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PubMedDate not supplied

Comorbidity of personality disorders with bipolar mood disorders.

The aim of the study was to assess the prevalence of personality disorders in a group of outpatients with bipolar I disorder. The Structured Clinical Interview for DSM-III-R Personality Disorders (SCID-II) was administered to 90 bipolar outpatients who met the DSM-III-R criteria and 58 control subjects. Of the patients and controls, 47.7% and 15.5%, respectively, had at least one personality disorder. At least one personality disorder in clusters A, B, and C and obsessive-compulsive, paranoid, histrionic, and borderline personality disorders were significantly more prevalent in bipolars. Suicide attempts were more frequent in patients with a history of personality disorder.

Adult↗
PubMed1999

Outcome for adjustment disorder with depressed mood: comparison with other mood disorders.

BACKGROUND: A review of the research literature on the diagnostic category of adjustment disorder indicates that its construct validity has not been established. Nevertheless, the diagnosis is made frequently, with an estimated incidence of 5-21% in psychiatric consultation services for adults. METHODS: Retrospective data was used to evaluate the construct validity of the adjustment disorder diagnostic category. The data primarily consisted of SF-36 Health Status Survey responses by a large group of adult psychiatric outpatients before treatment and again six months after beginning treatment. Subjects were divided into five diagnostic groups, and MANOVA, MANCOVA and chi square were used to clarify relationships among diagnoses, sociodemographic data and SF-36 scores. RESULTS: Diagnostic categories were significantly different at baseline, but did not differ in terms of outcome at six-months follow-up. There was a significant gender difference at baseline and a significant difference in gender distribution across diagnostic categories. LIMITATIONS: Structured interviews were not used for initial diagnoses, nor is there an estimate of the reliability of diagnoses among the clinicians. The patient attrition rate for six-months follow-up data was about 50%. Finally, patients received individualized treatment, with some patients receiving both medication and psychotherapy. CONCLUSIONS: Female patients were significantly more likely to be diagnosed with major depression or dysthymia than with an adjustment disorder. Females were also more likely than males to score lower on the mental health related scales of the SF-36 at admission. Patients diagnosed with an adjustment disorder scored higher on all SF-36 scales than did the other diagnostic groups at baseline and again at follow-up. There was no significant difference among diagnostic groups with regard to treatment outcome, suggesting that the adjustment disorder group can benefit as much as the other groups from treatment.

Adjustment Disorders↗
PubMed2006

Neural circuitry and neuroplasticity in mood disorders: insights for novel therapeutic targets.

SUMMARY: Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

Bipolar Disorder↗
PubMed2005

The involvement of G proteins and regulators of receptor-G protein coupling in the pathophysiology, diagnosis and treatment of mood disorders.

Biochemical research in mood disorders has focused, along the cascade of events involved in signal transduction, from studies at the level of the monoamine neurotransmitter to the level of the neurotransmitter receptors, and lately to information transduction mechanisms beyond receptors, involving the coupling of receptors with signal transducers. We review findings concerning (a) the involvement of G proteins, in the pathophysiology, diagnosis and treatment of mood disorders; (b) the importance of regulation of receptor-G protein coupling, G protein-coupled receptor kinases (GRKs), beta-arrestins, to the pathophysiology of mood disorders and the mechanism of action of antidepressants. We relate to the special complexity of mental disorders with regards to etiology and pathophysiological diagnosis as well as to the strength and limitations of the 'pharmacological bridge' approach governing studies to unravel the etiology of mental disorders. There are presently no established and reliable, sensitive and specific objective biological diagnostic markers in psychiatry that can serve as 'gold standards'. The future achievement of an objective biochemical differential diagnostic system for major mental disorders that will also enable an objective biological treatment monitoring is expected to be revolutionary for psychiatry with a magnitude similar to the impact of the discovery of psychopharmacological treatments for mental disorders more than 50 years ago.

Animals↗
PubMedDate not supplied

The Kahlbaum syndrome: a study of its clinical validity, nosological status, and relationship with schizophrenia and mood disorder.

