It is important to assess properly if the symptoms are caused by the therapy or by the failure of the CNS which is more often. It is proved that severe psychotic symptoms may be complication of steroid therapy only if daily dose is more than 40 mg of prednisone . But in chronic therapy the depression likewise in short therapy hypomania are more often than psychosis. Moreover the psychosis develops in irs 1-2 weeks of treatment . In our patient irst symptoms occurred after 9 years of curing. Until now there is only one case report of the patient with coexistence of schizo- phrenia and SLE. But in that patient the psychotic symptoms were irst and for a long time they were isolated. They occurred 14 years before other SLE symptoms, especially skin lesions, have occurred. After excluding lupus related to the antipsychotic drugs the authors suggested the participation of antibodies in pathogenesis of schizophrenia . There are several theories of the schizophrenia’s etiology such as the inluence of genetic, civilizational, prenatal, social and economic factors, usage of psychoactive substances, psychological, emotional and biochemical elements. However in the last few years the relation between disturbed immunological processes and schizophrenia has been raised .
and she was medicated with a low dose of an antipsychotic drug. Ater about 15 asymptomatic days, the patient presented again to the Child Psychiatry Service with allopsychic disorientation, psychomotor agitation, disorganized speech broken by irrational laughter that was inconsistent with the mood, disorganized think- ing, abnormalities of thought control and content, and bizarre egosyntonic visual hallucinations. A drug test on urine that was requested proved benign. Ater emergency administration of an antipsychotic drug, followed by short hospitalization for reassess- ment, a new evaluation of the patient’s mental state was made. She was found to be cognizant, cooperative and focused. Contact was reserved and she showed hypomimia. Her emotions were consistent with mild depression and blunted afect. She did not continue to show abnormalities of thought and sensory percep- tion. Her condition was relatively similar to her previous state and she had no memory of the episode. At this stage, a diagnosis of psychoticdisorder with symptoms of schizophrenia was made, in accordance with ICD-10. It was concluded from the assess- ment that she should be monitored long-term. Her antipsychotic medication was then adjusted, accordingly.
adversity, yet differences in the prefrontal cortex (PFC) were present . These findings seemingly disagree with those of Carballedo and colleagues , who observed an association between BDNF genotype and hippocampal volume when combining their sample of patients with depressive disorder (MDD) and healthy controls: for a given amount of exposure to childhood adversity, Met-allele carriers had a smaller hippocampal volume than Val homozygotes. The results in the present study suggest the absence of such interactions when alcohol consump- tion and drug use are included in the model, factors that have been demonstrated to affect brain structure [40–43]. Differences in sample characteristics, studied populations (MDD vs. psychoticdisorder), but also relevant inclusion of covariates and their E and G interactions  could explain the discrepancy in results.
The American Psychiatric Association (AMERICAN..., 1994) in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) characterized the Attention Deficit Hyperactivity Disorder (ADHD) by a pattern of behavior present in several configurations of the context of the individual, for example: school and home, which can result in performance problems in social, educational or work environments. Children diagnosed with ADHD should have at least six symptoms of those described in the handbook and older adolescents and adults aged above 17 years old should respond to at least five criteria. In the current DSM publication, in its fifth edition (AMERICAN..., 2013), the changes that occurred were: in DSM-IV, the symptoms should be present until 7 years old; in DSM-V, the individual’s ADHD symptoms must be present before 12 years old. This change is supported by substantial research published since 1994, which found no clinical differences among children identified at 7 years old or later, regarding stroke, severity, outcome, or response treatment. DSM-V does not include exclusion criteria for people with autism spectrum disorder since the symptoms of both diseases co-occur. However, symptoms of ADHD should not occur exclusively during the course of schizophrenia or other psychoticdisorder and should not be better accounted by another mental disorder such as depression, bipolar disorder, anxiety disorder, dissociative disorder, personality disorder or withdrawal or intoxication by medication.
