Exercise After Study Boosts Memory

There is significant interest in activities that may boost academic achievement in the classroom.

I previously posted on evidence that exercise prior to a learning task improved reading comprehension scores.

You can access that post by clicking HERE.

Now a study has compared two types of activities after a memorization task in male students.

In this study, 60 male students completed a learning task and then were randomized into one of three activities for one hour. The three activities were playing a violent video game, a period of running or a control period of conversation. After the activity period, subjects completed a memory test.

Subjects had salivary cortisol levels examined before and after the learning task at at the time of memory testing. 

All subjects had a increase in salivary cortisol levels after the learning phase, but only the running group demonstrated a continued rise in cortisol after the activity phase.

The subjects participating in a running activity performed better on the memory retention test than those in the violent video game and the conversation control groups.  There was no correlation between salivary cortisol levels and memory retention. 

The authors conclude that their finding has implications for scheduling exercise during the school day for children. They recommend physical exercise following intense learning cycles to promote improved learning efficiency.

Interestingly, in the United States many schools are cutting back on physical education activities due to budget constraints. Such cutbacks may contribute to declining performance on testing metrics.

Readers with more interest in this topic can access the free full text manuscript by clicking on the DOI link in the citation below.

Photo of monarch butterfly is from the author's files.

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Kindermann, H., Javor, A., & Reuter, M. (2016). Playing counter-strike versus running: The impact of leisure time activities and cortisol on intermediate-term memory in male students Cognitive Systems Research, 40, 1-7 DOI: 10.1016/j.cogsys.2016.01.002

Pathways to Substance Use and Abuse

Neuroscience medicine clinicians encounter patients every day who have both a mental and substance use disorder.

This co-occurrence, or comorbidity, complicates diagnosis, treatment and outcome.

The exact mechanism for this comorbidity issue is unclear.

A recent study out of Washington University in St. Louis and King's College London provides some insight into this comorbidity issue.

They examined participants in the Study of Addiction: Genetics and Environment (SAGE). These subjects provided genetic samples and psychiatric interviews to the research team.

Five psychiatric disorders were studied including attention deficit hyperactivity, autism spectrum disorder, major depression, bipolar disorder and schizophrenia. A initial finding ruled out any link between genetic risk for autism spectrum disorder and any substance use/abuse risk.

The remaining four psychiatric disorders did increase risk for substance use and abuse in a general manner. This means genetic risk for ADHD, bipolar disorder, major depression and schizophrenia all contribute to a general risk for substance use/abuse across all drug categories.

Additionally, the team reported some specific drug use/abuse with individual genetic risk for ADHD, bipolar disorder, major depression and schizophrenia. These specific pathways included:

• Major depression polygenetic risk score and non-problem cannabis use
• Major depression polygenetic risk score and severe cocaine dependence
• Schizophrenia polygenetic risk score and  non-problem cannabis use and severe cannabis dependence
• Schizophrenia polygenetic risk score and severe cocaine dependence

The take-home message from this study is that genetic risk for many psychiatric disorders also contributes to a increased risk for general substance use/abuse. Additionally, some psychiatric disorders appear to increase risk for specific substance use/abuse issues.

Prevention, assessment and treatment services need to address this relationship and the needs for each component of illness in those with comorbidity.

Individuals with more interest in this topic can access the free full-text manuscript by clicking on the link in the citation below.

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Image is an original graphic produced by me based on content in the manuscript.

Carey CE, Agrawal A, Bucholz KK, Hartz SM, Lynskey MT, Nelson EC, Bierut LJ, & Bogdan R (2016). Associations between Polygenic Risk for Psychiatric Disorders and Substance Involvement. Frontiers in genetics, 7 PMID: 27574527

Alzheimer's Disease: Atrophy Pattern and Symptoms

Memory impairment is a key symptom of Alzheimer's dementia common to patients with the condition.

However, additional cognitive and behavioral symptoms vary between patients with a clinical and pathological diagnosis of Alzheimer's disease.

A key area of research is focused on understanding factors that contribute to symptom variability in Alzheimer's disease.

A team of researchers from Singapore and Harvard Medical School recently published an important study on this topic.

They analyzed structural MRI images from a group of 188 subjects in the Alzheimer's Disease Neuroimaging Initiative.