Kahlbaum described catatonia as a disorder in which mood syndromes were the primary features and characteristic symptoms were the motor ones. However, after Kahlbaum this concept has not been taken into account and catatonia has been identified with motor features alone. In the present study, we assessed the clinical validity of Kahlbaum's concept of catatonia, its nosological position in relation to DSM-III-R, DSM-IV, and Leonhard's diagnostic criteria, and its relationships with schizophrenia and mood disorder. Of 567 patients consecutively admitted due to a functional psychotic disorder, 45 met criteria for catatonia according to Kahlbaum's concept (the Kahlbaum syndrome [KS]). Patients with the KS were differentiated from those with schizophrenia and mood disorders across a number of demographic and clinical variables, the differences being greater with the former than with the latter group. KS does not appear to fit any particular nosologic category, although this issue largely depends on whether schizophrenia and mood disorder are broadly or restrictively defined. When definitions of both disorders are most restrictive, as in the case of the Leonhard system, KS seems better accommodated as a "third psychosis". Overall, the data raise the possibility that KS is either a variant of mood disorder, or a distinct clinical entity.

Adult↗
PubMed2006

Galanin receptor antagonists : a potential novel pharmacological treatment for mood disorders.

The pathophysiology of mood disorders involves several genetic and social predisposing factors, as well as a dysregulated response to chronic stress. Accumulated evidence during the last two decades has implicated disturbances in brain serotonin and/or noradrenaline (norepinephrine) neurotransmission in the aetiology of depression. In fact, current pharmacological treatment for mood disorders is based on the use of drugs that act mainly by enhancing brain serotonin and noradrenaline neurotransmission by blockade of the active reuptake mechanism for these neurotransmitters. However, current antidepressant drugs have a delayed onset of therapeutic action, and a substantial number of patients do not respond adequately to them. In addition, these drugs have a number of adverse effects that limit patient compliance. In view of this, there is an intense search to identify novel (receptor) targets for antidepressant therapy. Recent studies have indicated that several neuropeptides and their receptors are potential candidates for the development of novel antidepressant treatment. In this context, galanin is of particular interest, since it is co-localised with serotonin in the dorsal raphe nucleus and with noradrenaline in the locus coeruleus, nuclei known to play a major role in affective disorders and in the action of antidepressant drugs. The actions of galanin are mediated by three receptor subtypes (GAL1, GAL2 and GAL3), which are coupled to different intracellular effector systems. Studies in rats have shown that galanin administered intracerebroventricularly is a potent inhibitor of mesencephalic serotonergic neurotransmission, as indicated by a long-lasting reduction in the release of serotonin in the hippocampus. This inhibitory effect is related to activation of the galanin receptors located on the dorsal raphe neurons. Moreover, intracerebroventricular galanin alters the gene expression of serotonin 5-HT1A autoreceptors in the dorsal raphe and also changes their functional activity. In addition, galanin produces a functional blockade of postsynaptic 5-HT1A receptor-mediated responses. Both pharmacological and genetic studies suggest a role for galanin in depression-like behaviour in rodent models. Transgenic mice overexpressing galanin under the control of the platelet-derived growth factor-beta promoter display increased immobility in the forced swim test. Intracerebroventricular administration of galanin in the rat increases depression-like behaviour, and this is fully blocked by the nonselective peptide galanin receptor antagonist M35. Importantly, M35 alone administered intracerebroventricularly produces an antidepressant-like effect. Recently, newly developed receptor-specific nonpeptidergic galanin GAL3 receptor antagonists (SNAP-37889 and SNAP-398299), which cross the blood-brain barrier after systemic administration, have shown antidepressant-like activity in several animal models. On the other hand, stimulation of the GAL2 receptor at the raphe level by local application of the GAL2 receptor agonist galanin (2-11) has been shown to increase serotonin levels in the hippocampus and dorsal raphe. These results indicate an important (mainly inhibitory) role of galanin as a regulator of brain serotonin and 5-HT1A receptor-mediated transmission, which may be of potential importance for understanding mood disorders and for the development of antidepressant drugs. Taken together, the present evidence suggests that antidepressant efficacy may be associated with compounds acting as antagonists at the GAL3 and/or possibly GAL1 receptors, and/or agonists at the GAL2 receptor.

Animals↗
PubMedDate not supplied

[Effect of comorbid substance use on neuropsychological performance in subjects with psychotic or mood disorders].

