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Introduction. Little is known about how metabolic comorbidity affects stress response during breast cancer (BRCa) after a recent diagnosis. Objective. To evaluate the physiological and psychological differences between the BRCa-RSxM groups and those with BRCa alone, and the influence of psychological variables and comorbidity in terms of stress response. Method. Comparative non-experimental causal-descriptive study. Fifty patients recently diagnosed with BRCa (25 with BRCa and 25 with BRCa-RSxM) in a convenience sample participated. Frontal muscle activity and skin conductance were recorded in response to stressful conditions. Quality of life, perceived stress, and coping strategies scales were used. Results. The presence of comorbidity (p = .001; p = .02), perceived stress (p = .004; p = .03), and social quality of life (p = .01; p = .01) influenced muscle activation and conductance during the emotional stressor (ES). Putting the stressful situation into perspective as a cognitive coping strategy was related to a decrease in activation (p = .04). An increase in physiological activation during the cognitive stressor (CS) was influenced by comorbidity (p = .05) and quality of social life (p = .01; p = .01). In turn, a decrease was influenced by the increase in age (p = .02). Discussion. Physiological vulnerability, coping strategies (behavioral and cognitive), and prior learning influenced the resulting reaction during the stressful situation. Conclusion. A metabolic disease, as a prelude to an oncological, may cause physiological vulnerability to respond adequately to stressful conditions. [ABSTRACT FROM AUTHOR]

Introduction. Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder affecting approximately 5% of the world population, with symptoms that may persist into adulthood. Despite the findings on the clinical course of this disorder, information regarding comorbidity patterns, psychosocial and executive functioning in adult life in those with and without ADHD in Latin American samples is scarce. Objective. The aim of this study is to compare the comorbidity pattern, psychosocial, and executive functioning of adults with and without ADHD from a clinical sample. Method. One hundred and fifty-one patients between 20 and 45 years, with screened positively on ASRS-V1.1, were invited to continue an evaluation process as part of clinical research program (PROMETEO): 1) K-SADS-PL Mx interview, 2) MINI-Plus interview, ASRS-V1-1 18 item version, BRIEF self-reported questionnaire, SCQA-ADHD, and 3) Individual case review by clinical expert in ADHD. Results. Individuals in the ADHD group had a higher average of comorbid disorders (2.5 SD 1.1 vs. 1.3 SD 1.0 respectively, F = .439; t = -6.621; df = 149; p < .001), more likelihood of procrastinating (OR = 6.5; 95% CI[2.6, 16.2]; z = 4.0) and were more likely to present difficulties in both the behavior regulation index (OR = 104.9; 95% CI[31.8, 345.7]; z = 7.65) and the metacognitive index (OR = 94.79; 95% CI[29.10, 308.76]; z = 7.56) compared to the non-ADHD group, regardless of gender. Discussion and conclusions. Our results indicate that the ADHD adult group presented with more comorbidity, and worse psychosocial and executive functioning than non-ADHD adults. [ABSTRACT FROM AUTHOR]

Introduction. Although an association between attention deficit hyperactivity disorder (ADHD) and personality disorders has been observed in adult population, no descriptions in Chilean adolescents have been reported. Objective. To explore personality profiles in Chilean adolescent patients diagnosed with ADHD. Method. Non-experimental, comparative design, convenience sample with 61 adolescent patients (13-19 years old) diagnosed with ADHD who completed the Millon Adolescent Clinical Inventory (MACI) questionnaire. Results compared parameters for the Chilean adolescent population and patients in the study. Attending psychiatrists completed a medical history file (comorbidities, pharmacological treatment and factors associated with mental health). Multivariate statistics, cluster analyses, and means comparison analyses were performed. This project was approved by the Ethics Committee of the University of Chile. Results. The personality profile of female adolescent patients with ADHD resembles that of the general female population, while the profile of the male patients is similar to that of the patient's parameter group. Cluster analysis identified two personality sub-profiles: 25% of the subjects belonged to cluster 1, which was characterized by higher scores for different personality traits, expressed concerns, and clinical syndromes, compared with subjects from cluster 2. There were no differences regarding gender, ADHD clinical presentation, use of medication, adverse childhood experiences (ACEs), type of school, grade retention, or, applicable only to the female group, comorbidities in belonging to cluster 1. Only the presence of comorbidity in male subjects was associated with cluster 1 membership. Discussion and conclusion. Adolescent patients diagnosed with ADHD differed significantly in some personality traits when compared to Chilean parameters for the MACI. Of the adolescents studied, 25% have maladaptive personality characteristics. [ABSTRACT FROM AUTHOR]

