders, Dr. Mulkey said while reporting her findings in a separate talk at the meeting. She acknowledged that the analysis was flawed by comparing the WIDEA outcomes of the Zika virus–exposed children to healthy children from either inner-city Chicago or Canada. Dr. Mulkey said that she and her associates plan to characterize a population of Zika virus–unexposed children in Colombia to use for future comparisons.
The study reported by Dr. Honein involved an enhanced surveillance program launched by the CDC in 2016 in three regions of Colombia and included 1,190 pregnancies accompanied by Zika symptoms in the mother and with a reported pregnancy outcome, including 1,185 live births. Nearly half of the Zika infections occurred during the first trimester, and 34% occurred during the second trimester. However, fewer than a third of the pregnant women underwent some type of laboratory testing to confirm their infection, either by serology or by a DNA-based assay, and of these 28% had a positive finding. Dr. Honein cautioned that many of the specimens that tested negative for Zika virus may have been false negatives.
The birth defects identified among the infants born from an apparently affected pregnancy included brain abnormalities, eye anomalies, and microcephaly, with 5% of the 1,185 live births showing one or more of these outcomes. The neurodevelopmental deficits identified during follow-up of 890 of the children out to 2 years included seizures; abnormalities of tone, movement, or swallowing; and impairments of vision or hearing.
WASHINGTON – Evidence continues to mount that infants born to moms infected with Zika virus during pregnancy can have neurodevelopmental abnormalities as they age even if they showed no defects at birth, based on follow-up of 890 Colombian children tracked by epidemiologists from the U.S. Centers for Disease Control and Prevention.
Among the 890 neonates born to mothers apparently infected with Zika during pregnancy and followed for up to 2 years, 40 of the 852 (5%) without a detectable birth defect at delivery went on to show some type of neurodevelopmental sequelae during up to 24 months of age, Margaret Honein, PhD, said at an annual scientific meeting on infectious diseases.
In addition, among the children without birth defects at delivery who received follow-up examinations out to about 2 years, the incidence of “alerts” for possible neurodevelopmental issues was 15%-20% for each of the four domains studied (gross motor, fine motor, hearing and language, and personal and social functions), said Dr. Honein, an epidemiologist and chief of the birth defects branch of the CDC. In contrast, 17 of the 38 children (45%) followed who had identifiable birth defects at delivery also showed neurodevelopmental abnormalities when reexamined as long as 2 years after birth. These possible neurodevelopmental abnormalities, designated as alerts, were identified in comparison with a contemporaneous cohort of children born to uninfected mothers in the same regions of Colombia and assessed by the CDC researchers.
This cohort of children born to mothers who became infected with Zika virus during the 2016 Colombian epidemic will not undergo any planned, additional follow-up beyond the initial 2 years, Dr. Honein noted.
The findings she reported were consistent with observations from a much smaller cohort of 70 infants born to Colombian mothers infected with Zika virus while pregnant who had a normal head circumference and a normal clinical examination at delivery. When assessed once or twice 4-18 months after birth, these 70 infants showed an overall greater than one standard deviation (z-score) drop in their scores on the Warner Initial Developmental Evaluation of Adaptive and Functional Skills (WIDEA) metric by 12 months after birth and continuing out to 18 months, said Sarah B. Mulkey, MD, a fetal-neonatal neurologist at Children’s National Health System in Washington. These deficits were especially pronounced in the mobility and social cognition domains of the four-domain WIDEA metric. The social cognition domain is an important predictor of later problems with executive function and other neurologic disorders, Dr. Mulkey said while reporting her findings in a separate talk at the meeting. She acknowledged that the analysis was flawed by comparing the WIDEA outcomes of the Zika virus–exposed children to healthy children from either inner-city Chicago or Canada. Dr. Mulkey said that she and her associates plan to characterize a population of Zika virus–unexposed children in Colombia to use for future comparisons.
The study reported by Dr. Honein involved an enhanced surveillance program launched by the CDC in 2016 in three regions of Colombia and included 1,190 pregnancies accompanied by Zika symptoms in the mother and with a reported pregnancy outcome, including 1,185 live births. Nearly half of the Zika infections occurred during the first trimester, and 34% occurred during the second trimester. However, fewer than a third of the pregnant women underwent some type of laboratory testing to confirm their infection, either by serology or by a DNA-based assay, and of these 28% had a positive finding. Dr. Honein cautioned that many of the specimens that tested negative for Zika virus may have been false negatives.
The birth defects identified among the infants born from an apparently affected pregnancy included brain abnormalities, eye anomalies, and microcephaly, with 5% of the 1,185 live births showing one or more of these outcomes. The neurodevelopmental deficits identified during follow-up of 890 of the children out to 2 years included seizures; abnormalities of tone, movement, or swallowing; and impairments of vision or hearing.
WASHINGTON – Evidence continues to mount that infants born to moms infected with Zika virus during pregnancy can have neurodevelopmental abnormalities as they age even if they showed no defects at birth, based on follow-up of 890 Colombian children tracked by epidemiologists from the U.S. Centers for Disease Control and Prevention.
Among the 890 neonates born to mothers apparently infected with Zika during pregnancy and followed for up to 2 years, 40 of the 852 (5%) without a detectable birth defect at delivery went on to show some type of neurodevelopmental sequelae during up to 24 months of age, Margaret Honein, PhD, said at an annual scientific meeting on infectious diseases.
In addition, among the children without birth defects at delivery who received follow-up examinations out to about 2 years, the incidence of “alerts” for possible neurodevelopmental issues was 15%-20% for each of the four domains studied (gross motor, fine motor, hearing and language, and personal and social functions), said Dr. Honein, an epidemiologist and chief of the birth defects branch of the CDC. In contrast, 17 of the 38 children (45%) followed who had identifiable birth defects at delivery also showed neurodevelopmental abnormalities when reexamined as long as 2 years after birth. These possible neurodevelopmental abnormalities, designated as alerts, were identified in comparison with a contemporaneous cohort of children born to uninfected mothers in the same regions of Colombia and assessed by the CDC researchers.
This cohort of children born to mothers who became infected with Zika virus during the 2016 Colombian epidemic will not undergo any planned, additional follow-up beyond the initial 2 years, Dr. Honein noted.
The findings she reported were consistent with observations from a much smaller cohort of 70 infants born to Colombian mothers infected with Zika virus while pregnant who had a normal head circumference and a normal clinical examination at delivery. When assessed once or twice 4-18 months after birth, these 70 infants showed an overall greater than one standard deviation (z-score) drop in their scores on the Warner Initial Developmental Evaluation of Adaptive and Functional Skills (WIDEA) metric by 12 months after birth and continuing out to 18 months, said Sarah B. Mulkey, MD, a fetal-neonatal neurologist at Children’s National Health System in Washington. These deficits were especially pronounced in the mobility and social cognition domains of the four-domain WIDEA metric. The social cognition domain is an important predictor of later problems with executive function and other neurologic disorders, Dr. Mulkey said while reporting her findings in a separate talk at the meeting. She acknowledged that the analysis was flawed by comparing the WIDEA outcomes of the Zika virus–exposed children to healthy children from either inner-city Chicago or Canada. Dr. Mulkey said that she and her associates plan to characterize a population of Zika virus–unexposed children in Colombia to use for future comparisons.
The study reported by Dr. Honein involved an enhanced surveillance program launched by the CDC in 2016 in three regions of Colombia and included 1,190 pregnancies accompanied by Zika symptoms in the mother and with a reported pregnancy outcome, including 1,185 live births. Nearly half of the Zika infections occurred during the first trimester, and 34% occurred during the second trimester. However, fewer than a third of the pregnant women underwent some type of laboratory testing to confirm their infection, either by serology or by a DNA-based assay, and of these 28% had a positive finding. Dr. Honein cautioned that many of the specimens that tested negative for Zika virus may have been false negatives.
The birth defects identified among the infants born from an apparently affected pregnancy included brain abnormalities, eye anomalies, and microcephaly, with 5% of the 1,185 live births showing one or more of these outcomes. The neurodevelopmental deficits identified during follow-up of 890 of the children out to 2 years included seizures; abnormalities of tone, movement, or swallowing; and impairments of vision or hearing.
REPORTING FROM ID WEEK 2019
Minimize blood pressure peaks, variability after stroke reperfusion
ST. LOUIS – Albuquerque. Investigators found that every 10–mm Hg increase in peak systolic pressure boosted the risk of in-hospital death 24% (P = .01) and reduced the chance of being discharged home or to a inpatient rehabilitation facility 13% (P = .03). Results were even stronger for peak mean arterial pressure, at 76% (P = .01) and 29% (P = .04), respectively; trends in the same direction for peak diastolic pressure were not statistically significant.
