The need to consider mood disorders, and especially chronic mania, in cases of Diogenes syndrome (squalor syndrome)

2010 ◽  
Vol 23 (3) ◽  
pp. 505-507 ◽  
Author(s):  
G. Fond ◽  
F. Jollant ◽  
M. Abbar

ABSTRACTWe report the case of a 69 year-old female patient who was hospitalized for Diogenes syndrome, defined by marked self-neglect, social withdrawal and excessive hoarding, leading to squalor. Somatic causes were eliminated. Her personal history showed an eight-year depressive episode followed by a 20-year hypomanic episode without remission, followed by a persistent manic episode associated with Diogenes syndrome for four years. The Diogenes syndrome was successfully treated with mood stabilizers. Mood disorders – in particular chronic mania (i.e. a manic episode lasting more than two years) – should be considered in cases of Diogenes syndrome and in current classifications.

CNS Spectrums ◽  
2016 ◽  
Vol 21 (S1) ◽  
pp. 25-33 ◽  
Author(s):  
Roger S. McIntyre ◽  
Yena Lee ◽  
Rodrigo B. Mansur

Mixed features specifier (MFS) is a new nosological entity defined and operationalized in the Diagnostic and Statistical Manual of Mental Disorders (DSM), 5th Edition. The impetus to introduce the MFS and supplant mixed states was protean, including the lack of ecological validity, high rates of misdiagnosis, and guideline discordant treatment for mixed states. Mixed features specifier identifies a phenotype in psychiatry with greater illness burden, as evidenced by earlier age at onset, higher episode frequency and chronicity, psychiatric and medical comorbidity, suicidality, and suboptimal response to conventional antidepressants. Mixed features in psychiatry have historical, conceptual, and nosological relevance; MFS according to DSM-5, is inherently neo-Kraepelinian insofar as individuals with either Major Depressive Disorder (MDD) or Bipolar Disorder (BD) may be affected by MFS. Clinicians are encouraged to screen all patients presenting with a major depressive episode (or hypomanic episode) for MFS. Although “overlapping symptoms” were excluded from the diagnostic criteria (eg, agitation, anxiety, irritability, insomnia), clinicians are encouraged to probe for these nonspecific symptoms as a possible proxy of co-existing MFS. In addition to conventional antidepressants, second generation antipsychotics and/or conventional mood stabilizers (eg, lithium) may be considered as first-line therapies for individuals with a depressive episode as part of MDD or BD with mixed features.


2019 ◽  
pp. S3-S15 ◽  
Author(s):  
M. ĽUPTÁK ◽  
J. HROUDOVÁ

Mitochondria primarily serve as source of cellular energy through the Krebs cycle and β-oxidation to generate substrates for oxidative phosphorylation. Redox reactions are used to transfer electrons through a gradient to their final acceptor, oxygen, and to pump hydrogen protons into the intermembrane space. Then, ATP synthase uses the electrochemical gradient to generate adenosine triphosphate (ATP). During these processes, reactive oxygen species (ROS) are generated. ROS are highly reactive molecules with important physiological functions in cellular signaling. Mitochondria play a crucial role in intracellular calcium homeostasis and serve as transient calcium stores. High levels of both, ROS and free cytosolic calcium, can damage mitochondrial and cellular structures and trigger apoptosis. Impaired mitochondrial function has been described in many psychiatric diseases, including mood disorders, in terms of lowered mitochondrial membrane potential, suppressed ATP formation, imbalanced Ca2+ levels and increased ROS levels. In vitro models have indicated that mood stabilizers affect mitochondrial respiratory chain complexes, ROS production, ATP formation, Ca2+ buffering and the antioxidant system. Most studies support the hypothesis that mitochondrial dysfunction is a primary feature of mood disorders. The precise mechanism of action of mood stabilizers remains unknown, but new mitochondrial targets have been proposed for use as mood stabilizers and mitochondrial biomarkers in the evaluation of therapy effectiveness.