Background. Although the presence of a gambling disorder (GD) together with another mental disorder poses special treatment challenges, such as relapses, severe outcomes for patients and families, and increased number of hospitalizations, there are only a few critical reviews in the literature. Objective. To review empirical evidence of psychological approaches to cope specifically with these dual disorders. Method. A narrative review of the relevant bibliography on this topic was carried out. A systematic search of original articles (2010-October 2017) was conducted in MEDLINE and PsycInfo. Key terms were: 1. gambling/gamblers, 2. treatment/intervention/therapy/therapeutics, and 3. dual diagnosis/comorbidity. Results. Current treatment for GD involves a number of different options, including inpatient treatments, intensive outpatient therapy, individual and group cognitive-behavioral options (CBT), self-help groups, and pharmacotherapy. Inpatient care is generally limited to patients with severe acute crises, treatment failures, and severe comorbid disorders, particularly depression and attempted suicide. Treatment for GD with other mental disorder needs more research. CBT, motivational enhancement therapy and self-help groups have some empirical support when GD is comorbid with other addiction, mood disorder, or schizophrenia. Programs that combine pharmacotherapy and psychosocial treatments for GD into a single comprehensive package are most likely to have good treatment outcomes, at least with regard to treatment retention. Discussion and conclusion. Interventions should be tailored to the needs of the patients. Future research should be concerned about the statistical power of the studies, implement motivational strategies for patients with poor medication adherence, and design measures to study treatment fidelity in the CBT groups. [ABSTRACT FROM AUTHOR]

Introduction. Descriptive data about co-occurrence of alcohol and cocaine consumption is scarce, despite its important prevalence. Dual disordes shows high prevalence in clinical samples, and patients report worse evolution and need more health services. Objective. To compare psychopathology in patients in treatment with lifetime alcohol and cocaine (Alc + Coc) substance use disorder (SUD) with subjects with alcohol but not cocaine (Alc) lifetime SUD and cocaine but not alcohol (Coc) SUD. Method. The sample consisted of 837 outpatients from Madrid, Spain, under treatment in substance misuse or mental health units. Two analyses were made: we compared subjects in the Alc + Coc (n = 366) to the Alc group (n = 162), and then to the Coc group (n = 122). Socio-demographic variables were addressed by interview. The Mini International Neuropsychiatric Interview (MINI) was used to evaluate Axis I disorders and the Personality Disorder Questionnaire (PDQ) to evaluate Personality Disorders (PD). Results. Compared to Alc group, patients in the Alc + Coc group were younger, had different socio-demographic characteristics, had more proportion of cannabis and opioid SUD, had less proportion of major depressive disorder, obsessive and depressive PD, more proportion of antisocial PD and lower suicide risk. Compared to the Coc group, they had more cannabis SUD and lower opioid SUD, showed higher prevalence of bipolar disorder, general anxiety disorder, paranoid, histrionic and dependent PD. Discussion and conclusion. We present a cross-sectional study describing comorbidity of dual disordes on treatment-seeking concurrent alcohol and cocaine problematic users. This concurrence showed different dual disordes prevalence profile than single users in some specific mental disorders. [ABSTRACT FROM AUTHOR]

Introduction Attention deficit hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder. The determination of the clinical features, adversity factors and level of functioning in siblings of probands with ADHD, known as a high risk (ADHD R Sib), could help us to establish the risk to which they are subjected. Objective To determine the frequency of ADHD and other psychiatric disorders in R Sib. Secondary objectives were to establish the psychosocial adversity factors that predict ADHD R Sib and determine the magnitude of effect on performance and other psychiatric disorders when siblings have ADHD (R Sib +) compared to those without ADHD (R Sib -). Material and methods This multicenter study is descriptive, transversal and analytical. The sample (n=84) was formed by adolescent siblings of probands with ADHD who shared both parents. Results While 45.2% (n=38) had ADHD, 17.9% (n=15) had no psychiatric disorder. Being a R Sib + increased at least four times the likelihood of having oppositional defiant disorder (OR=4.3, 95% CI 1.3-14.8). These data remained significant when adjusted for sex, age and number of adversities (RM 95=3, 1.8-10.9%). Being a R Sib+ increased almost five times the probability of academic dysfunction (OR=4.84, 95% CI 1.41-16.63). The overall average was 3.3 adversities (SD=1.4). Psychopathology in both parents was found in 51.2% of the sample (ES=0.055). Severe family dysfunction increased 2.5 times the probability of having ADHD in a R Sib (95% CI, 1.06- 6.25). When comparing the groups with three or more psychosocial adversities, there were no significant differences (81.6% vs. 65.2%, p=0.14). Conclusions The clinical study of R Sib for ADHD is necessary due to the different implications in terms of prevention, early care and prognosis improvement of these patients. [ABSTRACT FROM AUTHOR]

