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Testosterone deficiency in a Parkinson’s disease clinic: results of a survey
  1. M S Okun1,
  2. G P Crucian1,
  3. L Fischer2,
  4. B L Walter2,
  5. C M Testa2,
  6. J L Vitek2,
  7. M R DeLong2,
  8. J Hanfelt3,
  9. X Huang4
  1. 1Department of Neurology, McKnight Brain Institute, University of Florida, USA
  2. 2Department of Neurology, Emory University
  3. 3Department of Biostatistics, Emory University
  4. 4Department of Neurology, University of North Carolina, Chapel Hill
  1. Correspondence to:
 Dr Michael S Okun
 Movement Disorders Center, University of Florida, Brain Institute, PO Box 100236, Gainesville, FL 32610, USA;

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It has been shown recently that male patients with Parkinson’s disease who have testosterone deficiency may have symptoms resembling non-motor parkinsonian symptoms.12 Because of the similarity between the non-motor symptoms of Parkinson’s disease and the symptoms of testosterone deficiency, clinicians may fail to recognise and treat testosterone deficiency in patients with Parkinson’s disease.1 The identification of testosterone deficiency may have a significant impact on the long term course of the disease, as symptoms mistakenly labelled as non-motor parkinsonian manifestations could be relieved more effectively by testosterone replacement than by other treatments.

In this study we examined the prevalence of testosterone deficiency and testosterone deficiency symptoms among a group of patients with Parkinson’s disease presenting to our movement disorders clinic, to assess how common undiagnosed symptomatic testosterone deficiency was in this population. A mail-back survey was administered to all the patients seen in the clinic after a 12 month period where patients were seen, examined, and entered into a database. The surveys were returned by 91 of 137 male patients with Parkinson’s disease (66%). The diagnosis of idiopathic Parkinson’s disease was confirmed by a movement disorders specialist who applied the UK Brain Bank criteria3 and currently recommended guidelines for the diagnosis of Parkinson’s disease.4 We included in the survey two validated scales—the St Louis testosterone deficiency questionnaire5 and the Beck depression inventory.67 Additionally, historical information was obtained including the number of antidepressants the patients were exposed to in a lifetime, number of current antidepressants, history of testosterone deficiency, history of prostate cancer, and history of hormone replacement therapy. Forty two male patients with Parkinson’s disease who returned questionnaires had previously been identified as testosterone deficient by measurements of plasma testosterone concentrations.

The results of the survey are summarised in table 1. The average age of the male patients was 62 years. Nine per cent of the study population were on testosterone gel replacement therapy. Fifty of the 91 patients with Parkinson’s disease were screened with free testosterone levels during the 12 month period of the study. Half of the Parkinson’s disease patients (n = 25) who were screened for testosterone deficiency had a level of <70 pg/ml and were defined as having “low” testosterone. Ninety per cent of all male patients with Parkinson’s disease had a positive St Louis testosterone deficiency questionnaire (positive answers to more than three questions).

Table 1

Characteristics of 91 male patients with Parkinson’s disease who returned the questionnaire


The results of our survey indicate that testosterone deficiency is common in the elderly male population seen in a movement disorders clinic setting, and the prevalence is similar to that previously reported in the Baltimore longitudinal study of aging in the normal elderly population8 and in Parkinson’s disease.1 As the non-motor symptoms of Parkinson’s disease—including depression, anxiety, fatigue, decreased libido, sexual dysfunction, and a decreased enjoyment in life—directly overlap with those seen in male testosterone deficiency, separating testosterone deficiency from the non-motor symptoms of Parkinson’s disease can be difficult. This separation is important because specific treatment for testosterone deficiency is available and because these symptoms may not respond satisfactorily to antidepressant therapy.

Previous observations of refractory non-motor symptoms of Parkinson’s disease that responded to testosterone replacement suggested that patients were on or had been exposed to an increased number of antidepressants.1 Seidman and Rabkin found that testosterone deficiency—as also seen in thyroid hormone deficiency—may blunt responsiveness to antidepressants,9 prompting the investigators to examine whether patients with testosterone deficiency took more antidepressants than those without testosterone deficiency, as well as to examine whether deficiency scores correlated with the number of antidepressants. Our data did not suggest a difference in antidepressant use in the testosterone deficient Parkinson’s disease population; however, a prospective study will need to be done to confirm this observation. Overall, however, depression scores were not high in this study, which may either reflect aggressive treatment of depression in our Parkinson group, or suggest that testosterone deficiency does not present as major depression. Additionally, the study did not specifically screen for patients who were refractory to antidepressant treatment, and for those who had previously received aggressive treatment for depression. We suspect that testosterone deficiency, like thyroid deficiency, does affect the efficacy of antidepressants, but better prospective studies will be needed to examine this question.

Testosterone deficiency is a common, treatable, and largely unrecognised form of co-morbidity in Parkinson’s disease, and as demonstrated by this study is common in a movement disorders clinic setting. It may go undiagnosed when the symptoms are attributed to the non-motor manifestations of Parkinson’s disease. Additionally, a lack of a history of refractoriness to antidepressants, or lack of a positive depression screening questionnaire, should not dissuade practitioners from checking testosterone levels, as antidepressant responsive “depressive symptoms” seem to be common in testosterone deficiency.

Prospective epidemiological studies on this topic need to be undertaken, as this analysis of clinic patients suffered from both the bias of the researchers interested in testosterone deficiency, and the failure to get 100% return of the surveys. Additionally, a control group will need to be included in future analyses, and better screening devices with increased specificity for patients with Parkinson’s disease and testosterone deficiency will need to be developed. The issue of which type of testosterone assay is best, and how much the testosterone level matters if a patient is symptomatic, will also need to be examined.

Every practitioner who sees patients with Parkinson’s disease should be aware of this common treatable co-morbidity. The diagnosis of testosterone deficiency should be confirmed and prostate cancer excluded before initiating treatment.


We would like to thank the American Parkinson’s Disease Association and the Department of Neurology and McKnight Brain Institute for their generous support and help with the research described in this report.