Objective - Patients presenting with psychotic or mood disorders present with neuropsychological deficits such as executive and memory disturbance. Deficits of these functions have also been reported in patients presenting with alcohol use or substance use disorders. A large percentage of patients with non-affective psychotic or mood disorders present with a comorbid substance use disorder. These subjects are often a priori excluded from most neuropsychological studies. However, using such an exclusion criterion may induce a selection bias linked to the high prevalence of this dual diagnosis. It is therefore necessary to further explore the impact of substance abuse on neuropsychological performance in subjects with psychotic or mood disorders. Method - Patients consecutively hospitalized for a non-affective psychotic disorder or a mood disorder were included. A standardised method was used to collect information on addictive behaviour, clinical and social characteristics. DSM IV diagnoses, including those of substance use, were made using a structured diagnostic interview and all other available clinical and historical information collected during the hospital stay. Memory performance was tested using the Batterie d'Efficience Mnésique 84 (Battery of memory efficiency 84 items, BEM 84). Executive abilities were explored using the Wisconsin Card Sorting Test (WCST) and the Stroop test. ANCOVAs with cannabis use disorder or alcohol use disorder as main factor were used to examine associations with neuropsychological test scores. Results - We have included 77 patients fulfilling the diagnostic criteria for non-affective psychotic disorders (schizophrenia, schizoaffective disorder, delusional disorder, other psychotic disorder, n=35) or mood disorders (n=42). Among these patients, 27.3% presented with a lifetime history of alcohol abuse/dependence (current prevalence: 14.3%) and 23.4% presented with a lifetime history of cannabis abuse/dependence (current prevalence: 11.7%). We have assessed the specific impact of alcohol and cannabis use on neuropsychological performance. No significant differences on memory and executive performance were found between patients presenting with and without a lifetime history of alcohol abuse/dependence. These results were not modified after adjustement for potential confounding factors (age, gender, educational level, age at onset, diagnosis, current versus past addictive behaviour). Patients with a lifetime history of cannabis abuse/dependence had significantly higher (i.e. better performance) general BEM 84 score (F=3.89, df=1, p=0.05), higher complex figure delayed recall scores (F=6.62, df=1, p=0.01) and higher recognition scores (F=3.9, df=1, p=0.05) than patients presenting without a lifetime history of cannabis use. After adjustment on covariables (age, gender, educational level, age at onset, diagnosis, current versus past addictive behaviour), the differences on memory performance between the two groups were no longer significant, the differences found before adjustment were mainly explained by the confounding effect of age. Patients presenting with a lifetime history of cannabis abuse/dependence had significantly lower interference scores on the Stroop test than subjects without cannabis use (F=5.67, df=1, p=0.02). This finding was not modified after adjustment for confounding factors. Information on substance use was collected by interviewing the patient and was completed by using all other available source of information, but no urine testing was performed. Thus, substance use could have been underestimated or unrecognized in some patients. We did not distinguish patients who presented with substance abuse from those who presented with dependence because there were few of the latter. Distinguishing these two populations would be of interest because dependence may have a more deleterious effect than abuse in neuropsychological performances. Finally, we did not included normal control subjects so we can not assess if our cohort present with memory and executive deficits compared to normal subjects. Conclusion - Comorbid alcohol or cannabis abuse/dependence has limited effects on memory and executive abilities in subjects with psychotic or mood disorder. The only significant difference between subjects with and without a dual diagnosis was that subjects with cannabis use disorder performed poorly on the Stroop test. No other significant difference in executive and memory performance was found after adjustment for confounding factors. Since there is a high prevalence of a comorbid substance use disorder in subjects with psychotic or mood disorder, the exclusion of these patients in neuropsychological studies may not be systematically justified.

Adolescent↗
PubMed1990

[Mood disorders in adolescence].

Mood disorders are seen frequently in adolescents. They may range from normative developmental events through the gamut of psychopathologies--dysthymia, unipolar depression, bipolar disorder. This paper reviews the varied developmental and psychosocial factors that contribute to such disorders and discusses psychotherapeutic approaches that have proved helpful with such problems.

Adolescent↗
PubMed2006

Adolescent psychopharmacology: drugs for mood disorders.

This article reviews mood disorders in children and adolescents, the diagnostic criteria, and important differential diagnoses to be considered. Critical points in the treatment of mood disorders and comorbid conditions and the important role the primary care provider can play in their management are stressed. Warning signs to identify adolescents who may be at risk of attempting suicide are discussed.

