The association of affective disorder with Huntington's Disease in a case series and in families

Folstein, Susan E.; Abbott, Margaret H.; Chase, Gary A.; Jensen, Barbara; Folstein, Marshal F.

doi:10.1017/s0033291700047966

Cited by 209 publications

(84 citation statements)

References 21 publications

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“…In fact, Folstein et al [46] observed that depression might occur up to 5 years prior to onset of movement abnormalities. Shiwach [2] also found, in a sample of 110 patients with HD, that the lifetime prevalence of depression was almost 40%.…”

Section: Affective Disorders and Suicidementioning

confidence: 99%

“…Sertraline [44] Case series, 7 Improvement (marked in five, moderate in two); one patient treated concomitantly with risperidone for psychotic depression; two patients treated with lorazepam for sleep Fluoxetine [42] Open label trial, 8 Improvement in mood and function Fluoxetine and l-deprenyl [93] Case report, 1 with paranoia and aggression Improvement in all three psychiatric symptoms ECT [94] Retrospective case reports, 6 (five unipolar depressed patients; one bipolar depressed patient) Improvement in four of the unipolar patients and in the bipolar patient; patients with prominent delusions showed the most benefit; apathy showed the least improvement Clozapine [95] Case report, 1 with psychotic depression Improvement Sulpiride [96] Case report, 1 Improvement Phenelzine and isocarboxazid [97] Case series, 3 Improvement of mood; two of three patients showed improvement with concomitant psychosis Amoxapine [98] Case report, 1 Improvement ECT [46] Retrospective case reports, 2 Improvement TCA [43] Open trial, 6 Five of six patients improved, but only on neurovegetative symptoms TCA [99] Open trial, 10 Seven had some improvement of depression; sedation and anticholinergeric side effects seen in some, and some patients give neuroleptics Amytriptyline or chlorpromazine [100] Open trial, 4 (three given amytriptyline, one given chlorpromazine)…”

Section: Comments and Outcome On Target Symptomsmentioning

confidence: 99%

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An overview of psychiatric symptoms in Huntington’s disease

Anderson

Marder

2001

Curr Psychiatry Rep

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Huntington's disease (HD) is an inherited autosomal dominant disorder characterized by neurologic, cognitive, and psychiatric symptomatology. Psychiatric symptoms in HD are often amenable to treatment, and relief of these symptoms may provide significant improvement in quality of life. This review will briefly describe neurologic, neuropsychologic and brain imaging data, and then review psychiatric syndromes seen in HD and their treatment.

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Section: Affective Disorders and Suicidementioning

confidence: 99%

Section: Comments and Outcome On Target Symptomsmentioning

confidence: 99%

An overview of psychiatric symptoms in Huntington’s disease

Anderson

Marder

2001

Curr Psychiatry Rep

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“…The spectrum of psychiatric features characteristic of HD includes apathy, irritability, depression and anxiety, pathological impulse control, disinhibition and executive dysfunction (Folstein et al, 1983, Shiwach and Norbury, 1994, Julien et al, 2007, Wolf and Kloppel, 2013. One of only two available brain imaging studies investigating psychiatric progression in HD attributed increased levels of irritability in premanifest HD to reduced coupling between amygdalae and orbitofrontal cortex (Kloppel et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Longitudinal changes in the fronto-striatal network are associated with executive dysfunction and behavioral dysregulation in Huntington's disease: 30 months IMAGE-HD data

Poudel

Stout

et al. 2017

Cortex

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Neuropsychiatric disturbance−particularly executive dysfunction and behavioral dysregulation−is a common feature of Huntington's disease (HD), with implications for functional capacity and quality of life. No study to date has ascertained whether longitudinal change in brain activity is associated with neuropsychiatric deficits in HD. We used a set-response-shifting task together with functional magnetic resonance imaging to investigate 30-month longitudinal blood-oxygen level dependent (BOLD) signal changes in the fronto-striatal attentional control network in premanifest and symptomatic HD (pre-HD and symp-HD, respectively), relative to healthy control participants. We also assessed the extent to which changes in the BOLD signal over time were related to neuropsychiatric measures in the domains of executive dysfunction and behavioral dysregulation.Associations were also evaluated with clinical and disease severity. We found no longitudinal BOLD differences between pre-HD and controls over 30 months. In contrast, reduction in BOLD response over time was greater in symp-HD, relative to controls, in task-related areas (e.g., anterior cingulate cortex and striatum) and in regions from the default mode network (e.g., medial prefrontal cortex and posterior cingulate/precuneus). Moreover, when considered across both premanifest and symptomatic stages, longitudinal BOLD signal decline in the right dorsolateral prefrontal cortex and putamen was associated with executive dysfunction and behavioral dysregulation measures. In addition, longitudinal reduction in BOLD signal, in fronto-striatal and default mode networks, correlated with disease severity. These results suggest that longitudinal change in fronto-striatal and default mode networks may be useful in understanding the biological underpinnings of functional decline in HD.Such findings offer new avenues for targeted treatments in terms of minimizing psychiatric impairment and potentially maximizing cognitive function.

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“…[2,7]. Die psychiatrischen Manifestationen können dem Auftreten eindeutiger neurologischer Symptome dabei bis zu 20 Jahre vorausgehen [9]. Wie unsere Falldarstellungen zeigen, führt die enorme phänotypische Heterogenität einer HD sowie ihr mögliches spontanes Auftreten auch 10 Jahre nach der Charakterisierung der zugrunde liegenden genetischen Mutation im klinischen Alltag noch zu differenzialdiagnostischen Schwierigkeiten [30,10].…”

Section: Diskussionunclassified

Neuropsychiatrische Aspekte der Chorea Huntington

et al. 2004

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Huntington's disease (HD) is an autosomal, dominant, inherited disorder of the central nervous system with characteristic neurodegenerative alterations in the basal ganglia and cortex. Dependent on the individual CAG expansion load, disease onset occurs between the third or fourth decade of life, entailing an invariably lethal progression within 10 to 20 years. Although the clinical picture is characterized equally by cognitive and psychiatric disturbances, the apparent neurodegenerative alterations and presentation as a choreatic movement disorder account for the traditional link of Huntington's disease to the field of neurology. In contrast to the traditionally emphasized core features of chorea and dementia, recent empirical evidence points to the frequent emergence of nonchoreatic motor signs and subtle cognitive and psychiatric complaints, especially in asymptomatic gene carriers and early disease stages. The case studies presented here emphasize the spectrum of neuropsychiatric phenomena associated with HD and illustrate the resulting difficulties of differential diagnosis in clinical settings. Furthermore, current scientific knowledge of HD pleiotrophy is reviewed and the diagnostic power of specific neuropsychological approaches is explained.

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The association of affective disorder with Huntington's Disease in a case series and in families

Cited by 209 publications

References 21 publications

An overview of psychiatric symptoms in Huntington’s disease

An overview of psychiatric symptoms in Huntington’s disease

Longitudinal changes in the fronto-striatal network are associated with executive dysfunction and behavioral dysregulation in Huntington's disease: 30 months IMAGE-HD data

Neuropsychiatrische Aspekte der Chorea Huntington

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