The Spectrum of Mood Disorders: Bipolar I, Bipolar II, and Unipolar

Bipolar ◽  
2021 ◽  
pp. 29-64
Author(s):  
C. Raymond Lake
Keyword(s):  
2021 ◽  
pp. 000486742110200
Author(s):  
Gordon Parker

The 2020 College guidelines for mood disorders banish bipolar II disorder – despite its formal status in Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases manuals for more than two decades – and argue that there is no need to partition bipolar disorder into separate sub-types. Their single-entity model is seemingly based on opinion rather than any support from referenced scientific studies. The author challenges the Committee’s model of there being only one bipolar disorder and argues that it presents several clinical management risks, particularly of ‘over-treatment’.


CNS Spectrums ◽  
2009 ◽  
Vol 14 (8) ◽  
pp. 419-425 ◽  
Author(s):  
Mario Clerici ◽  
Beatrice Arosio ◽  
Emanuela Mundo ◽  
Elisabetta Cattaneo ◽  
Sara Pozzoli ◽  
...  

ABSTRACTIntroduction: An increasing amount of data suggests that dysregulation of the immune system, including the cytokine network, is associated with the etiology and pathophysiology of mood disorders. Genes encoding cytokines are highly polymorphic and single nucleotide polymorphisms, associated with increased or reduced cytokine production, have been described. The aim of this study was to define the genetic immunologic scenario associated with major depressive disorder (MDD) and bipolar disorder.Methods: Eighty-four Italian outpatients affected by bipolar disorder type I, bipolar disorder type II, or MDD, and 363 healthy controls were enrolled into the study. We analyzed allele and genotype distribution of −308 (G/A) tumor necrosis factor-α (TNF-α), +874 (T/A) interferon-γ (IFN-γ), -174 (G/C) interleukin (IL)-6, and −1082 (G/A) IL-10 promoter polymorphisms by Polymerase Chain Reaction Sequence Specific Primers technique.Results: We observed different genotype and allele distributions of TNF-α, IFN-γ, and IL-10 polymorphisms in the three groups of patients analyzed. In particular, bipolar II patients were characterized by an absence of adenine (A) high producer allele of TNF-α (P<.001) and a lower percentage of TT high producer genotype of IFN-γ (P <.001); bipolar I individuals showed reduced percentage of AA low producer genotype of IL-10 (P<.001). Both bipolar I and bipolar II patients not carrying guanine (G) high producer IL-6 allele showed a lower mean age at onset (P=.048).Conclusion: These data support the existence of a genetic profile related to pro-inflammatory cytokines in patients affected by mood disorders. The differences observed across the three clinical phenotypes suggest the presence of different pathogenetic mechanisms involved in the susceptibility of phenotypically different mood disorders.


1986 ◽  
Vol 31 (5) ◽  
pp. 436-441 ◽  
Author(s):  
J. Mark Levy ◽  
Ronald A. Remick

Eight female patients with rapid cycling mood disorders (at least four discrete affective episodes per year) were examined from a clinical perspective. Assessment suggested several different etiologies to the rapid cycling pattern in these patients. These included that the rapid mood swings were: a natural expression of the affective disorder, tricyclic induced, a result of frequent medication changes and/or poor medication compliance, and a combination of the aforementioned etiologies. All patients were helped significantly with treatment. Treatment was individualized for each patient's unique illness and possible etiological factors in the rapid cycling. Treatment strategies and guidelines include: i) A psychotherapeutic approach involving the patient and his family which emphasizes the lengthy nature of treatment before expected results; ii) The necessity of rigorous drug adherence, in) The sole use of “high dose” lithium therapy (> 1.2 MEQ/L) in some patients, and the consideration of “high dose” lithium in conjunction with tricyclics, MAO inhibitors or “adjuvant” medication in certain bipolar II patients; iv) The discontinuation of tricyclics in bipolar l rapid cyclers;v) The combination of lithium salts and carbamazepine or the use of carbamazepine alone in selected patients.


2006 ◽  
Vol 18 (2) ◽  
pp. 120-126 ◽  
Author(s):  
Po W. Wang ◽  
Napapon Sailasuta ◽  
Rebecca A. Chandler ◽  
Terence A. Ketter

