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During Lucid Dreams, the dreamer is aware, experiences the dream as if fully awake, and may control the dream content. The dreamer can start, stop, and restart dreaming, depending on the nature and pleasantness of the dream. For patients with Reward Deficiency Syndrome (RDS) behaviors, like Attention Deficit Hyperactivity Disorder (ADHD), Tourette's-Syndrome, and Posttraumatic Stress Disorder (PTSD), the dream content may be pleasant, unpleasant, or terrifying. A sample of psychiatric center patients identified as having RDS reported the effectiveness of a neuronutrient, dopamine agonist, KB200Z, in combating terrifying, lucid dreaming. These reports motivated the study of eight clinical cases with known histories of substance abuse, childhood abuse, and PTSD. The administration of KB200Z, associated with eliminating unpleasant or terrifying lucid dreams in 87.5% of the cases. Subsequently, other published cases have further established the possibility of the long-term elimination of terrifying dreams in PTSD and ADHD patients. Induction of dopamine homeostasis may mitigate the effects of neurogenetic and epigenetic changes in neuroplasticity, identified in the pathogenesis of PTSD and ADHD. The article explores how relief of terrifying lucid dreams may benefit from modulation of dopaminergic signaling activated by the administration of a neuronutrient. Recently, precision formulations of the KB220 neuronutrient guided by Genetic Addiction Risk Severity (GARS) test results have been used to repair inheritable deficiencies within the brain reward circuitry. The proposition is that improved dopamine transmodulational signaling may stimulate positive cognitive recall and subsequently attenuate the harmful epigenetic insults from trauma.

This is a review of research on “Precision Behavioral Management” of substance use disorder (SUD). America is experiencing a high prevalence of substance use disorder, primarily involving legal and illegal opioid use. A 3000% increase in treatment for substance abuse has occurred between 2000 and 2016. Unfortunately, present day treatment of opioid abuse involves providing replacement therapy with powerful opioids to, at best, induce harm reduction, not prophylaxis. These interventions do not enhance gene expression and restore the balance of the brain reward system’s neurotransmitters. We are proposing a generalized approach called “Precision Behavioral Management”. This approach includes 1) using the Genetic Addiction Risk Severity (GARS, a 10 candidate polymorphic gene panel shown to predict ASI-alcohol and drug severity) to assess early pre-disposition to substance use disorder; 2) using a validated reward deficiency syndrome (RDS) questionnaire; 3) utilization of the Comprehensive Analysis of Reported Drugs (CARD™) to assess treatment compliance and abstinence from illicit drugs during treatment, and, importantly; 4) utilization of a “Pro-dopamine regulator (KB220)” (via IV or oral [KB220Z] delivery systems) to optimize gene expression, restore the balance of the Brain Reward Cascade’s neurotransmitter systems and prevent relapse by induction of dopamine homeostasis, and; 5) utilization of targeted DNA polymorphic reward genes to direct mRNA genetic expression profiling during the treatment process. Incorporation of these events can be applied to not only the under-considered African-American RDS community, but all victims of RDS, as a demonstration of a paradigm shift that uniquely provides a novel putative “standard of care” based on DNA guided precision nutrition therapy to induce “dopamine homeostasis” and rebalance neurotransmitters in the Brain Reward Cascade. We are also developing a Reward Deficiency Syndrome Diagnostic Criteria (RDSDC) to assist in potential tertiary treatment.

Introduction: Polymorphic gene variants, particularly the genetic determinants of low dopamine function (hypodopaminergia), are known to associate with Substance Use Disorder (SUD) and a predisposition to PTSD. Addiction research and molecular genetic applied technologies supported by the National Institutes of Health (NIH) have revealed the complex functions of brain reward circuitry and its crucial role in addiction and PTSD symptomatology. Discussion: It is noteworthy that Israeli researchers compared mice with a normal immune system with mice lacking adaptive immunity and found that the incidence of PTSD increased several-fold. It is well established that raising endorphinergic function increases immune response significantly. Along these lines, Blum’s work has shown that D-Phenylalanine (DPA), an enkephalinase inhibitor, increases brain endorphins in animal models and reduces stress in humans. Enkephalinase inhibition with DPA treats Post Traumatic Stress Disorder (PTSD) by restoring endorphin function. The Genetic Addiction Risk Severity (GARS) can characterize relevant phenotypes, genetic risk for stress vulnerability vs. resilience. GARS could be used to pre-test military enlistees for adaptive immunity or as part of PTSD management with customized neuronutrient supplementation upon return from deployment. Conclusion: Based on GARS values, with particular emphasis on enhancing immunological function, pro-dopamine regulation may restore dopamine homeostasis. Recognition of the immune system as a “sixth sense” and assisting adaptive immunity with Precision Behavioral Management (PBM), accompanied by other supportive interventions and therapies, may shift the paradigm in treating stress disorders.

Millions of Americans experience pain daily. In 2017, opioid overdose claimed 64,000 lives increasing to 84,000 lives in 2020, resulting in a decrease in national life expectancy. Chronic opioid use results in dependency, drug tolerance, neuroadaptation, hyperalgesia, potential addictive behaviors, or Reward Deficiency Syndrome (RDS) caused by a hypodopaminergia. Evaluation of pain clinic patients with the Genetic Addiction Risk Score (GARS) test and the Addiction Severity Index (ASI- Media Version V) revealed that GARS scores equal to or greater than 4 and 7 alleles significantly predicted drug and alcohol severity, respectively. We utilized RT-PCR for SNP genotyping and multiplex PCR/capillary electrophoresis for fragment analysis of the role of eleven alleles in a ten-reward gene panel, reflecting the activity of brain reward circuitry in 121 chronic opioid users. The study consisted of 55 males and 66 females averaging ages 54 and 53 years of age, respectively. The patients included Caucasians, African Americans, Hispanics, and Asians. Inclusion criteria mandated that the Morphine Milligram Equivalent (MME) was 30–600 mg/day (males) and 20 to 180 mg/day (females) for treatment of chronic pain over 12 months. Ninety-six percent carried four or more risk alleles, and 73% carried seven or more risk alleles, suggesting a high predictive risk for opioid and alcohol dependence, respectively. These data indicate that chronic, legally prescribed opioid users attending a pain clinic possess high genetic risk for drug and alcohol addiction. Early identification of genetic risk, using the GARS test upon entry to treatment, may prevent iatrogenic induced opioid dependence.

Neuroscientists and psychiatrists working in the areas of “pain and addiction” are asked in this perspective article to reconsider the current use of dopaminergic blockade (like chronic opioid agonist therapy), and instead to consider induction of dopamine homeostasis by putative pro-dopamine regulation. Pro-dopamine regulation could help pharmaceutical opioid analgesic agents to mitigate hypodopaminergia-induced hyperalgesia by inducing transmodulation of dopaminergic signaling. An optimistic view is that early predisposition to diagnosis based on genetic testing, (pharmacogenetic/pharmacogenomic monitoring), combined with appropriate urine drug screening, and treatment with pro-dopamine regulators, could conceivably reduce stress, craving, relapse, enhance well-being and attenuate unwanted hyperalgesia. These concepts require intensive investigation. However, based on the rationale provided herein, there is a good chance that combining opioid analgesics with genetically directed pro-dopamine-regulation using KB220 (supported by 43 clinical studies). This prodopamine regulator may become a front-line technology with the potential to overcome, in part, the current heightened rates of chronic opioid-induced hyperalgesia and concomitant Reward Deficiency Syndrome (RDS) behaviors. Current research does support the hypothesis that low or hypodopaminergic function in the brain may predispose individuals to low pain tolerance or hyperalgesia.

