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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.

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.

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.

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.

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.

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.

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 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.

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.

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

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: To develop a functional MRI method for producing eye dominance histograms in humans at 1.5 Tesla (T). Methods: In the first set of experiments, 8 normal persons were tested. The eye dominance of each voxel within the person's visually activated primary visual cortex was determined with Student t statistics during a left eye versus right eye contrast. Eye dominance distribution was plotted, and the mean t statistic was used to describe the histogram asymmetry. In the second set of experiments, the effect of monocular optical blur and decreased luminance via filter was studied, and eye dominance distributions were similarly determined. Results: The eye dominance histogram in each of the 8 normals was approximately symmetric; the average mean t value was +0.13. All 4 subjects with the right eye blurred had histograms approximately symmetric or slightly shifted toward the left eye (average mean t = +0.56), and all 4 subjects with the right eye filtered had histograms dramatically shifted toward the left eye (average mean t = +2.22). The average mean t for the group with the right eye filtered was significantly different from that of the other 2 groups ( P Conclusions: With noninvasive methods in normal persons, functional magnetic resonance imaging techniques at 1.5 T were able to characterize the distribution of eye dominance of voxels in primary visual cortex, based upon their t statistic in the left eye versus right eye contrast. The method is sensitive to filtering but relatively insensitive to visual blur. This approach may have a future use in the study of amblyopia in humans.(J AAPOS 2002;6:40-8)