Introduction Historical perspective Mania/manic episode Hypomania/hypomanic episode Bipolar spectrum disorder Bipolar (affective) disorder 1: classification Bipolar (affective) disorder 2: clinical notes Bipolar (affective) disorder 3: aetiology Bipolar (affective) disorder 4: management principles Other issues affecting management decisions Treatment of acute manic episodes Treatment of depressive episodes...


2017 ◽  
Vol 41 (S1) ◽  
pp. S118-S118
Author(s):  
I. Ibanez Plans ◽  
E. Nieto ◽  
S. Biel

IntroductionThere are very few comparative controlled trials of risperidone versus olanzapine in manic patients. No previous naturalistic study has compared the efficacy of these two antipsychotics in the natural environment of manic inpatients.ObjectiveThe aim of this retrospective and naturalistic study was to evaluate the efficacy of acute treatment with risperidone vs. olanzapine in Bipolar I manic inpatients.Methods(1) Patients: the study includes all the inpatients diagnosed with bipolar I manic episode (DSM-IV) who were admitted during the years 2009 to 2014. Patients treated with risperidone and olanzapine concomitantly (n = 6) and patients not treated with risperidone or olanzapine (n = 129) were excluded.The patients finally included (n = 183) were separated in two groups:– treated with risperidone (n = 89);– treated with olanzapine (n = 94).(2) The Student-T test was used to compare, between the groups, the mean of scores in YMRS and CGI-S scales and the mean of length of stay.ResultsBaseline characteristics were similar between the groups. The majority of patients were also treated with mood stabilizers (46% with lithium and 45% with valproate).The mean decrease in CGI-S scores from baseline to the day of discharge was significantly (P < 0.003) higher in the risperidone group (−2.81 vs. −2.36). The length of stay was significantly (P < 0.004) lower in the olanzapine group (mean of 23.03 days vs. mean of 30.3).Conclusions(1) The CGI-S scores in manic patients treated with risperidone decreased more than in patients treated with olanzapine during admission. (2) The length of stay was significantly lower in patients treated with olanzapine.Disclosure of interestThe authors have not supplied their declaration of competing interest.


CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 272-284 ◽  
Author(s):  
Gonzalo Laje

Pharmacogenetics brought the promise of matching individuals with treatments that would be efficacious while minimizing adverse events. This has been long needed in psychiatry, where treatment options have been empirical and treatment choices have been made largely based on clinical judgment. The efficacy and tolerability of antidepressants, the most common drugs used in mood disorders, have been widely studied in pharmacogenetics. Genetic association studies have been reported for pharmacokinetic genes such as the CYP450 isoenzymes or MDR1, and pharmacodynamic genes such as the serotonin transporter (SLC6A4) or the serotonin 2A receptor (HTR2A). However, despite the large number of reports, clinically useful predictors are still scarce for antidepressant monotherapy. Pharmacogenetic predictors of efficacy for mood stabilizers such as lithium and anticonvulsants have not had a dissimilar fate, and clinically meaningful markers are yet to emerge. The lack of consistent results may be in part due to small samples of heterogeneous populations and lack of consensus on phenotype definitions. Current pharmacogenetic recommendations include testing for HLA-B*1502 when using carbamazepine in Asian ancestry populations to prevent Stevens–Johnson syndrome, CYP2D6 genotypes when using pimozide, and CYP2D6 in polypharmacy to minimize drug interactions. This review, which is aimed at clinicians, lays the basis for understanding strengths and weaknesses of pharmacogenetic studies and outlines current clinical uses of these biomarkers.


2017 ◽  
Vol 41 (S1) ◽  
pp. S206-S206
Author(s):  
K. Kulkarni ◽  
G. Devasthali ◽  
A. Purty ◽  
M. Kesavan ◽  
J. Reddy ◽  
...  