Background/Aims:This case series presents the novel Genetic Addiction Risk Score (GARS®) coupled with a customized pro-dopamine regulator matched to polymorphic reward genes having a hypodopaminergic risk.Methods:The proband is a female with a history of drug abuse and alcoholism. She experienced a car accident under the influence and voluntarily entered treatment. Following an assessment, she was genotyped using the GARS, and started a neuronutrient with a KB220 base indicated by the identified polymorphisms. She began taking it in April 2018 and continues.Results:She had success in recovery from Substance Use Disorder (SUD) and improvement in socialization, family, economic status, well-being, and attenuation of Major Depression. She tested negative over the first two months in treatment and a recent screening. After approximately two months, her parents also decided to take the GARS and started taking the recommended variants. The proband’s father (a binge drinker) and mother (no SUD) both showed improvement in various behavioral issues. Finally, the proband’s biological children were also GARS tested, showing a high risk for SUD.Conclusions:This three-generation case series represents an example of the impact of genetic information coupled with an appropriate DNA guided “Pro-Dopamine Regulator” in recovery and enhancement of life.

Background: The search for an accurate, gene-based test to identify heritable risk factors for Reward Deficiency Syndrome (RDS) was conducted based on hundreds of published studies about the role of dopamine in addictive behaviors, including risk for drug dependence and compulsive/impulsive behavior disorders. The term RDS was first coined by Blum’s group in 1995 to identify a group of behaviors with a common neurobiological mechanism associated with a polymorphic allelic propensity for hypodopaminergia. Objectives: To outline the process used to select risk alleles of reward genes for the Genetic Addiction Risk Score (GARS) test. Consequently, to address the limitations caused by inconsistent results that occur in many case-control behavioral association studies. These limitations are perhaps due to the failure of investigators to adequately screen controls for drug and alcohol use disorder, and any of the many RDS behaviors, including nicotine dependence, obesity, pathological gambling, and internet gaming addiction. Method: Review of the literature related to the function of risk alleles of reward genes associated with hypodopaminergia relevant case-control association studies for the selection of alleles to be measured by the Genetic Addiction Risk Score (GARS) test. Result: The prevalence of the DRD2 A1 allele in unscreened controls (33.3%), compared to “Super-Controls” [highly screened RDS controls (3.3%) in proband and family] is used to exemplify a possible solution. Conclusion: Unlike One Gene-One Disease (OGOD), RDS is polygenetic, and very complex. In addition, any RDS-related behaviors must be eliminated from the control group in order to obtain the best possible statistical analysis instead of comparing the phenotype with diseaseridden controls.

Reward Deficiency Syndrome (RDS) encompasses many mental health disorders, including a wide range of addictions and compulsive and impulsive behaviors. Described as an octopus of behavioral dysfunction, RDS refers to abnormal behavior caused by a breakdown of the cascade of reward in neurotransmission due to genetic and epigenetic influences. The resultant reward neurotransmission deficiencies interfere with the pleasure derived from satisfying powerful human physiological drives. Epigenetic repair may be possible with precision gene-guided therapy using formulations of KB220, a nutraceutical that has demonstrated pro-dopamine regulatory function in animal and human neuroimaging and clinical trials. Recently, large GWAS studies have revealed a significant dopaminergic gene risk polymorphic allele overlap between depressed and schizophrenic cohorts. A large volume of literature has also identified ADHD, PTSD, and spectrum disorders as having the known neurogenetic and psychological underpinnings of RDS. The hypothesis is that the true phenotype is RDS, and behavioral disorders are endophenotypes. Is it logical to wonder if RDS exists everywhere? Although complex, “the answer is blowin’ in the wind,” and rather than intangible, RDS may be foundational in species evolution and survival, with an array of many neurotransmitters and polymorphic loci influencing behavioral functionality.

In the United States, amid the opioid overdose epidemic, nonaddicting/nonpharmacological proven strategies are available to treat pain and manage chronic pain effectively without opioids. Evidence supporting the long-term use of opioids for pain is lacking, as is the will to alter the drug-embracing culture in American chronic pain management. Some pain clinicians seem to prefer classical analgesic agents that promote unwanted tolerance to analgesics and subsequent biological induction of the “addictive brain”. Reward genes play a vital part in modulation of nociception and adaptations in the dopaminergic circuitry. They may affect various sensory and affective components of the chronic pain syndromes. The Genetic Addiction Risk Severity (GARS) test coupled with the H-Wave at entry in pain clinics could attenuate pain and help prevent addiction. The GARS test results identify high-risk for both drug and alcohol, and H-Wave can be initiated to treat pain instead of opioids. The utilization of H-Wave to aid in pain reduction and mitigation of hedonic addictive behaviors is recommended, notwithstanding required randomized control studies. This frontline approach would reduce the possibility of long-term neurobiological deficits and fatalities associated with potent opioid analgesics.

Background: The risk for all addictive drug and non-drug behaviors, especially, in the unmyelinated Prefrontal Cortex (PFC) of adolescents, is important and complex. Many animal and human studies show the epigenetic impact on the developing brain in adolescents, compared to adults. Some reveal an underlying hyperdopaminergia that seems to set our youth up for risky behaviors by inducing high quanta pre-synaptic dopamine release at reward site neurons. In addition, altered reward gene expression in adolescents caused epigenetically by social defeat, like bullying, can continue into adulthood. In contrast, there is also evidence that epigenetic events can elicit adolescent hypodopaminergia. This complexity suggests that neuroscience cannot make a definitive claim that all adolescents carry a hyperdopaminergia trait. Objective: The primary issue involves the question of whether there exists a mixed hypo or hyper - dopaminergia in this population. Methods: Genetic Addiction Risk Score (GARS®) testing was carried out of 24 Caucasians of ages 12-19, derived from families with RDS. Results: We have found that adolescents from this cohort, derived from RDS parents, displayed a high risk for any addictive behavior (a hypodopaminergia), especially, drug-seeking (95%) and alcohol- seeking (64%). Conclusion: The adolescents in our study, although more work is required, show a hypodopaminergic trait, derived from a family with Reward Deficiency Syndrome (RDS). Certainly, in future studies, we will analyze GARS in non-RDS Caucasians between the ages of 12-19. The suggestion is first to identify risk alleles with the GARS test and, then, use well-researched precision, pro-dopamine neutraceutical regulation. This “two-hit” approach might prevent tragic fatalities among adolescents, in the face of the American opioid/psychostimulant epidemic.