Using a mathematical model known as latent Dirichlet allocation they were able to identify three distinct areas of atrophy of variable severity in their cohort. These three factors were found to be:

• Temporal atrophy: temporal cortex, hippocampus and amygdala
• Cortical atrophy: frontal, parietal, lateral temporal and lateral occipital cortex regions
• Subcortical atrophy: striatum, thalamus and cerebellum

Individual patterns of atrophy within subjects were found to be stable over time. This means the atrophy patterns are not just a reflection of the stage of the Alzheimer's disease.

As expected, patterns of atrophy correlated with neuropsychological domains of impairment. Temporal atrophy subjects had the greatest memory impairment. Cortical atrophy patients showed the most impairment in executive function. Subcortical atrophy subjects had lower levels of executive function and memory impairment and showed a slower rate of cognitive decline.

Patients tended to fall into factor groups where more than one area of atrophy was noted, i.e. cortical and temporal atrophy but not subcortical atrophy.

The authors note their findings support the heterogeneity of Alzheimer's disease affecting different cognitive and behavioral features as well as variability in disease progression.

This is an important study in understanding the clinical manifestation of Alzheimer's disease. Readers with more interest in this research can access the free full-text manuscript by clicking on the link in the citation below.

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Brain image highlighting regions of the subcortex is an iPad screen shot from the app Brain Tutor.

Zhang X, Mormino EC, Sun N, Sperling RA, Sabuncu MR, Yeo BT, & Alzheimer’s Disease Neuroimaging Initiative. (2016). Bayesian model reveals latent atrophy factors with dissociable cognitive trajectories in Alzheimer's disease. Proceedings of the National Academy of Sciences of the United States of America PMID: 27702899

Robin Williams and Lewy Body Disease

In a post last week, I highlighted a recent study examining clinical issues in the diagnosis of Lewy body dementia (LBD).

This study examined differentiating clinical and neuropsychological factors between LBD, Alzheimer's dementia and Parkinson's disease.

You can access this post by clicking HERE.

This topic received significant attention following the description of comedian Robin Williams' last years by his wife in the journal Neurology.

Robin Williams suffered from LBD and like many, his diagnosis was not made until autopsy.

I want to review some of the key clinical features shown by Robin Williams described by his widow's in his last few years.

Psychological symptoms/signs

• Anxiety
• Fear 
• Panic attacks
• Depression
• Paranoia
• Delusions
• Suicide

Cognitive symptoms/signs

• Memory impairment
• Fluctuating levels of memory/orientation

Physical symptoms/signs

• Constipation
• Urinary problems
• Heartburn
• Insomnia
• Poor sense of smell
• Sensitivity to anti-psychotic medications
• Tremor left hand
• Freezing of gait

Lab/Imaging

• Elevated serum cortisol levels
• Normal brain imaging (CT or MRI?)

Neuropathology

• 40% loss of dopamine neurons
• Lewy bodies throughout brain
• High concentration of Lewy bodies in brain amygdala

A clinical diagnosis of Parkinson's disease had been made for Robin and he had been placed on anti-Parkinson's medication. 

Signs and symptoms of LBD as outlined by Mayo Clinic staff  include:

• Visual and other hallucinations
• Movement disorder (signs of Parkinson's disease)
• Autonomic nervous system dysregulation (tachycardia, sweating, constipation, dizziness, falls)
• Cognitive problems (confusion, visuospatial problems, memory loss, fluctuating levels of attention)
• Sleep problems (REM sleep behavior problems)
• Depression/Apathy

As noted in Mrs. Williams' description, Robin Williams never reported visual hallucinations, a key symptom in LBD.  However, his clinical team felt is was quite possible visual hallucinations could have been present and simply not disclosed due to fear of how others would perceive the hallucinations.

The high concentration of Lewy bodies in the brain amygdala could explain some of the panic, fear and depression noted in the case history.

Suicide is not commonly noted in LBD although it has not been studied in great detail. I will examine this issue in a separate post.

Mrs. Williams has done a great service in writing this clinical history. She urges increased research into the causes and treatment for LBD. Additionally, her report again underscores the need for clinicians to be vigilant for the signs and symptoms of LBD.

I highly recommend reading about the clinical history of Robin Williams. You can access the free full-text report by clicking HERE.

Access the Mayo Clinic description of Lewy body dementia by clicking HERE.

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Photo of Robin William's Hollywood star is from a Creative Commons Wikipedia file authored by:
CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=2710421

Williams SS (2016). The terrorist inside my husband's brain Neurology, 87 (13), 1308-1311