Epigenetic Mechanisms in Obesity: Broadening Our Understanding of the Disease.

Now recognized as more than just the result of overeating or the consumption of poor-quality foods, obesity is understood to be a multifactorial disease, strongly correlated with a variety of environment-gene interactions. In addressing the complex public health issue of obesity, medical practitioners, along with their allied healthcare counterparts, face the challenge of reducing its prevalence by utilizing and sharing with patients the current, yet incomplete, scientific knowledge concerning the disease. While continued research is required to strengthen direct cause-effect relationships, substantial evidence links post-translational modifications such as DNA methylation and histone modifications of several candidate "obesity" genes to the predilection for obesity. Additional evidence supports the influence of maternal diet during the gestational period, individual diet, and other lifestyle and genetic factors in obesity. The purpose of this review is to synthesize the current information concerning epigenetic modifications that appear to support, or result from, the development of obesity. Such mechanisms may serve as therapeutic targets for developing novel prevention and/or treatment strategies for obesity or as epigenetic biomarkers for monitoring recovery.

Pheochromocytoma: A Troublesome Tumor.

This report presents the case of a 45-year-old man with a history of episodic headaches, palpitations, and sweating for the past six months. His blood pressure on admission was 170/100 mmHg. The patient was diagnosed with pheochromocytoma confirmed by elevated levels of plasma catecholamines and metanephrines. CT imaging revealed a 3 cm mass in the left adrenal gland with evidence of local invasion into the surrounding tissues. The patient underwent a laparoscopic adrenalectomy and was discharged on the third postoperative day with normal blood pressure. Histopathological examination confirmed the diagnosis of pheochromocytoma. The patient was followed for six months postoperatively with the resolution of symptoms and no evidence of tumor recurrence on imaging. Recurrence involves complex environment-gene interactions that are poorly understood. The diagnosis of pheochromocytoma could take several weeks to several years mainly because the symptoms are nonspecific and episodic. Although sudden death is rare, the debilitations associated with pheochromocytoma are often multisystemic with cardiovascular, emotional, and metabolic components. This case report highlights the importance of early diagnosis, appropriate management, and follow-up for pheochromocytoma.

An Integrated Review of Carpal Tunnel Syndrome: New Insights to an Old Problem.

Carpal tunnel syndrome (CTS) is a common entrapment neuropathy characterized by pain, numbness, and impaired function of the hand due to compression of the median nerve at the level of the wrist. Although CTS can develop from repetitive strain, injury, or medical conditions, there are also congenital and genetic risk factors that can predispose individuals to the condition. With respect to anatomical factors, some individuals are born with a smaller carpal tunnel, which increases their susceptibility to median nerve compression. Variations in specific genes, such as those encoding proteins involved in extracellular matrix remodeling, inflammation, and nerve function, have also been linked to an increased risk for CTS. CTS is associated with a high cost of health care maintenance and loss of work productivity. Therefore, it is vital that primary care physicians fully understand the anatomy, epidemiology, pathophysiology, etiology, and risk factors of CTS, so they can be proactive in prevention, diagnosing, and guiding proper treatment. This integrated review also provides insights into how biological, genetic, environmental, and occupational factors interact with structural elements to determine who is most likely to acquire and suffer from CTS. Keeping health practitioners abreast of all the factors that could impact CTS should go a long way in decreasing the health care and socioeconomic burden of CTS.

A Study of Diurnal Cortisol Adaptations in Sleep-Deprived Firefighters During a 72-Hour Work Shift: A Case Series.

Seventy percent of US firefighters are overweight or obese. The combination of sleep deprivation and exposure to traumatic events during 72-hour work shifts, commonly employed in emergency responders, is thought to put firefighters at high risk for a variety of stress-related diseases and suicide. Previous studies suggest that the cortisol awakening response (CAR) may be increased in sleep-deprived emergency responders. This case series was designed to investigate the variations in CAR and associations with measurements of salivary cortisol and testosterone, blood glucose and triglyceride, and blood pressure during a 72-hour work shift. Measurements were made at 08:00 and 20:00 in five participants (one normal weight normotensive, three obese hypertensive, and one morbidly obese normotensive male). Data were characterized by the regression statistic R2 computed from the relationship between diurnal measurement and concentration, with significance at R2≥0.4. The predominant AM CAR adaptation response consisted of no significant 72-h change (flat response) in salivary cortisol (R2<0.4), found in three of the five participants (60%). The normal-weight participant's 72-h AM CAR adaptation was characterized as incremental (R2=0.91), and markedly different than that of the four obese firefighters who exhibited either a flat response (R2<0.4, 60%) or, in one subject, a decremental response (R2=0.40, 20%). The predominant 72-h PM cortisol adaptation was found to be decremental (R2=0.78-0.97) in three of the five participants (60%), including the normal weight subject (R2=0.78). Diurnal salivary cortisol and testosterone exhibited normal physiological circadian variations (P=0.01, AM>PM and P=0.1, AM>PM, respectively). Blood glucose and triglyceride also showed physiological circadian variations (P=0.02 AM

