Hamilton Rating Scale for Depression

Hamilton, Max

doi:10.1037/t04100-000

Cited by 591 publications

(673 citation statements)

References 0 publications

Supporting

Mentioning

636

Contrasting

Unclassified

Order By: Relevance

“…All subjects were Caucasians of central European descent. Standardized clinical assessment with the Structured Clinical Interview I (First et al, 2001) (Derogatis, 1983); State-Trait-Anxiety Inventory (STAI) (Spielberger et al, 1970)] and depression [Center for Epidemiological Studies Depression Scale (CES-D) (Radloff, 1997); Hamilton Rating Scale for Depression (HAMD) (Hamilton, 1986)] as well as personality [Temperament and Character Inventory (TCI) (Cloninger et al, 1994)] and education were assessed (Table 1).…”

Section: Methodsmentioning

confidence: 99%

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Smolka¹,

Schumann²,

Wrase³

et al. 2005

J. Neurosci.

403

281

View full text Add to dashboard Cite

Catechol-O-methyltransferase (COMT) degrades the catecholamine neurotransmitters dopamine, epinephrine, and norepinephrine. A functional polymorphism in the COMT gene (val 158met) accounts for a fourfold variation in enzyme activity. The low-activity met 158 allele has been associated with improved working memory but with higher risk for anxiety-related behaviors. Using functional magnetic resonance imaging, we assessed the effects of COMT genotype on brain activation by standardized affective visual stimuli (unpleasant, pleasant, and neutral) in 35 healthy subjects. The analysis of genotype effects was restricted to brain areas with robust activation by the task. To determine gene-dose effects, the number of met 158 alleles (0, 1, or 2) was correlated with the blood oxygen level-dependent (BOLD) response elicited by pleasant or unpleasant stimuli compared with neutral stimuli. COMT genotype had no significant impact on brain activation by pleasant stimuli but was related to the neural response to unpleasant stimuli: reactivity to unpleasant stimuli was significantly positively correlated with the number of met 158 alleles in the limbic system (left hippocampus, right amygdala, right thalamus), connected prefrontal areas (bilateral ventrolateral prefrontal cortex, right dorsolateral prefrontal cortex), and the visuospatial attention system (bilateral fusiform gyrus, left inferior parietal lobule). Genotype explained up to 38% of interindividual variance in BOLD response elicited by unpleasant stimuli. We conclude that (1) genetic variations can account for a substantial part of interindividual variance in task-related brain activation and that (2) increased limbic and prefrontal activation elicited by unpleasant stimuli in subjects with more met 158 alleles might contribute to the observed lower emotional resilience against negative mood states.

show abstract

Section: Methodsmentioning

confidence: 99%

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Smolka¹,

Schumann²,

Wrase³

et al. 2005

J. Neurosci.

403

281

View full text Add to dashboard Cite

show abstract

“…The rating scales that were used comprised: the Hamilton Rating Scale for Depression (Hamilton, 1986) and Beck's Depression Inventory (BDI-II) (Beck et al, 1961). The 28-item short form of the Childhood Trauma Questionnaire Short Form (CTQ-SF) was used to assess adversity during childhood and teenage years (Bernstein and Fink, 1998).…”

Section: Rating Instrumentsmentioning

confidence: 99%

Single-Nucleotide Polymorphism of the FKBP5 Gene and Childhood Maltreatment as Predictors of Structural Changes in Brain Areas Involved in Emotional Processing in Depression

Tozzi

Carballedo

Wetterling

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

The gene expressing the FK506 binding protein 51 (FKBP5) is involved in the regulation of glucocorticoid receptor sensitivity. The rs1360780 SNP in this gene (T allele vs C homozygous) has been found to be associated with major depressive disorder (MDD). The aim of our study was to investigate whether this polymorphism might be associated with altered brain structure and function in a cohort of 40 patients with MDD and 43 healthy controls. A functional magnetic resonance imaging (fMRI) emotional attention task was employed. Diffusion tensor imaging (DTI) was also conducted, extracting mean diffusivity (MD) and fractional anisotropy (FA) from brain areas that showed functional differences between patients expressing the two alleles of the rs1360780 SNP. Finally, the effect of the interaction of childhood adversity as measured by the Childhood trauma Questionnaire (CTQ) and rs1360780 allele status was analyzed in relation to DTI measures using a general linear model. All results presented are family-wise error (FWE) corrected. Functional interactions were found between genotype and diagnosis (po0.01). Patients carrying the high-risk allele, compared with patients not carrying it, showed reduced activity in the rolandic operculum, Heschl gyrus, insula, parahippocampal gyrus, posterior cingulate cortex, inferior frontal gyrus (po0.05 for all measures); and increased MD and reduced FA measures in many of these regions (po0.05). An interaction between CTQ scores and allele status was associated with DTI changes in the insula, rolandic operculum, and inferior frontal gyrus. Here, the presence of both the high-risk allele and higher CTQ scores was associated with higher MD and lower FA values (po0.05). In conclusion, MDD patients expressing the T allele of rs1360780, compared with C homozygous patients, exhibit functional and structural differences in areas involved in emotional perception and inhibition. The interaction between the T allele and childhood maltreatment explained our structural findings in these regions, suggesting that their altered maturation and function might be influenced by early chronic stress in the presence of this genetic trait.