Also, every 10–mm Hg increase in blood pressure variability again increased the risk of dying in the hospital, whether it was systolic (33%; P = .002), diastolic (33%; P = .03), or mean arterial pressure variability (58%; P = .02). Higher variability also reduced the chance of being discharged home or to a rehab 10%-20%, but the findings, although close, were not statistically significant.
Neurologists generally do what they can to control blood pressure after stroke, and the study confirms the need to do that. What’s new is that the work was limited to reperfusion patients – intravenous thrombolysis with alteplase in 83.5%, mechanical thrombectomy in 60%, with some having both – which has not been the specific focus of much research.
“Be much more aggressive in terms of making sure the variability is limited and limiting the peaks,” especially within 24 hours of reperfusion, said lead investigator and stroke neurologist Dinesh Jillella, MD, of Emory University, Atlanta, at the annual meeting of the American Neurological Association. “We want to be much more aggressive [with these patients]; it might limit our worse outcomes,” Dr. Jillella said. He conducted the review while in training at the University of New Mexico.
What led to the study is that Dr. Jillella and colleagues noticed that similar reperfusion patients can have very different outcomes, and he wanted to find modifiable risk factors that could account for the differences. The study did not address why high peaks and variability lead to worse outcomes, but he said hemorrhagic conversion might play a role.
It is also possible that higher pressures could be a marker of bad outcomes, as opposed to a direct cause, but the findings were adjusted for two significant confounders: age and the National Institutes of Health Stroke Scale score, which were both significantly higher in patients who did not do well. But after adjustment, “we [still] found an independent association with blood pressures and worse outcomes,” he said.
Higher peak systolic pressures and variability were also associated with about a 15% lower odds of leaving the hospital with a modified Rankin Scale score of 3 or less, which means the patient has some moderate disability but is still able to walk without assistance.
Patients were 69 years old on average, and about 60% were men. The majority were white. About a third had a modified Rankin Scale score at or below 3 at discharge, and about two-thirds were discharged home or to a rehabilitation facility; 17% of patients died in the hospital.
Differences in antihypertensive regimens were not associated with outcomes on univariate analysis. Dr. Jillella said that, ideally, he would like to run a multicenter, prospective trial of blood pressure reduction targets after reperfusion.
There was no external funding, and Dr. Jillella didn’t have any relevant disclosures.
ST. LOUIS – Albuquerque. Investigators found that every 10–mm Hg increase in peak systolic pressure boosted the risk of in-hospital death 24% (P = .01) and reduced the chance of being discharged home or to a inpatient rehabilitation facility 13% (P = .03). Results were even stronger for peak mean arterial pressure, at 76% (P = .01) and 29% (P = .04), respectively; trends in the same direction for peak diastolic pressure were not statistically significant.
Also, every 10–mm Hg increase in blood pressure variability again increased the risk of dying in the hospital, whether it was systolic (33%; P = .002), diastolic (33%; P = .03), or mean arterial pressure variability (58%; P = .02). Higher variability also reduced the chance of being discharged home or to a rehab 10%-20%, but the findings, although close, were not statistically significant.
Neurologists generally do what they can to control blood pressure after stroke, and the study confirms the need to do that. What’s new is that the work was limited to reperfusion patients – intravenous thrombolysis with alteplase in 83.5%, mechanical thrombectomy in 60%, with some having both – which has not been the specific focus of much research.
“Be much more aggressive in terms of making sure the variability is limited and limiting the peaks,” especially within 24 hours of reperfusion, said lead investigator and stroke neurologist Dinesh Jillella, MD, of Emory University, Atlanta, at the annual meeting of the American Neurological Association. “We want to be much more aggressive [with these patients]; it might limit our worse outcomes,” Dr. Jillella said. He conducted the review while in training at the University of New Mexico.
What led to the study is that Dr. Jillella and colleagues noticed that similar reperfusion patients can have very different outcomes, and he wanted to find modifiable risk factors that could account for the differences. The study did not address why high peaks and variability lead to worse outcomes, but he said hemorrhagic conversion might play a role.
It is also possible that higher pressures could be a marker of bad outcomes, as opposed to a direct cause, but the findings were adjusted for two significant confounders: age and the National Institutes of Health Stroke Scale score, which were both significantly higher in patients who did not do well. But after adjustment, “we [still] found an independent association with blood pressures and worse outcomes,” he said.
Higher peak systolic pressures and variability were also associated with about a 15% lower odds of leaving the hospital with a modified Rankin Scale score of 3 or less, which means the patient has some moderate disability but is still able to walk without assistance.
Patients were 69 years old on average, and about 60% were men. The majority were white. About a third had a modified Rankin Scale score at or below 3 at discharge, and about two-thirds were discharged home or to a rehabilitation facility; 17% of patients died in the hospital.
Differences in antihypertensive regimens were not associated with outcomes on univariate analysis. Dr. Jillella said that, ideally, he would like to run a multicenter, prospective trial of blood pressure reduction targets after reperfusion.
There was no external funding, and Dr. Jillella didn’t have any relevant disclosures.
ST. LOUIS – Albuquerque. Investigators found that every 10–mm Hg increase in peak systolic pressure boosted the risk of in-hospital death 24% (P = .01) and reduced the chance of being discharged home or to a inpatient rehabilitation facility 13% (P = .03). Results were even stronger for peak mean arterial pressure, at 76% (P = .01) and 29% (P = .04), respectively; trends in the same direction for peak diastolic pressure were not statistically significant.
Also, every 10–mm Hg increase in blood pressure variability again increased the risk of dying in the hospital, whether it was systolic (33%; P = .002), diastolic (33%; P = .03), or mean arterial pressure variability (58%; P = .02). Higher variability also reduced the chance of being discharged home or to a rehab 10%-20%, but the findings, although close, were not statistically significant.
Neurologists generally do what they can to control blood pressure after stroke, and the study confirms the need to do that. What’s new is that the work was limited to reperfusion patients – intravenous thrombolysis with alteplase in 83.5%, mechanical thrombectomy in 60%, with some having both – which has not been the specific focus of much research.
“Be much more aggressive in terms of making sure the variability is limited and limiting the peaks,” especially within 24 hours of reperfusion, said lead investigator and stroke neurologist Dinesh Jillella, MD, of Emory University, Atlanta, at the annual meeting of the American Neurological Association. “We want to be much more aggressive [with these patients]; it might limit our worse outcomes,” Dr. Jillella said. He conducted the review while in training at the University of New Mexico.
What led to the study is that Dr. Jillella and colleagues noticed that similar reperfusion patients can have very different outcomes, and he wanted to find modifiable risk factors that could account for the differences. The study did not address why high peaks and variability lead to worse outcomes, but he said hemorrhagic conversion might play a role.
It is also possible that higher pressures could be a marker of bad outcomes, as opposed to a direct cause, but the findings were adjusted for two significant confounders: age and the National Institutes of Health Stroke Scale score, which were both significantly higher in patients who did not do well. But after adjustment, “we [still] found an independent association with blood pressures and worse outcomes,” he said.
Higher peak systolic pressures and variability were also associated with about a 15% lower odds of leaving the hospital with a modified Rankin Scale score of 3 or less, which means the patient has some moderate disability but is still able to walk without assistance.
Patients were 69 years old on average, and about 60% were men. The majority were white. About a third had a modified Rankin Scale score at or below 3 at discharge, and about two-thirds were discharged home or to a rehabilitation facility; 17% of patients died in the hospital.
Differences in antihypertensive regimens were not associated with outcomes on univariate analysis. Dr. Jillella said that, ideally, he would like to run a multicenter, prospective trial of blood pressure reduction targets after reperfusion.
There was no external funding, and Dr. Jillella didn’t have any relevant disclosures.
REPORTING FROM ANA 2019
Neurologists publish consensus statement on stridor in MSA
The statement was published Oct. 1 in Neurology. In addition to reviewing the literature on the topic and providing recommendations, the authors described several areas for future research.
MSA is a rare neurodegenerative disorder that entails autonomic failure, cerebellar ataxia, and parkinsonism. Laryngeal stridor has a high positive predictive value in the diagnosis of MSA, but consensus about its definition and clinical implications had not been established previously. The Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) delle Scienze Neurologiche di Bologna (Italy) convened a consensus conference of experts in 2017 to determine diagnostic criteria for stridor in MSA, define its prognostic value, suggest treatment options, and indicate subjects for future research. The neurologists reviewed studies of any design that reported original data. They based their statements on 34 published articles, most of which were class III or IV.
