The Hamilton Depression Scale

Bech, Per; Allerup, Peter; Gram, Lars F.; Reisby, N; Rosenberg, Raben; Jacobsen, O.; Nagy, Ádám

doi:10.1111/j.1600-0447.1981.tb00676.x

Cited by 341 publications

(92 citation statements)

References 22 publications

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“…This implies that studies based on the observed effect sizes from the core subscales would require approximately one-third less patients than studies based on the HAM-D total score [17]. This is consistent with previous findings from our group that the 6-item HAM-D, a unidimensional core subscale called the Melancholia scale, yielded larger effect sizes after antidepressant treatment than the 17-item version and other longer versions [18, 19]. Even certain self-rating scales have outperformed the HAM-D. For example, in a study comparing 300 mg of imipramine with 150 mg of imipramine, the self-rating scale Symptom Rating Test (SRT) discriminated significantly between the two doses, but not the total HAM-D score and the SRT had been developed specifically to increase the sensitivity of outcome measures of depression and anxiety [15, 20].…”

Section: The Search For a Culpritsupporting

confidence: 82%

The Problem of the Placebo Response in Clinical Trials for Psychiatric Disorders: Culprits, Possible Remedies, and a Novel Study Design Approach

Fava¹,

Evins²,

Dorer

et al. 2003

Psychother Psychosom

390

422

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The placebo response is a major issue in clinical trials for psychiatric disorders. Possible contributing factors to this problem include diagnostic misclassification, issues concerning inclusion/exclusion criteria, outcome measures’ lack of sensitivity to change, measurement errors, poor quality of data entry and verification, waxing and waning of the natural course of illness, regression toward the mean phenomenon, patient and clinician expectations about the trial, study design issues, non-specific therapeutic effects, and high attrition. Over the past few decades, researchers have attempted to reduce the placebo effect in a variety of ways. Unfortunately, approaches with very little or no benefit have included restricting enrollment to selected populations, rater training, requirement of same rater, and placebo lead-in phases. Some benefits, although often marginal, have been derived from standardizing diagnostic procedures, managing clinicians’ overestimation of change, simplification of study visits and assessments, minimizing non-specific, therapeutic effects, extending trial duration, reducing number of sites, increasing the sensitivity of outcome measures, and reducing the number of treatment arms. Thus far, there has been no attempt to develop new study designs aimed at reducing the placebo effect. We are proposing a novel study design, called ‘Sequential Parallel Comparison Design’, suitable for double-blind, placebo-controlled trials in psychiatric disorders. This design is aimed at reducing both the overall placebo response rate and the sample size required for such trials. Its usefulness in clinical research needs to be tested empirically. If this study design were to be found to meet its stated goals, this could markedly facilitate the process of clinical development of new compounds for the treatment of psychiatric disorders.

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Section: The Search For a Culpritsupporting

confidence: 82%

The Problem of the Placebo Response in Clinical Trials for Psychiatric Disorders: Culprits, Possible Remedies, and a Novel Study Design Approach

Fava¹,

Evins²,

Dorer

et al. 2003

Psychother Psychosom

390

422

View full text Add to dashboard Cite

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“…All raters were blind to the sequence of testing. Behavioral ratings consisted of the modified 6-item version of the original 17-item Hamilton Rating Scale for Depression (HRSD-6; Bech et al 1981) and the Hamilton Rating Scale for Anxiety (HRSA; Hamilton 1959). The item regarding insomnia was excluded from the HRSA.…”

Section: Behavioral Ratingsmentioning

confidence: 99%

Tryptophan depletion in SSRI-recovered depressed outpatients

et al. 2001

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Rationale: Recently, a number of studies have challenged the finding that acute tryptophan depletion (TD) increases depressive symptoms in medicated, formerly depressed patients. The present study examined the effects of acute nutritional TD on remitted depressed patients currently treated with selective serotonin reuptake inhibitors. In an attempt to clarify conflicting earlier findings, the effects of a number of clinical variables on outcome were also investigated. Methods: Ten patients underwent TD in a double-blind, controlled, balanced crossover fashion. The control session followed the procedure of Krahn et al. (1996 Neuropsychopharmacology 15:325-328). Sessions were 5-8 days apart. Results: TD was significantly related to increased scores on clinicianrated depression and anxiety scales, and on self-rated depression, anxiety, and somatic symptoms. The control challenge had no effect, despite the fact that the reductions in plasma tryptophan during the control session were unexpectedly high. Some evidence was found for a threshold in the relationship between reduction of plasma tryptophan and mood response. Conclusions: The mood effect of TD in medicated, formerly depressed patients was confirmed. A threshold may exist for mood effects following TD, implying that recent negative findings may have been caused by insufficient depletion. No other predicting or mediating factors were identified, although the variable "history of response pattern to medication" deserves further study.

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“…The psychometric validity in terms of unidimensionality (total score a sufficient statistic) was then documented in a new study using the Rasch analysis [31]. This showed that the HAM-D 6 but not the HAM-D 17 fulfilled the Rasch analysis, indicating that the total score is a sufficient statistic.…”

Section: The Clinimetric Classification Of the Hamilton Scalesmentioning

confidence: 99%

Fifty Years with the Hamilton Scales for Anxiety and Depression

Bech

2009

Psychother Psychosom

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From the moment Max Hamilton started his psychiatric education, he considered psychometrics to be a scientific discipline on a par with biochemistry or pharmacology in clinical research. His clinimetric skills were in operation in the 1950s when randomised clinical trials were established as the method for the evaluation of the clinical effects of psychotropic drugs. Inspired by Eysenck, Hamilton took the long route around factor analysis in order to qualify his scales for anxiety (HAM-A) and depression (HAM-D) as scientific tools. From the moment when, 50 years ago, Hamilton published his first placebo-controlled trial with an experimental anti-anxiety drug, he realized the dialectic problem in using the total score on HAM-A as a sufficient statistic for the measurement of outcome. This dialectic problem has been investigated for more than 50 years with different types of factor analyses without success. Using modern psychometric methods, the solution to this problem is a simple matter of reallocating the Hamilton scale items according to the scientific hypothesis under examination. Hamilton’s original intention, to measure the global burden of the symptoms experienced by the patients with affective disorders, is in agreement with the DSM-IV and ICD-10 classification systems. Scale reliability and obtainment of valid information from patients and their relatives were the most important clinimetric innovations to be developed by Hamilton. Max Hamilton therefore belongs to the very exclusive family of eminent physicians celebrated by this journal with a tribute.

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The Hamilton Depression Scale

Cited by 341 publications

References 22 publications

The Problem of the Placebo Response in Clinical Trials for Psychiatric Disorders: Culprits, Possible Remedies, and a Novel Study Design Approach

The Problem of the Placebo Response in Clinical Trials for Psychiatric Disorders: Culprits, Possible Remedies, and a Novel Study Design Approach

Tryptophan depletion in SSRI-recovered depressed outpatients

Fifty Years with the Hamilton Scales for Anxiety and Depression

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