show abstract

“…The Hamilton Rating Scale for Depression (HDRS) was developed by Hamilton and the original scale has 17 items measuring the severity of depression (15). The reliability and validity of the Turkish form has been examined (16).…”

Section: Assessment Toolsmentioning

confidence: 99%

Yatarak Tedavi Gören Bipolar Bozukluk Hastalarında Dissosiyatif Bozukluk Eştanısı Olan ve Olmayan Hasta Gruplarının Karşılaştırılması

Bakım

Baran

Güleken³

et al. 2016

Aile Hekimliği Ve Palyatif Bakım

View full text Add to dashboard Cite

Introduction: This study aims to compare sociodemographic characteristics of the patients with bipolar disorder (BD) with and without comorbid dissociative disorder (DD) and to investigate the eventual effect of the comorbidity on the treatment. Methods:We enrolled a total of 149 patients diagnosed with BD and treated as inpatients consecutively in Şişli Etfal Hospital, Psychiatry Clinic between 2010 and 2011. For the patients who were diagnosed with DD using SCID-D and with BD using SCID-I, sociodemographic characteristics, YMRS, HAM-D, BPRS, DES scores and duration and number of hospital stays were evaluated. Results: 23 patients (15.4%) had dissociative disorder not otherwise specified (DD-NOS), 4 patients (2.6%) had dissociative identity disorder (DID) and 1 patient (0.6%) had dissociative amnesia. BD patients with comorbid DD were found to be predominantly female (p=0.015) and younger (p=0.002) and to have significantly higher DES scores than BD patients without DD (p<0.001). The total score of DES was correlated with duration hospital stay (p=0.001, Spearman r=0.336) in the total sample. Total HAM-D score at the time of admission was significantly higher in the comorbidity group (p=0.027), and suicide item was found to be significantly higher both at admission and at discharge (p<0.001 and p=0.035). Among BPRS scores at admission, hallucinatory behavior item was found to be higher in the comorbidity group (p=0.019). Among YMRS scores both at admission and at discharge, velocity and amount of speech item (p=0.027) and insight item at admission (p=0.006) was found to be significantly higher in the pure bipolar group (p=0.018). Conclusion:In patients with BD, DD comorbidity should be investigated. The BD patients with DD comorbidity tend to be female and younger, and show higher depression scores, leading to a prolonged hospital stay. In the presence of dissociation comorbidity, attempts and number of suicides and hallucinatory behaviors seem to be increased.

show abstract

Hamilton Rating Scale for Depression

Cited by 591 publications

References 0 publications

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Single-Nucleotide Polymorphism of the FKBP5 Gene and Childhood Maltreatment as Predictors of Structural Changes in Brain Areas Involved in Emotional Processing in Depression

Yatarak Tedavi Gören Bipolar Bozukluk Hastalarında Dissosiyatif Bozukluk Eştanısı Olan ve Olmayan Hasta Gruplarının Karşılaştırılması

Contact Info

Product

Resources

About

Hamilton Rating Scale for Depression

Cited by 591 publications

References 0 publications

Catechol-O-Methyltransferaseval158metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Catechol-O-Methyltransferaseval158metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Single-Nucleotide Polymorphism of the FKBP5 Gene and Childhood Maltreatment as Predictors of Structural Changes in Brain Areas Involved in Emotional Processing in Depression

Yatarak Tedavi Gören Bipolar Bozukluk Hastalarında Dissosiyatif Bozukluk Eştanısı Olan ve Olmayan Hasta Gruplarının Karşılaştırılması

Contact Info

Product

Resources

About

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex

Catechol-O-Methyltransferaseval¹⁵⁸metGenotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex