Myelinolysis cases presenting with manic attack after rapid correction of hyponatremia: Two cases.

OBJECTIVE: Myelinolysis is a neurological condition that can display diverse psychiatric symptoms, with electrolyte imbalance, alcoholism and malnutrition being the frequent causes. Rapid correction of hyponatremia may trigger pontine and extra-pontine myelinolysis. CASES: This paper examines two cases: one of hyponatremia after antihypertensive use and the other of myelinolysis due to rapid correction of hyponatremia. Since myelinolysis appeared as a manic episode, the patients sought treatment at the psychiatry outpatient clinic. Further tests were conducted to rule out organic causes and the diagnosis was confirmed prior to referring the patients to the neurology clinic. CONCLUSION: Psychiatrists should be meticulous in excluding organic causes in first-episode mania and consider these possibilities in the differential diagnosis for the pertinent patient group.

Study of the different sleep disturbances during the prodromal phase of depression and mania in bipolar disorders.

BACKGROUND: One of the challenges in bipolar disorder (BD) lies in early detection of the illness and its recurrences, to improve prognosis. Sleep disturbances (SD) have been proposed as reliable predictive markers of conversion. While preliminary studies have explored the relationship between SD and the onset of mood episodes, the results remain heterogeneous and a few have specifically examined patients' perception of prodromal symptoms and their progression until the episode occurs. Identifying prodromes represents a crucial clinical challenge, as it enables early intervention, thereby reducing the severity of BD. Therefore, the objective of this study is to better characterize and evaluate the progressive nature of SD as prodromal symptoms of mood episodes, and patients' perception of it. METHODS: Patients diagnosed with BD, either hospitalized or seeking treatment for a (hypo)manic or depressive episode benefited from standardized questionnaires, structured interviews, and self-report questionnaires to evaluate SD prior to the current episode, as well as sociodemographic and clinical information. RESULTS: Out of the 41 patients included, 59% spontaneously reported SD prior to the episode, appearing 90 days before depression and 35 days before mania (pre-indexed/spontaneous reports: 51.22% insomnia complaints, 4.88% hypersomnolence complaints, 7.32% parasomnias, 2.44% sleep movements). After inquiry about specific SD, the percentage of patients reporting prodromal SD increased significantly to 83%, appearing 210 days before depression and 112.5 days before mania (post-indexed reports: 75.61% presented with insomnia complaints appearing 150 days before depression and 20 days before mania, 46.34% had hypersomnolence complaints appearing 60 days before depression, 43.9% had parasomnias appearing 210 days before depression and 22.5 days before mania, 36.59% had sleep movements appearing 120 days before depression and 150 days before mania). Of note, bruxism appeared in 35% of patients before mania, and restless legs syndrome in 20% of patients before depression. CONCLUSION: This study highlights the very high prevalence of SD prior to a mood episode in patients with BD with differences between depressive and manic episodes. The more systematic screening of sleep alterations of the prodromal phase improved the recognition and characterization of different symptoms onset by patients. This underscores the need for precise questioning regarding sleep patterns in patients, to better identify the moment of transition toward a mood episode, referred to as "Chronos syndrome". The study emphasizes the importance of educating patients about the disorder and its sleep prodromal symptoms to facilitate early intervention and prevent recurrences.

[THE ROLE OF STRESS IN MANIC-PSYCHOTIC EPISODE DURING THE TERROR ATTACK OF OCTOBER 7 - CASE REPORT].

INTRODUCTION: The bio-psycho-social model is mostly used to understand the etiology and pathogenesis of psychiatric disorders. Even though in our era, the biological factors became more dominant in the field, the stress-diathesis model is quite acceptable to explain and understand the evolution of psychotic as well as affective disorders. BACKGROUND: In this case report we present a patient, in her late 40's, admitted to our department with a manic-psychotic episode for the first time in her life, after the massive terror attack of October 7, and in which we suggest that the signs and symptoms might be explained using the psycho-dynamic theory. CONCLUSIONS: We conclude suggesting that the equilibrium of the bio-psycho-social model, should be adjusted in the context of time and space, especially during a situation of catastrophic scale in the patient environment. DISCUSSION: Although stress is a risk factor for the development of affective disorders and especially manic-psychotic episodes, there is scarce literature to support it. On the other hand, psycho-dynamic theories sometimes consider stressful life events as a causative factor for the development of depressive as well as manic episodes.