Not all patients presenting with symptoms that are typical of the prodromal phase will develop a psychoticdisorder and the predictive validity of these symptoms has great variation across studies. Prodromal phase symptoms alone, regardless of the increased risk for psychosis that they represent, may be enough to fulill the criteria for the diagnosis of a mental disorder (deined as a syndrome or behavioral or psychological pattern associated with clinically signiicant suffering and impaired global functioning), which could also justify the need and the right of the patient to receive assistance (not necessarily pharmacological). 14
Recent studies have not been able to detect substantial associations between JTC and para- noid or delusional symptomatology [23,26–30] and some studies did not find differences in the prevalence of JTC in patients versus controls . On balance, although an association with psychosis is likely, the literature on JTC does not permit a definitive conclusion as to whether it relates more to psychotic symptoms, such as delusions, or diagnostic categories associated with trait psychosis proneness . As a trait, it could contribute to the formation of delusions and be part of the vulnerability of psychoticdisorder; as a state, it could be a factor mediating the maintenance of transdiagnostic delusionality . In order to further examine the trait-or-state issue it may be productive to examine JTC in relation to low grade, or subclinical, psychotic experiences in other diagnostic categories. For example, anorexia patients did not display ele- vated JTC and JTC was not associated with level of delusionality in this group . Similarly, patients with body dysmorphic disorder (BDD) did not display elevated JTC relative to con- trols although poor insight in BDD was associated with elevated JTC . Patients with obses- sive-compulsive disorder did not display elevated JTC, howevwr, JTC was associated with delusionality in this group .
HE is an uncommon clinical syndrome. Diagnosis of this rare disorder requires positive anti TPO level and exclusion of other cases for encephalopathy. Prevalance is reported 2,1/100.000 and male/female ratio for adults is 1:4. Until present approxi- mately 130 cases were reported and most of these cases were female. In contrast to female predominance of these cases our patient was male.
In bipolar disorder (BD), during either manic or depressive episodes, a rapid thought process may be a core feature. This feature is frequently associated with ruminative characteristics of thought. Several studies have shown that patients in a depressive state increase rumination after experiencing negative affect, especially when they have low positive affect in daily life. 1 Therefore, rumina- tion is considered to be an indicator of the onset and severity of depressive episodes, in addition to mediating differences in depressive symptoms between men and women. 2 However, rumination in BD or mania is much less studied.
ticar a SCN utilizados no meio científico interna- cional e em processo de validação no Brasil. Por conseguinte, possivelmente no futuro poder-se-á aferir a SCN, tendo-se, inclusive, a possibilidade de estudar a alocação da maior parte da cota alimentar no curso do dia entre diferentes culturas e níveis sociais. É evidente que faz parte do pro- cesso diagnóstico diferenciar a SCN de outros transtornos alimentares, pois nem todos os sujeitos com queixa de comer à noite apresentam SCN. Pois a alocação da maior parte da fração alimentar para o turno da noite ocorre também em trans- tornos alimentares relacionados ao sono, como a sleep-related eating disorder, a bulimia nervosa e o transtorno do comer compulsivo 1 . Os critérios
study assessing the role of behavioral inhibition in the development of social anxiety disorder during adolescence. That study, which followed 2242 students for 4 years, with a mean age of 15 years in the first evaluation, showed that, although childhood behavioral inhibition does not always become a social anxiety disorder in adolescence, the risk for social anxiety disorder in adolescence is possibly 4 to 5-fold for those with childhood behavioral inhibition. The association between behavioral inhibition and social anxiety disorder was also described in a study by Schwartz et al 23 which evaluated
hood anxiety disorders had significantly higher rates of comorbid depression in adult life. This result agrees with a longitudinal epidemiological study of adolescents and young adults that found that social phobia in nondepressed individu- als was associated with an increased likelihood of depressive disorder onset during the follow-up. 13 Patients with comorbid
The study was conducted from February to May 2017 and involved patients attending the outpatient clinic of the department of psychiatry of a tertiary-level teaching hospital. The study protocol was approved by the institutional ethics committee of Government Medical College, Manjeri. Remitted subjects with BD aged between 18 and 60 years who fulfilled criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) for BD were included in the study after providing written informed consent (obtained from patient and caregiver). Clinical remission of BD was established based on treatment records, information from the patient and caregivers, and on a score <8 on both the Hamilton Depression Rating Scale (HDRS) and the Young Mania Rating Scale (YMRS). Patients with schizophrenia, schizoaffective disorder, major depressive disorder, mental retardation, epilepsy, cerebrovascular accidents or sensory impairments were excluded.
Recently, Ronald Pies developed a comprehensive screening questionnaire that aimed to screen the whole spectrum of bipolar disorders, including the so-called soft bi- polarity cases. Hence, this instrument was named the bipolar spectrum diagnostic scale. The sensitivity and speciicity of the instrument was assessed on 68 outpatients with bipolar spectrum disorder. The sensitivity was 0.76 and the speciic- ity was 0.85 9 .
