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Psychiatric disorders in preclinical Huntington’s disease
  1. Camille L Julien1,
  2. Jennifer C Thompson1,
  3. Sue Wild2,
  4. Pamela Yardumian2,
  5. Julie S Snowden1,
  6. Gwen Turner2,
  7. David Craufurd3
  1. 1Cerebral Function Unit, Greater Manchester Neuroscience Centre, Hope Hospital, Salford, UK
  2. 2Department of Clinical Genetics, St James’ Hospital, Leeds, UK
  3. 3Academic Unit of Medical Genetics and Regional Genetic Service, University of Manchester and St Mary’s Hospital, Manchester, UK
  1. Correspondence to:
 Dr David Craufurd
 Academic Unit of Medical Genetics and Regional Genetic Service, St Mary’s Hospital, Hathersage Road, Manchester M13 0JH, UK; david.craufurd{at}manchester.ac.uk

Abstract

Background: Psychiatric symptoms are a common feature of Huntington’s disease (HD) and often precede the onset of motor and cognitive impairments. However, it remains unclear whether psychiatric changes in the preclinical period result from structural change, are a reaction to being at risk or simply a coincidental occurrence. Few studies have investigated the temporal course of psychiatric disorder across the preclinical period.

Objectives: To compare lifetime and current prevalence of psychiatric disorder in presymptomatic gene carriers and non-carriers and to examine the relationship of psychiatric prevalence in gene carriers to temporal proximity of clinical onset.

Methods: Lifetime and current psychiatric histories of 204 at risk individuals (89 gene carriers and 115 non-carriers) were obtained using a structured clinical interview, the Composite International Diagnostic Interview. Psychiatric disorders were classified using both standardised diagnostic criteria and a more subtle symptom based approach. Follow-up of gene carriers (n = 51) enabled analysis of the role of temporal proximity to clinical onset.

Results: Gene carriers and non-carriers did not differ in terms of the lifetime frequency of clinical psychiatric disorders or subclinical symptoms. However, gene carriers reported a significantly higher rate of current depressive symptoms. Moreover, the rate of depression increased as a function of proximity to clinical onset.

Conclusions: Affective disorder is an important feature of the prodromal stages of HD. The findings indicate that depression cannot be accounted for by natural concerns of being at risk. There is evidence of a window of several years in which preclinical symptoms are apparent.

  • CIDI, Composite International Diagnostic Interview
  • DSM-III, Diagnostic and Statistical Manual of Mental Disorders 3rd edition
  • HD, Huntington’s disease
  • QNE, quantitated neurological examination

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Footnotes

  • See Editorial Commentary, p 913

  • Published Online First 18 December 2006

  • Competing interests: None.

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