The authors defined stridor in MSA as “a strained, high-pitched, harsh respiratory sound, mainly inspiratory, caused by laryngeal dysfunction leading to narrowing of the rima glottidis.” Stridor may occur exclusively during sleep or during sleep and wakefulness. It may be recognized during a clinical examination, through witness report, or through an audio recording. Neurologists may consider laryngoscopy to exclude mechanical lesions or functional vocal cord abnormalities related to other neurologic conditions, wrote the authors. Drug-induced sleep endoscopy and video polysomnography also may be considered.
Whether stridor, or certain features of stridor, affects survival in MSA is uncertain. “Stridor within 3 years of motor or autonomic symptom onset may shorten survival,” according to the statement. “However, identification of stridor onset may be difficult.” Moreover, stridor during wakefulness is considered to reflect a more advanced stage of disease, compared with stridor during sleep. Although stridor can be distressing for the patient and his or her caregivers, its influence on health-related quality of life has yet to be determined, according to the statement.
Continuous positive airway pressure (CPAP) during sleep can be a useful symptomatic treatment and should be considered a first-line therapy for stridor, wrote the authors. Tracheostomy, another effective symptomatic treatment, bypasses upper-airway obstruction at the larynx. “Persistent and severe stridor may require tracheostomy,” according to the statement. It is not certain whether CPAP improves survival in patients with MSA and stridor, and tracheostomy may improve survival. The literature contains insufficient evidence about whether minimally invasive procedures or botulinum toxin injections are effective symptomatic treatments for stridor, wrote the authors.
During their review of the literature, the authors identified what they considered to be several research gaps. The diagnosis of stridor remains challenging, and investigators should develop a questionnaire for detecting stridor, they wrote. A smartphone application also could be developed to recognize stridor automatically. “The relationship between stridor and other breathing disorders (i.e., central apneas and breathing rate abnormalities) and their respective contributions to disease prognosis and survival should be determined through a multicenter prospective study,” according to the statement. Finally, randomized controlled trials comparing CPAP and tracheostomy for various degrees of stridor could guide physicians’ choice of treatment.
The IRCCS funded the study. One of the authors is a section editor for Neurology, and other authors reported receiving honoraria from various companies such as Novartis, Sanofi, and UCB.
The statement was published Oct. 1 in Neurology. In addition to reviewing the literature on the topic and providing recommendations, the authors described several areas for future research.
MSA is a rare neurodegenerative disorder that entails autonomic failure, cerebellar ataxia, and parkinsonism. Laryngeal stridor has a high positive predictive value in the diagnosis of MSA, but consensus about its definition and clinical implications had not been established previously. The Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) delle Scienze Neurologiche di Bologna (Italy) convened a consensus conference of experts in 2017 to determine diagnostic criteria for stridor in MSA, define its prognostic value, suggest treatment options, and indicate subjects for future research. The neurologists reviewed studies of any design that reported original data. They based their statements on 34 published articles, most of which were class III or IV.
The authors defined stridor in MSA as “a strained, high-pitched, harsh respiratory sound, mainly inspiratory, caused by laryngeal dysfunction leading to narrowing of the rima glottidis.” Stridor may occur exclusively during sleep or during sleep and wakefulness. It may be recognized during a clinical examination, through witness report, or through an audio recording. Neurologists may consider laryngoscopy to exclude mechanical lesions or functional vocal cord abnormalities related to other neurologic conditions, wrote the authors. Drug-induced sleep endoscopy and video polysomnography also may be considered.
Whether stridor, or certain features of stridor, affects survival in MSA is uncertain. “Stridor within 3 years of motor or autonomic symptom onset may shorten survival,” according to the statement. “However, identification of stridor onset may be difficult.” Moreover, stridor during wakefulness is considered to reflect a more advanced stage of disease, compared with stridor during sleep. Although stridor can be distressing for the patient and his or her caregivers, its influence on health-related quality of life has yet to be determined, according to the statement.
Continuous positive airway pressure (CPAP) during sleep can be a useful symptomatic treatment and should be considered a first-line therapy for stridor, wrote the authors. Tracheostomy, another effective symptomatic treatment, bypasses upper-airway obstruction at the larynx. “Persistent and severe stridor may require tracheostomy,” according to the statement. It is not certain whether CPAP improves survival in patients with MSA and stridor, and tracheostomy may improve survival. The literature contains insufficient evidence about whether minimally invasive procedures or botulinum toxin injections are effective symptomatic treatments for stridor, wrote the authors.
During their review of the literature, the authors identified what they considered to be several research gaps. The diagnosis of stridor remains challenging, and investigators should develop a questionnaire for detecting stridor, they wrote. A smartphone application also could be developed to recognize stridor automatically. “The relationship between stridor and other breathing disorders (i.e., central apneas and breathing rate abnormalities) and their respective contributions to disease prognosis and survival should be determined through a multicenter prospective study,” according to the statement. Finally, randomized controlled trials comparing CPAP and tracheostomy for various degrees of stridor could guide physicians’ choice of treatment.
The IRCCS funded the study. One of the authors is a section editor for Neurology, and other authors reported receiving honoraria from various companies such as Novartis, Sanofi, and UCB.
The statement was published Oct. 1 in Neurology. In addition to reviewing the literature on the topic and providing recommendations, the authors described several areas for future research.
MSA is a rare neurodegenerative disorder that entails autonomic failure, cerebellar ataxia, and parkinsonism. Laryngeal stridor has a high positive predictive value in the diagnosis of MSA, but consensus about its definition and clinical implications had not been established previously. The Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) delle Scienze Neurologiche di Bologna (Italy) convened a consensus conference of experts in 2017 to determine diagnostic criteria for stridor in MSA, define its prognostic value, suggest treatment options, and indicate subjects for future research. The neurologists reviewed studies of any design that reported original data. They based their statements on 34 published articles, most of which were class III or IV.
The authors defined stridor in MSA as “a strained, high-pitched, harsh respiratory sound, mainly inspiratory, caused by laryngeal dysfunction leading to narrowing of the rima glottidis.” Stridor may occur exclusively during sleep or during sleep and wakefulness. It may be recognized during a clinical examination, through witness report, or through an audio recording. Neurologists may consider laryngoscopy to exclude mechanical lesions or functional vocal cord abnormalities related to other neurologic conditions, wrote the authors. Drug-induced sleep endoscopy and video polysomnography also may be considered.
Whether stridor, or certain features of stridor, affects survival in MSA is uncertain. “Stridor within 3 years of motor or autonomic symptom onset may shorten survival,” according to the statement. “However, identification of stridor onset may be difficult.” Moreover, stridor during wakefulness is considered to reflect a more advanced stage of disease, compared with stridor during sleep. Although stridor can be distressing for the patient and his or her caregivers, its influence on health-related quality of life has yet to be determined, according to the statement.
Continuous positive airway pressure (CPAP) during sleep can be a useful symptomatic treatment and should be considered a first-line therapy for stridor, wrote the authors. Tracheostomy, another effective symptomatic treatment, bypasses upper-airway obstruction at the larynx. “Persistent and severe stridor may require tracheostomy,” according to the statement. It is not certain whether CPAP improves survival in patients with MSA and stridor, and tracheostomy may improve survival. The literature contains insufficient evidence about whether minimally invasive procedures or botulinum toxin injections are effective symptomatic treatments for stridor, wrote the authors.
During their review of the literature, the authors identified what they considered to be several research gaps. The diagnosis of stridor remains challenging, and investigators should develop a questionnaire for detecting stridor, they wrote. A smartphone application also could be developed to recognize stridor automatically. “The relationship between stridor and other breathing disorders (i.e., central apneas and breathing rate abnormalities) and their respective contributions to disease prognosis and survival should be determined through a multicenter prospective study,” according to the statement. Finally, randomized controlled trials comparing CPAP and tracheostomy for various degrees of stridor could guide physicians’ choice of treatment.
The IRCCS funded the study. One of the authors is a section editor for Neurology, and other authors reported receiving honoraria from various companies such as Novartis, Sanofi, and UCB.
FROM NEUROLOGY
MRI saves money, better than CT in acute stroke
ST. LOUIS – , according to a review from Johns Hopkins University, Baltimore.
MRI as the first scan leads to “a definitive diagnoses sooner and helps you manage the person more rapidly and appropriately, without negatively affecting outcomes even in stroke patients who receive endovascular therapy,” said neurologist and senior investigator Argye Hillis, MD, director of the Center of Excellence in Stroke Detection and Diagnosis at Hopkins. “Consider skipping the CT and getting an MRI, and get the MRI while they are still in the emergency room.”
Almost all emergency departments in the United States are set up to get a CT first, but MRI is known to be the better study, according to the researchers. MRI is much more sensitive to stroke, especially in the first 24 hours, and pinpoints the location and extent of the damage. It can detect causes of stroke invisible to CT, with no radiation, and rule out stroke entirely, whereas CT can rule out only intracranial bleeding. Increasingly in Europe, MRI is the first study in suspected stroke, and new EDs in the United States are being designed with an in-house MRI, or one nearby.