The current addiction crisis has destroyed a multitude of lives, leaving millions of fatalities worldwide in its wake. At the same time, various governmental agencies dedicated to solving this seemingly never-ending dilemma have not yet succeeded or delivered on their promises. We understand that addictive behavioral seeking is a multi-faceted neurobiological and spiritually complicated phenomenon. However, although the substitution replacement approach, especially to treat Opioid Use Disorder (OUD), has importance for harm reduction in the short term, it does not bring about a harm-free recovery or prevention. Instead, we propose a promising novel approach that uses genetic risk testing with induction of dopamine homeostasis and an objective Brain Health Check during youth. Our model involves a six-hit approach known as the "Reward Dysregulation Syndrome Solution System," which can identify addiction risk and target the root cause of addiction, dopamine dysregulation. While we applaud all past sophisticated neurogenetic and neuropharmacological research, our opinion is that in the long term, addiction scientists and clinicians might characterize preaddiction using tests; for example, administering the validated RDSQuestionarre29, genetic risk assessment, a modified brain health check, or diagnostic framing of mild to moderate Substance Use Disorder (SUD). The preaddiction concept could incentivize the development of interventions to prevent addiction from developing in the first place and target and treat neurotransmitter imbalances and other early indications of addiction. WC 222.

INTRODUCTION: Polymorphic gene variants, particularly the genetic determinants of low dopamine function (hypodopaminergia), are known to associate with Substance Use Disorder (SUD) and a predisposition to PTSD. Addiction research and molecular genetic applied technologies supported by the National Institutes of Health (NIH) have revealed the complex functions of brain reward circuitry and its crucial role in addiction and PTSD symptomatology. DISCUSSION: It is noteworthy that Israeli researchers compared mice with a normal immune system with mice lacking adaptive immunity and found that the incidence of PTSD increased several-fold. It is well established that raising endorphinergic function increases immune response significantly. Along these lines, Blum’s work has shown that D-Phenylalanine (DPA), an enkephalinase inhibitor, increases brain endorphins in animal models and reduces stress in humans. Enkephalinase inhibition with DPA treats Post Traumatic Stress Disorder (PTSD) by restoring endorphin function. The Genetic Addiction Risk Severity (GARS) can characterize relevant phenotypes, genetic risk for stress vulnerability vs. resilience. GARS could be used to pre-test military enlistees for adaptive immunity or as part of PTSD management with customized neuronutrient supplementation upon return from deployment. CONCLUSION: Based on GARS values, with particular emphasis on enhancing immunological function, pro-dopamine regulation may restore dopamine homeostasis. Recognition of the immune system as a “sixth sense” and assisting adaptive immunity with Precision Behavioral Management (PBM), accompanied by other supportive interventions and therapies, may shift the paradigm in treating stress disorders.

This article describes a unique therapeutic precision intervention, a formulation of enkephalinase inhibitors, enkephalin, and dopamine-releasing neuronutrients, to induce dopamine homeostasis for detoxification and treatment of individuals genetically predisposed to developing reward deficiency syndrome (RDS). The formulations are based on the results of the addiction risk severity (GARS) test. Based on both neurogenetic and epigenetic evidence, the test evaluates the presence of reward genes and risk alleles. Existing evidence demonstrates that the novel genetic risk testing system can successfully stratify the potential for developing opioid use disorder (OUD) related risks or before initiating opioid analgesic therapy and RDS risk for people in recovery. In the case of opioid use disorders, long-term maintenance agonist treatments like methadone and buprenorphine may create RDS, or RDS may have been in existence, but not recognized. The test will also assess the potential for benefit from medication-assisted treatment with dopamine augmentation. RDS methodology holds a strong promise for reducing the burden of addictive disorders for individuals, their families, and society as a whole by guiding the restoration of dopamine homeostasisthrough anti-reward allostatic neuroadaptations. WC 175.

Background Addictive-like behaviors (e.g., hoarding and shopping) may be the result of the cumulative effects of dopaminergic and other neurotransmitter genetic variants as well as elevated stress levels. We, therefore, propose that dopamine homeostasis may be the preferred goal in combating such challenging and unwanted behaviors, when simple dopaminergic activation through potent agonists may not provide any resolution. Case presentation C.J. is a 38-year-old, single, female, living with her mother. She has a history of substance use disorder as well as attention deficit hyperactivity disorder, inattentive type. She had been stable on buprenorphine/naloxone combination and amphetamine, dextroamphetamine mixed salts for many years when unexpectedly she lost her job for oversleeping and not calling into work. KB200z (a pro-dopamine compound) was added to her regimen for complaints of low drive and motivation. After taking this nutraceutical for 4 weeks, she noticed a marked improvement in her mental status and many behaviors. She noted that her shopping and hoarding addictions had appreciably decreased. Furthermore, her lifelong history of terrifying lucid dreams was eliminated. Finally, she felt more in control; her locus of control shifted from external to more internal. Discussion The hypothesis is that C.J.'s reported, behavioral, and psychological benefits resulted from the pro-dopamine-regulating effect of KB220Z across the brain reward system. Conclusions This effect, we surmise, could be the result of a new dopamine balance, across C.J.'s brain reward system. Dopamine homeostasis is an effect of KB220Z seen in both animal and human placebo-controlled fMRI experiments.

Parkinson's disease (PD) is primarily considered to be a progressive degenerative motor disease associated with the degeneration of striatal dopamine neurons. However, increasing evidence has suggested progressive cognitive and psychiatric changes as well. Forty-six patients with PD, ranging in severity from Hoehn and Yahr (H-Y) score of 1:4, were recruited from a clinic specializing in PD. Various cognitive and neuropsychological measures were used to discover if there were indeed differences due to the progression of PD. As H-Y stage significantly increased, so did age and levodopa equivalency dose of medications, both independent of one another. Years of education had a significant negative relationship with H-Y score. Measures of general cognition divulged a significant decrease as H-Y score increased. Finally, as H-Y score increased, magical ideation decreased, and religious group social support increased. Mechanistically, the significant cognitive decline occurring with H-Y staging may be linked to a reduced dopaminergic function. Significant cognitive and neuropsychological changes are associated with the progression of PD and its possible relationship to Reward Deficiency Syndrome (RDS).

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys cognitive skills and the ability to perform the simplest tasks. More than 5 million Americans are afflicted with Alzheimer’s; a disorder which ranks third, just behind heart disease and cancer, as a cause of death for older people. With no real cure and in spite of enormous efforts worldwide, the disease remains a mystery in terms of treatment. Importantly, African Americans are two times as likely as Whites to develop late-onset Alzheimer’s disease and less likely to receive timely diagnosis and treatment. Dopamine function is linked to normal cognition and memory and carriers of the DRD2 Taq1A A1 allele have significant loss of D2 receptor density in the brain. Recent research has shown that A1 carriers have worse memory performance during long-term memory (LTM) updating, compared to non-carriers or A2-carriers. A1-carriers also show less blood oxygen level dependent (BOLD) activation in left caudate nucleus which is important for Long Term Memory (LTM) updating. This latter effect was only seen in older adults, suggesting magnification of genetic effects on brain functioning in the elderly. Moreover, the frequency of the A1 allele is 0.40 in African-Americans, with an approximate prevalence of the DRD2 A1 allele in 50% of an African American subset of individuals. This is higher than what is found in a non-screened American population (≤28%) for Reward Deficiency Syndrome (RDS) behaviors. Based on DRD2 known genetic polymorphisms, we hypothesize that the DRD2 Taq1A A1 allele magnifies the risk of Alzheimer’s in aging African Americans. Research linking this high risk for Alzheimer’s in the African American population, with DRD2/ANKK1-TaqIA polymorphism and neurocognitive deficits related to LTM, could pave the way for novel, targeted pro-dopamine homeostatic treatment.

