The use of animals for therapeutic benefit is well-established. For example, for individuals with a disability such as blindness, trained service dogs can enhance the ability to live independently and participate fully in society. An emotional support animal (ESA) is an untrained animal that is used to support a person disabled by an emotional or mental disorder. For an animal to qualify as an ESA, a mental health or medical professional needs to write a letter saying that the animal is needed for the mental health of the person with the disability. This article describes the legal framework for service animals and ESAs, as well as the differences between them. We summarize information about the Americans with Disabilities Act, the Fair Housing Act, the Air Carrier Access Act, and other laws governing an individual's right to be accompanied by a support animal. We also summarize the clinical research on ESAs and argue that, although there are few studies on the clinical effectiveness of ESAs, a broader body of research indicates that animals may have positive clinical effects on medical and mental illness. Finally, we suggest there is a need for further research and provider education on ESAs.

Study objectives

To investigate whether subjective sleep quality is associated with brain volume independent of comorbid psychiatric conditions.

Design

Cross-sectional.

Setting

Department of Veterans Affairs (VA) Medical Center.

Participants

One hundred forty-four Gulf War Veterans (mean age 45 years; range: 31-70 years; 14% female).

Interventions

None.

Measurements and results

Total cortical, lobar gray matter, and hippocampal volumes were quantified from 1.5 Tesla magnetic resonance images using Freesurfer version 4.5. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). Multiple linear regressions were used to determine the association of sleep quality with total and regional brain volumes. The global PSQI score was positively correlated with lifetime and current posttraumatic stress disorder (PTSD) and current depressive symptoms (P < 0.001) and was higher in veterans with Gulf War Illness, trauma exposure, and those using psychotropic medication (P ≤ 0.03). After adjusting for these comorbid variables, age, intracranial volume, and multiple comparisons, global PSQI was inversely associated with total cortical and frontal gray matter volume (adjusted P ≤ 0.03). Within the frontal lobe, total PSQI was inversely associated with the superior and middle frontal, orbitofrontal, anterior cingulate, and frontal pole volumes (adjusted P ≤ 0.02). Examination of the 3-factor structure of the PSQI revealed that the associations were driven by perceived sleep quality.

Conclusions

Poorer subjective sleep quality was associated with reduced total cortical and regional frontal lobe volumes independent of comorbid psychiatric conditions. Future work will be needed to examine if effective treatment of disturbed sleep leads to improved structural and functional integrity of the frontal lobes.

Purpose of review

Posttraumatic stress disorder (PTSD) is associated with increased risk for dementia, yet mechanisms are poorly understood.

Recent findings

Recent literature suggests several potential mechanisms by which sleep impairments might contribute to the increased risk of dementia observed in PTSD. First, molecular, animal, and imaging studies indicate that sleep problems lead to cellular damage in brain structures crucial to learning and memory. Second, recent studies have shown that lack of sleep might precipitate the accumulation of harmful amyloid proteins. Finally, sleep and PTSD are associated with elevated inflammation, which, in turn, is associated with dementia, possibly via cytokine-mediated neural toxicity and reduced neurogenesis. A better understanding of these mechanisms may yield novel treatment approaches to reduce neurodegeneration in PTSD. The authors emphasize the importance of including sleep data in studies of PTSD and cognition and identify next steps.

Posttraumatic stress disorder (PTSD) is associated with smaller volumes of the hippocampus, as has been demonstrated by meta-analyses. Proposed mechanistic relationships are reviewed briefly, including the hypothesis that sleep disturbances mediate the effects of PTSD on hippocampal volume. Evidence for this includes findings that insomnia and restricted sleep are associated with changes in hippocampal cell regulation and impairments in cognition. We present results of a new study of 187 subjects in whom neither PTSD nor poor sleep was associated with lower hippocampal volume. We outline a broad research agenda centered on the hypothesis that sleep changes mediate the relationship between PTSD and hippocampal volume.

Study objectives

To investigate interactions between high and low amounts of sleep and other predictors of cognitive performance.

Methods

We used four cognitive tests to determine whether sleep time interacted with age, personal history of a memory problem, parental history of a memory problem, or personal concerns about memory and were associated with cognitive performance. Data were collected from an internet-based cohort study. We used an ordinary least squares regression with restricted cubic splines, controlling for demographic variables and comorbidities.

Results

We found significant nonlinear interactions between (1) total sleep time and age and (2) total sleep time and personal history of a memory problem and cognitive performance. Short and long sleep durations and self-reported memory complaints were associated with poorer performance on a test of attention and this was true to a greater degree in younger and older adults. A repeat analysis excluding subjects reporting dementia was significant only for the test of attention.

Conclusions

These results extend existing data on sleep duration and cognition across the lifespan by combining in a single study the results from four specific cognitive tests, both younger and older adults, and four self-reported risk factors for cognitive impairment. Longitudinal studies with biomarkers should be undertaken to determine whether causal mechanisms, such as inflammation or amyloid buildup, account for these associations.