Combating depression in Huntington's disease: Effective antidepressive treatment with venlafaxine XR

University Clinic of Psychiatry bUniversity Clinic of Neurosurgery, Graz Medical University, Auenbruggerplatz 31, Graz, Austria.
International clinical psychopharmacology (Impact Factor: 2.46). 01/2010; 25(1):46-50. DOI: 10.1097/YIC.0b013e3283348018
Source: PubMed


Patients with Huntington's disease (HD) often suffer from psychiatric symptoms including affective disorder, psychosis, irritability, and apathy, which may be present in all stages of the disease. However--despite the obvious likelihood that these symptoms may be reduced by antidepressive treatments--to date, the effectiveness of such treatments in HD has only ever been examined in case studies. Twenty-six HD patients (17 men), with a diagnosis of major depression, were studied. The symptoms of HD and depression were systematically measured using the Beck Depression Inventory and the Hamilton Rating Scale for Depression both at baseline and after 4 weeks of treatment with venlafaxine XR. After 4 weeks of venlafaxine XR treatment, the symptoms of depression in HD patients decreased significantly relative to baseline. However, approximately one in five patients developed significant venlafaxine-related side effects (nausea and irritability). Venlafaxine XR is highly effective in the treatment of depression in HD, although it may produce unpleasant side effects. Further studies are required to establish the most suitable treatment for depression in HD.

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    • "Case studies report benefits of selective serotonin reuptake inhibitors (SSRIs), selective noradrenergic reuptake inhibitors (SNRIs) (venlafaxine), atypical antipsychotics (olanzepine), monoamine oxidase inhibitors (MAOI), tetracyclic, and tricyclic antidepressants on small numbers of patients (Patel et al., 1996; Squitieri et al., 2001; Bonelli et al., 2003; Ciammola et al., 2009). A study of 26 HD patients with diagnoses of major depression treated with venlafaxine for 4 weeks showed significant improvement albeit a high rate of side effects such as irritability (Holl et al., 2010). In a more recent study by Rowe et al. (2012) of 787 prodromal HD participants, it was reported that 20% of prodromal patients were prescribed antidepressants with the vast majority using SSRIs (e.g., paroxetine, fluoxetine, and sertraline). "
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    ABSTRACT: Huntington's disease (HD) is an autosomal dominant disorder caused by a tandem repeat expansion encoding an expanded tract of glutamines in the huntingtin protein. HD is progressive and manifests as psychiatric symptoms (including depression), cognitive deficits (culminating in dementia), and motor abnormalities (including chorea). Having reached the twentieth anniversary of the discovery of the "genetic stutter" which causes HD, we still lack sophisticated insight into why so many HD patients exhibit affective disorders such as depression at very early stages, prior to overt appearance of motor deficits. In this review, we will focus on depression as the major psychiatric manifestation of HD, discuss potential mechanisms of pathogenesis identified from animal models, and compare depression in HD patients with that of the wider gene-negative population. The discovery of depressive-like behaviors as well as cellular and molecular correlates of depression in transgenic HD mice has added strong support to the hypothesis that the HD mutation adds significantly to the genetic load for depression. A key question is whether HD-associated depression differs from that in the general population. Whilst preclinical studies, clinical data, and treatment responses suggest striking similarities, there are also some apparent differences. We discuss various molecular and cellular mechanisms which may contribute to depression in HD, and whether they may generalize to other depressive disorders. The autosomal dominant nature of HD and the existence of models with excellent construct validity provide a unique opportunity to understand the pathogenesis of depression and associated gene-environment interactions. Thus, understanding the pathogenesis of depression in HD may not only facilitate tailored therapeutic approaches for HD sufferers, but may also translate to the clinical depression which devastates the lives of so many people.
    Frontiers in Neurology 07/2013; 4:81. DOI:10.3389/fneur.2013.00081
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    ABSTRACT: Several studies have suggested a greater risk of suicide in Huntington disease (HD); however, unique risk factors for suicide in HD are not established. We sought to determine risk factors for suicidal behavior, defined as suicide or attempted suicide, in prodromal HD. From the prospective PREDICT-HD cohort, we identified 735 cases with HD gene expansion but no manifest symptoms of HD and 194 non-gene-expanded controls. In survival analysis, a number of potential risk factors for suicidal behavior were assessed, including symptoms of depression, hopelessness, substance abuse, marital status, gender, and psychiatric history. During a mean of 3.7 years of prospective follow-up, 12 cases (1.6%) attempted suicide and 1 completed suicide (0.1%). No suicides were observed among controls. In univariate Cox proportional hazards regression models, a history of suicide attempts (HR 8.5, 95% CI 2.8-26.1, p < 0.0002) and a Beck Depression Inventory II score >13 (HR 7.2, 95% CI 2.3-22.0, p < 0.0006) were associated with suicidal behavior. These risk factors had independent effects in multivariate models. A history of incarceration in the past 2 years was also associated (HR 12.5, 95% CI 2.7-56.6, p < 0.002), though uncommon. No further risk factors were identified. A history of suicide attempts and the presence of depression are strongly predictive of suicidal behavior in prodromal HD. As these risk factors are among the most robust risk factors for suicide, established suicide risk factors appear applicable to those with prodromal HD.
    Neurodegenerative Diseases 06/2011; 8(6):483-90. DOI:10.1159/000327754 · 3.51 Impact Factor
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    ABSTRACT: Huntington disease (HD) has traditionally been considered a movement disorder, but cognitive and psychiatric symptoms also prominently factor into its clinical presentation. Depression is one of the most common psychiatric disturbances in HD, with its prevalence highest in manifest disease during stage 2, but it is also present during the illness prodrome (the period before manifestation of motor symptoms). Identification and treatment of depression in individuals with the HD mutation is an essential part of clinical management in this population, especially owing to the high risk of suicide. This article summarizes what is currently known about the presentation and treatment of depression in the early stages of HD and provides advice to clinicians treating this population.
    10/2011; 1(5):407-414. DOI:10.2217/nmt.11.45
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