The ED at Hopkins’ main campus in downtown Baltimore already has an MRI, and uses it first whenever possible. The problem has been that MRI techs are available only during weekdays, so physicians have to default back to CT at night and on weekends. The impetus for the review, presented at the annual meeting of the American Neurological Association, was to see if savings from unnecessary admissions prevented by MRI would be enough to offset the cost of around-the-clock staffing for the MRI scanner.
Dr. Hillis and her team reviewed 320 patients with suspected ischemic stroke who were seen at the main campus in 2018 and had CT in the ED, and then definitive diagnosis by MRI, which is the usual approach in most U.S. hospitals.
A total of 134 patients had a final diagnosis on MRI that did not justify admission; techs were available to give 75 of them MRIs in the ED after the CT, and those patients were sent home. Techs were not available, however, for 59 patients and since the CT was not able to rule out stroke, those patients were admitted. The cost of those 59 admissions was $814,016.
The cost of the noncontrast CTs for the 75 patients who were sent home after definitive MRI imaging was $28,050, plus an additional $46,072 for those who had CT neck/head angiograms. Altogether, skipping the CT and going straight to the MRI would have saved Hopkins $888,138 in 2018, enough to cover round-the-clock MRI staffing in the ED, which is now the plan at the main campus.
Once the facility moves to 24-and-7 MRI coverage, the next step in the project is to compare stroke outcomes with Johns Hopkins Bayview Medical Center, also in Baltimore, which will continue to do CT first. “We know MRI first is cheaper. We want to see if we have better outcomes. If we find they’re much better, I think many hospitals will say it’s worth the 5 minutes longer it takes to get to the MRI scanner,” Dr. Hillis said.
Stroke mimics among the 134 patients included peripheral nerve palsy and migraine, but also people simply faking it for a hot meal and a warm bed. “Its pretty common, unfortunately,” she said.
The average age for stroke admissions at Hopkins is 55 years, with as many men as women.
There was no industry funding, and Dr. Hillis didn’t have any relevant disclosures.
ST. LOUIS – , according to a review from Johns Hopkins University, Baltimore.
MRI as the first scan leads to “a definitive diagnoses sooner and helps you manage the person more rapidly and appropriately, without negatively affecting outcomes even in stroke patients who receive endovascular therapy,” said neurologist and senior investigator Argye Hillis, MD, director of the Center of Excellence in Stroke Detection and Diagnosis at Hopkins. “Consider skipping the CT and getting an MRI, and get the MRI while they are still in the emergency room.”
Almost all emergency departments in the United States are set up to get a CT first, but MRI is known to be the better study, according to the researchers. MRI is much more sensitive to stroke, especially in the first 24 hours, and pinpoints the location and extent of the damage. It can detect causes of stroke invisible to CT, with no radiation, and rule out stroke entirely, whereas CT can rule out only intracranial bleeding. Increasingly in Europe, MRI is the first study in suspected stroke, and new EDs in the United States are being designed with an in-house MRI, or one nearby.
The ED at Hopkins’ main campus in downtown Baltimore already has an MRI, and uses it first whenever possible. The problem has been that MRI techs are available only during weekdays, so physicians have to default back to CT at night and on weekends. The impetus for the review, presented at the annual meeting of the American Neurological Association, was to see if savings from unnecessary admissions prevented by MRI would be enough to offset the cost of around-the-clock staffing for the MRI scanner.
Dr. Hillis and her team reviewed 320 patients with suspected ischemic stroke who were seen at the main campus in 2018 and had CT in the ED, and then definitive diagnosis by MRI, which is the usual approach in most U.S. hospitals.
A total of 134 patients had a final diagnosis on MRI that did not justify admission; techs were available to give 75 of them MRIs in the ED after the CT, and those patients were sent home. Techs were not available, however, for 59 patients and since the CT was not able to rule out stroke, those patients were admitted. The cost of those 59 admissions was $814,016.
The cost of the noncontrast CTs for the 75 patients who were sent home after definitive MRI imaging was $28,050, plus an additional $46,072 for those who had CT neck/head angiograms. Altogether, skipping the CT and going straight to the MRI would have saved Hopkins $888,138 in 2018, enough to cover round-the-clock MRI staffing in the ED, which is now the plan at the main campus.
Once the facility moves to 24-and-7 MRI coverage, the next step in the project is to compare stroke outcomes with Johns Hopkins Bayview Medical Center, also in Baltimore, which will continue to do CT first. “We know MRI first is cheaper. We want to see if we have better outcomes. If we find they’re much better, I think many hospitals will say it’s worth the 5 minutes longer it takes to get to the MRI scanner,” Dr. Hillis said.
Stroke mimics among the 134 patients included peripheral nerve palsy and migraine, but also people simply faking it for a hot meal and a warm bed. “Its pretty common, unfortunately,” she said.
The average age for stroke admissions at Hopkins is 55 years, with as many men as women.
There was no industry funding, and Dr. Hillis didn’t have any relevant disclosures.
ST. LOUIS – , according to a review from Johns Hopkins University, Baltimore.
MRI as the first scan leads to “a definitive diagnoses sooner and helps you manage the person more rapidly and appropriately, without negatively affecting outcomes even in stroke patients who receive endovascular therapy,” said neurologist and senior investigator Argye Hillis, MD, director of the Center of Excellence in Stroke Detection and Diagnosis at Hopkins. “Consider skipping the CT and getting an MRI, and get the MRI while they are still in the emergency room.”
Almost all emergency departments in the United States are set up to get a CT first, but MRI is known to be the better study, according to the researchers. MRI is much more sensitive to stroke, especially in the first 24 hours, and pinpoints the location and extent of the damage. It can detect causes of stroke invisible to CT, with no radiation, and rule out stroke entirely, whereas CT can rule out only intracranial bleeding. Increasingly in Europe, MRI is the first study in suspected stroke, and new EDs in the United States are being designed with an in-house MRI, or one nearby.
The ED at Hopkins’ main campus in downtown Baltimore already has an MRI, and uses it first whenever possible. The problem has been that MRI techs are available only during weekdays, so physicians have to default back to CT at night and on weekends. The impetus for the review, presented at the annual meeting of the American Neurological Association, was to see if savings from unnecessary admissions prevented by MRI would be enough to offset the cost of around-the-clock staffing for the MRI scanner.
Dr. Hillis and her team reviewed 320 patients with suspected ischemic stroke who were seen at the main campus in 2018 and had CT in the ED, and then definitive diagnosis by MRI, which is the usual approach in most U.S. hospitals.
A total of 134 patients had a final diagnosis on MRI that did not justify admission; techs were available to give 75 of them MRIs in the ED after the CT, and those patients were sent home. Techs were not available, however, for 59 patients and since the CT was not able to rule out stroke, those patients were admitted. The cost of those 59 admissions was $814,016.
The cost of the noncontrast CTs for the 75 patients who were sent home after definitive MRI imaging was $28,050, plus an additional $46,072 for those who had CT neck/head angiograms. Altogether, skipping the CT and going straight to the MRI would have saved Hopkins $888,138 in 2018, enough to cover round-the-clock MRI staffing in the ED, which is now the plan at the main campus.
Once the facility moves to 24-and-7 MRI coverage, the next step in the project is to compare stroke outcomes with Johns Hopkins Bayview Medical Center, also in Baltimore, which will continue to do CT first. “We know MRI first is cheaper. We want to see if we have better outcomes. If we find they’re much better, I think many hospitals will say it’s worth the 5 minutes longer it takes to get to the MRI scanner,” Dr. Hillis said.
Stroke mimics among the 134 patients included peripheral nerve palsy and migraine, but also people simply faking it for a hot meal and a warm bed. “Its pretty common, unfortunately,” she said.
The average age for stroke admissions at Hopkins is 55 years, with as many men as women.
There was no industry funding, and Dr. Hillis didn’t have any relevant disclosures.
REPORTING FROM ANA 2019
Key clinical point: Getting an MRI first for suspected stroke, instead of a CT, saves money by avoiding unnecessary admissions and might lead to better outcomes.
Major finding: An MRI-first approach at a busy ED in downtown Baltimore would have saved $888,138 in 1 year.
Study details: Review of 320 patients with suspected ischemic strokes.
Disclosures: There was no industry funding, and the senior investigator did not have any relevant disclosures.
Source: Sherry E et al. ANA 2019. Abstract M123.