Aldosterone Synthase Inhibitors and Dietary Interventions: A Combined Novel Approach for Prevention and Treatment of Cardiovascular Disease.

Systemic hypertension (HTN) is the hallmark of cardiovascular disease and the forerunner of heart failure. These associations have been established over decades of research on essential HTN. Advancements in the treatment of patients diagnosed with HTN, consisting of alpha- or beta-adrenergic receptor blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, thiazide, or aldosterone receptor blockers known as anti-mineralocorticoids, in the presence or absence of low sodium salt diets, often fail to control blood pressure adequately to prevent morbidity and mortality. Low sodium diets have had limited success in controlling HTN because low sodium intake is associated with renin-angiotensin-aldosterone system upregulation. Therefore, upregulating aldosterone secretion, sodium, and water retention which, in turn, moves the blood pressure back toward the range of HTN dictated by the baroreceptor reset value, as a compensatory mechanism, especially in resistant HTN. These impediments to blood pressure control in HTN may have been effectively circumvented by the advent of a new class of drugs known as aldosterone synthase inhibitors, represented by baxdrostat. The mechanism of action of baxdrostat as an aldosterone synthase inhibitor demonstrates the inextricable linkage between sodium and blood pressure regulation. Theoretically, combining a low sodium diet with the activity of this aldosterone synthesis inhibitor should alleviate the adverse effect of renin-angiotensin-aldosterone system upregulation. Aldosterone synthesis inhibition should also decrease the oxidative stress and endothelial dysfunction associated with HTN, causing more endothelial nitric oxide synthesis, release, and vasorelaxation. To the best of our knowledge, this is the first systematic review to summarize evidence-based articles relevant to the use of a novel drug (aldosterone synthase inhibitor) in the treatment of HTN and cardiovascular disease. Making the current database of relevant information on baxdrostat and other aldosterone synthase inhibitors readily available will, no doubt, aid physicians and other medical practitioners in their decision-making about employing aldosterone synthase inhibitors in the treatment of patients.

Postprandial Hypotension: An Underreported Silent Killer in the Aged.

Orthostatic hypotension (OH) is one of the most common autonomic dysfunctions, with high prevalence in populations of elderly, hypertensive, diabetic, or Parkinson's patients. Evidence is emerging that OH co-occurs with postprandial hypotension (PPH); a greater prevalence of PPH than of OH is reported for Parkinson's disease patients. OH is diagnosed by measuring the blood pressure changes associated with postural changes and often produces alterations in consciousness or other such bothersome symptoms as fainting. PPH is diagnosed by measuring the blood pressure changes associated with ingesting high carbohydrate test meals. Because of the time lag between food ingestion and absorption, PPH is often not reported as symptomatic and, therefore, not diagnosed as PPH. OH and PPH are independent predictors for all causes of mortality. Relative underdiagnosis may qualify PPH as a "silent killer" disease. This review is aimed at providing updates on the epidemiology, pathophysiology, and clinical aspects associated with the diagnosis and treatment of PPH. Highlighting the current gaps in knowledge and research about PPH is expected to make medical practitioners more cognizant of the dangers of underdiagnosis and motivate future research to identify individuals and populations at high risk for PPH and its sequelae.

A Case of Guillain-Barré Syndrome With Multiple Causative Factors in a Young Male.