Nitrated meat products are associated with mania in humans and altered behavior and brain gene expression in rats.

Mania is a serious neuropsychiatric condition associated with significant morbidity and mortality. Previous studies have suggested that environmental exposures can contribute to mania pathogenesis. We measured dietary exposures in a cohort of individuals with mania and other psychiatric disorders as well as in control individuals without a psychiatric disorder. We found that a history of eating nitrated dry cured meat but not other meat or fish products was strongly and independently associated with current mania (adjusted odds ratio 3.49, 95% confidence interval (CI) 2.24-5.45, p < 8.97 × 10-8). Lower odds of association were found between eating nitrated dry cured meat and other psychiatric disorders. We further found that the feeding of meat preparations with added nitrate to rats resulted in hyperactivity reminiscent of human mania, alterations in brain pathways that have been implicated in human bipolar disorder, and changes in intestinal microbiota. These findings may lead to new methods for preventing mania and for developing novel therapeutic interventions.

Poststroke Bipolar Disorder.

ABSTRACT: Various diseases that impact different systems and organs in the body may trigger manic episodes. Strokes are often associated with psychiatric symptoms, particularly depressive and, more rarely, manic. We herein report a case of bipolar disorder secondary to cerebrovascular disease in a 67-year-old man with no personal or family history of psychiatric illness who, at the age of 64, had a bilateral ischemic stroke in the middle cerebral artery territory. About 20 days after this stroke, he experienced a manic episode. Three years later, he experienced a second manic episode, with another hospitalization in a psychiatric ward. With this case, we intend to emphasize that, although rare, the diagnosis of mania after stroke should not be forgotten, and most important, one should be aware of the recurrence of affective episodes just as in non-medical-caused bipolar disorder.

Deep brain stimulation of the subthalamic nucleus in obsessive-compulsives disorders: long-term follow-up of an open, prospective, observational cohort.

BACKGROUND: Obsessive-compulsive disorder (OCD) is a major cause of disability in western country and responsible for severe impairment of quality of life. About 10% of patients present with severe OCD symptoms and require innovative treatment such as deep brain stimulation (DBS). Among possible targets, the non-motor subthalamic nucleus (STN) is a key node of the basal ganglia circuitry, strongly connected to limbic cortical areas known to be involved in OCD. METHOD: We analysed, in a prospective, observational, monocentric, open label cohort, the effect of chronic non-motor STN-DBS in 19 patients with treatment-resistant OCD consecutively operated in a single centre. Severity of OCD was evaluated using the Yale and Brown Obsessive-Compulsive Scale (YBOCS). YBOCS scores at 6, 12 and 24 months postoperatively were compared with baseline. Responders were defined by >35% improvement of YBOCS scores. Global Assessment Functioning (GAF) scale was used to evaluate the impact of improvement. RESULTS: At a 24-month follow-up, the mean YBOCS score improved by 53.4% from 33.3±3.5 to 15.8±9.1 (95% CI 11.2-20.4; p<0.0001). Fourteen out of 19 patients were considered as responders, 5 out of 19 being improved over 75% and 10 out of 19 over 50%. GAF scale improved by 92% from 34.1±3.9 to 66.4±18.8 (95% CI 56.7-76.1; p=0.0003). The most frequent adverse events consisted of transient DBS-induced hypomania and anxiety. CONCLUSION: Chronic DBS of the non-motor STN is an effective and relatively safe procedure to treat severe OCD resistant to conventional management.

Reporting trigger factors for (hypo)manic episodes in bipolar disorder: association with personality and prognosis.