Background:Animal models of depression and psychopharmacological mechanisms of action suggest the importance of the gamma-amino butyric acid (GABA) system in the pathophysiology of mood disorders. Mood stabilizers have overlapping effects on GABAergic neurotransmission, and antidepressant use has been associated with alterations in GABAB receptor function. Magnetic resonance spectroscopy (MRS) provides an opportunity to noninvasively assess cerebral GABA concentrations in anterior paralimbic circuits that have been implicated in mood disorders.Methods:In bipolar disorder patients and healthy control subjects, we used MRS with a modified GABA-edited point resolved spectroscopy sequence (TE 68 ms, TR 1500 ms, 512 averages, total scan time 26 min) to assess GABA in an 18-cm3 occipital voxel. In addition, in another cohort of bipolar disorder patients and healthy control subjects, we similarly assessed GABA in a 12.5-cm3 medial prefrontal/anterior cingulate (MPF/AC) voxel. The concentration of GABA was referenced to creatine (Cr) from unedited spectra.Results:In bipolar patients and controls, we consistently detected 3.0 p.p.m. GABA peaks in occipital lobe and MPF/AC. In 16 bipolar (nine bipolar I and seven bipolar II) disorder patients, compared with six healthy control subjects, mean occipital GABA/Cr concentration was 61% higher. In addition, in 15 bipolar (five bipolar I, nine bipolar II, and one bipolar not otherwise specified) disorder patients, compared with six healthy control subjects, mean MPF/AC GABA/Cr concentration tended to be 41% higher.Conclusions:Patients with bipolar disorders may have increased cerebral GABA concentrations. Although this was more evident in the occipital lobe, MPC/AC GABA disturbance may be of greater potential interest in view the more established role of MPF/AC in affective processing. Additional studies are warranted to assess changes in GABAergic neurotransmission and the influences of diagnosis, mood state, and medication status in bipolar disorder patients.


2016 ◽  
Vol 33 (S1) ◽  
pp. S210-S210
Author(s):  
R. Khemakhem ◽  
W. Homri ◽  
D. Karoui ◽  
M. Mezghani ◽  
L. Mouelhi ◽  
...  

IntroductionSeveral studies have explored the vulnerability to mood disorders that constitute some personality traits.AimsTo study the potential relationship between mood disorders and personality disorders.ObjectiveWe hypothesized that personality disorders can be related to severe mood disorders.MethodsThis was a retrospective study including the period from January 2000 till September 2015 and related to patients in whom the diagnosis of mood disorder and personality one were retained according to the criteria of the DSM-IV TR while the sociodemographic and clinical were collected by a pre-established railing.ResultsWe included 28 patients (15 ♂, 13 ♀). The average age was 38 years. Eighteen (64.3%) patients (7 ♂, 11 ♀) are unemployed. Fifteen patients (10 ♂, 5 ♀) were schooled until secondary level. Seventeen patients (60.7%) were married. The bipolar I disorder (BD I) was most frequently founded (50%), followed by the major depressive disorder in 25% (n = 7) then by the bipolar II disorder in 21.4% (n = 6). A case of dysthymia was also noted. Half of the personality disorders were the borderline type, followed by the histrionic type in 28.6% (n = 8) then by the antisocial in 17.9% (n = 5) and finally one patient presented a paranoiac personality. The antisocial personality was significantly associated with the BD I (P = 0.011) and half of the patients with a pathological personality, presented a depressive symptomatology.ConclusionThe personality disruption is a factor of severity of the thymic disorders. Consequences on the management of patients and their response to treatments remain available.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Author(s):  
Harvinder Singh ◽  
Brian Frankel

In this chapter the topics that are reviewed include major depressive disorder, persistent depressive disorder (dysthymia), unspecified depressive disorder, bipolar I disorder, bipolar II disorder, cyclothymic disorder and unspecified bipolar disorder


2016 ◽  
Vol 33 (S1) ◽  
pp. S334-S334
Author(s):  
E.J. Kim

ObjectiveIt has been suggested that the features of childhood ADHD are significantly associated with adult mood disorders. Some genetic factors may be common to both ADHD and mood disorders underlie the association between these two phenotypes. The present study aimed to determine whether a genetic role may be played by the serotonin transporter-linked polymorphic region (5-HTTLPR) in the childhood ADHD features of adult patients with mood disorders.MethodsThe present study included 232 patients with MDD, 154 patients with BPD, and 1288 normal controls. Childhood ADHD features were assessed with the Korean version of the Wender Utah Rating Scale. The total score and the scores of three factors (impulsivity, inattention, mood instability) from the WURS-K were analyzed to determine whether they were associated with the 5-HTTLPR genotype.ResultsIn the BPD II group, the 5-HTTLPR genotype was significantly associated with the total score (P = 0.029) and the impulsivity factor (P = 0.004) on the WURS-K. However, the inattention and mood instability factors were not associated with the 5-HTTLPR genotype, and the MDD and normal control groups did not exhibit any significant associations between the WURS-K scores and the 5-HTTLPR genotype.ConclusionThe present findings suggest that the 5-HTTLPR genotype may play a role in the impulsivity component of childhood ADHD in patients with BPD II. Because of a small sample size and a single candidate gene, further studies investigating other candidate genes using a larger sample are warranted to more conclusively determine any common genetic links.Disclosure of interestThe author has not supplied his declaration of competing interest.


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