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Obsessive-compulsive phenomenon and Parkinson's disease
  1. P Sharma1,
  2. N Gupta1
  1. 1Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh-160 012, India
  1. Correspondence to:
 Professor N Gupta;
 tinysam{at}glide.net.in
  1. M Alegret2,
  2. C Junqué2,
  3. P Vendrell2,
  4. F Valldeoriola3,
  5. M J Marti3,
  6. E Tolosa3
  1. 2Department of Psychiatry and Clinical Psychobiology, Univeristat de Barcelona, IDIBAPS, Casanova 143, E-08036 Barcelona, Spain
  2. 3Parkinson's and Movement Disorders Unit, Institut Clinic de Malalties del Sistema Nerviós (ICMSN), Department of Neurology, Hospital Clinic Universitari, School of Medicine, Barcelona, Spain

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    Alegret et al1 have systematically studied patients with Parkinson's disease for presence of “obsessive-compulsive traits”. This study is based on the evidence that Parkinson's disease and obsessive-compulsive disorder have neuroanatomical overlap in terms of frontobasal ganglia circuitary involvement. Anatomical specificity of obsessive-compulsive disorder or obsessive-compulsive phenomenon has been previously studied in Tourette's syndrome, Huntington's chorea, Sydenham's chorea etc, but not in Parkinson's disease.2 The authors, through a cross sectional design, found significantly high scores on the Maudsley obsessive-compulsive Inventory (MOCI) and Leyton obsessional inventory (LOI) in severe Parkinson's disease. However, the presentation and interpretation of results merits further elucidation and clarification.

    The aim has been mentioned as to “ . . .systematically investigate obsessive-compulsive traits in Parkinson's disease”, using MOCI and LOI. Although LOI is used to assess both obsessional symptoms and traits,3 MOCI is used to investigate the different types and rate severity of obsessive-compulsive complaints in patients with obsessive-compulsive disorder.3,4 Also, traits are defined as enduring patterns of perceiving, relating to, and thinking about the environment and oneself that are exhibited in a wide range of important social and personal contents5 and are part and parcel of the personality of any person. On the other hand, obsessive-compulsive disorder is a clinical disorder characterised by recurrent obsessions or compulsions that causes distress or impairment.5 Hence the MOCI is used to assess the obsessive-compulsive symptoms in patients with obsessive-compulsive disorder and is not applicable for obsessive-compulsive traits or neurotic patients with no obsessional symptoms.3,4 This issue needs discussion as the authors have interchangeably used the terms “traits”, “phenomenon”, and “symptoms” leading to considerable semantic confusion. Also, it raises the query as to what is being actually assessed. Are the authors assessing obsessive-compulsive traits or obsessive-compulsive symptoms? To our mind, the attempt has been to assess obsessive-compulsive phenomena (both traits and symptoms); traits using LOI and symptoms using MOCI.

    Secondly, it is mentioned that “patients with mild Parkinson's disease had no obsessive-compulsive symptoms”. A closer look at the table presented shows that the MOCI total score was 4.83 (SD 3.57) in controls compared with 4.12 (SD 3.15) in patients with mild Parkinson's disease. If such is the case, then the controls demonstrated more (though statistically comparable) obsessive-compulsive symptoms than patients with mild Parkinson's disease. This issue has not been highlighted and discussed. Another related issue is the absence of a cut off score on MOCI that can differentiate between presence or absence of obsessive-compulsive symptoms.3,4 Hence, the above statement by the authors is itself not tenable.

    Thirdly, it has been suggested that obsessive-compulsive symptoms appeared late during progression of Parkinson's disease (based on correlation between years of evolution and MOCI global score). Keeping in mind the previous issue, this suggestion should be modified to: patients with longer duration of Parkinson's disease had greater severity (rather than emergence) of obsessive-compulsive symptoms. Additionally, a correlation between MOCI total score and stage of Parkinson's disease can just simply be interpreted as: the more progressive the Parkinson's disease, the more prominent/severe is the obsessive-compulsive symptomatology. The assertion that obsessive-compulsive symptoms appeared late during disease progression can only be made if there is a correlation between duration of illness and severity of Parkinson's disease.

    Fourthly, the statement “slowness might be expected . . .did not increase” is conceptually not tenable as the slowness characteristic of Parkinson's disease can in no way be equated (or compared) with the slowness in obsessive-compulsive disorder (or obsessive-compulsive slowness); as evidenced from items of slowness and repetition of MOCI.4 Also, the obsessive-compulsive slowness is related to obsessions5 whereas the slowness in Parkinson's disease has no such cognitive basis.

    Lastly, a very interesting and important finding in this study has been that no patient with Parkinson's disease had obsessive-compulsive disorder. Hence, the link between these two may be lacking. But, at the neuroanatomical level, the basic psychopathology seems to be somewhat similar. It may be that a pathoplastic effect is exerted by the frontal and temporal lobes on some basic dysfunction of basal ganglia leading to differing clinical manifestations. This study, indeed, opens up new vistas of research for understanding the neurobiological basis of obsessive-compulsive disorder.

    REFERENCES

    Authors' reply

    We are grateful to Sharma and Gupta for their comments.

    (1) We concur with them that the term “phenomena” may be the most appropiate to describe our results because they included measures of traits and symptoms. Patients with Parkinson's disease may show both symptoms and traits. There are several studies suggesting the presence of a characteristic premorbid personality profile in Parkinson's disease. Similarly to obsessive-compulsive disorder, patients with Parkinson's disease demonstrated a previous tendency to inflexibility and mental rigidity.1 In addition, it has been shown that basal ganglia lesions and induced parkinsonism produce obsessive-compulsive disorder symptomatology.2 We think, acordingly, that the use of both MOCI and LOI was pertinent. On the other hand, despite the fact that traits and symptoms can be well differentiated in clinical diagnoses, there is also some evidence supporting a continuum hypothesis.3,4

    (2) It is true that the mean of the MOCI scores of patients with mild Parkinson's disease was slightly lower than that of the controls, but without statistical relevance. Thus, we considered it inappropiate to include that issue in the discussion.

    (3) Regarding the issue of co-ocurrence of severity of Parkinson's disease and obsessive-compulsive disorder phenomena, in addition to the correlation reported in the paper we found that the duration of illness was highly correlated with Parkinson's disease severity (r=0.66; p<0.0001), supporting the view that obsessive-compulsive disorder phenomena appeared late during disease progression. Moreover, patients with more than 10 years of evolution (n=37) significantly differed from patients with less than 10 years of evolution (n= 35) in MOCI scores (7.37 (SD 4.28) v 4.91 (SD 3.62) (t=−2.6, p=0.007).

    (4) We agree with Sharma and Gupta regarding the absence of a clear explanation about the link between Parkinson's disease and obsessive-compulsive disorder. We think that although both pathologies share frontostriatal dysfunction, there is not a direct relation because obsessive-compulsive disorder phenomena are not present in the early stages of the disease. Within basal ganglia dysfunctions we suspect that obsessive-compulsive disorder is more closely related to dyskinetic motor symptoms such as Huntington's disease. Dyskinesia also appears with progression of Parkinson's disease. Moreover, MOCI scores in obsessive-compulsive disorder improve after pallidotomy similarly to dyskinetic manifestations.5

    (5) Finally, the Sharma and Gupta hypothesis claiming a pathoplastic effect exerted by frontal and temporal lobes on some basal ganglia dysfunction is suggestive although perhaps somewhat speculative in the light of the available evidence.

    REFERENCES

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