Psychology

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.

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. (J. of Att. Dis. 2013; 17

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.

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.

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.

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.

It has been over 27 years since Blum & Noble discovered the first association of the DRD2 A1 allele in severe alcoholism, suggesting reward as the real phenotype, not alcoholism. This has been acknowledged by an explosion of research in the arena of Psychiatric Genetics. To date, a PubMed search listed 6,839 studies (5-15-17). The A1 allele has been associated with substance use disorders other than alcoholism, including cocaine, nicotine dependence, polysubstance abuse and many Reward Deficiency Syndrome (RDS) behaviors substance and non-substance related. Certainly following extensive controversy, the emerging evidence suggests that the
DRD2 is a reinforcement or reward gene. In fact, it could represent one of the most prominent single-gene determinants of susceptibility to severe substance abuse/reward deficiency. While, however, the environment
through epigenetic impact and other genes, when combined, still play the larger role, targeting the DRD2 gene through the novel genetic rewriting of the DNA code at the mRNA level may hold the greatest promise to date for potentially “curing” the RDS phenotype.

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.

ARTICLE INFO ABSTRACT Mood disorders including major depressive disorder (MDD) are one of the most important causes of disability for human health cardiovascular diseases, dementia, lung cancer, and diabetes. The comorbidity of depression and substance use disorder and depression, a definitive human gene map of depression still eludes the field of psychiatric genetics. Certainly, GWAS and candidate approaches are on future. It is our contention that one approach involves the induc easier said than done. In this treatise, we are suggesting a novel therapeutic modality that includes DNA genotyping based on a Genetic Addiction Risk Score (GARS) test and concomitant alteration of a Pro-dopamine Regula genes across the brain reward circuitry in the prefrontal cortex and mesolimbic systems. Copyright©2017, Kenneth Blum et al. This is an open access article distributed under the distribution, and reproduction in any medium, provided the original work is properly cited.

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).