Guillain-Barré syndrome (GBS), an immune-mediated disease of the peripheral nervous system, is mainly characterized by rapidly progressive ascending weakness of the limbs with reduced or absent deep tendon reflexes. The exact cause of GBS is unknown, but it often occurs after a gastrointestinal or respiratory infection. The present study represents a case of GBS in which multiple antecedent antigenic stimuli may have contributed to the development of GBS. The patient, a 28-year-old immunocompetent man with no significant medical history, presented to the emergency department (ED) with acute ascending flaccid paralysis that persisted for a few days. His initial symptoms included tingling in his legs, which started at his shin and calf and developed into numbness, which extended to his upper limbs and arms. A CT scan of the lumbar and cervical spine indicated minor L4-L5 and L5-S1 disc herniation as well as slight bulging in C5-C6 and C7. The patient was discharged but returned to the ED for urgent treatment the next day after he weakened rapidly, losing the ability to walk or maintain balance. Based on his clinical presentation of ascending weakness and generalized hyporeflexia, he was diagnosed with GBS. Abnormal liver function and positive blood tests for anti-cytomegalovirus (anti-CMV) and anti-Epstein-Barr virus (anti-EBV) IgG and IgM antibodies diagnosed hepatitis, CMV, and EBV, respectively. The patient was treated with intravenous immunoglobulin therapy (IVIG; 27 g/day) and antiviral medicine (ganciclovir; 340 mg IV/day) for five days. His nonexistent deep tendon reflexes began to improve two to three days following treatment. He was able to ambulate longer distances with a walker, and his upper extremities regained full strength. This case highlights the importance of a multiple-treatment approach to the treatment of GBS, wherein multiple antigenic triggering factors may be involved.

Cardiac Rehabilitation and Cardiopulmonary Fitness in Children and Young Adults With Congenital Heart Diseases: A Critically Appraised Topic.

Public health guidelines and a myriad of studies have proven that exercise is beneficial in the alleviation of various cardio-metabolic diseases. Congenital heart disease (ConHD) is one of the most frequently occurring congenital structural malfunctions in the pediatric population, affecting nine of every 1,000 live births. Only a few studies have established the impact of a structured exercise program on cardiopulmonary fitness in diverse groups of patients with ConHD. It is also alarming to know that a substantial number of these patients and their caregivers often remain very wary of exercise. Anxiety about exercise may increase the risk of developing morbid obesity and other long-term health complications of ConHD. The present review of a critically appraised topic is undertaken to answer the question, "Does structured exercise intervention (cardiac rehabilitation) improve cardiorespiratory fitness in children and young adults with ConHD?" Exercise science and the medical literature were searched for studies that engaged the use of aerobic exercise in patients with different ConHD diagnoses. The search yielded four studies after screening with the inclusion and exclusion criteria, which were further narrowed to three studies after a full-text review. These studies yielded results showing significant increments in peak exercise workload, duration, power output, peak oxygen uptake, or improved tissue oxygenation and muscle strength after an exercise training intervention. It is noteworthy that a group identified as "cyanotic palliated" exhibited the most significant impairment both at baseline and after the exercise intervention. This review provides level 1b medical evidence that a structured exercise program may improve cardiopulmonary fitness in patients with ConHD, which is likely to be beneficial to their overall physical, motor, and psychosocial development. The results of this review may be useful for alleviating the anxiety of patients and their caregivers about participation in structured exercise programs. This review should also motivate future research investigations to develop clinical guidelines for the management of patients with ConHD by adding exercise prescriptions to their daily therapeutic regimens.

Epigenetics and Pain: New Insights to an Old Problem.

Physicians and neuroscientists have long observed that factors such as thoughts, emotions, and expectations can influence the perception of pain. Pain can be described as an unpleasant sensation that causes physical discomfort and emotional distress. It alerts an individual to seek help and is the main complaint that brings individuals to physicians. Though it is associated with probable tissue damage, such damage may be subtle, sometimes involving the release of algesic chemicals, and also influenced by attitudes, beliefs, personality, and social factors. The perception of pain may vary due to a multitude of these factors influencing the ascending sensory impulse propagation to the primary somatosensory cortex. The genetics and epigenetics of pain modulators have been previously studied, but there is a lack of application in the everyday management and treatment of pain due to the paucity of valid evidence-based data. We used the PubMed database as our primary tool for researching current literature on this topic. The MeSH terms used included: gene modification, epigenetics, genes, pain, analgesia, "types of pain, and theories of pain. The results were filtered as follows: publications within the last 10 years, generalized pain studies regarding the biopsychosocial aspect of pain, pertinent genes, and epigenetic modulation of those genes; 52 publications were selected for review. By addressing the external factorial causes and the appropriate application of epigenetic principles which affect pain perception, it is hoped that this review will motivate future advancements in the management of acute and/or chronic pain.