The presence of a psychiatric disorder in parents is associated with increased frequency of psychopathology in their offsprings. Children of parents diagnosed with bipolar disorder (BD) are at greater risk and lower function. However, it has not yet been determined precisely which clinical and sociodemographic factors are associated with the presentation of psychiatric disorders in this group of children and adolescents at risk. Under this framework, the aim of this study was to determine the clinical and sociodemographic variables associated with a lower function. We recruited 61 children and adolescents with ages ranging from six to 17. All of them were the children of parents with BD who were patients attended at the National Institute of Psychiatry Ramón de la Fuente Muñiz. Clinical evaluation was developed by the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children Present and Lifetime Version (K-SADS-PL), and Children's Global Assesment Scale (C-GAS) scale was used to established the overall functioning. Of the 61 evaluated 62.3% were women, the lowest function (defined by <81 points C-GAS) was found in 44.3% of women vs. 18% men (x2=3.29, p<0.043). Comorbidity with major depressive disorder or attention deficit hyperactivity disorder or oppositional defiant disorder conferred ten times greater risk of lower global function. Being a woman gives three times higher risk for a lower global function. Conclusion We found that the comorbid externalizing disorders and depression, as well as the female gender characteristics are linked to lower function in children and adolescents of parents with BD. [ABSTRACT FROM AUTHOR]

Substance use disorders have a high degree of comorbidity with other psychiatric disorders; it has been reported that the prevalence of comorbidity is higher in psychiatric (20-50%) and addiction (50-75%) treatment settings than in household or student populations. Because of limited treatment alternatives and greater treatment needs, Mutual-Aid groups have become relevant in the last decades. A modality of Mutual-Aid for addiction treatment that has proliferated in Mexico has taken the form of residential Mutual-Aid centers called "anexos" in Spanish. The objective of this study was to estimate the prevalence of lifetime comorbidity between substance use disorders and psychiatric disorders in those who attended these residential Mutual-Aid centers. The initial sample consisted of 535 male participants diagnosed with a substance use disorder, but only 346 fulfilled the inclusion criteria to continue with the evaluation. Only males were included as the participating centers only admit males. Psychiatric diagnosis was evaluated with the Composite International Diagnostic Interview (WMH-CIDI) using DSM-IV criteria. The results showed that 75.72% met criteria for any comorbid psychiatric disorder, the most frequent being attention deficit and conduct disorders, followed by anxiety disorders, separation anxiety disorders, mood disorders, impulse control disorders and least frequently eating disorders. While the study is limited by its non-representative sample, the findings provide valuable information for a hidden population for which there is a dearth of information and points to the need for integrative services which address both addiction and comorbid psychiatric disorders simultaneously. [ABSTRACT FROM AUTHOR]

Obsessive-compulsive disorder (OCD) is a prevalent neuropsychiatric disorder in children, adolescents and adults. Prevalence rates of 2% to 4% have been reported. Despite the presence of effective treatments, underdiagnosis in children and adolescents is frequent. In addition, OCD is frequently comorbid with externalizing disorders such as attention deficit hyperactivity disorder (ADHD) and anxiety disorders such as generalized anxiety disorder (GAD), panic disorder, social phobia and separation anxiety disorder. Comorbidity with affective disorders is frequent too. The OCD association with major depressive disorder (MDD) increases in adolescence, reaching similar rates in adults. The comorbidity and other clinical variables, such as the duration of illness, have been mentioned as predictors of severity and treatment response. An erratic family functioning has also been associated to the severity of the illness. The aim of this study was to determine if there were differences in demographic variables (sex and age), clinical variables (age onset of the illness and comorbid disorders) and family functioning between children and adolescents with mild/moderate vs. severe OCD. Methods In a comparative cross sectional design, 60 children and adolescents aged 