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An intraneuronal parasite infecting approximately one-third of the world’s population, Toxoplasma gondii has been associated with markers of cardiovascular disease. In this study, we used data from the Center for Disease Control and Prevention’s National Health and Nutrition Examination Survey to investigate associations between T. gondii and blood pressure and hypertension. Multiple regression modelling adjusted for a range of covariates showed that T. gondii was associated with lowered probability of elevated blood pressure, with lower probability of Stages 1 and 2 hypertension, and with lower systolic and diastolic blood pressure. These findings suggest that T. gondii might alter hemodynamic regulation, although the clinical relevance of these associations requires additional investigation.

Several viral, bacterial, and parasitic diseases have been associated with cognitive function and neuropsychiatric outcomes in humans, including human T-cell lymphotropic virus 1 (HTLV-1). In this study, we sought to further generalize previously reported associations of cognitive function and depression with HTLV-1 seropositivity and serointensity using a community-based sample of adults aged approximately 40 to 70 years (mean = 55.3 years) from the United Kingdom. In this sample, the results of adjusted linear regression models showed no associations of HTLV-1 seropositivity or serointensity with reasoning, pairs-matching, or reaction-time cognitive tasks or with depression. In addition, neither age, sex, educational attainment, nor income moderated associations of HTLV-1 seropositivity or serointensity with cognitive function or depression. In this middle-aged to older middle-aged adult community sample, HTLV-1 seropositivity and serointensity do not appear to be associated with reasoning, pairs-matching, and reaction-time tasks or with depression.

Background The hippocampus is important for memory processing. Several neuropsychiatric diseases including Alzheimer’s disease are associated with reduced hippocampal volume, and further the hippocampus appears vulnerable to environmental insult. Air pollution has been associated with cardiovascular disease, abnormal brain structure, and cognitive deficits. Objective Because of hippocampal vulnerability to environmental insults and based on the association between exposure to air pollution and cognitive function and brain structure, we evaluated the association between exposure to toxins in air pollution and left and right hippocampal volume using brain-imaging and air-pollution data from the UK Biobank, a large community-based dataset. Methods We used regression modelling to evaluate the association between exposure to nitrogen dioxide, nitrogen oxides, PM 2.5 , PM 2.5-10 , and PM 10. and left and right hippocampal volume controlling for age, sex, body-mass index, overall health, alcohol use, smoking, educational attainment, socioeconomic status, inverse distance from the nearest major road, and a measure of total brain volume. Results In these models, PM 2.5 concentration was associated with smaller left hippocampal volume. None of the other measures of air pollution was associated with either left or right hippocampal volume, although interaction models provided some evidence that sex might moderate the relationship between air pollution and hippocampal volume. In adjusted models, age, sex, educational attainment, income, overall health, current smoking, alcohol intake, and body-mass index were associated with hippocampal volume. Conclusions PM 2.5 at levels found in the United Kingdom was associated with smaller left hippocampal volume. Additional associations between several covariates and hippocampal volumes indicate that hippocampal volume might be associated with several potentially modifiable variables.

Infecting much of the world's population, the herpesviridae virus cytomegalovirus has been associated with lower cognitive function in some but not all studies. In this study, we further investigate associations between cytomegalovirus and cognitive function in a community-based sample of adults aged 40 to 70 years (M = 55.3; SD = 8.1) from the United Kingdom. Adjusted multiple-regression modeling showed no significant associations between cytomegalovirus and performance on nine cognitive tasks. Further, in adjusted interaction models, age, sex, educational attainment, and income did not moderate associations between cytomegalovirus and cognitive function. In this community-based adult sample, cytomegalovirus was not associated with cognitive function.