OBJECTIVE: To investigate external factors that trigger manic and hypomanic relapses and how this is associated with personality and clinical outcome measured as number of affective episodes over a 7-year period. METHOD: This is a prospective cohort study of 204 meticulously characterized Swedish bipolar disorder patients. Personality was evaluated at baseline using the Swedish universities Scales of Personality in 170 patients, and 90 patients were followed up after approximately 7 years in order to evaluate clinical outcomes. RESULTS: We found that 44% of the patients reported trigger factors, including sleep disturbance, work- or family-related issues, medication, and illicit drug use. There were no significant differences in any of the personality traits when comparing the 74 patients that reported triggers with the 90 patients that did not. At 7-year follow-up, there was no difference between the groups in number of affective episodes (depressive, hypomanic, manic, or mixed), involuntary commitments, suicide attempts, or self-harm incidents since baseline. CONCLUSIONS: Around 40% of the patients reported external triggers for manic and hypomanic episodes. However, this was neither associated with personality traits nor number of affective episodes at 7-year follow-up.

Association of Etiological Factors for Hypomanic Symptoms, Bipolar Disorder, and Other Severe Mental Illnesses.

Importance: Subsyndromal hypomanic symptoms are relatively common in the general population and are linked to the onset of bipolar disorder. Little is known about their etiology and whether this is shared with the etiology of bipolar disorder or other mental illnesses. Objective: To examine the genetic and environmental architecture of hypomanic symptoms in a nonclinical youth sample and compare estimates at varying severity levels and their association with diagnosed bipolar disorder. Design, Setting, and Participants: This cohort study used phenotypic and genetic data from the Child and Adolescent Twin Study in Sweden and included individuals with International Statistical Classification of Diseases and Related Health Problems, Tenth Revision diagnosis of psychiatric disorders from national registries for residents of Sweden. Associations between hypomania and polygenic risk scores for bipolar disorder, major depressive disorder and schizophrenia were also investigated. Analysis began November 2018 and ended October 2021. Main Outcomes and Measures: Hypomanic symptoms were assessed using the parent-rated Mood Disorders Questionnaire when the twins were aged 18 years. Bipolar disorder diagnosis and/or lithium prescription were ascertained from national registries for residents of Sweden. Polygenic risk scores for psychiatric disorders were calculated using independent discovery genetic data. Results: A total of 8568 twin pairs aged 18 years (9381 [54.7%] female) were included in the study. The hypomania heritability estimate was 59% (95% CI, 52%-64%) for male individuals and 29% (95% CI, 16%-44%) for female individuals. Unique environmental factors accounted for 41% (95% CI, 36%-47%) of the hypomania variance in male individuals and 45% (95% CI, 40%-50%) in female individuals. Shared environmental factors were only detected for female individuals and explained 26% (95% CI, 13%-38%) of the variance. The heritability estimates were fairly consistent across different hypomania severity groups. Moderate genetic (0.40; 95% CI, 0.21-0.58) and shared environmental (0.41; 95% CI, 0.03-0.75) correlations between hypomania and diagnosed bipolar disorder were found. Hypomania was significantly associated with the polygenic risk scores for schizophrenia (ß = 0.08; SE = 0.026; P = .002) and major depressive disorder (ß = 0.09; SE = 0.027; P = .001) but not bipolar disorder (ß = 0.017; SE = 0.03; P = 0.57) (bipolar disorder I [ß = 0.014; SE = 0.029; P = .64] or bipolar disorder II [ß = 0.045; SE = 0.027; P = .10]). Conclusions and Relevance: Higher heritability for hypomania was found for male compared with female individuals. The results highlight the shared etiologies between hypomanic symptoms, bipolar disorder, major depression, and schizophrenia in youths. Future research should focus on identifying specific shared genetic and environmental factors. These findings support a possible dimensional model of bipolar disorder, with hypomania representing a continuous trait underlying the disorder.

Precursors of self-reported subclinical hypomania in adolescence: A longitudinal general population study.