6 to 17 years, who met criteria for OCD and were drug naive, were assessed. Subjects who were unable to complete the interviews or had severe neurological or medical comorbidities were excluded. Subjects were recruited at the inpatients and outpatients services of the Child Psychiatric Hospital Dr. Juan N. Navarro (HPIJNN). Trained physicians interviewed the subjects and their parents using the Schedule for Affective Disorders and Schizophrenia for School-Age Children Present and Lifetime version (K-SADS-PL), the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS), the Global Assessment of Functioning Scale (GAS) and the family APGAR rating scale. Based on CY-BOCS scores, the sample was divided in mild/moderate OCD (CY-BOCS < 30 points) and severe OCD (CY-BOCS > 30 points). Statistical analyses: Descriptive statistics (frequencies, means, standard deviation) and comparative (t student and Chi square) were used. Univariate analysis and linear regression were conducted for assessing factors associated with OCD severity. Results The sample had a mean age of 12.57±2.91 years old, they were 71.7% male. The mean duration of their illness was 19±10.75 months. The average score of CY-BOCS was 22.76±8.66, family APGAR 14.68±6.02 and GAS 54.91±15.05. A relative with OCD symptoms was reported by 23.3% of the sample; in these relatives, the most common symptoms were those related to contamination fears and washing (16%), symmetry and order (6.6%), checking (3.3%) and hoarding (1.6%). The mean number of comorbid disorders was 3.16±1.68. The most frequent were MDD, ADHD and GAD. The internalizing disorders were reported as secondary to OCD. The most common obsessions in the sample were those related to contamination and germs 60% (n=37), followed by fears to harm 58% (n=35), somatic 26.7% (n=16) and symmetry 20% (n=12). The most common compulsions were washing 50% (n=30), repeating 43% (n=26) and checking 35% (n=21). Six subjects reported contamination thoughts or rituals-related enuresis and encopresis (fear of contamination when using the bathroom or doing it only at a specific time). The main reason for attention seeking was the presence of anxiety or depressive symptoms (48%), externalized symptoms (27%), OCD symptoms (20%) and psychotic symptoms (5%). The KSADS-PL interview showed that 26% (n=16), 33% (n=20) and 43% (n=26) of the sample reported academic, social and family dysfunction respectively. When the sample was divided according to their severity, 81.7% (n= 48) belonged to the mild/moderate OCD group and 18.3% (n=11) to the severe OCD group; this had a shorter duration of illness (16.54±5.3, vs. 19.73±11.5 months; t= 0.913, df=58, p=0.003). The comparison of demographic characteristics, OCD in family members, and family functioning showed no differences between severity groups. Significant differences on rituals between groups were found, since they were reported in 45% of the severe OCD group and in 4% of the mild/moderate OCD group (?²=14.9, df=1, p= 0.001). Although the severe OCD group had shorter duration of illness, some symptoms were present for a longer time than in the mild/moderate OCD group: checking (12.6±3 vs. 2.4±4.3 months, t=3.58, df=58, p=0.001), repeating (8.3±12 vs. 3.4±5.1 months, t=2.1, df=58, p=0.03) and the inclusion of others in their rituals (20.34±1.7 vs. 2.6±4.4 months, t=2, df=58, p=0.049). Two patients of the mild/ moderate OCD group and one of the severe OCD group were affected with schizophreniform disorder. Psychotic symptoms secondary to OCD were found only in the severe OCD group (45.5%). The main reason for attention seeking of the severe OCD group was the presence of obsessions and compulsions, and in the mild/ moderate OCD group the presence of internalized disorders. Univariate analysis showed that counting compulsions (F=7.27, p=0.01) and rituals (F=17.24, p=0.000) were related to OCD severity. However, the linear regression model showed that only the presence of rituals predicted the severity of OCD (B=0.591, t=4.1, p<0.001). Discussion The studied sample represents 2.7% of the patients who were evaluated during a seven-month period at the HPIJNN, the inclusion of a screening instrument for OCD would be helpful for the identification of obsessions and compulsions in clinical samples of children and adolescents. The demographic characteristics of the present sample were similar to those reported in previous studies of pediatric OCD. The duration of illness reported by this sample suggests an age of onset around 10 years old; the frequency of obsessions and compulsions reported were also similar to those in other samples. In particular, compulsions without obsessions and the rituals involving others. Almost all the studied patients had comorbid disorders, which in many cases lead their attention seeking. It has been observed that subjects with severe obsessions regarding contamination and aggression seek for help more frequently than patients with other symptoms. Rituals were more frequently seen in patients with severe OCD; these symptoms have been associated to alterations in executive functions and have been related with psychosocial dysfunction. Conclusions: Subjects of the mild/moderate OCD group sought attention mainly due to the symptoms of comorbid disorders. Subjects with severe OCD had a shorter duration of illness and more frequency of psychotic symptoms. In the present sample, rituals predicted the severity of OCD (B=0.591, t=4.1, p<0.001). [ABSTRACT FROM AUTHOR]