Retraining Working Memory to Reduce PTSD Symptoms
Working memory (WM)—the function that allows us to temporarily store information and use it for cognitive tasks like learning, reasoning, and comprehension—is thought to play an important role in managing anxiety and intrusive symptoms of posttraumatic stress disorder (PTSD). Researchers have found inefficient filtering of threatening material from WM and increased storage of task-irrelevant threat distractors are associated with elevated anxiety. Thus, veterans with high levels of anxiety may disproportionately allocate cognitive resources toward threatening stimuli, and have trouble keeping threatening thoughts from entering WM and staying there. People with PTSD also have been shown to have problems using WM in emotional contexts, making it hard for them to deal with stressful situations in work and personal life. Some research has suggested that WM training that incorporates affective stimuli may increase the ability to use WM in emotional contexts. In a pilot study, researchers from Medical College of Wisconsin and University of Wisconsin-Milwaukee expanded on that possibility by testing 2 kinds of WM training in 21 veterans with elevated PTSD symptoms.
Participants completed a pretest, 15 sessions of at-home computerized training, a posttest, and a 1-month follow-up session. The computerized tests included tasks to measure WM capacity, such as solving math questions while trying to remember a set of unrelated numbers. The participants were then assigned to active emotional WM training (n-back) or control emotional WM training (1-back). The n-back training involved constant updating of information stored in WM and shifting between visual and auditory stimuli using 8 different faces and 8 different negative words. The training sessions started at the 1-back level and increased in difficulty level by level with performance with > 95% accuracy, or were scaled back with performance with < 75% accuracy. The control training was the same but consisted only of 1 level.
Overall, the researchers say, contrary to their hypothesis, they did not find a significant difference in results from the 2 groups. But they did find that both trainings had an overall “significant and sizable” impact on PTSD symptoms in both groups: 73% of the n-back group and 60% of the 1-back group had a reduction of ≥ 10 points on the PTSD Checklist total scores, which the researchers say is considered a clinically meaningful change. Moreover, both groups showed a clinically meaningful reduction in symptoms at follow-up: 55% and 40%, respectively.
It was interesting, the researchers say, that both groups showed improvement, especially with the 1-back intervention, which they had used as a “minimally effective” control condition. They also note that, anecdotally, the participants found both interventions “quite challenging.” It may be that in this population even the 1-back intervention is enough to detectably reduce symptoms, the researchers say. They were also encouraged to see that the n-back condition (marginally) outperformed the 1-back condition in improving reexperiencing symptoms, theoretically the most relevant training target of WM-focused intervention. The researchers believe that their study yields useful pilot data, suggesting that n-back training can have a clinical impact primarily by reducing reexperiencing symptoms, which are highly likely to indicate the presence of impaired WM functioning.
Working memory (WM)—the function that allows us to temporarily store information and use it for cognitive tasks like learning, reasoning, and comprehension—is thought to play an important role in managing anxiety and intrusive symptoms of posttraumatic stress disorder (PTSD). Researchers have found inefficient filtering of threatening material from WM and increased storage of task-irrelevant threat distractors are associated with elevated anxiety. Thus, veterans with high levels of anxiety may disproportionately allocate cognitive resources toward threatening stimuli, and have trouble keeping threatening thoughts from entering WM and staying there. People with PTSD also have been shown to have problems using WM in emotional contexts, making it hard for them to deal with stressful situations in work and personal life. Some research has suggested that WM training that incorporates affective stimuli may increase the ability to use WM in emotional contexts. In a pilot study, researchers from Medical College of Wisconsin and University of Wisconsin-Milwaukee expanded on that possibility by testing 2 kinds of WM training in 21 veterans with elevated PTSD symptoms.
Participants completed a pretest, 15 sessions of at-home computerized training, a posttest, and a 1-month follow-up session. The computerized tests included tasks to measure WM capacity, such as solving math questions while trying to remember a set of unrelated numbers. The participants were then assigned to active emotional WM training (n-back) or control emotional WM training (1-back). The n-back training involved constant updating of information stored in WM and shifting between visual and auditory stimuli using 8 different faces and 8 different negative words. The training sessions started at the 1-back level and increased in difficulty level by level with performance with > 95% accuracy, or were scaled back with performance with < 75% accuracy. The control training was the same but consisted only of 1 level.
Overall, the researchers say, contrary to their hypothesis, they did not find a significant difference in results from the 2 groups. But they did find that both trainings had an overall “significant and sizable” impact on PTSD symptoms in both groups: 73% of the n-back group and 60% of the 1-back group had a reduction of ≥ 10 points on the PTSD Checklist total scores, which the researchers say is considered a clinically meaningful change. Moreover, both groups showed a clinically meaningful reduction in symptoms at follow-up: 55% and 40%, respectively.
It was interesting, the researchers say, that both groups showed improvement, especially with the 1-back intervention, which they had used as a “minimally effective” control condition. They also note that, anecdotally, the participants found both interventions “quite challenging.” It may be that in this population even the 1-back intervention is enough to detectably reduce symptoms, the researchers say. They were also encouraged to see that the n-back condition (marginally) outperformed the 1-back condition in improving reexperiencing symptoms, theoretically the most relevant training target of WM-focused intervention. The researchers believe that their study yields useful pilot data, suggesting that n-back training can have a clinical impact primarily by reducing reexperiencing symptoms, which are highly likely to indicate the presence of impaired WM functioning.
Working memory (WM)—the function that allows us to temporarily store information and use it for cognitive tasks like learning, reasoning, and comprehension—is thought to play an important role in managing anxiety and intrusive symptoms of posttraumatic stress disorder (PTSD). Researchers have found inefficient filtering of threatening material from WM and increased storage of task-irrelevant threat distractors are associated with elevated anxiety. Thus, veterans with high levels of anxiety may disproportionately allocate cognitive resources toward threatening stimuli, and have trouble keeping threatening thoughts from entering WM and staying there. People with PTSD also have been shown to have problems using WM in emotional contexts, making it hard for them to deal with stressful situations in work and personal life. Some research has suggested that WM training that incorporates affective stimuli may increase the ability to use WM in emotional contexts. In a pilot study, researchers from Medical College of Wisconsin and University of Wisconsin-Milwaukee expanded on that possibility by testing 2 kinds of WM training in 21 veterans with elevated PTSD symptoms.
Participants completed a pretest, 15 sessions of at-home computerized training, a posttest, and a 1-month follow-up session. The computerized tests included tasks to measure WM capacity, such as solving math questions while trying to remember a set of unrelated numbers. The participants were then assigned to active emotional WM training (n-back) or control emotional WM training (1-back). The n-back training involved constant updating of information stored in WM and shifting between visual and auditory stimuli using 8 different faces and 8 different negative words. The training sessions started at the 1-back level and increased in difficulty level by level with performance with > 95% accuracy, or were scaled back with performance with < 75% accuracy. The control training was the same but consisted only of 1 level.
Overall, the researchers say, contrary to their hypothesis, they did not find a significant difference in results from the 2 groups. But they did find that both trainings had an overall “significant and sizable” impact on PTSD symptoms in both groups: 73% of the n-back group and 60% of the 1-back group had a reduction of ≥ 10 points on the PTSD Checklist total scores, which the researchers say is considered a clinically meaningful change. Moreover, both groups showed a clinically meaningful reduction in symptoms at follow-up: 55% and 40%, respectively.
It was interesting, the researchers say, that both groups showed improvement, especially with the 1-back intervention, which they had used as a “minimally effective” control condition. They also note that, anecdotally, the participants found both interventions “quite challenging.” It may be that in this population even the 1-back intervention is enough to detectably reduce symptoms, the researchers say. They were also encouraged to see that the n-back condition (marginally) outperformed the 1-back condition in improving reexperiencing symptoms, theoretically the most relevant training target of WM-focused intervention. The researchers believe that their study yields useful pilot data, suggesting that n-back training can have a clinical impact primarily by reducing reexperiencing symptoms, which are highly likely to indicate the presence of impaired WM functioning.
FDA approves Reyvow for acute migraine treatment
The Food and Drug Administration has approved lasmiditan (Reyvow) for acute treatment of migraines with and without auras in adults.
The agency’s Oct. 11 announcement said the approval is based on results from a pair of randomized, double-blind, placebo-controlled trials that included 3,177 adult patients with a history of migraine with and without aura. The percentage of patients whose pain and most bothersome migraine symptom (nausea, light sensitivity, or sound sensitivity) resolved after 2 hours was higher in patients receiving lasmiditan than in patients receiving placebo.
Lasmiditan is a serotonin 5-hydroxytryptamine1F–receptor agonist, giving it a unique mechanism of action as compared with other migraine treatments.
The most common adverse events associated with lasmiditan include dizziness, fatigue, paresthesia, and sedation. There is a risk of driving impairment while taking the medication, and patients are advised not to operate or drive machinery for 8 hours after taking lasmiditan.