Infecting approximately one-third of the world’s human population, Toxoplasma gondii has been associated with cognitive function. Here, we sought to further characterize the association between Toxoplasma gondii and cognitive function in a community sample of adults aged approximately 40 to70 years. Using adjusted linear regression models, we found associations of Toxoplasma gondii seropositivity with worse reasoning (b = -.192, p < .05) and matrix pattern completion (b = -.681, p < .01), of higher anti-Toxoplasma gondii p22 antibody levels with worse reasoning (b = -.078, p < .01) and slower Trails (numeric) performance (b = 5.962, p < .05), of higher anti-Toxoplasma gondii sag1 levels with worse reasoning (b = -.081, p < .05) and worse matrix pattern completion (b = -.217, p < .05), and of higher mean of the anti-Toxoplasma gondii p22 and sag1 levels with worse reasoning (b = -.112, p < .05), slower Trails (numeric) performance (b = 9.195, p < .05), and worse matrix pattern completion (b = -.245, p < .05). Neither age nor educational attainment moderated associations between the measures of Toxoplasma gondii seropositivity or serointensity. Sex, however, moderated the association between the sag1 titer and digit-symbol substitution and the association between the mean of the p22 and sag1 levels and digit-symbol substitution, and income moderated the association between Toxoplasma gondii seropositivity and numeric memory and the association between the p22 level and symbol-digit substitution. Based on the available neuropsychological tasks in this study, Toxoplasma gondii seropositivity and serointensity were associated with some aspects of poorer executive function in adults., Author summary Toxoplasma gondii is a parasite that reproduces in cats but that can infect other animals and humans. Toxoplasma gondii has an affinity for the brain and infection results in a long-term immune response that may have negative effects. Animal models have shown that Toxoplasma gondii can affect behavior and cognition (thinking). In humans, the association is less clear, but there are associations between infection and variety of psychiatric and neurological conditions such as schizophrenia and epilepsy. Toxoplasma gondii may even increase the risk of dementia. If true, it is possible that the presence of this infection may affect thinking long before the onset of dementia. We sought to determine if the presence of antibodies in the blood to Toxoplasma gondii, which is the immune system’s response to past infections, might be associated with performance on measures of cognition. We analyzed a large dataset, the UK Biobank, which includes measures of cognition and blood test results for antibodies to Toxoplasma gondii. We found that both the presence of antibodies as well as the amount of these antibodies were related to some aspects of cognition, particularly problem solving and reasoning in otherwise healthy adults ages 40 to 69 years.

Objective Insomnia is associated with suicidality, although the mechanisms of this association are unclear. This study sought to replicate previous findings showing that insomnia symptoms but not sleep duration are associated with frequency of suicidal ideation in adults. We further investigated whether depression or sleep duration moderates the association between insomnia symptoms and frequency of suicidal ideation. Materials and Methods We used the 2005–2006 cycle of the National Health and Nutrition Examination Survey to replicate previously reported findings from the 2007–2008 cycle. We used ordered logistic regression to determine whether insomnia symptoms were associated with frequency of suicidal ideation independently of depression and other potential confounds. To extend these findings, we tested whether depression or sleep duration moderated the association between insomnia symptoms and frequency of suicidal ideation. We further replicated these findings in parallel analyses using the combined data from the 2005–2006 and 2007–2008 cycles. Results This study replicated previous results showing that insomnia symptoms are associated with frequency of suicidal ideation in the NHANES 2005–2006 cycle (OR = 1.09, p < 0.05), even after adjusting for potentially confounding variables, including depression. Neither depression nor sleep duration moderated this association. Difficulty with sleep maintenance insomnia symptoms were most robustly associated with frequency of suicidal ideation (OR ≥ 1.97, p < 0.05). Sleep duration was not robustly associated with suicidal ideation. Conclusions In this study, we found that insomnia symptoms were uniquely associated with frequency of suicidal ideation. This association cannot be explained by the shared association with depression or sleep duration.

Objective: We investigated two hypotheses: First, incident CHD, defined as myocardial infarction or definite angina, leads to faster long-term cognitive decline. Second, among those with CHD, treatment with CABG surgery or PCI leads to slower long-term cognitive decline. Methods: The Cardiovascular Health Study is a cohort of US adults aged 65+. Global cognitive ability was assessed annually up to 9 times from 1990 to 1998 with the 100-point Modified Mini-Mental State Examination (3MS). We estimated trajectories of 3MS scores in the absence of stroke, adjusting for demographics, health behaviors, and comorbidities. For hypothesis 1, we compared 3MS trajectory after incident CHD with 3MS trajectory in the absence of CHD, censoring at first receipt of CABG/PCI. For hypothesis 2, among participants with CHD, we compared 3MS trajectory after first receipt of CABG/PCI with 3MS trajectory without CABG/PCI. Results: For hypothesis 1, of 4,122 participants, 398 had incident CHD during a mean of 5.9 years of follow-up. Figure Panel A shows model-predicted mean 3MS trajectories without CHD (blue) and after incident CHD (red) diagnosed at ages 70, 75, 80, or 85. Model-predicted 3MS score declined faster after incident CHD, especially for CHD diagnosed at age 80 or later. For example, after incident CHD at age 85, predicted 5-year decline in mean 3MS score through age 90 was 13.9 points (95% CI: 11.0, 16.7) versus 8.9 points (95% CI: 8.1, 9.7) among those without CHD. For hypothesis 2, of 1,183 participants who had prevalent or incident CHD, 118 had their first CABG/PCI during a mean of 4.1 years of follow-up. Model-predicted 3MS score declined faster after first receipt of CABG/PCI ( Figure Panel B ). Conclusions: Older adults diagnosed with incident CHD had faster average cognitive decline than those without CHD. However, treatment with CABG/PCI did not slow cognitive decline among those with CHD. This finding may be due to adverse effects of CABG/PCI on brain health or CABG/PCI recipients having more severe CHD or more cerebral atherosclerosis.