In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle ´9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It adua;lly contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, ´-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effeds that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of on interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal tendions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated. [ABSTRACT FROM AUTHOR]

The pleasant sensation experienced when, for example eating or having sex is regulated by the motivation-rewarding system. This rewarding sensation makes the subject to repeat the behavior in order to obtain the reinforcer once more. This system can be corrupted by drugs of abuse by triggering an «intense feeling of pleasure» and inducing plastic changes. In normal conditions, a natural reinforcer is a stimulus generating a benefit to the organism. For example, food will provide energy and structure among many other benefits. Sex, in turn, accomplishes the function of giving new beings to the species and to create boundaries between subjects to generate groups and culture. Due to these facts, it is crucial to reinforce this kind of behaviors. They are crucial for the subject's life. In contrast, drugs do not produce any benefit to the subject or group. Although in ancient times human beings used drugs as a means to develop and practice their mysticism, such practice is no longer associated with the use of drugs. With the exception of present time aboriginal communities, none of the regular users in our countries consume drugs with ritualmystical purposes. Hence, we have to accept that drugs are of no use for human beings. They do not help us as species to have more adapted, intelligent or developed subjects in our communities. However, their ability to stimulate the rewarding system makes them popular and dangerous to the individual's health and life. The motivation-rewarding system is regulated by numerous neurotransmitters, among them dopamine, that is released in the nucleus accumbens (NAc) and synthesized by the neurons located in the ventral tegmetal area (VTA). There are other substances that modulate the activity of the dopaminergic neurons in the VTA, such as serotonin, acetylcholine, gamma-aminobutyric acid (GABA) and glutamate. The activation of the VTA and its consequent activation of the NAc enhance the release of neuromodulators such as endorphins and endocannabinoids, thus generating the subjective sensation of pleasure. All these interactions trigger the activity of memory systems generating a memory trace encoding the characteristics of the substance or behavior causing pleasure. This occurs in the context that the brain accepts these substances or behaviors as beneficial to the organism. The punishment system is also a very important system working in tight communication with the pleasure system. Fear is one of the most critical adapting behaviors for any subject in the animal kingdom. Fear helps us to avoid dangerous stimulus and behaviors. There is also pleasure involved in escaping this kind of situations. It seems like there is an interaction between the motivation-rewarding and the punishment systems. As a result, there is a balance at times in favor of pleasure, at times in favor of punishment depending on the quality of the stimulus. This balance gives the valence to the emotion triggered by the stimulus. A stimulus with a positive valence will increase the probability of exhibiting the behavior displayed to obtain it, while a stimulus with a negative valence will increase the probability of exhibiting the behavior displayed to avoid it. In this context, the so-called non-natural reinforcers such as drugs of abuse act directly on the pleasure system. For example, nicotine acts on the nicotinic receptor of ACh, alcohol, on the receptor of GABAa and glutamate (NMDA), marihuana on the endocannabinoid receptor (CB1R), located in the motivationrewarding system triggering an «intense sensation of pleasure». However, two main shortcomings make drugs of abuse dangerous: first, their effect is short and, second, they do not convey any beneficial effect to the organism whatsoever. Brain mechanisms not very well defined detect this lack of benefit; hence, the motivation-rewarding system reduces its response by means of at least two plastic changes, reducing the availability of receptors (epigenetic changes induced by the drug) and by increasing the activity of the punishment system to maintain the balance. As a result, the subject does not experience the same pleasure with the same dose of the drug. In the clinic we call this phenomenon tolerance. If the individual insists in pursuing the same intensity of pleasure, he/she has to consume more of the drug, forcing the brain to strengthen its plastic changes. In