The brain regions tied to pleasure can be triggered by engaging in sex, eating tasty food, watching a movie, accomplishments at school and athletics, consuming drugs, and noble efforts to help the community, the country, and the world. It is noteworthy that research suggests that the latter type of satisfaction, supporting the community, may result in the most substantial positive effects on our immune system. However, these pathways for these effects are not understood. Berridge and Kringelbach have suggested that pleasure is mediated by well-developed mesocorticolimbic circuitry and serves adaptive functions. In affective disorders, anhedonia (lack of pleasure) or dysphoria (negative affect) can result from a breakdown of that hedonic system. Most importantly, human neuroimaging investigations indicate that surprisingly similar circuitry is activated by quite diverse pleasures, suggesting a common neural pathway shared by all rewarding stimuli and behaviors. Over many years the controversy of dopamine involvement in pleasure/reward has led to confusion in terms, such as trying to separate motivation from pure pleasure (i.e., wanting versus liking). We take the position that animal studies cannot provide real clinical information that is described by self-reports in humans. On November 23rd, 2017, evidence for our concerns was revealed. A brain system involved in everything from addiction to autism appears to have evolved differently in humans than in apes, as reported by a large research team in the journal Science. To reiterate, the new findings by Sousa et al., also suggest the importance of not over-relying on rodent and even non-human primate studies. Extrapolations, when it comes to the concept of pleasure, dopamine, and reinforcement, are not supported by these data. Human experience and study are now much more critical and important. Extrapolations from non-humans to humans may be more fiction than fact. While this statement is bold it should not at all suggest that animal date is unimportant, that is not the case. It is extremely valuable in many aspects and we must encourage the development of animal models for disease. However, we must be cautious in our interpretation of results without leaping to conclusions that may be explained by follow-up human experiments and subsequent data. We are further proposing that in terms of overcoming a never –ending battle related to the current drug epidemic, the scientific community should realize that disturbing dopamine homeostasis by taking drugs or having a system compromised by genes or other epigenetic experiences, should be treated by alternative therapeutic modalities, expressed in this article as a realistic key goal. Application of genetic addiction risk (GARS™) testing and pro-dopamine regulation (KB220) should be considered along with other promising technologies including cognitive behavioral therapy, mind fullness, brain spotting and trauma therapy. Basic scientists have worked very hard to dis-entangle pleasure from incentive salience and learning signals in brain reward circuitry, but this work may be limited to animal models and rodents. A different consideration regarding the human reward systems is required.

We hypothesize that major depressive disorder (MDD), especially anhedonia, (excluding bipolar) should be included as a subtype of Reward Deficiency Syndrome (RDS) following more extensive genetic and molecular neurobiological research. RDS, first coined by Blum in 1995, is a failure of the reward system that usually confers satisfaction, resulting in behaviors such as overeating, heavy cigarette smoking, drug and alcohol abuse (substance use disorder [SUD]), hoarding, internet addiction, gambling, and hyperactivity. RDS is caused by hypodopaminergia. We suggest that the inclusion of MDD within RDS will assist in more appropriate treatment in the addiction recovery community, whereby the goal of achieving dopamine stabilization or homeostasis will result in better clinical outcomes. One therapeutic technique to achieve this laudable goal is via epigenetic induction involving the administration of gene expression modulators that may have a positive impact on reversing hypodopaminergia, SUD, and anhedonia. We hereby encourage further research into dopaminergic homeostasis in SUD with MDD that will guide future drug development programs.

A research participant came to our lab with self-proclaimed, ecstatic, Kundalini meditative experiences. Using neurophenomenology and functional magnetic resonance imaging (fMRI), we were able to identify brain activation in the left prefrontal cortex [primarily in left Brodmann׳s areas (BAs) 46 and 10, but also extending into BAs 11, 47, and 45] associated with this experience. The Phenomenology of Consciousness Inventory provided evidence that this was a perceived altered state of consciousness. Additionally, the Physio-Kundalini Syndrome Index strongly suggested that what he was experiencing was indeed Kundalini. The feelings of joy, happiness and the left prefrontal brain region found in this study are consistent with many published neuroimaging and electrophysiological studies of meditation. This case study suggests that using first-person subjective experience within a phenomenological reduction process can be combined with neuroimaging to divulge objective brain regions associated with such experiences. Furthermore, this provides evidence that at least in this participant, the Kundalini experience is associated with brain activation in the left prefrontal cortex. Future research is needed to confirm these results in a large group study, perhaps contrasting brain activation of those who experience spontaneously emerging Kundalini with trained Kundalini practitioners.

Post-traumatic stress disorder (PTSD) is a severe polygenic disorder triggered by environmental factors. Many polymorphic genes, particularly the genetic determinants of hypodopaminergia (low dopamine function), associate with a predisposition to PTSD as well as substance use disorder. Support from the National Institutes of Health for neuroimaging research and molecular, genetic applied technologies has improved understanding of brain reward circuitry functions that have inspired the development of new innovative approaches to their early diagnosis and treatment of some PTSD symptomatology and addiction. This review presents psychosocial and genetic evidence that vulnerability or resilience to PTSD can theoretically be impacted by dopamine regulation. From a neuroscience perspective, dopamine is widely accepted as a major neurotransmitter. Questions about how to modulate dopamine clinically in order to treat and prevent PTSD and other types of reward deficiency disorders remain. Identification of genetic variations associated with the relevant genotype-phenotype relationships can be characterized using the Genetic Addiction Risk Score (GARS®) and psychosocial tools. Development of an advanced genetic panel is under study and will be based on a new array of genes linked to PTSD. However, for now, the recommendation is that enlistees for military duty be given the opportunity to voluntarily pre-test for risk of PTSD with GARS, before exposure to environmental triggers or upon return from deployment as part of PTSD management. Dopamine homeostasis may be achieved via customization of neuronutrient supplementation "Precision Behavioral Management" (PBM™) based on GARS test values and other pro-dopamine regulation interventions like exercise, mindfulness, biosensor tracking, and meditation.

The well-researched pro-dopamine regulator KB220 and variants result in increased functional connectivity in both animal and human brains, and prolonged neuroplasticity (brain cell repair) having been observed in rodents. Moreover, in addition to increased functional connectivity, recent studies show that KB220Z increases overall brain connectivity volume, enhances neuronal dopamine firing, and eliminates lucid dreams in humans over a prolonged period. An unprecedented number of clinical studies validating this patented nutrigenomic technology in re-balancing brain chemistry and optimizing dopamine sensitivity and function have been published. On another note, it is sad that unsuspecting consumers could be deceived and endangered by false promises of knock-off marketers with look- and- sound-alike products. Products containing ingredients having potential dangers (i.e., combinations of potent D2 agonists including L-Dopa and L-Theanine) threaten the credibility and reputation of validated, authentic, and ethical products. We encourage clinicians and neuroscientists to continue to embrace the concept of “dopamine homeostasis” and search for safe, effective, validated and authentic means to achieve a lifetime of recovery, instead of reverting to anti-dopaminergic agents doomed to fail in the war against the devastating drug epidemic, or promoting powerful D2 agonists that compromise needed balance.