A 56-year-old schizoaffective obese woman, with arterial hypertension and mild chronic obstructive pulmonary disease was frustrated in previous attempts to quit smoking, either with the aid of psychosocial treatment alone or combined with nicotine gum and patch. Bupropion had to be discontinued due to the irruption of manic symptoms. Her mother had bipolar I disorder. From age 18 (first psychiatric hospitalization), haloperidol was the main antipsychotic drug for thirty years. She did not want to quit during these initial years, and smoked up to 100 cigarettes per day. Adherence to psychiatric treatment was incomplete, with eight life- threatening suicide attempts. In subsequent years, haloperidol was substituted for lithium plus ziprasidone, improving compliance and stability. Thirty months later, she started to express a desire to quit cigarettes. Varenicline was titrated from 0.5mg once a day to 1mg twice a day, and the first month passed with only minor mood changes. In the second month, the following escalating mixed symptomatology built up rapidly: increased energy, logorrhea, grandiosity, irritability, impulsivity, voices commenting on her, paranoid ideation, nihilistic ideas about the future, intense self- criticism, frequent crying, and continuous suicidal ideation, with a specific plan. She recovered with 6 bilateral, bitemporal ECT sessions. As for the consequences attributable to varenicline, she later evaluated such treatment as highly beneficial and valuable to
Angiotensin II seems to regulate dopamine neurotransmission as well . In BD pathophysiology the dopamine hypothesis is re- lated to the presence of a dopamine dysregulation syndrome underlying this disorder. According to this hypothesis an increased dopaminergic drive is related to symptoms of mania and the con- verse to depression . Dopamine brain levels are influenced by angiotensin, because AngII receptors are found on the soma and terminals of mesolimbic dopaminergic neurons and within this dopaminergic pathway AngII binding to AT1Rs facilitates dopa- mine release. Indeed, in vitro pretreatment with candesartan, an AT1R blocker was able to attenuate dopamine release induced by amphetamine in caudate-putamen and nucleus accumbens slices showing, thus, that AT1R activation is related to the neuroadapta- tive changes induced by amphetamine . Of note, the repeated amphetamine administration is broadly used as an animal model of mania [22,50].
design reliable screening tests and screening criteria that could help to predict conversion to bipolar disorder. However, reliable clinical scales to assess prodromal symptoms are still lacking. To date, the predictive value of four clinical scales has been tested in longitudinal studies: the General Behavior Inventory, a self- report measure useful to discriminate between mood and be- havioral disorders; the Child Behavior Checklist–Pediatric Bipolar Disorder, a proﬁle consisting of severe aggression, inattention, and mood instability; the Hypomanic Personality Scale; and the Hypomania Checklist–32 Revised scale (73–78). Higher scores on the depression scale of the General Behavior Inventory (74), higher scores on the Hypomanic Personality Scale (75, 76), and positive subthreshold hypomanic symptoms identiﬁed by the Hypomania Checklist–32 (77) were related to an increased risk of future mood disorder among bipolar offspring. In turn, the Child Behavior Checklist–Bipolar seems useful for predicting comorbid and impairing psychopathology rather than any one speciﬁc DSM-IV diagnosis (73, 78). It is worth mentioning that most participants without the Child Behavior Checklist–Bipolar phenotype did not manifest bipo- lar disorder, attention deﬁcit hyperactivity disorder (ADHD), cluster B personality disorder, or multiple psychiatric comorbid conditions at young-adult follow-up assessment (negative pre- dictive values of 86% to 95%) (78). An abbreviated version of the General Behavior Inventory, the Seven Up Seven Down, has also been proposed, but it failed to predict new onset of bipolar disorder (79).
Currently the two main treatments in clinical practice for major depression disorder (MDD), generalized anxiety disorder (GAD) and obsessive-compulsive disorder (OCD) are antidepressants and psychotherapy. Many studies examining the use of antidepressants in the treatment of psychiatric disorders focus on the underlying neurobiological mechanisms, whereas most studies on psychotherapy focus on its effects on symptom manage- ment and psychosocial function. Few studies have examined the role of psychotherapy in improving neuro- biological function (1-3), with even fewer studies compar- ing the difference between the two therapies in terms of their effects on neurobiological function.