Mood disorders are common mental illnesses. Among the factors associated with major depression are exposures to infectious diseases including hepatitis C, influenza, varicella-zoster, and herpes viruses. In this study, we sought to evaluate further associations between viral exposure and depression. From the US Center for Disease Control's National Health and Nutrition Examination Survey, we obtained data about depression status, antidepressant use, exposure to hepatitis A, hepatitis B, herpes simplex virus type 1, herpes simplex virus type 2, human immunodeficiency virus, and cytomegalovirus, and sociodemographic variables and evaluated associations between depression and viral exposure in adjusted multivariable models. Herpes simplex virus type 2 was associated with an increased risk of depression, whereas hepatitis A, hepatitis B, and herpes simplex virus type 1 were not. Higher cytomegalovirus antibody levels were associated with depression in subjects seropositive for cytomegalovirus. In conclusion, exposure to herpes simplex virus type 2 and possibly cytomegalovirus are associated with depression in an adult US sample.

Caused by the neuroinvasive nematodes Toxocara canis and Toxocara cati, human toxocariasis has a worldwide distribution with seroprevalence in humans associated with low socioeconomic status and low educational attainment. Third-stage Toxocara larvae can invade human tissues, including the brain and spine, where they can result in encephalitis, meningitis, and inflammation. Toxocara infection in animal models has been associated with cognitive and behavioural changes. In humans, preliminary cross-sectional research suggests that Toxocara seropositivity is associated with worse cognitive function in children and adults. Additional preliminary cross-sectional findings suggest associations between Toxocara seropositivity and neuropsychiatric function, including schizophrenia and neurologic conditions such as epilepsy. Given the widespread distribution of human toxocariasis and early evidence suggesting that it can be associated with cognitive and neuropsychiatric function in humans, additional research regarding the effects of toxocariasis on the human brain is required.

BackgroundAir pollution has been associated with cognitive function and brain volume. While most previous research has examined the association between air pollution and brain volume in cortical structures or total brain volume, less research has investigated associations between exposure to air pollution and subcortical structures, including the thalamus. Further, the few available previous studies investigating associations between air pollution and thalamic volume have shown mixed results.MethodsIn this study, we evaluated the association between PM2.5, PM2.5-10, PM10, nitrogen dioxide, and nitrogen oxides and volume of the thalamus in adults using the UK Biobank resource, a large community-based sample, while adjusting for multiple covariates that could confound an association between air pollution and thalamic volume.ResultsIn adjusted models, the left but not right thalamus volume was significantly inversely associated with PM2.5-10, although there were no significant associations between PM2.5, PM10, nitrogen dioxide, and nitrogen oxides with either left or right thalamic volumes. In addition, interactions between age and PM2.5-10 and PM10 were inversely associated with thalamic volume, such that thalamic volume in older people appeared more vulnerable to the adverse effects of PM2.5-10 and PM10, and interactions between educational attainment and PM2.5, nitrogen dioxide, and nitrogen oxides and between self-rated health and PM2.5-10 were positively associated with thalamic volume, such that higher educational attainment and better self-rated health appeared protective against the adverse effects of air pollution on the thalamus.ConclusionThese findings suggest a possible association between thalamic volume and air pollution particularly in older people and in people with comparatively low educational attainment at levels of air pollution found in the United Kingdom.

Associated with numerous cognitive and behavioral functions and with several diseases, the prefrontal cortex is vulnerable to environmental insult. Among other factors, toxins in air pollution have been associated with damage to the prefrontal cortex in children and older adults. We used data from the UK Biobank to assess further associations between an array of toxins in air pollution and gray matter in the prefrontal cortex including the left and right frontal poles, left and right superior frontal gyri, left and right frontal medial cortex, left and right orbitofrontal cortex, and left and right frontal opercula, using multivariate models adjusted for covariates that possibly could confound the association between air pollution and volume of prefrontal gray matter. The results showed inverse associations between PM 2.5, PM 10, and nitrogen oxides and prefrontal volume in models adjusted for age, sex, education, socioeconomic status, race-ethnicity, self-rated overall health, body mass index, total brain volume, smoking status, and alcohol use frequency. Education appeared to moderate the association between air pollution and prefrontal volume. The data in these analyses came from regions whose mean PM 2.5 was near the upper limit and whose mean PM 10 was under those recommended by the World Health Organization. These findings suggest that comparatively low levels of air pollution might be associated with reduced volume of the prefrontal cortex.