Epigenetic Influences on Wound Healing and Hypertrophic-Keloid Scarring: A Review for Basic Scientists and Clinicians.

Primary care physicians and dermatologists are challenged by patients affected by keloid or hypertrophic scarring resulting from accidental wounding, surgical incisions, tattooing, or "branding" procedures to demonstrate their association with a specific culture, fraternity, or cult. The dysregulated wound healing associated with keloids and hypertrophic scarring adversely affects genetically susceptible individuals, especially persons of color with Fitzpatrick Skin types IV-VI. Although the specific mechanisms of bulky hypertrophic/keloid scarring and its association with oxidative stress and inflammation remain unclear, the current knowledge base is sufficient to provide some guidance to health practitioners who must serve, treat, and counsel affected individuals. This review focuses on providing insight to healthcare professionals about the role of epigenetics, oxidative stress, poor local oxygenation, and its relationship to impaired wound healing. The goal is to promote further research on bulky hypertrophic and keloid scarring for its prevention and to develop evidence-based clinical guidelines for optimal treatment.

Electroencephalographic Signature of Negative Self Perceptions in Medical Students.

Frontal alpha asymmetry (fAA) is purported to be a neurophysiological marker for anxiety and depression. Higher left frontal alpha EEG voltage is associated with lower left and higher right frontal cerebral cortical activation, indicative of right-sided fAA. This pilot study tests the hypothesis that greater left-sided frontal alpha voltage is associated with negative thoughts about oneself. A group of eight healthy 28-41-year-old right-handed male medical students were subjected to an extensive interactive self-report inventory (ISI) evaluating perceptions of their psychosocial interactions. Quantitative EEG (qEEG) was performed with eyes closed. Computations of fAA and related parameters were based on measurements in the alpha bandwidth (8-13 Hz) at the left frontal F7 and right frontal F8 scalp electrodes. fAA was the percent difference between mean voltages at F8 minus that at F7. Significance of associations between fAA and the ISI scores was determined by Pearson's product-moment correlation coefficient, at P≤0.05. "Depressed" scores were positively correlated with right-sided fAA (P=0.01). "Relaxed" (P=0.05), "regulated" (P=0.02), "cooperative" (P=0.05) and "dependent scores" (P=0.004) were negatively correlated with right-sided fAA. These findings imply that right-sided fAA may be associated with more perceptions of "depressed" psychosocial interactions involving negative thoughts about oneself, as well as, more reliance on others ("dependence" score), less sharing ("cooperative" ISI score), less trust ("regulated" ISI score) and less initiative ("relaxed" ISI score). These results support the hypothesis that right-sided fAA may identify individuals with a predilection for negative thoughts about themselves and other negatively-valenced perceptions of their psychosocial interactions.

Pancoast tumor presenting with multiple joint pains: a case report.

BACKGROUND: Pancoast tumors represent a unique subset of lung cancers wherein a primary neoplasm arises in the lung's apex and invades the surrounding soft tissues. One of the main challenges in the diagnosis and treatment of these apical lung cancers is that they are usually not visualized on initial chest x-ray and, by the time the patient presents with symptoms, the tumor has almost always invaded nearby structures. CASE PRESENTATION: Herein we report a case of a 58-year-old nonsmoking African American male who presented to the neurology clinic with a history of multiple chronic joint pains. The patient complained of shoulder pain that traveled into his right arm and right finger and had worsened over the past 9 months. The patient also reported decreased right proximal strength and swelling of his right hand. Magnetic resonance imaging of the shoulder and cervical region showed mild cervical spondylosis and a questionable right apical mass. A subsequent high-resolution computed tomography scan of the chest revealed a large right apical lung mass, with chest wall invasion and erosion of the adjacent ribs. Biopsy of the mass confirmed poorly differentiated non-small cell lung cancer. Radiation therapy was initiated, and the patient's pain improved significantly. Given the size of the tumor, chemotherapy was recommended by the oncology team. The patient decided against chemotherapy. CONCLUSION: This case highlights the importance of early diagnosis by expanding the differential diagnosis in patients presenting with weakness, sensory loss, and shoulder pain beyond radiculopathy or joint-related diseases. A comprehensive history and careful examination may lead to an earlier diagnosis, more appropriate treatment, and better outcome in cases of Pancoast tumor presenting with neuropathic or musculoskeletal pain.