Following 25 years of extensive research by many scientists worldwide, a panel of ten reward gene risk variants, called the Genetic Addiction Risk Score (GARS), has been developed. In unpublished work, when GARS was compared to the Addiction Severity Index (ASI), which has been used in many clinical settings, GARS significantly predicted the severity of both alcohol and drug dependency. In support of early testing for addiction and other RDS subtypes, parents caught up in the current demographic of 127 people, both young and old, dying daily from opiate/opioid overdose, need help. In the past, families would have never guessed that their loved ones would die or could be in real danger due to opiate addiction. Author, Bill Moyers, in Parade Magazine, reported that as he traveled around the United States, he found many children with ADHD and other spectrum disorders like Autism, and noted that many of these children had related conditions like substance abuse. He called for better ways to identify these children and treat them with approaches other than addictive pharmaceuticals. To our knowledge, GARS is the only panel of genes with established polymorphisms reflecting the Brain Reward Cascade (BRC), which has been correlated with the ASI-MV alcohol and drug risk severity score. While other studies are required to confirm and extend the GARS test to include other genes and polymorphisms that associate with an hypodopaminergic trait, these results provide clinicians with a non-invasive genetic test. Genomic testing, such as GARS, can improve clinical interactions and decision-making. Knowledge of precise polymorphic associations can help in the attenuation of guilt and denial, corroboration of family gene-o-grams; assistance in risk-severity-based decisions about appropriate therapies, including pain medications and risk for addiction; choice of the appropriate level of care placement (i.e., inpatient, outpatient, intensive outpatient, residential); determination of the length of stay in treatment; determination of genetic severity-based relapse and recovery liability and vulnerability; determination of pharmacogenetic medical monitoring for better clinical outcomes (e.g., the A1 allele of the DRD2 gene reduces the binding to opioid delta receptors in the brain, thus, reducing Naltrexone's clinical effectiveness); and supporting medical necessity for insurance scrutiny.

The slaughters in Las Vegas and Sutherland Springs demand explanation, in the face of the ineffable. An understanding of the shooters' motives could restore our trust in our mutually cooperative existence. In this short communication we provide post-hoc rationale of both Stephen Paddock (Las Vegas mass shooting) and Devin Kelley (Southerland Springs mass shooting) and hypothesize that these shooters had genetically induced "Reward Deficiency Syndrome" (RDS) and a hypodopaminergia trait/state. In this particular case we are in pursuit of trying to obtain postmortem samples of mass shooters for subsequent epigenetic and neurogenetic analyses. It is our contention that early genetic identification of RDS and its pathological behaviors including hyper - sexuality, violence, a love for guns, even in children, could be a giant step forward in potentially saving lives.

It is universally agreed that dopamine is a major neurotransmitter in terms of reward dependence, however, there remains controversy regarding how to modulate its role clinically to treat and prevent relapse for both substance and non-substance-related addictive behaviors. It is also agreed by most that there is a need to provide early genetic identification possibly through a novel researched technology referred to Genetic Addiction Risk Score(GARS).™ The existing FDA-approved medications promote blocking dopamine, however, we argue that a more prudent paradigm shift should be biphasic-short-term blockade and long-term upregulation, enhancing functional connectivity of brain reward. It is critical to understand that the real phenotype is not any specific drug or non -drug addictive behavior, but instead is Reward Deficiency Syndrome (RDS). Thus the true phenotype of all addictive behaviors is indeed RDS. Finally, we are suggesting that one way to combat the current out of control Opioid /Alcohol crisis worldwide is to seriously reconsider treating RDS by simply supplying powerful narcotic agents (e.g. Buprenorphine). This type of treatment will only keep people addicted. A more reasonable solution involving genetic testing, urine drug screens using Comprehensive Analysis of Reported Drugs (CARD) and dopamine homeostasis we call " Precision Addiction Management" ™ seems parsonomiuos.

It is a reality that globally opioid deaths have soared for men and women of all social, economic status and age from heroin and fentanyl overdoses. Specifically, in the United States, deaths from narcotic overdoses have reached alarming metrics since 2010. In fact, the Fentanyl rise is driven by drug dealers who sell it as heroin or who use it to lace cocaine or to make illegal counterfeit prescription opioids. The President's Commission on the crisis has linked the death toll as equivalent to "September 11th every three weeks." In fact, The U.S. Centre for Disease Control (CDC) released data showing that opioid-related overdoses were up 15% in the first three quarters of 2016 compared to 2015. Various governmental organizations including NIDA, are actively seeking solutions. However, we argue that unless the scientific community embraces genetic addiction risk coupled with potential precision or personalized medicine to induce "dopamine homeostasis" it will fail. We now have evidence that a ten-gene and eleven single nucleotide polymorphism (SNP) panel predicts Addiction Severity Index (ASI) for both alcohol and drugs of abuse (e.g., Opioids). In a large multi-addiction centre study involving seven diverse treatment programs, the genetic addiction risk score (GARS

It is well-known that Native Americans (NA) clinically present with a very high rate of alcoholism and other drugs of abuse. It is also known that NA also display a very high rate of suicide compared to other ethnic groups. Furthermore, individuals with various psychiatric disorders (e.g., depression) also have higher rates of suicide that are frequently alcohol related. Males are as much as four times more likely to die from suicide than females. Studies comparing Native to other populations within the same geographic regions in North America divulged, almost universally, that alcohol involvement is higher among Native suicides than among the local, non-Native people. Unfortunately, suicide is the eighth leading cause of death in the U.S. and is the third cause of death in those ages 15–24. With these disappointing statistics, we are hereby proposing that because of such a high genetic risk as supported by the work of Barr and Kidd showing that NA carriers the DRD2 A1 allele at the rate of 86%, compared to a highly screened reward deficiency free control of only 3%. It seems reasonable that early identification, especially in children, be tested with the Genetic Addiction Risk Score (GARS) and concomitantly be offered the precision pro-dopamine regulator (KB220PAM), one that matches their unique brain polymorphisms involving serotonergic, endorphinergic, glutaminergic, gabaergic and dopaminergic pathways among others. We believe that using the Precision Addiction Management (PAM) platform at an early age may be prophylactic, while in adults PAM may reduce substance craving affecting tertiary treatment and even relapse and mortality prevention.