Background Helicobacter pylori (H. pylori) infection is associated with cognitive deficits in humans, an association potentially mediated or moderated by folate concentration or inflammation. Materials and Methods We used the National Health and Nutrition Examination Survey (NHANES) datasets to examine whether folate concentration or inflammation mediates or moderates the relationship between H. pylori and cognitive function. Models were performed using linear, Poisson, and zero-inflated Poisson regression, and we performed separate analyses for groups aged 20–59 and 60–90 years with sample sizes ranging from 700 to 1700. Results We did not find evidence of mediation in either age group. In the 20- to 59-year group, interactions between H. pylori and ferritin (p values ranging from .004 to .039) were associated with worse processing speed, better working memory, and worse reaction time. Interactions between H. pylori and fibrinogen (p values ranging from .023 to .045), C-reactive protein (CRP) (p = .023), and the inflammatory index (p = .045) were associated with worse processing speed. In 60- to 90-year-olds, H. pylori interacted with ferritin and the inflammatory index to predict fewer mathematical errors (p values of .036 and .023). Interactions with folate (p values of .016 and .006) and C-reactive protein (p values ranging from

The intracellular protozoal parasite Toxoplasma gondii has been associated with worsened cognitive function in animal models and in humans. Despite these associations, the mechanisms by which Toxoplasma gondii might affect cognitive function remain unknown, although Toxoplasma gondii does produce physiologically active intraneuronal cysts and appears to affect dopamine synthesis. Using data from the UK Biobank, we sought to determine whether Toxoplasma gondii is associated with decreased prefrontal, hippocampal, and thalamic gray-matter volumes and with decreased total gray-matter and total white-matter volumes in an adult community-based sample. The results from adjusted multivariable regression modelling showed no associations between Toxoplasma gondii and prefrontal, hippocampal, and thalamic brain gray-matter volumes. In contrast, natural-log transformed antibody levels against the Toxoplasma gondii p22 (b = -3960, 95-percent confidence interval, -6536 to -1383, p < .01) and sag1 (b = -4863, 95-percent confidence interval, –8301 to -1425, p < .01) antigens were associated with smaller total gray-matter volume, as was the mean of natural-log transformed p22 and sag1 titers (b = -6141, 95-percent confidence interval, -9886 to -2397, p < .01). There were no associations between any of the measures of Toxoplasma gondii and total white-matter volume. These findings suggest that Toxoplasma gondii might be associated with decreased total gray-matter in middle-aged and older middle-aged adults in a community-based sample from the United Kingdom.

Chronic pain is a common clinical condition that has a high lifetime prevalence, with significant morbidity and medical cost. An often overlooked aspect of chronic pain is the cognitive consequences. Findings on chronic pain and cognitive function reveal several important factors. First, patients with chronic pain appear to have worse cognitive functioning than do healthy controls, particularly in the areas of attention, processing speed, and executive functioning. Second, the duration and intensity of chronic pain appear to be negatively correlated with cognitive function. Third, chronic pain appears to affect cognitive functioning in a multifactorial fashion. That is, there appears to be a strong overlap between neural networks devoted to attention and areas of the brain associated with pain processing. There also seem to be both general and etiology-specific focal and regional brain-volume loss associated with pain and some evidence of a reversal of these morphological changes with the cessation of pain. Finally, long-term opioid medication use may have an effect on cognition, but the actual effect is difficult to elucidate given confounding factors such as interaction effects with other medications, the type of opioid, dosage, time of dose, and length of dose.

Characterized by alterations in mood, both major depression and bipolar disorder are also associated with deficits in neuropsychological function across several cognitive domains, including impaired attention, executive function, language, and processing speed. The majority of findings indicate that these deficits are likely present early in the course of affective disorders and can even persist after the resolution of the mood disturbance. The cognitive deficits in major depression and bipolar disorder appear to contribute to the disability associated with major depression and bipolar disorder. While the medications used to treat affective disorders might contribute to some of the cognitive impairments found in affective disorders, they do not appear to account for all of the cognitive impairments. The causes of the cognitive deficits associated with major depression remain unknown, although several possible causes require consideration. Abnormal function of the neural circuits associated with major depression and bipolar disorder might contribute not only to abnormal mood regulation but also to deficits in cognition. The association between affective disorders and cognitive function and mechanisms of this association require additional study.

This chapter discusses the epidemiological scope of Obstructive Sleep Apnea (OSA) and the characteristics and cause of cognitive impairments in OSA. OSA is a common medical condition and a significant public health concern, with increased rates in males and increased risk associated with obesity and age. Both observational and clinical research studies have examined the impact of OSA on neuropsychological outcomes, with evidence of both objective impairments and patient-reported impairments. Additional secondary factors are associated with OSA risk, and OSA is related to multiple medical comorbidities. The impact of OSA on cognitive function appears to be related to inflammation, cerebrovascular injury, and oxyhemoglobin desaturation. While language function is relatively resilient in OSA, executive functioning, memory, and visual-spatial functioning appear to be impaired. Cognitive impairments are correlated with morphological and volumetric changes on brain imaging, with evidence of some degree of recovery of structure and functioning with long-term consistent CPAP treatment.