Case Report: Ulcerative Colitis with Multiple Dural Venous Thrombosis.

Background Cerebral sinus vein thrombosis (CVT) is a rare but serious complication associated with ulcerative colitis (UC), an idiopathic autoimmune inflammatory disease of the gastrointestinal tract. Management approaches for CVT remain unclear but may include anticoagulation and surgical thrombectomy. Herein, we report a case of a 23-year-old male who developed CVT with a history of UC. The patient was presented to Howard University Hospital when he slipped and fell. On arrival at the hospital, he complained of a headache with an aching sensation, associated with light/sound sensitivity. The patient had a history of uncontrolled UC. He had positive bloody diarrhea, lower abdominal pain, but denied any other neurological deficit. Computed tomography of the head showed left frontoparietal lobe hypodensities. Neurological exam was nonfocal. Vital signs were within normal range, but the patient experienced some memory loss and personality changes. Subsequent diagnosis of CVT was made with magnetic resonance angiography and magnetic resonance venography. Immediate treatment with low-molecular-weight intravenous heparin (18 IU/kg) was introduced. His UC was managed with methylprednisolone (60 mg IV daily), proton pump inhibitors, mesalamine, ciprofloxacin, and metronidazole. His condition gradually improved. On discharge, he was prescribed prednisone, azathioprine for his UC, levetiracetam for seizure, and warfarin with an INR goal of 2-3. In conclusion, the sudden onset and/or acute worsening of neurological status such as headache and mental confusion in a patient with UC should alert the treating physician about the possibility of CVT so that timely intervention could be employed to prevent disabling and potentially lethal sequelae of this disease.

Autoimmune Mechanisms of Interferon Hypersensitivity and Neurodegenerative Diseases: Down Syndrome.

Down syndrome (DS), also known as trisomy 21 (T21), is associated with interferon (IFN) hypersensitivity, as well as predilections for Alzheimer's dementia (AD) and various autoimmune diseases. IFN-α and IFN-γ receptors are encoded on chromosome 21 (Ch21). It remains unclear how other Ch21 genes contribute to the neuropathological features of DS/T21. This study tests the hypothesis that identifying IFN-stimulated response element (ISRE) control sites on Ch21 will mark novel candidate genes for DS/T21-related IFN hypersensitivity and neuropathology not previously reported to be associated with IFN functions. We performed whole chromosome searches of online databases. The general ISRE consensus and gamma interferon activation consensus sequences (GAS) were used for identifying IFN-stimulated response elements. Candidate genes were defined as those possessing two or more ISRE and/or GAS control sites within and/or upstream of the transcription start site. A literature search of gene functions was used to select the candidate genes most likely to explain neuropathology associated with IFN hypersensitivity. DOPEY2, TMEM50B, PCBP3, RCAN1, and SIM2 were found to meet the aforementioned gene search and functional criteria. These findings suggest that DOPEY2, TMEM50B, PCBP3, RCAN1, and SIM2 are genes which may be dysregulated in DS/T21 and may therefore serve as novel targets for treatments aimed at ameliorating the neuropathological features of DS/T21. Future studies should determine whether these genes are dysregulated in patients with DS, DS-related AD, and autoimmune diseases.

Vitamin D and Demyelinating Diseases: Neuromyelitis Optica (NMO) and Multiple Sclerosis (MS).

Vitamin D deficiency is prevalent in all ages regardless of climate or geographical location and evidence is emerging that the incidence of autoimmune diseases is increasing worldwide. Women make up a large proportion of autoimmune disease diagnoses, underscoring the importance of fully elucidating the complex synergistic relationships between estrogens and vitamin D. Vitamin D receptor-activating drugs appear to enhance remyelination in patients diagnosed with multiple sclerosis (MS) and other demyelinating diseases such as neuromyelitis optica (NMO). This review is intended to update health practitioners about the potential role of vitamin D deficiency demyelination and to motivate future research on dietary recommendations for vitamin D in preventing and treating demyel1nating diseases.