this context, we can say that these systems are defending themselves against the action of the drug. Then, why do subjects insist in pursuing the effect of drugs? Very likely because the substrate of the subject's disorder resides anywhere in the brain but in the pleasure system. If so, this indicates that drug addiction is a disorder caused by another disease, very likely a psychiatric one. Several factors contribute to generate drug addiction, i. e. social, psychological and genetic. Genes contribute in different ways to generate the subject's vulnerability to suffer an addiction. A gene mutation (alteration in genetic information) or a given polymorphism (the existence of multiple alleles of a gene in a population) can produce a dysfunctional protein or alter its normal levels. Such changes may make some individuals vulnerable to the initial use of drugs of abuse. However, those genes facilitating adjustments in the motivation-rewarding system that occur after the repeated consumption of drugs of abuse seem to be functioning normally, as we can infer from the development of tolerance. The heritability of these genes, making subjects vulnerable to addiction, has been studied in many ways, including studies of families, adoptees, and twins (monozygotic and dizygotic). From these studies it has been possible to calculate the heritability index, a measure which indicates how much variance of a trait in a specific sample is associated to genetic factors and how much to the environment. The heritability index has a range from 1, meaning the maximum genetic influence, to 0, meaning the maximum environment influence. At present, a significant number of genes have been involved in facilitating addiction to drugs, and also very important, to the response to treatment for rehabilitation. The expression of the genes is regulated by a series of processes called epigenesis. Epigenetic changes can be a result of the interaction between genes and environment. This interaction results in chemical processes that modify chromatin structure. For example, cytosine nucleotide methylation causes chromatin condensation, which interferes with gene transcription; hence, the protein encoded by this gene will be reduced, and the function in which it participates will be altered. As an example, when the methylation of the gene encoding for the glucocorticoid receptor occurs in rats, it reduces the bioavailability of this receptor and increases the release of corticosterone when rats are stressed. At the behavioral level, rats seem to be more stressed most of the time as compared with rats without methylation of this gene. Almost every stimulus in the environment is a potential promoter of epigenesis. Epigenesis is important to occur, since it is an adaptive response of the organism to the environment. It seems like the switches of the genes are turned on or off according to environment circumstances. These genetic changes will be ultimately expressed as plastic changes pursuing the right adaptation of the subject to the environment. Parental care seems to be one crucial contributor to these epigenetic modifications. For example, when a mother-rat provides poor care (feeding, grooming, and physical contact) to its litter during the neonate period, facilitates the methylation of genes, as it has been proved for the glucocorticoid receptor. These changes generate subjects with poor stress management and less capability for learning. Likewise, it makes them susceptible to drug addiction. These results highlight the importance of parental care as provider of a healthy environment, which is modeling the expression of their genes, hence their behavior. In this review we are discussing the interaction between genes and environment and the function of the brain to generate drug addiction. Although not exhaustive, this review pursues to discuss relevant and state-of-the art information to help the reader to understand those mechanisms subserving this debilitating disease. [ABSTRACT FROM AUTHOR]

During the last years obsessive-compulsive disorder (OCD) has been reported with increased prevalence in pediatric population; this is due to the development of more specific assessment methods. This evolution in the evaluation tools has given rise to the possibility of characterizing OCD presentation in children and adolescents. In childhood, OCD is a chronic and distressing disorder that can lead to severe impairments in social, academic and family functioning. Current diagnosis criteria for pediatric OCD are the same than those used in adults. During all life span, obsessive and compulsive symptoms are necessary to establish the presence of the disorder. There are several different clinical manifestations among age groups, different evolution among children, adolescents and adults; all these represent a diagnostic and therapeutic challenge for the clinician. Several classifications incorporate pediatric OCD, especially those related to the familiar presentation form and patterns of comorbidity, mainly with tics disorders. At least 50% of children and adolescents with Gilles de la Tourette syndrome develop obsessive compulsive symptoms