Many studies have found some deficits in cognitive function in anorexia nervosa. While deficits in memory appear to be associated with anorexia nervosa, a more consistent finding is that anorexia nervosa appears to be associated with impairments in a variety of measures of executive function, and it is not clear how the cognitive impairments that are associated with anorexia might change with treatment and weight restoration. Overall, additional research is required to understand fully the associations between cognitive function and anorexia nervosa. The cognitive function of people with bulimia nervosa is even less clear. Many of the available studies show few if any differences between bulimia nervosa and healthy controls across a range of cognitive domains. Bulimia nervosa in the context of a history of anorexia nervosa might be associated with worse executive function than people with bulimia nervosa without a history of anorexia nervosa. Additional research is necessary to understand the relationships between bulimia nervosa and cognition.

While this chapter focuses on the cognitive consequences of cerebrovascular disease, it is also important to know that cerebrovascular disease is not a unitary condition but rather multiple conditions that affect the cerebrovascular health of the brain. These include obvious conditions such as ischemic and intracerebral hemorrhagic stroke, aneurysms, arteriovenous malformations, cardiac arrest, and carotid-artery occlusion and stenosis. In addition, cerebrovascular disease often leads to conditions primarily based on the cognitive consequences of these conditions, which would include vascular cognitive impairment and vascular dementia. This chapter will include a brief discussion of cardiovascular disease and epidemiology, followed by a discussion of the specifics of cerebrovascular disease, including mechanisms of action and cognitive ramifications. We will then briefly discuss treatment for cerebrovascular disease, and the chapter will conclude with a case example detailing the cognitive effects of vascular cognitive impairment.

A number of pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma, and acute respiratory distress syndrome (ARDS), not only effect the lungs but have well-described effects on the brain and behavior. Many individuals with pulmonary disorders experience new and often severe morbidities including cognitive impairments and psychological disorders such as depression and anxiety. These morbidities last for years and in the case of COPD and asthma may worsen with increased disease severity. This chapter will describe the cognitive impairments in patients with COPD, asthma, and ARDS. The chapter will also discuss mechanisms of injury, including hypoxia which is a common mechanism across these disorders. Finally, the chapter will discuss treatments for cognitive impairments with an emphasis on cognitive rehabilitation.

Deficits in attention and executive function appear to be fundamental aspects of attention-deficit, hyperactivity disorder, although impairment in executive function might not occur in all individuals who have attention-deficit, hyperactivity disorder. A crucial aspect of attention-deficit, hyperactivity disorder, though, is impairment in inhibitory response. Deficits in working memory, an aspect of executive function, are also associated with attention-deficit, hyperactivity disorder. Other cognitive deficits in addition to attention, inhibitory response, and working memory are associated with attention-deficit, hyperactivity disorder. These additional areas of deficits can include intellectual function and language.

Carbon monoxide (CO) poisoning is one of the most common types of poisoning in the USA and can be either acute or chronic. CO poisoning is diagnosed through examination of the patients’ history and is confirmed by an elevated carboxyhemoglobin level. The symptoms of CO poisoning are often nonspecific including headache, nausea, vomiting, or other flu-like symptoms which are often misdiagnosed. Many patients with CO poisoning develop new cognitive impairments that can occur immediately after the poisoning or can appear within 40 days of the CO poisoning known as delayed neurologic sequelae. Individuals with CO poisoning develop new morbidities including cognitive impairments and psychological disorders (depression and anxiety). Cognitive impairments occur in a variety of cognitive domains and vary in severity. This chapter will describe the cognitive impairments following CO poisoning, mechanism of injury including the role of hypoxia, and treatment for cognitive impairments.

Although generally conceptualized as involving primarily abnormal anxiety regulation, the anxiety disorders as a group along with obsessive–compulsive disorder and post-traumatic stress disorder also appear associated with deficits in cognitive function in several cognitive domains, including attention, executive function, language, memory, and processing speed. The association between cognitive deficits and anxiety varies across the various types of anxiety disorders, with some disorders having a greater association than others. It is unclear how treatment affects the cognitive deficits associated with the anxiety disorders and the causes of the cognitive impairments associated with the anxiety disorders remain to be identified. As is the case with the mood disorders, it is feasible that the abnormal function of the neural circuits associated with the anxiety disorders could contribute to cognitive impairments. Additional research is required to explore more fully cognitive function in anxiety disorders, obsessive–compulsive disorder, and post-traumatic stress disorder and how deficits in cognition contribute to the disorders and to the disability that can accompany these conditions.