Norepinephrine stabilizes translation-dependent, homosynaptic long-term potentiation through mechanisms requiring the cAMP sensor Epac, mTOR and MAPK.

Neuromodulators regulate higher-order cognitive processes including learning and memory through modulation of synaptic transmission and plasticity. Norepinephrine is a neuromodulator that is secreted throughout the brain in response to novelty or increased arousal, which alters neural circuits by increasing the modifiability of CNS synapses. Norepinephrine activates metabotropic receptors, initiating complex intracellular signalling cascades that can promote enduring changes in synaptic strength including long-term potentiation (LTP). In particular, activation of beta-adrenergic receptors (ß-ARs) by norepinephrine enhances LTP through downstream engagement of signalling cascades which upregulate protein synthesis at synapses. Here, we sought to determine the select signalling pathways recruited by norepinephrine to promote homosynaptic LTP at hippocampal synapses in mice. Application of norepinephrine initiated a long-lasting form of homosynaptic LTP that requires protein synthesis. Norepinephrine-mediated enhancement of LTP was reduced by inhibition of mammalian target of rapamycin and exchange protein directly activated by cAMP (Epac) but not cAMP-dependent protein kinase A, suggesting that the endogenous ß-AR ligand norepinephrine may preferentially recruit Epac signalling to promote enduring changes in synaptic strength. These findings advance our understanding of the mechanisms through which norepinephrine regulates synaptic plasticity associated with formation of new memories.

Mood Responses to Passive and Active Motion Leg Cycling Exercise in Healthy Sedentary Young Adults.

Previous studies suggest that passive motion exercise (PME) may be useful for overcoming exercise limitations associated with a sedentary lifestyle, orthopedic disorders, and various other debilitating conditions. Negative mood response is one of the factors that limit a person's ability to exercise. Therefore, this study tests the hypothesis that the mood response associated with PME is not different than the mood response associated with active motion exercise (AME). Eight women and seven men participated in the study and were administrated the Profile of Mood States (POMS) during modes of PME and AME in a randomized order. Outcome of the POMS consisted of the total mood disturbance score [(feelings of tension + depression + fatigue + anger + confusion) - vigor]. ANOVA was used to determine significance of differences in total mood disturbance, oxygen uptake (V.O2), and middle cerebral blood flow velocity (MCAv) at baseline and immediately after 30-minute conditions of PME and AME. Postexercise total mood disturbance score was significantly decreased for both conditions (PME baseline 29.2 ± 5.2 vs. postexercise 16.4 ± 6.8, P < 0.05) and AME baseline 22.4 ± 4.4 vs. postexercise 13.1 ± 5.2, P < 0.05). These senses of changes in feelings were associated with significant physiological increases in V.O2 and MCAv during both PME and AME (P < 0.05). These results demonstrate that physiological and mood responses to passive and active motion cycling exercise are not different. Future studies should determine whether passive motion cycling exercise is a useful preventive medicine strategy for overcoming various disease-related exercise limitations and counteracting the adverse effects of sedentary lifestyles.

Associations of Alpha and Beta Interhemispheric EEG Coherences with Indices of Attentional Control and Academic Performance.

Introduction. Heretofore, research on optimizing academic performance has suffered from an inability to translate what is known about an individual's learning behaviors to how effectively they are able to use the critical nodes and hubs in their cerebral cortex for learning. A previous study from our laboratory suggests that lower theta-beta ratios (TBRs) measured by EEG may be associated with higher academic performance in a medical school curriculum. METHODS: In this study, we tested the hypothesis that TBR and academic performance may be correlated with EEG coherence, a measure of brain connectivity. We analyzed the interhemispheric coherences of the subjects involved in our prior study. TBR and coherence measurements were made at 19 scalp electrode recording sites and 171 electrode combinations with eyes open and closed (EO, EC). Control data were acquired during a session of acclimation to the research protocol 3 d before an initial examination in anatomy-physiology (control exam) and were repeated five weeks later, 3 d before a second exam covering different anatomy-physiology topics (comparison exam). RESULTS: Between the control and comparison exams, beta coherences increased significantly at the frontal pole, frontal, parietal, midtemporal, posterior temporal, and occipital recording sites under the EO condition and at the inferior frontal, central, midtemporal, and posterior temporal sites under the EC condition. Alpha coherences increased significantly at the same sites and under the same EO/EC conditions as found for the beta coherences. The beta coherences were negatively correlated with the TBR and were positively correlated with the comparison exam score at the midfrontal electrode site (F3-F4) but only under the EO condition. Beta and alpha coherences at the midfrontal, inferior frontal midtemporal, posterior temporal, and occipital sites were also negatively correlated with the average TBR under the EO condition. CONCLUSIONS: Lower TBR, an indicator of attentional control, was associated with higher alpha and beta interhemispheric coherences measured with eyes open at sites overlying the frontal, temporal, and occipital cortices. Changes in EEG coherences and TBRs might be useful as neurophysiological measures of neuroplasticity and the efficacy of strategies for preventing academic underachievement and treatments for improving academic performance.