Prescriptions for Benzodiazepines (BZDs) have risen continually. According to national statistics, the combination of BZDs with opioids has increased since 1999. BZDs (sometimes called "benzos") work to calm or sedate a person by raising the level of the inhibitory neurotransmitter GABA in the brain. In terms of neurochemistry, BZDs act at the GABAA receptors to inhibit excitatory neurons, reducing VTA glutaminergic drive to reduce dopamine release at the Nucleus accumbens. Benzodiazepine Use Disorder (BUD) is very difficult to treat, partly because BZDs are used to reduce anxiety which paradoxically induces hypodopaminergia. Considering this, we are proposing a paradigm shift. Instead of simply targeting chloride channel direct GABAA receptors for replacement or substitution therapy, we propose the induction of dopamine homeostasis. Our rationale is supported by the well-established notion that the root cause of drug and non-drug addictions (i.e. Reward Deficiency Syndrome [RDS]), at least in adults, involve dopaminergic dysfunction and heightened stress. This proposition involves coupling the Genetic Addiction Risk Score (GARS) with a subsequent polymorphic matched genetic customized Pro-Dopamine Regulator known as KB220ZPBM (Precision Behavioral Management). Induction of dopamine homeostasis will be clinically beneficial in attempts to combat BUD for at least three reasons: 1) During detoxification of alcoholism, the potential induction of dopamine regulation reduces the need for BZDs; 2) A major reason for BZD abuse is because people want to achieve stress reduction and subsequently, the potential induction of dopamine regulation acts as an anti-stress factor; and 3) BUD and OUD are known to reduce resting state functional connectivity, and as such, potential induction of dopamine regulation enhances resting state functional connectivity. Future randomized placebo-controlled studies will investigate this forward thinking proposed novel modality.

Buprenorphine and naloxone (bup/nal), a combination partial mu receptor agonist and low-dose delta mu antagonist, is presently recommended and used to treat opioid-use disorder. However, a literature review revealed a paucity of research involving data from urine drug tests that looked at compliance and abstinence in one sample.Statistical analysis of data from the Comprehensive Analysis of Reported Drugs (CARD) was used to assess compliance and abstinence during treatment in a large cohort of bup/nal patients attending chemical-dependency programs from eastern USA in 2010 and 2011.Part 1: Bup/nal was present in 93.4% of first (n = 1,282; p.0001) and 92.4% of last (n = 1,268; p.0001) urine samples. Concomitantly, unreported illicit drugs were present in 47.7% (n = 655, p =.0261) of samples. Patients who were compliant to the bup/nal prescription were more likely than noncompliant patients to be abstinent during treatment (p =.0012; odds ratio = 1.69 with 95% confidence interval (1.210, 2.354). Part 2: An analysis of all samples collected in 2011 revealed a significant improvement in both compliance (p2.2 × 10

The interaction of neurotransmitters and genes that control the release of dopamine is the Brain Reward Cascade (BRC). Variations within the BRC, whether genetic or epigenetic, may predispose individuals to addictive behaviors and altered pain tolerance. This discussion authored by a group of concerned scientists and clinicians examines the Genetic Addiction Risk Score (GARS), the first test to accurately predict vulnerability to pain, addiction, and other compulsive behaviors, defined as Reward Deficiency Syndrome (RDS). Innovative strategies to combat epidemic opioid, iatrogenic prescription drug abuse and death, based on the role of dopaminergic tone in pain pathways, are proposed. Sensitivity to pain may reside in the mesolimbic projection system, where genetic polymorphisms associate with a predisposition to pain vulnerability or tolerance. They provide unique therapeutic targets that could assist in the treatment of pain, and identify risk for subsequent addiction. Pharmacogenomic testing of candidate genes like CB1, mu receptors, and PENK might result in pharmacogenomic, personalized solutions, and improved clinical outcomes. Genetically identifying risk for all RDS behaviors, especially in compromised populations, may be a frontline tool to assist municipalities to provide better resource allocation.

The principal vector of Lyme disease in the United States is Ixodes scapularis: black legged or deer ticks. There is increased evidence that those infected may be plagued by anxiety or depression as well. Researchers have identified transcripts coding for two putative cytosolic sulfotransferases in these ticks, which recognized phenolic monoamines as their substrates. It is hypothesized that protracted Lyme disease sequelae may be due to impairment of dopaminergic function of the brain reward circuitry. The subsequent recombinant proteins exhibited sulfotransferase function against two neurotransmitters: dopamine and octopamine. This, in itself, can reduce dopamine function leading to many Reward Deficiency Syndrome behaviors, including depression and possibly, anxiety. In fact, it was shown that activity of Ixosc Sult 1 and Sult 2 in the Ixodid tick salivary glands might contain inactivation of the salivation signal through sulfonation of either dopamine or octopamine. This infraction results in a number of clinically observed mood changes, such as anxiety and depression. In fact, there are common symptoms observed for both Parkinson and Lyme diseases. The importance of understanding the mechanistic and neurobiological effects of Lyme on the central nervous system (CNS) provides the basis for pro-dopamine regulation as a treatment. WC 195.

There is no question that America is experiencing a horrific opiate/opioid epidemic whereby thousands of people are unfortunately dying, and the rate of people seeking treatment is at all -time high. One major problem can be linked to the fact that legal prescriptions for powerful opioid analgesics reached 297 million in 2016. One company that manufactures Oxycontin generated $3.1 billion in revenue in 2017. Moreover, that deaths from prescription drug overdoses have been called the “silent epidemic†for many years.

Following 25 years of extensive research by many scientists worldwide, a panel of ten reward gene risk variants, called the Genetic Addiction Risk Score (GARS), has been developed. In unpublished work, when GARS was compared to the Addiction Severity Index (ASI), which has been used in many clinical settings, GARS significantly predicted the severity of both alcohol and drug dependency. In support of early testing for addiction and other RDS subtypes, parents caught up in the current demographic of 127 people, both young and old, dying daily from opiate/opioid overdose, need help. In the past, families would have never guessed that their loved ones would die or could be in real danger due to opiate addiction. Author, Bill Moyers, in Parade Magazine, reported that as he traveled around the United States, he found many children with ADHD and other spectrum disorders like Autism, and noted that many of these children had related conditions like substance abuse. He called for better ways to identify these children and treat them with approaches other than addictive pharmaceuticals.

We are currently in a genomics era with important implications for the field of psychiatry. An understanding of DNA, as well as polymorphic changes affecting the brain’s reward circuitry, has provided a new way of approaching and thinking about addictive behaviors. Our current goal is to provide a foundation for more accurate genetic diagnoses as well, as the application of dopamine agonist therapy (pro-dopamine regulation), in order to balance dopaminergic activation. Based upon our extensive research, we are proposing a novel approach which challenges the Addiction recovery field to utilize these tools by introducing them into inpatient/outpatient addiction treatment programs The following tools, we hope, will change the recovery landscape: The Genetic Addiction Risk Score (GARS™) for Reward Deficiency Syndrome (RDS) diagnoses; the Comprehensive Analysis Of Reported Drugs (CARD™) to establish compliance of prescribed medications and abstinence during treatment; natural Dopamine agonistic therapy (KB220™); mRNA (patent pending) to resolve pre-and post-candidate gene expressions in Reward Deficiency Syndrome (RDS). As a result we have dubbed, this paradigm shift as: “The Reward Deficiency Solutions System (RDSS™).”Wc 180Keywords: Genome, Genetic Addiction Risk Score (GARS), KB220 variants, Pro-Dopamine Regulation, Pain, Opiate/opioid epidemic