“Reyvow is a new option for the acute treatment of migraine, a painful condition that affects one in seven Americans. We know that the migraine community is keenly interested in additional treatment options, and we remain committed to continuing to work with stakeholders to promote the development of new therapies for the acute and preventive treatment of migraine,” said Nick Kozauer, MD, acting deputy director of the division of neurology products in the FDA’s Center for Drug Evaluation and Research.
Eli Lilly, the drug’s manufacturer, said in a news release that “the recommended controlled substance classification for Reyvow is currently under review by the Drug Enforcement Administration and is expected within 90 days of today’s FDA approval, after which Reyvow will be available to patients in retail pharmacies” in oral doses of 50 mg, 100 mg, and 200 mg.
The Food and Drug Administration has approved lasmiditan (Reyvow) for acute treatment of migraines with and without auras in adults.
The agency’s Oct. 11 announcement said the approval is based on results from a pair of randomized, double-blind, placebo-controlled trials that included 3,177 adult patients with a history of migraine with and without aura. The percentage of patients whose pain and most bothersome migraine symptom (nausea, light sensitivity, or sound sensitivity) resolved after 2 hours was higher in patients receiving lasmiditan than in patients receiving placebo.
Lasmiditan is a serotonin 5-hydroxytryptamine1F–receptor agonist, giving it a unique mechanism of action as compared with other migraine treatments.
The most common adverse events associated with lasmiditan include dizziness, fatigue, paresthesia, and sedation. There is a risk of driving impairment while taking the medication, and patients are advised not to operate or drive machinery for 8 hours after taking lasmiditan.
“Reyvow is a new option for the acute treatment of migraine, a painful condition that affects one in seven Americans. We know that the migraine community is keenly interested in additional treatment options, and we remain committed to continuing to work with stakeholders to promote the development of new therapies for the acute and preventive treatment of migraine,” said Nick Kozauer, MD, acting deputy director of the division of neurology products in the FDA’s Center for Drug Evaluation and Research.
Eli Lilly, the drug’s manufacturer, said in a news release that “the recommended controlled substance classification for Reyvow is currently under review by the Drug Enforcement Administration and is expected within 90 days of today’s FDA approval, after which Reyvow will be available to patients in retail pharmacies” in oral doses of 50 mg, 100 mg, and 200 mg.
The Food and Drug Administration has approved lasmiditan (Reyvow) for acute treatment of migraines with and without auras in adults.
The agency’s Oct. 11 announcement said the approval is based on results from a pair of randomized, double-blind, placebo-controlled trials that included 3,177 adult patients with a history of migraine with and without aura. The percentage of patients whose pain and most bothersome migraine symptom (nausea, light sensitivity, or sound sensitivity) resolved after 2 hours was higher in patients receiving lasmiditan than in patients receiving placebo.
Lasmiditan is a serotonin 5-hydroxytryptamine1F–receptor agonist, giving it a unique mechanism of action as compared with other migraine treatments.
The most common adverse events associated with lasmiditan include dizziness, fatigue, paresthesia, and sedation. There is a risk of driving impairment while taking the medication, and patients are advised not to operate or drive machinery for 8 hours after taking lasmiditan.
“Reyvow is a new option for the acute treatment of migraine, a painful condition that affects one in seven Americans. We know that the migraine community is keenly interested in additional treatment options, and we remain committed to continuing to work with stakeholders to promote the development of new therapies for the acute and preventive treatment of migraine,” said Nick Kozauer, MD, acting deputy director of the division of neurology products in the FDA’s Center for Drug Evaluation and Research.
Eli Lilly, the drug’s manufacturer, said in a news release that “the recommended controlled substance classification for Reyvow is currently under review by the Drug Enforcement Administration and is expected within 90 days of today’s FDA approval, after which Reyvow will be available to patients in retail pharmacies” in oral doses of 50 mg, 100 mg, and 200 mg.
Pediatric stroke thrombectomy study sheds light on off-label procedure
based on data from a retrospective, multicenter study of 73 patients.
Children with high scores on the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) or large-vessel occlusion in the anterior or posterior circulation are at increased risk for morbidity and mortality, but the safety of thrombectomy in children has not been well studied. Several randomized trials have showed its safety and efficacy in adults, wrote Peter Sporns, MD, of the Institute of Clinical Radiology at Universitätsklinikum Muenster (Germany), and colleagues.
In a study published in JAMA Neurology, Dr. Sporns and coauthors reviewed data from pediatric patients aged younger than 18 years who underwent endovascular recanalization between Jan. 1, 2000, and Dec. 31, 2018, at 25 stroke centers in Europe and 2 in the United States.
The primary outcome was change in the PedNIHSS scores and the endovascular recanalization involved “a combination of techniques using distal thrombaspiration and/or clot retrievers,” the researchers wrote.
Neurologic outcomes improved from a median PedNIHSS score of 14.0 at hospital admission to 4.0 at day 7. The average time from stroke onset to hospital admission was 3 hours, and the median time from stroke onset to recanalization was 4 hours.
“The rapidity of recanalization across the large number of centers in the Save ChildS study is a commendable achievement, establishing feasibility for acute pediatric stroke treatment within the short window of time for embolectomy at centers prepared for this event,” wrote Christine Fox, MD, of the University of California, San Francisco, and Nomazulu Dlamini, MBBS, PhD, of the Hospital for Sick Children, Toronto, in an accompanying editorial.
In addition, the median modified Rankin Scale score was 1.0 at discharge and at 6 and 24 months, and the median Pediatric Stroke Outcome Measure score was 1.0 at discharge and 0.5 at 6 and 24 months.
The median age of the patients was 11 years, and approximately half were boys (51%). A total of 63 children (86%) were treated for anterior circulation occlusion, and 10 (14%) were treated for posterior circulation occlusion; (22%) received concomitant intravenous thrombolysis.
Transient vasospasm was the only observed periprocedural complication, seen in four patients, and all cases resolved without clinical sequelae. One patient with a history of a heart anomaly died of cardiac arrest after recanalization. No vascular complications were reported, and the proportion of symptomatic intracerebral hemorrhage events was 1.37 per 100 observations, compared with 2.79 in a meta-analysis of adult studies.
The main limitation of the study was its retrospective design, as well as the absence of a control group, the researchers noted. However, the results “may support clinicians’ practice of off-label thrombectomy in childhood stroke in the absence of high-level evidence.”
The editorial authors emphasized that safety concerns remain despite the relatively low level of complications observed in the current study. “The safety of thrombectomy in children with suspected focal cerebral arteriopathy or bilateral arteriopathies is a particular concern because of the potential to further injure an acutely inflamed or chronically diseased vessel,” they wrote.
“We should be cautious about the interpretation of long-term outcome measures in the Save ChildS study,” Dr. Fox and Dr. Dlamini added, noting that additional multicenter studies are needed “to advance our knowledge of pediatric stroke and inform best practices.”
Dr. Sporns had no financial conflicts to disclose; several coauthors disclosed relationships with multiple pharmaceutical companies. Dr. Fox and Dr. Dlamini had no financial conflicts to disclose.
SOURCES: Sporns P et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3403; Fox C, Dlamini N. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3412.
based on data from a retrospective, multicenter study of 73 patients.
Children with high scores on the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) or large-vessel occlusion in the anterior or posterior circulation are at increased risk for morbidity and mortality, but the safety of thrombectomy in children has not been well studied. Several randomized trials have showed its safety and efficacy in adults, wrote Peter Sporns, MD, of the Institute of Clinical Radiology at Universitätsklinikum Muenster (Germany), and colleagues.
In a study published in JAMA Neurology, Dr. Sporns and coauthors reviewed data from pediatric patients aged younger than 18 years who underwent endovascular recanalization between Jan. 1, 2000, and Dec. 31, 2018, at 25 stroke centers in Europe and 2 in the United States.
The primary outcome was change in the PedNIHSS scores and the endovascular recanalization involved “a combination of techniques using distal thrombaspiration and/or clot retrievers,” the researchers wrote.
Neurologic outcomes improved from a median PedNIHSS score of 14.0 at hospital admission to 4.0 at day 7. The average time from stroke onset to hospital admission was 3 hours, and the median time from stroke onset to recanalization was 4 hours.
“The rapidity of recanalization across the large number of centers in the Save ChildS study is a commendable achievement, establishing feasibility for acute pediatric stroke treatment within the short window of time for embolectomy at centers prepared for this event,” wrote Christine Fox, MD, of the University of California, San Francisco, and Nomazulu Dlamini, MBBS, PhD, of the Hospital for Sick Children, Toronto, in an accompanying editorial.
In addition, the median modified Rankin Scale score was 1.0 at discharge and at 6 and 24 months, and the median Pediatric Stroke Outcome Measure score was 1.0 at discharge and 0.5 at 6 and 24 months.