Adolescent↗
PubMed1998

Hormone measures in reproductive endocrine-related mood disorders: diagnostic issues.

Mood disturbances have been identified in association with changes in levels of reproductive hormones. The use of hormonal measures in the diagnosis of reproductive endocrine-related mood disorders is highly variable, ranging from necessary in perimenopausal depression to irrelevant in premenstrual syndrome. This article describes our view of the use of hormonal measures for diagnostic and research purposes in perimenopausal depression and premenstrual syndrome. We suggest that the understanding of these disorders lies in as yet unidentified contextual factors rather than in hormonal excesses or deficiencies.

Female↗
PubMed2005

Treating mood disorders during pregnancy: safety considerations.

Mood disorders in pregnancy may have a negative effect on self care and pregnancy outcome that affects the mother directly and the child indirectly. Thus, some women may require pharmacological treatment. Pharmacotherapy of mood disorders during pregnancy implies specific considerations. This paper presents an updated review of available studies on the treatment of mood disorders and present knowledge on teratogenicity, neonatal effects and long-term neurobehavioural effects for the different psychotropic drugs, including treatment with selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), other antidepressants, benzodiazepines, lithium, carbamazepine/valproic acid, lamotrigine and novel antipsychotics. However, the existing knowledge on the use of antidepressants and mood stabilising agents during pregnancy is hampered by a lack of results from randomised controlled trials.SSRIs and TCAs have not been associated with an increased risk of major malformations, but poor neonatal adaptation has been described. Benzodiazepines used in the first trimester have been associated with orofacial clefts. Mood stabilisers such as lithium, carbamazepine and valproic acid (sodium valproate) are associated with an increased risk of fetal malformations. Both benzodiazepines and lithium may cause adaptation problems in the newborn. In utero exposure to novel antipsychotics has not been associated with congenital malformations; however, the data are still limited. The knowledge about long-term neurobehavioural effects in the offspring is still limited for all agents and requires further investigation. Possible adverse effects of fetal exposure must be balanced against the adverse effects of an untreated maternal mood disorder.

Adult↗
PubMed2003

Mood disorders following traumatic brain injury.

Mood disorders are a frequent complication of traumatic brain injury that exerts a deleterious effect on the recovery process and psychosocial outcome of brain injured patients. Prior psychiatric history and impaired social support have been consistently reported as risk factors for developing mood disorders after traumatic brain injury (TBI). In addition, biological factors such as the involvement of the prefrontal cortex and probably other limbic and paralimbic structures may play a significant role in the complex pathophysiology of these disorders. Preliminary studies have suggested that selective serotonin reuptake inhibitors such as sertraline, mood stabilizers such as sodium valproate, as well as stimulants and ECT may be useful in treating these disorders. Mood disorders occurring after TBI are clearly an area of neuropsychiatry in which further research in etiology as well as treatment is needed.

Adult↗
PubMed1990

The spectrum of mood disorders.

The problem of classifying mood disorders still lacks an acceptable solution. Interrater reliability studies have shown that this problem is more prevalent in mood disorders compared with other psychiatric conditions. Historically the problem originates from the distinction between Geisteskrankheiten and Gemütskrankheiten (mental and mood disorders) because the domain covered by the word mood has been progressively reduced. The fact that neurotic disorders are "emotional disorders" further complicates this field. The words anxiety and depression refer to a disorder, to a symptom, and to everyday feelings. A failure or difficulty in the distinction between these three meanings leads to nosological confusion. In recent years, the notion of a spectrum of mood disorders has gained acceptance. According to this, the diverse disorders are placed on a point that is more or less close to one of the extremes. Something similar occurs in the unipolar-bipolar distinction, in which the bipolar II or atypical and bipolar III occupy a central place on the spectrum. Cluster analysis and other mathematical techniques have helped to clarify the outlook, but there is a need for a biopsychosocial perspective and for a deeper understanding of the natural history of these disorders.

Adult↗
PubMed2001

Mood disorders and suicide.