or OCD in adulthood and almost a half of early-onset OCD subjects have a tics history. These findings support the notion that tics disorders are the comorbidity more closely related with early-onset OCD, giving elements to consider this association as a specific pediatric OCD subtype. In this age group population, comorbidity has been reported as high as in adulthood; some diagnoses are especially prevalent during childhood and others during adolescence. On the whole, anxiety disorders are frequent with OCD, generalized anxiety disorder, panic attack, social phobia and anxiety separation disorder. Comorbidity related with affective disorders is high too. The OCD association with major depressive disorder (MDD) in childhood is low but increases in adolescence; MDD reaches similar adult comorbidity rates in adolescence. Higher comorbidity prevalence of MDD has been found more related to the duration of OCD-illness than early-onset. Bipolar disorder (BD) is another frequent comorbid entity with great clinical relevance. When BD is the main diagnosis, comorbidity with OCD shows a prevalence of 16%; when OCD is the main diagnosis, comorbidity with BD shows a prevalence of 44%, showing an unidirectional relation. Some studies have shown even higher comorbidity prevalence of BD when considering bipolar spectra dimension as hypomania and cyclothymic disorder (30% and 50%, respectively) in OCD samples. Adults with OCD and BD comorbidity have more frequent episodic form, a greater number of concurrent mayor depressive episodes and a higher rate of religious or sexual obsessions. Adults with OCD without BD comorbidity show more rituals and compulsions. A recent study in pediatric population with BD and OCD found that BD type II was the must common related diagnosis, when age was considered, subjects with bipolar disorder resulted to have an earlier onset of OCD. Other comorbid diagnoses frequently reported in this early-onset OCD population are externalizing disorders as attention deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD). Children and adolescents with OCD have high rates of commorbid ADHD; this co-occurrence seems to be bidirectional. There is a consistent preponderance of males in most epidemiological studies. The onset of ADHD preceded the onset of OCD and the onset of OCD was earlier when ADHD was comorbid. Children with OCD plus ADHD compared with peers with OCD without ADHD show higher attentional and social problems, as well as aggressive high scores. [ABSTRACT FROM AUTHOR]

Attention deficit hyperactivity disorder (ADHD) can present itself with a wide variety of comorbid psychiatric entities and can easily be misdiagnosed with disorders such as the pediatric bipolar disorder (PedBP), making early detection and treatment difficult. The main objective of this review is to evaluate the relationship between PedBP and ADHD. Several studies have addressed this association, establishing a high rate of comorbidity, from 57% to 93%. The risk of developing PedBP in ADHD population has also been studied, documenting a ten-fold increase risk in both genders compared with age-matched healthy controls. Pediatric bipolar disorder is still a diagnostic entity which is hard to recognize and differentiate from other disorders, even with the current international diagnostic criteria. Individuals with ADHD with a current depressive episode, suicide attempts and/or substance abuse and that carry a family load (mainly parents) for bipolar disorder are at increased risk of actually having this disorder. Several researchers have compared clinical symptoms expressed in children with ADHD and PedBP. They have found that children with PebBP exhibit higher frequency of elated mood, increased energy, thought disorder, flight of ideas, increased speed in speech and irritability than those with ADHD. Other authors report higher rates of thought disorders, anxiety, depression, aggression and delinquent behavior amongst children with PedBP than those with ADHD. It has also been reported that children with PedBP compared to those with ADHD present higher rates of euphoria, grandiosity, racing thoughts and decreased need for sleep. Yet another study found that euphoria and increased energy distinguished youths with PedBP from those with other psychiatric disorders, and found that with the group of depressed patients exhibit higher rates of suicidal thoughts and behavior than other diagnostic groups. Some cues to diagnose and differentiate PedBP and ADHD have been proposed: ADHD symptoms appearing suddenly or later in life, loss of therapeutic response to stimulants in a previous responder, intermittent symptoms, emergence of elated mood and decreased need for sleep, severe mood shifting, hallucinations or thought disorders, family history of bipolar disorder and lack of response to adequate treatment. Three of the seven criteria for bipolar disorder are shared with ADHD (distractibility, increased goal directed activity and talkativeness), making the clinical distinction between ADHD and early onset PedBP a difficult task. In fact, most children diagnosed with PedBP present symptoms and behavior compatible with