In addition to the positive and negative features, deficits in cognition appear to be an important aspect of schizophrenia and are found in many cognitive domains, including attention, executive function, language, memory, processing speed, and visuospatial ability. The cognitive impairments associated with schizophrenia are present across the lifespan and occur in populations with schizophrenia across the world independent of geography and culture, although they might be more severe in men than in women. Despite considerable effort, there do not appear to be to date effective treatments for the cognitive deficits associated with schizophrenia. The severe functional burden associated with the cognitive impairments of schizophrenia and lack of effective treatments indicate the need for additional research into cognitive function in schizophrenia and ways to prevent and to treat the cognitive deficits associated with schizophrenia.

Traumatic brain injury (TBI) represents a common occurrence that places the brain at risk. This chapter first deals with the various definitional issues related to TBI, where the principal definitional challenges occur with mild injuries, often referred to as concussions. While the majority who sustain a mild TBI recover and may not have any lasting effects from the injury, even mild injuries may increase the risk of neuropsychiatric disorders later in life. One explanation for the adverse effects of TBI is the vulnerability of certain brain regions in the frontal and temporal lobes that relate to emotional and cognitive control. Moderate-to-severe TBI is association with considerable risk for adverse outcome and major disability. The chapter reviews some neuroimaging findings that demonstrate brain damage and how such neuropathology relates to changes in physical functioning, cognition, and behavior. How brain injuries may affect different domains of cognitive and behavioral functioning are discussed. The chapter concludes with an exploration of contemporary treatment for the physical, emotional, and cognitive effects from TBI.

Diabetes is a common endocrine disease and a common public health concern. Diabetes is associated with vascular burden and morphological brain change, and the increased risk of cerebrovascular disease appears to mediate much of the association, between diabetes and cognitive deficits. Such cognitive deficits appear to have a greater effect on processing speed and executive function than on other cognitive domains. Understanding the cognitive ramifications of diabetes may be important considering findings that cognitive impairment, particularly executive function, predicts diabetes knowledge, the number of appointments kept for diabetes treatment, insulin-adjustment skills, abilities to perform glucose checks and insulin injections, and general treatment compliance. Fortunately, there appears to be some evidence that medical treatment and lifestyle modification may mitigate the cognitive impairments that can be associated with diabetes.

Some substances and prescribed medications appear to be associated with cognitive impairments across a variety of cognitive domains, although comparatively few studies address associations between drug use and cognitive function, and in some cases, the clinical importance of some of the associations between drug use and cognitive function remains unclear. However, the available findings indicate that some medications and illicit drugs are indeed associated with cognitive deficits. The importance of pharmacotherapy for many diseases as well as the widespread use of drugs and substances suggests that awareness of the potential for drugs and substances to be associated with cognitive deficits is a critical part of drug use and development.

Each chapter of the Brain at Risk has explored different ways in which the brain is vulnerable for disease and/or various disorders, including ones that are acquired. Some of the latest research is presented in an informative way describing risk and mitigating factors that influence the expression and course of some of the more common major medical and environmental factors that alter behavior, emotional functioning, and cognition. Emphasis throughout each chapter is on a summation of the latest research on some of the most common major neuropsychological and neuropsychiatric disorders, highlighting the current understanding of each disease or disorder. Some general recommendations for improving outcome associated with some conditions are offered.

Due to a combination of advancing medical technology and the increasing age of the adult population, more adults are pursuing surgical intervention, particularly elective surgery, than ever before. Postoperative cognitive decline (POCD) describes either a transient or chronic change in cognitive function that comes as a result of anesthesia or surgical intervention and that and can occur at any age. POCD has a significant impact on functioning and quality of life. While there is variable reporting of POCD outcomes, it appears that POCD particularly affects executive function and memory. Emerging evidence suggests that modification to certain surgical procedures and methods to reduce inflammation during surgery might improve cognitive outcomes after surgery. Although an understanding of POCD, its risk and protective factors, and its duration is still in its infancy, neuropsychology can offer a valuable assessment of the risk of POCD and represents a valuable contribution to the presurgical evaluation.

Most commonly thought of as an autoimmune condition, multiple sclerosis (MS) represents the most common demyelinating condition and is, in fact, the most common neurological condition among young- and middle-aged adults. Multiple sclerosis has a significant negative impact on physical, perceptual, and cognitive functioning. Although reduced processing speed and difficulties with episodic memory are the most common neuropsychological consequences of MS, the aim of this chapter is to broadly discuss the neuropathology and epidemiology of MS and the broad cognitive functioning among individuals with MS. While patients with MS are typically maintained on medications, there is less research efficacy on cognitive rehabilitation techniques, although alternative treatments, such as exercise and mood treatment, show some promise in treating cognitive deficits in MS.

Caused by the parasitic nematodes Toxocara canis and cati, toxocariasis in humans can result in covert toxocariasis, ocular toxocariasis, visceral larval migrans, and neurotoxocariasis. A common infection, toxocariasis exposure varies widely within and between countries, with a previous estimate of Toxocara seroprevalence using data from 1988 to 1994 in the United States of approximately 13%. Age, poverty, sex, educational attainment, ethnicity, and region have been associated with Toxocara seroprevalence. In this study, we sought to determine the seroprevalence of and factors associated with Toxocara seropositivity in the United States using data from the National Health and Nutrition Examination Survey from 2011 to 2014 to provide a more recent estimate of Toxocara seroprevalence in the United States. We found an overall Toxocara seroprevalence of 5.1%. Increasing age, male sex, low educational attainment, low income, and immigration status each was associated with Toxocara seropositivity. Mexican Americans had reduced odds of exposure. These findings show that exposure to Toxocara continues in the United States and that several demographic factors influence the risk of exposure.

The intracellular parasite Toxoplasma gondii (Nicolle et Manceaux, 1908) infects humans resulting in acute toxoplasmosis, an infection that in immunocompetent people is typically mild but results in persistent latent toxoplasmosis. In that T. gondii appears to affect dopamine synthesis and because addicting drugs affect midbrain dopamine transmission, latent toxoplasmosis could influence substance use. Using both the third and continuous National Health and Nutrition Examination Surveys from the US Centers for Disease Control and Prevention, we used logistic regression to test for associations between T. gondii seropositivity and subject self-report of having ever used tobacco, alcohol, marijuana, cocaine, heroin, or methamphetamine. In the third NHANES dataset, which included data for tobacco, alcohol, marijuana and cocaine, T. gondii seropositivity was associated with a reduced likelihood of self-reported marijuana (OR = 0.71 [95% CI: 0.58; 0.87]; p = 0.001) and cocaine use (OR = 0.72 [95% CI: 0.56; 0.91]; p = 0.006). In the continuous National Health and Nutrition Examination Surveys dataset, which included data for all six substances, T. gondii seropositivity was associated with a reduced likelihood of self-reported tobacco (OR = 0.87 [95% CI: 0.76; 1.00]; p = 0.044), marijuana (OR = 0.60 [95% CI: 0.50; 0.72]; p < 0.001), heroin (OR = 0.60 [95% CI: 0.42; 0.85]; p = 0.005) and methamphetamine use (OR = 0.54 [95% CI: 0.38; 0.77]; p = 0.001). We observed interactions between sex and T. gondii seropositivity in the prediction of self-reported use of tobacco and alcohol. Further, T. gondii seropositivity appeared to remove the protective effect of education and economic status against self-reported cigarette smoking. These findings suggest that T. gondii seropositivity may be inversely associated with some but not all types of substance use in US adults.

Background: The apicomplexan protozoa Toxoplasma gondii (TG) is a successful parasite infecting ~30% of the human population, with some evidence to suggest it is more frequent in individuals with schizophrenia. TG has an affinity for the central nervous system and has been linked to cognitive and behavioral changes in rodents as well as humans. It is believed this mechanism contributes to the presentation of some schizophrenia cases. Given the relative absence of neurobiological studies, the aim of this project was to examine the influence of TG status on cortical thickness and cognitive function in a sample of schizophrenia and healthy individuals both seropositive and negative for the parasite. Methods: Schizophrenia (SCZ) = 77 (5 TG positive) and healthy control volunteers (CON) = 36 (11 TG positive) with clinical, cognitive, imaging, and available blood samples were used for the study. At least a 1-cc aliquot of serum from each subject was used for micro-enzyme-linked immunosorbent assay (ELISA) using a commercially available research kit for quantitative immunoenzymatic determination of anti-TG immunoglogulin G (IgG)-class antibodies. Cognitive and clinical functioning was assessed using a standardized battery. Structural T1-weighted images were processed using the FreeSurfer toolkit. Analyses included analysis of variance models examining differences in cortical thickness and cognition between TG seropositive (+) and negative (−) groups per condition (SCZ and CON); and Pearson correlation models of anti-TG IgG antibody titer values with thickness and behavioral variables within each condition group. Results: No significant differences in cortical thickness or cognition were observed in SCZ(+) vs SCZ(−), as well as CON(+) vs CON(−) groups, with the exception of visuospatial reasoning in CON. When correlating against anti-TG IgG titer values and cognition, significant negative relationships were noted with visuospatial reasoning (r = −.39, P = .02) and verbal memory (r = −.36, P = .03) in CON but none in SCZ. Titer values were significantly correlated with cortical thickness of the superior parietal region in SCZ (RH: r = −.24, P = .03) and at a trend level in CON (LH: r = −.31, P = .06; RH: r = −.30, P = .07). Conclusion: To our knowledge, this is the first study to examine cortical thickness in relation to cognitive function in a sample of SCZ and CON subjects with both seropositive and negative TG status. Results revealed the presence of TG appeared to primarily disrupt posterior association cortex and related functions (e.g., visuospatial reasoning) most prominently in healthy individuals but to a minor extent in schizophrenia patients. Overall, our findings suggest TG appears to exert greater influence over the neurobiology of nonpsychiatric individuals relative to psychosis, although addition research is warranted. Small seropositive sample sizes likely underpowered our ability to detect other effects.

