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Psychiatric disorders in pre-clinical Huntington's disease
  1. Camille L Julien (camille.julien{at}manchester.ac.uk)
  1. Greater Manchester Neuroscience Centre, United Kingdom
    1. Jennifer C Thompson (jennifer.thompson{at}manchester.ac.uk)
    1. Greater Manchester Neuroscience Centre, United Kingdom
      1. Sue Wild (sue.wild{at}leedsth.nhs.uk)
      1. St James' Hospital Leeds, United Kingdom
        1. Pamela Yardumian (pamela.yardumian{at}leedsth.nhs.uk)
        1. St James' Hospital Leeds, United Kingdom
          1. Julie S Snowden (julie.snowden{at}manchester.ac.uk)
          1. Greater Manchester Neuroscience Centre, United Kingdom
            1. Gwen Turner (gwen.turner{at}doctors.org.uk)
            1. St James' Hospital Leeds, United Kingdom
              1. David Craufurd (david.craufurd{at}manchester.ac.uk)
              1. University of Manchester, United Kingdom

                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 pre-clinical period result from structural change or are a reaction to being at risk or simply a coincidental occurrence. Few studies have investigated the temporal course of psychiatric disorder across the pre-clinical period.

                Objectives: To compare lifetime and current prevalence of psychiatric disorder in pre-clinical 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 (CIDI). 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 sub-clinical symptoms. However, gene carriers did report 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.

                • Huntington Disease
                • pre-clinical
                • psychiatric aspects

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