ObjectiveContemporary treatment guidelines recommend use of second-generation antipsychotics (SGAs) either as mono therapy or in combination with mood stabilizers as first-line treatment. While these drugs have been established to have superior efficacy compared to placebo, there is very less data comparing these antipsychotics with one another. We sought to study differences in the five-year outcome of first episode of mania (FEM) treated with olanzapine or risperidone, either alone or in combination with mood stabilizer.MethodsWe conducted a retrospective chart review of patients diagnosed with FEM (ICD-10) in the year 2008 (n = 88) at our centre. We selected the data of patients prescribed either olanzapine or risperidone for the purpose of this analysis. We extracted data about time to recovery and recurrence after FEM, total episodes, drug compliance and response, and number of follow-up visits from 2008 to 2013. The study was approved by the Institute Ethics Committee.ResultsA total of 88 patients received diagnosis of FEM in the year 2008, of which 50 (56.8%) received risperidone and 35 (39.8%) received olanzapine. The two groups were comparable in socio-demographic and clinical symptomatology of FEM (all P > 0.08). Complete recovery was significantly more in the olanzapine group than the risperidone group (χ2 = 4.84, P < 0.05).ConclusionOur study indicates that risperidone and olanzapine, either alone or in combination with mood stabilizers have a similar impact on the five-year course of BD following a first manic episode. However, olanzapine is associated with more complete recovery from FEM than risperidone.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2005 ◽  
Vol 162 (4) ◽  
pp. 799-802 ◽  
Author(s):  
Jitschak G. Storosum ◽  
Tamar Wohlfarth ◽  
Christine C. Gispen-de Wied ◽  
Don H. Linszen ◽  
Berthold P.R. Gersons ◽  
...  

CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 231-241 ◽  
Author(s):  
Mark J. Niciu ◽  
Dawn F. Ionescu ◽  
Daniel C. Mathews ◽  
Erica M. Richards ◽  
Carlos A. Zarate

The etiopathogenesis and treatment of major mood disorders have historically focused on modulation of monoaminergic (serotonin, norepinephrine, dopamine) and amino acid [γ-aminobutyric acid (GABA), glutamate] receptors at the plasma membrane. Although the activation and inhibition of these receptors acutely alter local neurotransmitter levels, their neuropsychiatric effects are not immediately observed. This time lag implicates intracellular neuroplasticity as primary in the mechanism of action of antidepressants and mood stabilizers. The modulation of intracellular second messenger/signal transduction cascades affects neurotrophic pathways that are both necessary and sufficient for monoaminergic and amino acid–based treatments. In this review, we will discuss the evidence in support of intracellular mediators in the pathophysiology and treatment of preclinical models of despair and major depressive disorder (MDD). More specifically, we will focus on the following pathways: cAMP/PKA/CREB, neurotrophin-mediated (MAPK and others), p11, Wnt/Fz/Dvl/GSK3β, and NFκB/ΔFosB. We will also discuss recent discoveries with rapidly acting antidepressants, which activate the mammalian target of rapamycin (mTOR) and release of inhibition on local translation via elongation factor stimulation. Throughout this discourse, we will highlight potential intracellular targets for therapeutic intervention. Finally, future clinical implications are discussed.


2004 ◽  
Vol 6 (2) ◽  
pp. 143-155

There is increasing evidence from a variety of sources that severe mood disorders are associated with regional reductions in brain volume, as well as reductions in the number, size, and density of glia and neurons in discrete brain areas. Although the precise pathophysiology underlying these morphometric changes remains to be fully elucidated, the data suggest that severe mood disorders are associated with impairments of structural plasticity and cellular resilience. In this context, it is noteworthy that a growing body of data suggests that the glutamaiergic system (which is known to play a major role in neuronal plasticity and cellular resilience) may be involved in the pathophysiology and treatment of mood disorders. Glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) GluR1 receptor trafficking plays a critical role in regulating various forms of neural plasticity. It is thus noteworthy that recent studies have shown that structurally dissimilar mood stabilizers lithium and valproate regulate GluR1 receptor subunit trafficking and localization at synapses. These studies suggest that regulation of glutamatergically mediated synaptic plasticity may play a role in the treatment of mood disorders, and raises the possibility that agents more directly affecting synaptic GluR1 represent novel therapies for these devastating illnesses.


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