Latent infection from Toxoplasma gondii (T. gondii) is widespread worldwide and has been associated with cognitive deficits in some but not all animal models and in humans. We tested the hypothesis that latent toxoplasmosis is associated with decreased cognitive function in a large cross-sectional dataset, the National Health and Nutrition Examination Survey (NHANES). There were 4178 participants aged 20-59 years, of whom 19.1% had IgG antibodies against T. gondii. Two ordinary least squares (OLS) regression models adjusted for the NHANES complex sampling design and weighted to represent the US population were estimated for simple reaction time, processing speed and short-term memory or attention. The first model included only main effects of latent toxoplasmosis and demographic control variables, and the second added interaction terms between latent toxoplasmosis and the poverty-to-income ratio (PIR), educational attainment and race-ethnicity. We also used multivariate models to assess all three cognitive outcomes in the same model. Although the models evaluating main effects only demonstrated no association between latent toxoplasmosis and the cognitive outcomes, significant interactions between latent toxoplasmosis and the PIR, between latent toxoplasmosis and educational attainment, and between latent toxoplasmosis and race-ethnicity indicated that latent toxoplasmosis may adversely affect cognitive function in certain groups.

Purpose (1) To assess the prevalence of rural primary care physician (PCP) bypass, a behavior in which residents travel farther than necessary to obtain health care, (2) To examine the role of community and non-health-care-related characteristics on bypass behavior, and (3) To analyze spatial bypass patterns to determine which rural communities are most affected by bypass. Methods Data came from the Montana Health Matters survey, which gathered self-reported information from Montana residents on their health care utilization, satisfaction with health care services, and community and demographic characteristics. Logistic regression and spatial analysis were used to examine the probability and spatial patterns of bypass. Results Overall, 39% of respondents bypass local health care. Similar to previous studies, dissatisfaction with local health care was found to increase the likelihood of bypass. Dissatisfaction with local shopping also increases the likelihood of bypass, while the number of friends in a community, and commonality with community reduce the likelihood of bypass. Other significant factors associated with bypass include age, income, health, and living in a highly rural community or one with high commuting flows. Conclusions Our results suggest that outshopping theory, in which patients bundle services and shopping for added convenience, extends to primary health care selection. This implies that rural health care selection is multifaceted, and that in addition to perceived satisfaction with local health care, the quality of local shopping and levels of community attachment also influence bypass behavior.

BackgroundInfectious diseases might affect cognitive aging and dementia risk, possibly via neuroinflammation. Similarly, risk factors for cardiovascular and cerebrovascular diseases are associated with cognitive function and dementia. We hypothesized that cardiovascular risk factors moderate the association of exposure to infectious diseases with cognitive function.MethodsWe studied 5662 participants aged 20 to 59 years from the third National Health and Nutrition Examination Survey (1988-1994) in the United States. We used linear regression to investigate whether the Framingham general cardiovascular risk index moderated the association of infection burden based on exposure to eight different infectious diseases with cognitive functioning as measured by the Symbol Digit Substitution, Serial Digit Learning, and Reaction Time tests.ResultsThe multiplicative interaction between the infection-burden index and the cardiovascular-risk index was associated with performance on the Symbol Digit Substitution (B = .019 [95% CI: .008, .031], p < .001) but not on the Serial Digit Learning (B = .034 [95% CI: -.025, .094]) or for Reaction Time (B = -.030 [95% CI: -.848, .787]). Participants with a lower cardiovascular risk appeared to be more resilient against the potential adverse effects of higher infection burden on the Symbol Digit Substitution task.ConclusionsParticipants at zero risk for a cardiovascular event in the next 10 years had no differences in processing speed with increasing exposure to infectious disease, whereas participants with higher risk for a cardiovascular event had worse processing speed with increased exposure to infectious disease.

Studies of traumatic brain injury (TBI) among adult populations demonstrate that such injuries can lead to aggressive behaviors. Related findings suggest that incarcerated individuals have high rates of brain injuries. Such studies suggest that traumatic brain injury may be related to the etiology and recidivism of criminal behavior. Relatively few studies have examined the prevalence of TBI using a delinquent juvenile sample. In order to assess the relationship between TBI and juvenile offender status, the current study used meta-analytic techniques to examine the odds of having a TBI among juvenile offenders. Across 9 studies, we found that approximately 30% of juvenile offenders have sustained a previous brain injury. Across 5 studies that used a control group, a calculated summary odds ratio of 3.37 suggests that juvenile offenders are significantly more likely to have a TBI compared to controls. Results suggest that the rate of TBIs within the juvenile offender population is significant and that there may be a relationship between TBIs and juvenile criminal behavior.