qEEG Measures of Attentional and Memory Network Functions in Medical Students: Novel Targets for Pharmacopuncture to Improve Cognition and Academic Performance.

OBJECTIVES: Attentional and memory functions are important aspects of neural plasticity that, theoretically, should be amenable to pharmacopuncture treatments. A previous study from our laboratory suggested that quantitative electroencephalographic (qEEG) measurements of theta/beta ratio (TBR), an index of attentional control, may be indicative of academic performance in a first-semester medical school course. The present study expands our prior report by extracting and analyzing data on frontal theta and beta asymmetries. We test the hypothesis that the amount of frontal theta and beta asymmetries (fTA, fBA), are correlated with TBR and academic performance, thereby providing novel targets for pharmacopuncture treatments to improve cognitive performance. METHODS: Ten healthy male volunteers were subjected to 5-10 min of qEEG measurements under eyes-closed conditions. The qEEG measurements were performed 3 days before each of first two block examinations in anatomy-physiology, separated by five weeks. Amplitudes of the theta and beta waveforms, expressed in µV, were used to compute TBR, fTA and fBA. Significance of changes in theta and beta EEG wave amplitude was assessed by ANOVA with post-hoc t-testing. Correlations between TBR, fTA, fBA and the raw examination scores were evaluated by Pearson's product-moment coefficients and linear regression analysis. RESULTS: fTA and fBA were found to be negatively correlated with TBR (P<0.03, P<0.05, respectively) and were positively correlated with the second examination score (P<0.03, P=0.1, respectively). CONCLUSION: Smaller fTA and fBA were associated with lower academic performance in the second of two first-semester medical school anatomy-physiology block examination. Future studies should determine whether these qEEG metrics are useful for monitoring changes associated with the brain's cognitive adaptations to academic challenges, for predicting academic performance and for targeting phamacopuncture treatments to improve cognitive performance.

Environmental Enrichment and Brain Neuroplasticity in the Kainate Rat Model of Temporal Lobe Epilepsy.

BACKGROUND AND PURPOSE: Environmental enrichment (EE) improves brain function and ameliorates cognitive impairments; however, whether EE can reverse the learning and memory deficits seen following seizures remains unknown. METHODS: We tested the hypothesis that EE augments neurogenesis and attenuates the learning and memory deficits in rats subjected to kainate-induced seizures in hippocampus, amygdala and motor cortex. EE consisted of daily exposures immediately after KA lesioning (early EE) and after a 60-day period (late EE). Morphometric counting of neuron numbers (NN), dendritic branch-points and intersections (DDBPI) were performed. Spatial learning in a T-maze test was described as percent correct responses and memory in a passive-avoidance test was calculated as time spent in the small compartment where they were previously exposed to an aversive stimulus. RESULTS: EE increased NN and DDBPI in the normal control and in the KA-lesioned rats in all brain areas studied, after both early and late exposure to EE. Late EE resulted in significantly fewer surviving neurons than early EE in all brain areas (p < 0.0001). EE increased the percent correct responses and decreased time spent in the small compartment, after both early and late EE. The timing of EE (early vs. late) had no effect on the behavioral measurements. CONCLUSIONS: These findings demonstrate that, after temporal lobe and motor cortex epileptic seizures in rats, EE improves neural plasticity in areas of the brain involved with emotional regulation and motor coordination, even if the EE treatment is delayed for 60 days. Future studies should determine whether EE is a useful therapeutic strategy for patients affected by seizures.