Symptoms of subclinical hypomania (SHM) are common in the general population of adolescents and young adults. SHM are most often transient yet might be risk markers of later bipolar disorder. The current study aimed to assess the clinical correlates of SHM at age 11 in the general population, examine the continuity of SHM from age 11-age 16 and explore the clinical precursors of age 16 SHM. As part of the Copenhagen Child Cohort 2000, 1,632 preadolescents participated in the examination of SHM and various clinical correlates at age 11, 893 were re-assessed for SHM at age 16 years. At age 11, SHM, psychotic experiences and depressive symptoms were assessed by semi-structured psychopathological interviews. Furthermore, the participants were diagnostically assessed by the Development and Well-Being Assessment and interviewed about sleep length. At age 16, SHM was assessed by self-report, using the Hypomania Checklist-32. Cannabis use occurring at age 15 or earlier was assessed at age 16. At age 11, SHM was associated with depressive disorders (Relative Risk [RR] = 2.96 [95% CI 1.26-6.96]), interview-based depressive symptoms (RR = 9.22 [5.93-14.34]), neurodevelopmental disorders (RR = 2.94 [1.66-5.20]), psychotic experiences (RR = 4.51 [2.90-7.01]) and insufficient sleep (RR = 2.10 [1.28-3.43]. In the longitudinal analyses, age 16 SHM was preceded by age 11 SHM (RR = 1.89 [1.02-3.49]), psychotic experiences (RR = 2.06, [1.28-3.33]), emotional disorders (RR = 1.77, [1.02-3.09]) and cannabis use (RR = 3.14, [1.93-5.10]), after mutual adjustment and adjustment for sex, and sociodemographic factors. In conclusion, age 11 SHM was statistically significantly associated with other types of psychopathology in cross-sectional analyses and showed some continuity with later self-reported SHM at age 16. Particularly early psychotic experiences and cannabis use stood out as independent precursors of self-reported SHM and might constitute important risk markers for the development of future SHM and bipolar disorder. An important potential caveat of the current study includes the self-report assessment of SHM.

Treatment of Electroconvulsive Therapy-Emergent Hypomania and Mania: A Systematic Review of the Literature.

Objective: Electroconvulsive therapy (ECT)-emergent hypomania/mania is a clinically significant problem that has lacked evidence-based guidelines for effective management. The aim of this systematic literature review is to compile the current published literature on treating ECT-emergent hypomania/mania to help guide treatment course in patients with unipolar and bipolar depression.Data Sources: MEDLINE/PubMed was searched for studies published from 1980 through August 2020 that evaluated the treatment of ECT-emergent hypomania/mania. Search terms included Boolean combinations of the following: mania, hypomania, ECT, ECT induced mania, and ECT induced hypomania.Study Selection: There were 1,662 articles reviewed, and all published studies detailing the treatment of ECT-emergent hypomania/mania written in English that met inclusion criteria were included. Due to the limited number of articles, there were no restrictions.Data Extraction: Two reviewers extracted relevant articles and assessed each study based on inclusion criteria.Results: The literature review identified 12 articles that described the treatment course of ECT-emergent hypomania/mania in 17 patients. There were 9 patients who had no known history of manic or hypomanic episodes and were diagnosed with unipolar depression and 8 patients diagnosed with bipolar disorder. There were 4 primary treatment courses identified: continuing ECT alone, continuing ECT in conjunction with lithium, discontinuing ECT with no medication treatment, or discontinuing ECT and starting a medication.Conclusions: The available data are insufficient to support definitive conclusions; however, potential treatment guidelines are suggested within the review to providers based on the limited data available.

Preliminary Findings Associate Hippocampal 1H-MR Spectroscopic Metabolite Concentrations with Psychotic and Manic Symptoms in Patients with Schizophrenia.

BACKGROUND AND PURPOSE: Previous hippocampal proton MR spectroscopic imaging distinguished patients with schizophrenia from controls by elevated Cr levels and significantly more variable NAA and Cho concentrations. This goal of this study was to ascertain whether this metabolic variability is associated with clinical features of the syndrome, possibly reflecting heterogeneous hippocampal pathologies and perhaps variability in its "positive" (psychotic) and "negative" (social and emotional deficits) symptoms. MATERIALS AND METHODS: In a sample of 15 patients with schizophrenia according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, we examined the association of NAA and Cho levels with research diagnostic interviews and clinical symptom ratings of the patients. Metabolite concentrations were previously obtained with 3D proton MR spectroscopic imaging at 3T, a technique that facilitates complete coverage of this small, irregularly shaped, bilateral, temporal lobe structure. RESULTS: The patient cohort comprised 8 men and 7 women (mean age, 39.1 [SD, 10.8] years, with a mean disease duration of 17.2 [SD, 10.8] years. Despite the relatively modest cohort size, we found the following: 1) Elevated Cho levels predict the positive (psychotic, r = 0.590, P = .021) and manic (r = 0.686, P = .005) symptom severity; and 2) lower NAA levels trend toward negative symptoms (r = 0.484, P = .08). No clinical symptoms were associated with Cr level or hippocampal volume (all, P ≥ .055). CONCLUSIONS: These preliminary findings suggest that NAA and Cho variations reflect different pathophysiologic processes, consistent with microgliosis/astrogliosis and/or lower vitality (reduced NAA) and demyelination (elevated Cho). In particular, the active state-related symptoms, including psychosis and mania, were associated with demyelination. Consequently, their deviations from the means of healthy controls may be a marker that may benefit precision medicine in selection and monitoring of schizophrenia treatment.