The median age of the patients was 11 years, and approximately half were boys (51%). A total of 63 children (86%) were treated for anterior circulation occlusion, and 10 (14%) were treated for posterior circulation occlusion; (22%) received concomitant intravenous thrombolysis.
Transient vasospasm was the only observed periprocedural complication, seen in four patients, and all cases resolved without clinical sequelae. One patient with a history of a heart anomaly died of cardiac arrest after recanalization. No vascular complications were reported, and the proportion of symptomatic intracerebral hemorrhage events was 1.37 per 100 observations, compared with 2.79 in a meta-analysis of adult studies.
The main limitation of the study was its retrospective design, as well as the absence of a control group, the researchers noted. However, the results “may support clinicians’ practice of off-label thrombectomy in childhood stroke in the absence of high-level evidence.”
The editorial authors emphasized that safety concerns remain despite the relatively low level of complications observed in the current study. “The safety of thrombectomy in children with suspected focal cerebral arteriopathy or bilateral arteriopathies is a particular concern because of the potential to further injure an acutely inflamed or chronically diseased vessel,” they wrote.
“We should be cautious about the interpretation of long-term outcome measures in the Save ChildS study,” Dr. Fox and Dr. Dlamini added, noting that additional multicenter studies are needed “to advance our knowledge of pediatric stroke and inform best practices.”
Dr. Sporns had no financial conflicts to disclose; several coauthors disclosed relationships with multiple pharmaceutical companies. Dr. Fox and Dr. Dlamini had no financial conflicts to disclose.
SOURCES: Sporns P et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3403; Fox C, Dlamini N. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3412.
based on data from a retrospective, multicenter study of 73 patients.
Children with high scores on the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) or large-vessel occlusion in the anterior or posterior circulation are at increased risk for morbidity and mortality, but the safety of thrombectomy in children has not been well studied. Several randomized trials have showed its safety and efficacy in adults, wrote Peter Sporns, MD, of the Institute of Clinical Radiology at Universitätsklinikum Muenster (Germany), and colleagues.
In a study published in JAMA Neurology, Dr. Sporns and coauthors reviewed data from pediatric patients aged younger than 18 years who underwent endovascular recanalization between Jan. 1, 2000, and Dec. 31, 2018, at 25 stroke centers in Europe and 2 in the United States.
The primary outcome was change in the PedNIHSS scores and the endovascular recanalization involved “a combination of techniques using distal thrombaspiration and/or clot retrievers,” the researchers wrote.
Neurologic outcomes improved from a median PedNIHSS score of 14.0 at hospital admission to 4.0 at day 7. The average time from stroke onset to hospital admission was 3 hours, and the median time from stroke onset to recanalization was 4 hours.
“The rapidity of recanalization across the large number of centers in the Save ChildS study is a commendable achievement, establishing feasibility for acute pediatric stroke treatment within the short window of time for embolectomy at centers prepared for this event,” wrote Christine Fox, MD, of the University of California, San Francisco, and Nomazulu Dlamini, MBBS, PhD, of the Hospital for Sick Children, Toronto, in an accompanying editorial.
In addition, the median modified Rankin Scale score was 1.0 at discharge and at 6 and 24 months, and the median Pediatric Stroke Outcome Measure score was 1.0 at discharge and 0.5 at 6 and 24 months.
The median age of the patients was 11 years, and approximately half were boys (51%). A total of 63 children (86%) were treated for anterior circulation occlusion, and 10 (14%) were treated for posterior circulation occlusion; (22%) received concomitant intravenous thrombolysis.
Transient vasospasm was the only observed periprocedural complication, seen in four patients, and all cases resolved without clinical sequelae. One patient with a history of a heart anomaly died of cardiac arrest after recanalization. No vascular complications were reported, and the proportion of symptomatic intracerebral hemorrhage events was 1.37 per 100 observations, compared with 2.79 in a meta-analysis of adult studies.
The main limitation of the study was its retrospective design, as well as the absence of a control group, the researchers noted. However, the results “may support clinicians’ practice of off-label thrombectomy in childhood stroke in the absence of high-level evidence.”
The editorial authors emphasized that safety concerns remain despite the relatively low level of complications observed in the current study. “The safety of thrombectomy in children with suspected focal cerebral arteriopathy or bilateral arteriopathies is a particular concern because of the potential to further injure an acutely inflamed or chronically diseased vessel,” they wrote.
“We should be cautious about the interpretation of long-term outcome measures in the Save ChildS study,” Dr. Fox and Dr. Dlamini added, noting that additional multicenter studies are needed “to advance our knowledge of pediatric stroke and inform best practices.”
Dr. Sporns had no financial conflicts to disclose; several coauthors disclosed relationships with multiple pharmaceutical companies. Dr. Fox and Dr. Dlamini had no financial conflicts to disclose.
SOURCES: Sporns P et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3403; Fox C, Dlamini N. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3412.
FROM JAMA NEUROLOGY
Increased Parkinson’s disease risk seen with bipolar disorder
Patients with bipolar disorder may be at increased risk of Parkinson’s disease in later life, according to a systematic review and meta-analysis published in JAMA Neurology.
Patrícia R. Faustino, MD, from the faculty of medicine at the University of Lisboa (Portgual), and coauthors reviewed and analyzed seven articles – four cohort studies and three cross-sectional studies – that reported data on idiopathic Parkinson’s disease in patients with bipolar disorder, compared with those without. The meta-analysis found that individuals with a previous diagnosis of bipolar disorder had a 235% higher risk of being later diagnosed with Parkinson’s disease. Even after removing studies with a high risk of bias, the risk was still 3.21 times higher in those with bipolar disorder, compared with those without.
“The pathophysiological rationale between bipolar disorder and Parkinson’s disease might be explained by the dopamine dysregulation hypothesis, which states that the cyclical process of bipolar disorder in manic states leads to a down-regulation of dopamine receptor sensitivity (depression phase), which is later compensated by up-regulation (manic state),” the authors wrote. “Over time, this phenomenon may lead to an overall reduction of dopaminergic activity, the prototypical Parkinson’s disease state.”
Subgroup analysis revealed that subgroups with shorter follow-up periods – less than 9 years – had a greater increase in the risk of a later Parkinson’s disease diagnosis. The authors noted that this could represent misdiagnosis of parkinsonism – possibly drug induced – as Parkinson’s disease. The researchers also raised the possibility that the increased risk of Parkinson’s disease in patients with bipolar disorder could relate to long-term lithium use, rather than being a causal relationship. “However, treatment with lithium is foundational in bipolar disorder, and so to separate the causal effect from a potential confounder would be particularly difficult,” they wrote.
One of the studies included did explore the use of lithium, and found that lithium monotherapy was associated with a significant increase in the risk of being diagnosed with Parkinson’s disease or taking antiparkinsonism medication, compared with antidepressant therapy. However the authors commented that the diagnostic code may not differentiate Parkinson’s disease from other causes of parkinsonism.
Given their findings, the authors suggested that, if patients with bipolar disorder present with parkinsonism features, it may not necessarily be drug induced. In these patients, they recommended an investigation for Parkinson’s disease, perhaps using functional neuroimaging “as Parkinson’s disease classically presents with nigrostriatal degeneration while drug-induced parkinsonism does not.”
Two authors declared grants and personal fees from the pharmaceutical sector. No other conflicts of interest were reported.
SOURCE: Faustino PR et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3446.
Patients with bipolar disorder may be at increased risk of Parkinson’s disease in later life, according to a systematic review and meta-analysis published in JAMA Neurology.
Patrícia R. Faustino, MD, from the faculty of medicine at the University of Lisboa (Portgual), and coauthors reviewed and analyzed seven articles – four cohort studies and three cross-sectional studies – that reported data on idiopathic Parkinson’s disease in patients with bipolar disorder, compared with those without. The meta-analysis found that individuals with a previous diagnosis of bipolar disorder had a 235% higher risk of being later diagnosed with Parkinson’s disease. Even after removing studies with a high risk of bias, the risk was still 3.21 times higher in those with bipolar disorder, compared with those without.
“The pathophysiological rationale between bipolar disorder and Parkinson’s disease might be explained by the dopamine dysregulation hypothesis, which states that the cyclical process of bipolar disorder in manic states leads to a down-regulation of dopamine receptor sensitivity (depression phase), which is later compensated by up-regulation (manic state),” the authors wrote. “Over time, this phenomenon may lead to an overall reduction of dopaminergic activity, the prototypical Parkinson’s disease state.”