a simultaneous ADHD. The role of ADHD as a prodromic, phenocopy, comorbid condition and/or as a misdiagnosis for PedBP can be further clarified by: 1. case follow-up to determine if comorbid diagnosis can predict the course or determine a prognosis factor; and 2. family genetic studies which are convenient for the evaluation of complex comorbid conditions. Some studies have suggested that this comorbid syndrome may possess a specific genotype, as well a particular course, a pattern of treatment response and may represent a distinctive clinical condition. High comorbidity BPD, both in adult and child and adolescent populations, runs a similar pattern to that of other important diagnostic categories in child and adolescent psychiatry. From a clinical perspective, these findings support the notion of avoiding hierarchical diagnoses. Furthermore, it questions the vision of categorical entities as it is proposed in the current diagnostic classification (ICD and DSM). Currently, when we talk about ADHD, we cannot separate it from other disruptive behavior disorders, such as conduct disorder (CD) and oppositional-defiant disorder (ODD). Epidemiological studies show that 40% to 70% of children with ADHD have CD or ODD, and some of them also present comorbid internalizing disorders.… [ABSTRACT FROM AUTHOR]

The differentiation between the symptoms of anxiety and depression is one of the most important problems in psychology as the dilemma profoundly affects the diagnosis and clinical intervention. According to the epidemiological data there is a strong comorbidity between the two types of disorder. Nevertheless, it is not known which one of them precedes or predisposes to the other. The comorbidity could be also caused by the confusion between the two. There are many common symptoms and some of them traditionally attributed to the anxiety are also present in depression and vice versa. Additionally, in some cases the symptoms themselves could constitute complete clinical charts. Taking into account the above description, one of the most important current preoccupations in psychology and psychopathology is the identification of the symptoms which would be characteristic for each disorder. Although there is clinical evidence on an overlap between the symptoms, the current manuals describe two disorders and the clinical differences are crucial. One of the possible explanations of the overlap between the symptoms of anxiety and depression has been classically attributed to comorbidity which means the presence of both charts in many clinical cases. Different sources indicate that the presence of anxiety in early ages can generate certain vulnerability to develop later-age major depression. On the other hand, other studies indicate that the cases in which both, depression and anxiety are present, tend to chronify and are more resistant to treatment. In this case both disorders are present but there is no sufficient evidence to determinate which one of them would be the principal diagnosis and which one would be secondary. For this reason, the explanations are confused and neither the researchers nor clinicians are satisfied. On the other hand, the concurrence of symptoms has been attributed to the instruments utilized for the evaluation. The disorders also depend on the tools for their measure which follow a theoretical model to explain the aetiology, course, prognosis and associated symptomatology. This way, the implicit bias of the instruments is to privilege a specific aspect which depends on the definition of disorders without taking into account the other aspects. According the description above, the evaluation, especially in case of depression, is characterized by multiplicity of instruments and diversity of contents which are evaluated. Thus, it is difficult to establish the characteristic symptoms as in many cases only some of them coincide when utilizing different tools. Moreover, many symptoms which are detected by scales of depression are also present in anxiety disorders. This difficulty is one of the most important problems in clinics as it affects the validity and reliability of the tools which assess the disorders. The importance of the instructions given to the subjects should also be emphasized. In many cases they lead to the confusion of the measures of frequency and severity which is related to the classical discussion about the dimensional or categorical character of depression. Some authors state that the consideration of depression as a dimensional disorder makes possible to understand that some charts, as for example the anxiety disorders, can appear as a consequence of certain vulnerability generated by the depression. One of the alternatives to explain the presence of symptoms shared by the anxiety and depression is to consider the existence of a factor of negative affect which would be present in both types of disorder. This point of view is derived from the correspondence between some common symptoms in depression and anxiety observed in clinics. Additionally, some items included in the self-report questionnaires and scales are the same for the two disorders.… [ABSTRACT FROM AUTHOR]