This multi-center study of dual diagnosis (DD) programs involved 804 residential patients with co-occurring alcohol and mental health disorders. The Addiction Severity Index was administered at admission and at one, six, and 12 months after discharge. Repeated measures analysis showed the intoxication rate per month stabilized between months six and 12 with 68% still in remission and an 88% mean reduction from baseline (F = 519, p < .005). A comparison between patients with and without weekly relapse produced significant differences in hospitalization (odds ratio 11.3:1; 95% C.I., 5.5 to 23.2). Eight ANCOVAs used mean intoxication days per month after discharge as the outcome variable, pre-admission intoxication days per month as a covariate, and eight variables associated with relapse (e.g. depression) as factors. Patients with these factors at admission did not have significantly higher intoxication rates after discharge than patients without them. This suggests that these DD programs successfully integrated treatment of both disorders and explained their effectiveness. Co-occurring DSM IV mood disorders such as anxiety and depression as well as drug abuse involving opioids or cocaine fell between 66 and 95% at months one, six, and twelve.

Recent studies suggest changes in religious cognition in a subgroup of patients with Parkinson’s disease [PD (e.g., Butler et al., 2011)]. It is unclear whether this deficit extends to both doctrinal and experiential categorization forms of religious cognition. Kapogiannis et al. (2009b) dissociated experiential and doctrinal religious knowledge to different neural networks using fMRI. We examined Kapogiannis’ dissociation against the background of PD side of onset (LOPD, ROPD), assessing performance both On- and Off-medication. In the behavioral portion of the study, we used a statement classification task in combination with scholar derived test sets for experiential and doctrinal religious knowledge categorization in conjunction with neuropsychological measures. In the neuroimaging portion of the study, we expanded on Kapogiannis’ study by examining the same networks in PD. The behavioral data revealed that all groups rated (categorized) the scholar derived tests of experiential and doctrinal significantly differently than the scholars. All groups, including the scholars, classified more phrases as doctrinal than experiential. Religious cognition differed in the PD groups: those with PD Off-medication and LOPD Off-medication comprehended scholar defined experiential phrases with more difficulty, making them more likely to be classified as mixed or doctrinal. This was in contrast to the subjective frequency of classification of phrases as experiential paired with a cognitive decline in PD Off-medication; whereas PD On-medication showed a positive correlation with cognitive state and subjective doctrinal classification. For ROPD, cognitive state was associated with subjective experiential and doctrinal frequency of classification. With more intact intellect, there was a greater likelihood of classifying phrases subjectively as mixed, and the converse for experiential. Furthermore, religiosity negatively predicted subjective doctrinal frequency in LOPD, with the converse in ROPD. In fcMRI in PD, we found resting state functional intrinsic connectivity of reward networks associated with classification of statements using seeds in bilateral nucleus accumbens in PD. For experiential regressors, there was a negative correlation in bilateral frontal lobes paired with a positive correlation in left occipital visual areas (BAs 17, 18). For doctrinal regressors, there was a positive correlation in right BA 20. Keywords: Doctrinal; Experiential; Parkinson’s disease; Religious cognition; Functional connectivity.

Purpose: We studied the functional magnetic resonance imaging (fMRI) of the visual cortex in order to activate preferentially the parvocellular (PC) or the magnocellular (MC) visual system by manipulation of the spatiotemporal characteristics of the stimuli. Then we applied this technique to a patient with amblyopia to see how these two visual systems are affected in amblyopia. Methods: We acquired the fMRI at 1.5 T in 8 normal subjects and in one patient with anisometropic amblyopia, each receiving their best refractive correction. Each subject underwent experimentation under five conditions. The MC stimulus had a low contrast, a large check size, and a high temporal frequency. The PC stimulus had a high contrast, a small check size, and a low temporal frequency. After the activation in each condition had been determined by contrasting the visual stimulation conditions with the condition at rest, the inter-eye difference was determined. Results: In normal subjects, the activation map showed different vis...

Alice in Wonderland Syndrome was originally coined by Dr. John Todd in 1955. The syndrome is named after the sensations experienced by the character Alice in Lewis Carroll's novel Alice's Adventures in Wonderland. Alice in Wonderland Syndrome consists of metamorphopsia (seeing something in a distorted fashion), bizarre distortions of their body image, and bizarre perceptual distortions of form, size, movement or color. Additionally, patients with Alice in Wonderland Syndrome can experience auditory hallucinations and changes in their perception of time. Currently, there is no known specific cause of Alice in Wonderland Syndrome. However, theories point to infections such as the Epstein-Barr virus, medications such as topiramate and associated migraines. Neuroimaging studies have revealed brain regions involved with the manifestation of symptoms. These include the temporo-parietal junction within the temporal lobe and the visual pathway, specifically the occipital lobe. There are no current treatments for Alice in Wonderland Syndrome. Further research is needed to find better treatments for Alice in Wonderland Syndrome and to elucidate the exact cause or causes of Alice in Wonderland Syndrome.

We theorise that in some cases Attention Deficit Hyperactivity Disorder (ADHD) predisposes to narcolepsy and hypersomnia, and that there may be a shared pathophysiology with various addictions [Reward Deficiency Syndrome (RDS)]. Reticence to acknowledge such connections may be due to a narrow nosological framework. Additionally, we theorise that the development of narcolepsy on a baseline of ADHD/RDS leads to an additional assault on the dopaminergic reward system in such individuals. In this study, we propose to test these hypotheses by using a combination of broad genetic screening, and neuroimaging with and without pharmacological intervention, in those with pure ADHD, pure narcolepsy, and the combined ADHD-narcolepsy phenotype. Results of this proposed study may reveal a common pathophysiology of ADHD, narcolepsy and RDS, and perhaps an additional compromise to the reward system in those with combined ADHD-narcolepsy. If the evidence supports the hypothesis that indeed there is a shared pathophysiology for narcolepsy with RDS and thus its subtype ADHD, early intervention/preventative treatment amongst those with ADHD may be beneficial with the putative dopaminergic compound KB220Z™.

Purpose Motion perception abnormalities and extrastriate abnormalities have been suggested in amblyopia. Functional MRI (fMRI) and motion stimuli were used to study whether interocular differences in activation are detectable in motion-sensitive cortical areas in patients with anisometropic amblyopia. Methods We performed fMRI at 1.5 T 4 control subjects (20/20 OU), 1 with monocular suppression (20/25), and 2 with anisometropic amblyopia (20/60, 20/800). Monocular suppression was thought to be form fruste of amblyopia. The experimental stimulus consisted of expanding and contracting concentric rings, whereas the control condition consisted of stationary concentric rings. Activation was determined by contrasting the 2 conditions for each eye. Results Significant fMRI activation and comparable right and left eye activation was found in V3a and V5 in all control subjects (Average z -values in L vs R contrast 0.42, 0.43) and in the subject with monocular suppression ( z = 0.19). The anisometropes exhibited decreased extrastriate activation in their amblyopic eyes compared with the fellow eyes ( z s = 2.12, 2.76). Conclusions Our data suggest motion-sensitive cortical structures may be less active when anisometropic amblyopic eyes are stimulated with moving rings. These results support the hypothesis that extrastriate cortex is affected in anisometropic amblyopia. Although suggestive of a magnocellular defect, the exact mechanism is unclear.