Subgroup analysis revealed that subgroups with shorter follow-up periods – less than 9 years – had a greater increase in the risk of a later Parkinson’s disease diagnosis. The authors noted that this could represent misdiagnosis of parkinsonism – possibly drug induced – as Parkinson’s disease. The researchers also raised the possibility that the increased risk of Parkinson’s disease in patients with bipolar disorder could relate to long-term lithium use, rather than being a causal relationship. “However, treatment with lithium is foundational in bipolar disorder, and so to separate the causal effect from a potential confounder would be particularly difficult,” they wrote.
One of the studies included did explore the use of lithium, and found that lithium monotherapy was associated with a significant increase in the risk of being diagnosed with Parkinson’s disease or taking antiparkinsonism medication, compared with antidepressant therapy. However the authors commented that the diagnostic code may not differentiate Parkinson’s disease from other causes of parkinsonism.
Given their findings, the authors suggested that, if patients with bipolar disorder present with parkinsonism features, it may not necessarily be drug induced. In these patients, they recommended an investigation for Parkinson’s disease, perhaps using functional neuroimaging “as Parkinson’s disease classically presents with nigrostriatal degeneration while drug-induced parkinsonism does not.”
Two authors declared grants and personal fees from the pharmaceutical sector. No other conflicts of interest were reported.
SOURCE: Faustino PR et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3446.
Patients with bipolar disorder may be at increased risk of Parkinson’s disease in later life, according to a systematic review and meta-analysis published in JAMA Neurology.
Patrícia R. Faustino, MD, from the faculty of medicine at the University of Lisboa (Portgual), and coauthors reviewed and analyzed seven articles – four cohort studies and three cross-sectional studies – that reported data on idiopathic Parkinson’s disease in patients with bipolar disorder, compared with those without. The meta-analysis found that individuals with a previous diagnosis of bipolar disorder had a 235% higher risk of being later diagnosed with Parkinson’s disease. Even after removing studies with a high risk of bias, the risk was still 3.21 times higher in those with bipolar disorder, compared with those without.
“The pathophysiological rationale between bipolar disorder and Parkinson’s disease might be explained by the dopamine dysregulation hypothesis, which states that the cyclical process of bipolar disorder in manic states leads to a down-regulation of dopamine receptor sensitivity (depression phase), which is later compensated by up-regulation (manic state),” the authors wrote. “Over time, this phenomenon may lead to an overall reduction of dopaminergic activity, the prototypical Parkinson’s disease state.”
Subgroup analysis revealed that subgroups with shorter follow-up periods – less than 9 years – had a greater increase in the risk of a later Parkinson’s disease diagnosis. The authors noted that this could represent misdiagnosis of parkinsonism – possibly drug induced – as Parkinson’s disease. The researchers also raised the possibility that the increased risk of Parkinson’s disease in patients with bipolar disorder could relate to long-term lithium use, rather than being a causal relationship. “However, treatment with lithium is foundational in bipolar disorder, and so to separate the causal effect from a potential confounder would be particularly difficult,” they wrote.
One of the studies included did explore the use of lithium, and found that lithium monotherapy was associated with a significant increase in the risk of being diagnosed with Parkinson’s disease or taking antiparkinsonism medication, compared with antidepressant therapy. However the authors commented that the diagnostic code may not differentiate Parkinson’s disease from other causes of parkinsonism.
Given their findings, the authors suggested that, if patients with bipolar disorder present with parkinsonism features, it may not necessarily be drug induced. In these patients, they recommended an investigation for Parkinson’s disease, perhaps using functional neuroimaging “as Parkinson’s disease classically presents with nigrostriatal degeneration while drug-induced parkinsonism does not.”
Two authors declared grants and personal fees from the pharmaceutical sector. No other conflicts of interest were reported.
SOURCE: Faustino PR et al. JAMA Neurol. 2019 Oct 14. doi: 10.1001/jamaneurol.2019.3446.
FROM JAMA NEUROLOGY
Forgetting the Stuff That Dreams Are Made On
Why do we forget some dreams and remember others? Researchers in a study funded by the National Institute of Neurological Disorders and Stroke say our dream memory may be controlled by a group of neurons commonly associated with appetite. Their findings could shed light on a wide range of memory-related conditions, including posttraumatic stress disorder (PTSD) and Alzheimer disease.
Studies have already shown that sleep helps the brain store new memories and eliminate excess information. Recent mouse studies have found that during sleep the brain prunes synaptic connections made between neurons involved in some types of learning.
But this study shows how that might happen.
The researchers have previously demonstrated that narcolepsy might be linked to the loss of hypocretin/orexin-making neurons in the hypothalamus. In this study, they looked at neighboring cells that produce melanin-concentrating hormone (MCH), which is involved in the control of both sleep and appetite. A majority (53%) of hypothalamic MCH cells fired in mice during REM sleep; 35% fired when they were awake, and 12% fired at both times.
Those cells also may play a role in learning and memory, the researchers suggest. To test their theory that MCH cells might help the brain store memories, they used “genetic tools” to turn MCH neurons on and off during memory tests.
Surprisingly, the researchers say, pharmacogenetic activation—turning on the MCH cells—worsened memory; genetic ablation—turning them off—improved memory. Further experiments suggested MCH neurons exclusively played this role during REM sleep.
The results suggest that MCH neurons help the brain actively forget new, possibly unimportant information. “Since dreams are thought to primarily occur during REM sleep,” says Thomas Kilduff, PhD, senior author of the study, “the sleep stage when the MCH cells turn on, activation of these cells may prevent the content of a dream from being stored in the hippocampus—consequently, the dream is quickly forgotten.”
Why do we forget some dreams and remember others? Researchers in a study funded by the National Institute of Neurological Disorders and Stroke say our dream memory may be controlled by a group of neurons commonly associated with appetite. Their findings could shed light on a wide range of memory-related conditions, including posttraumatic stress disorder (PTSD) and Alzheimer disease.
Studies have already shown that sleep helps the brain store new memories and eliminate excess information. Recent mouse studies have found that during sleep the brain prunes synaptic connections made between neurons involved in some types of learning.
But this study shows how that might happen.
The researchers have previously demonstrated that narcolepsy might be linked to the loss of hypocretin/orexin-making neurons in the hypothalamus. In this study, they looked at neighboring cells that produce melanin-concentrating hormone (MCH), which is involved in the control of both sleep and appetite. A majority (53%) of hypothalamic MCH cells fired in mice during REM sleep; 35% fired when they were awake, and 12% fired at both times.
Those cells also may play a role in learning and memory, the researchers suggest. To test their theory that MCH cells might help the brain store memories, they used “genetic tools” to turn MCH neurons on and off during memory tests.
Surprisingly, the researchers say, pharmacogenetic activation—turning on the MCH cells—worsened memory; genetic ablation—turning them off—improved memory. Further experiments suggested MCH neurons exclusively played this role during REM sleep.
The results suggest that MCH neurons help the brain actively forget new, possibly unimportant information. “Since dreams are thought to primarily occur during REM sleep,” says Thomas Kilduff, PhD, senior author of the study, “the sleep stage when the MCH cells turn on, activation of these cells may prevent the content of a dream from being stored in the hippocampus—consequently, the dream is quickly forgotten.”
Why do we forget some dreams and remember others? Researchers in a study funded by the National Institute of Neurological Disorders and Stroke say our dream memory may be controlled by a group of neurons commonly associated with appetite. Their findings could shed light on a wide range of memory-related conditions, including posttraumatic stress disorder (PTSD) and Alzheimer disease.
Studies have already shown that sleep helps the brain store new memories and eliminate excess information. Recent mouse studies have found that during sleep the brain prunes synaptic connections made between neurons involved in some types of learning.
But this study shows how that might happen.
The researchers have previously demonstrated that narcolepsy might be linked to the loss of hypocretin/orexin-making neurons in the hypothalamus. In this study, they looked at neighboring cells that produce melanin-concentrating hormone (MCH), which is involved in the control of both sleep and appetite. A majority (53%) of hypothalamic MCH cells fired in mice during REM sleep; 35% fired when they were awake, and 12% fired at both times.
Those cells also may play a role in learning and memory, the researchers suggest. To test their theory that MCH cells might help the brain store memories, they used “genetic tools” to turn MCH neurons on and off during memory tests.
Surprisingly, the researchers say, pharmacogenetic activation—turning on the MCH cells—worsened memory; genetic ablation—turning them off—improved memory. Further experiments suggested MCH neurons exclusively played this role during REM sleep.
The results suggest that MCH neurons help the brain actively forget new, possibly unimportant information. “Since dreams are thought to primarily occur during REM sleep,” says Thomas Kilduff, PhD, senior author of the study, “the sleep stage when the MCH cells turn on, activation of these cells may prevent the content of a dream from being stored in the hippocampus—consequently, the dream is quickly forgotten.”