Graves' disease presenting with hypomania and paranoia to the acute psychiatry service.

This manuscript describes the case of a young woman, with no prior psychiatric history, who developed hypomania and paranoia as the principal presenting features of Graves' disease. After starting treatment with carbimazole and propranolol, symptoms resolved without the use of antipsychotic drugs. Close liaison between psychiatry and endocrinology services was essential. This demonstrates that treating underlying thyrotoxicosis in patients presenting with psychiatric symptoms may lead to recovery without the use of antipsychotic medication. While agitation, irritability and mood lability are well-recognised thyrotoxic symptoms, psychosis is a rare presenting feature of Graves' disease. All patients with agitation, delirium or psychiatric symptoms should have thyroid function checked as part of initial tests screening for organic disease. In new or relapsing psychiatric conditions, it is important to ask patients, their carers or relatives about symptoms of hypothyroidism or thyrotoxicosis.

Effects of tamoxifen and glutamate and glutamine levels in brain regions in repeated sleep deprivation-induced mania model in mice.

Protein kinase C inhibitor tamoxifen reduces symptoms of acute mania in bipolar patients and mania-like behaviors in animals. Memory impairment and altered levels of glutamate and glutamate/glutamine ratio have been reported in mania. Tamoxifen suppresses glutamate release which plays an important role in memory. The present study evaluated whether tamoxifen's activity participates in its antimanic efficacy in repeated sleep deprivation mania model. Mice were divided into control and 24-h sleep-deprived groups and were treated with vehicle or 1 mg/kg tamoxifen twice daily for 8 days. Sleep deprivation was repeated three times at intervals of 2 days. Square crossing and rearing were recorded as measures of locomotor activity. Memory and risk taking behavior were evaluated using novel object recognition and staircase tests, respectively. Glutamate and glutamine levels were measured in the frontal cortex and hippocampus. Behavioral tests were conducted 24 h after the second or immediately after the third sleep deprivations. Sleep deprivation increased locomotor activity and risk taking. Glutamate and glutamine levels and glutamate/glutamine ratio in the frontal cortex and hippocampus were unaffected. Locomotor hyperactivity was prevented by tamoxifen treatment. No change in the recognition index suggested lack of memory impairment in the model. These findings confirm the relevance of repeated sleep deprivation as a mania model and tamoxifen as an antimanic agent. However, future research is needed to further address lack of memory impairment in the model and lack of glutamatergic influence on the model and antimanic effect of tamoxifen.

SARS-CoV-2-associated first episode of acute mania with psychotic features.

Despite neuropsychiatric outcomes of SARS-CoV-2 infection are now under close scrutiny, psychoneuroimmunological characteristics of COVID-19 and precise pathophysiology of neuropsychiatric manifestations of the infection are still obscure. Moreover, there still exists a shortfall in demonstrating specific clinical manifestations of the brain involvement of the virus. Here, we presented a 33-year-old female patient with COVID-19, reporting acute-onset paranoid delusions symptoms, insomnia and irritability. Cranial MRI showed an hyperintense signal in the splenium of the corpus callosum with decreased apparent diffusion coefficient, which might possibly indicate the presence of cytotoxic edema related to the brain involvement of the infection. Following the completion of SARS-CoV-2 treatment, both cytotoxic edema and psychiatric symptoms resolved. In light of this report, we suggest that either heightened immune response and direct viral infection that SARS-CoV-2 may lead to such psychiatric manifestations and neuropsychiatric monitoring should be performed in patients with COVID-19. Prompt recognition of psychiatric consequences of COVID-19 may help clinicians provide guidance for differential diagnosis and manage them accordingly.