The neural correlate of object recognition in non-canonical views is uncertain, but there is evidence for involvement of neural pathways, possibly separate from those used for object recognition in canonical views.Boxcar functional MRI (fMRI) techniques were used to detect neural activity while eight normal subjects were instructed to identify digital photographs of objects in non-canonical and canonical orientations.The right angular gyrus, the left inferior temporal gyrus, and the right cerebellum showed significant fMRI activity during non-canonical as opposed to canonical viewing.Subjects recognizing objects in non-canonical orientations engage in a process separate from, or in addition to, the process used in recognizing objects in canonical orientations.

Functional magnetic resonance imaging (fMRI) can detect lateral geniculate nucleus (LGN) activation. We studied LGN function in 5 patients with retrogeniculate homonymous hemianopia using fMRI at 4.0 Tesla during binocular visual stimulation. Decreased activation of visual cortex and LGN on the side of the lesion was observed in all 5 patients. These findings suggest that retrogeniculate lesions are associated with decreased activation of the LGN, due to retrograde degeneration or a functional decrease caused by decreased feedback from ipsilateral visual cortex.

Functional magnetic resonance imaging (fMRI), which is a technique useful for non-invasive mapping of brain function, is well suited for studying the visual system. This review highlights current clinical applications and research studies involving patients with visual deficits. Relevant reports regarding the investigation of the brain's role in visual processing and some newer fMRI techniques are also reviewed. Functional magnetic resonance imaging has been used for presurgical mapping of visual cortex in patients with brain lesions and for studying patients with amblyopia, optic neuritis, and residual vision in homonymous hemianopia. Retinotopic borders, motion processing, and visual attention have been the topics of several fMRI studies. These reports suggest that fMRI can be useful in clinical and research studies in patients with visual deficits.

Purpose: To investigate the reproducibility of visual activation by checkerboard stimulation, we used functional magnetic resonance imaging (fMRI) at 4 Tesla (T). Methods: Four subjects were studied with fMRI at 4 T during checkerboard visual stimulation. The functional images were realigned and spatially normalized to the standard brain. For each subject, statistical parametric maps were made for each study, and the reproducibility was determined based on the number of supra-threshold voxels (Z > 3.5, 4.5, and 5.5). Results: The mean ratio for the number of supra-threshold (Z > 4.5) voxels was 0.75, and the mean ratio for the overlapping voxels was 0.61. Restricting the region of interest within the posterior half of the brain improved reproducibility values at the low threshold (Z > 3.5), but did not improve the values at the higher thresholds. Conclusions: Despite the fact that more than half of the supra-threshold voxels were found to be active for the repeated scans, visual activation with checkerboard stimulation seems to be less reproducible than that by flash stimulation.

Functional magnetic resonance imaging (fMRI) at very high field strengths provides functional brain mapping with the enhanced signal to noise ratio and the larger blood oxygenation level-dependent (BOLD) effect. We report activated areas in the standard space detected by fMRI at 4 Tesla (T) during simple visual stimulation.Twelve healthy young subjects were scanned using a 4 T scanner during binocular flashing visual stimulation. Functional images were realigned to the first scan and then spatially normalized. Individual and group data analyses were performed to identify areas of visual activation.Activation of the bilateral primary visual cortex (V1/V2) was observed along the entire calcarine fissure in all subjects. The activated area extended to the extrastriate cortex in all subjects. Activation of the bilateral lateral geniculate nucleus (LGN) was detected in all subjects. The group data showed activation of the bilateral primary visual cortex and the bilateral lateral geniculate nucleus.Robust activation of the vision-related areas was successfully obtained in all subjects using a 4 T magnetic resonance scanner. These results suggest that fMRI at very high field strengths may be effective in showing visual system physiology, and that it can be a promising method to assess visual function of human subjects.

We present the functional magnetic resonance imaging findings at 4 Tesla in a 49-year-old male patient with a right thalamic tumor and left homonymous hemianopia. Markedly asymmetric activation of the lateral geniculate nucleus and visual cortex was found, and a pregeniculate or geniculate lesion was suspected from these findings. Functional magnetic resonance imaging at a high magnetic field can be useful in localizing a lesion responsible for visual loss.

Objective: This study examined the retrospective history of childhood ADHD symptomatology in an adult narcoleptic population (Narcolepsy Group [NG]: n = 161) compared with a control group (CG: n = 117). Method: Both groups completed the Wender Utah Rating Scale (WURS), a retrospective self-report questionnaire indicating the presence of childhood ADHD symptomatology in adults. Results: Childhood ADHD symptoms were significantly greater in NG than CG ( p < .001). Joint prevalence calculations of childhood ADHD symptomatology in NG were more than 8 to 15 times greater than expected. Among NG, those individuals with a greater score on the WURS, indicative of childhood ADHD symptomatology, also had shorter sleep onsets on the Multiple Sleep Latency Test, a common objective measure of sleepiness, t(97) = −7.11, p < .05. Conclusion: It appears that self-reported childhood ADHD symptomatology history among adult narcoleptics is common. Future research is warranted with adult narcoleptics to elucidate the true nature of this.

Background Parkinson's disease (PD) usually emerges with a unilateral side-of-onset (left-onset: LOPD; right-onset: ROPD; Marinus & van Hilten, 2015) due to an asymmetrical degeneration of striatal dopaminergic neurons (Donnemiller et al., Brain, 135, 2012, 3348). This has led to a body of research exploring the cognitive, neuropsychological, and clinical differences between LOPD and ROPD (e.g., Verreyt et al., Neuropsychology Review, 21, 2011, 405). Methods Thirty ROPD and 14 LOPD cases were drawn from a Boston clinic specializing in PD. Various cognitive and neuropsychological measures were used in an attempt to discover if there were indeed any differences between LOPD and ROPD in this cohort. Results For LOPD, duration of illness was found to be significantly greater than that of ROPD. However, further testing was able to confirm that despite this difference, it was not the cause of the other significant differences found. Furthermore, this increased duration was consistent with a previous study (Munhoz et al., Parkinsonism and Related Disorders, 19, 2013, 77). Performance on the Digit Span Backward (DSB) was found to be significantly poorer in LOPD than ROPD, suggesting compromised executive function in LOPD. Additionally, LOPD had significantly greater anxiety on the DASS Anxiety scales than ROPD. However, unlike Foster et al (Cognitive and Behavioral Neurology, 23, 2010, 4), this increased anxiety could not account for the poorer performance on the DSB for LOPD. Finally, ROPD had significantly greater magical ideation than LOPD, which can be explained by the theory put forth by Brugger and Graves (European Archives of Psychiatry, 247, 1997, 55). Conclusion Clear and significant differences between LOPD and ROPD were found within our cohort. LOPD showed greater impairment of working memory, greater anxiety, and greater duration of illness—all independent of one another; whereas, those with ROPD had greater magical ideation, also independent of any other variables.