The mood disorders unipolar major depression and bipolar disorder increase the risk of suicidal ideation, attempted suicide, and death by completed suicide. This article reviews the epidemiologic data on the relationship between mood disorders and suicide, with an emphasis on the substantial risk of suicide, while reassessing older data that may no longer apply. Widespread underdiagnosis and undertreatment of major depression and bipolar disorder contribute to an unacceptable risk of suicide, a preventable tragedy.

Adult↗
PubMed2002

Readmission rates for adjustment disorders: comparison with other mood disorders.

BACKGROUND: The diagnostic category of adjustment disorders continues to receive little attention in the research literature despite its estimated incidence of 5-21% in psychiatric consultation services for adults and 7.1% in inpatient admissions. METHODS: Ten years of readmission data were reviewed for six diagnostic categories: adjustment disorders, major depressive disorder (single episode and recurrent), dysthymia, any anxiety disorder and depression NOS. Cox regression analysis was used. RESULTS: Admission diagnosis was a significant predictor of readmission, with adjustment disorders resulting in significantly fewer readmissions than the group as a whole, and major depression recurrent resulting in significantly more readmissions. LIMITATIONS: Structured interviews were not used for the establishment of admission diagnoses. CONCLUSIONS: Readmission rates in this sample support the construct validity of the adjustment disorders category. The category includes a significant minority of patients admitted to psychiatric hospitalization.

Adjustment Disorders↗
PubMed2003

Occult mood disorders in 104 consecutively presenting children referred for the treatment of attention-deficit/hyperactivity disorder in a community mental health clinic.

OBJECTIVE: To ascertain the prevalence of mood disorders among consecutively evaluated prepubertal children presenting for the treatment of attention-deficit/hyperactivity disorder (ADHD) in a community mental health clinic. METHOD: 104 children received systematic assessments designed to identify individuals meeting the DSM-IV criteria for major depressive disorder (MDD), mania, and ADHD. "Standard" and "modified" criteria for mania were employed. Modified criteria, in an effort to minimize false-positive diagnoses of mania, required the presence of euphoria and/or flight of ideas. A child meeting the criteria for MDD or either set of criteria for mania was categorized as having a mood disorder. Mood disorders in first-degree relatives were assessed using a systematic interview. Data were gathered from 2000 to 2002. RESULTS: Sixty-two children (59.6%) had a mood disorder. Compared with those who did not have a mood disorder, they were 3.3 times more likely (54.8% vs. 16.7%) to have a family history of any affective disorder (p <.0001) and 18.3 times more likely (43.5% vs. 2.4%) to have a family history of bipolar disorder (p <.0001). Twenty (32.3%) of the children with and none without a mood disorder had psychotic features (p <.0001). Compared with those meeting only the standard criteria for mania, those meeting the modified criteria were 9.1 times more likely (69.8% vs. 7.7%) to have a family history of an affective disorder (p <.0001) and 7.3 times more likely (55.8% vs. 7.7%) to have a family history of bipolar disorder (p =.002). CONCLUSION: Children who presumably have ADHD often have unrecognized affective illness. Our findings support the view that children meeting the modified criteria for mania have veritable bipolar disorder. These findings, which were derived in the course of delivering routine clinical services in a community mental health clinic, are consistent with those obtained in research settings suggesting that children presenting with ADHD often have occult mood disorders, especially unrecognized bipolarity. We suggest that clinicians encountering children with prominent features of ADHD inquire about the presence of euphoria and flight of ideas. We submit that the presence of these "classic" manifestations of mania strongly suggests the presence of occult bipolarity, even if course of illness otherwise markedly deviates from "classic" descriptions.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

Ten-year stability of personality disorders among outpatients with mood disorders.

One of the core propositions in most clinical and descriptive models of personality disorders (PDs) is that these conditions are stable over time. However, the available empirical literature suggests that PDs are far less stable than these models imply. The present study examines the 10-year stability of PDs in a sample of depressed outpatients who were assessed for the full range of Axis II conditions across 5 assessments. Three primary issues are addressed: (a) the stability of categorical PD diagnoses, (b) the relative stability of dimensional PD traits, and (c) the absolute stability of PD traits. The stability of PD diagnoses was poor to fair, and the stability of dimensional PD traits was fair to moderate. Growth curve analyses revealed complex patterns of change in absolute scores for PD traits across the 10-year interval. Stability of PDs was generally comparable to that of anxiety disorder diagnoses and normal personality traits.

Adolescent↗