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 Table of Contents    
EDITORIAL  
Year : 2013  |  Volume : 55  |  Issue : 2  |  Page : 103-105
Screening for disease, psychological testing, and psychotherapy Looking behind the mirror


1 Department of Psychiatry, JSS Medical College Hospital, Mysore, Karnataka, India
2 Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India

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Date of Web Publication7-May-2013
 

How to cite this article:
Sathyanarayana Rao T S, Andrade C. Screening for disease, psychological testing, and psychotherapy Looking behind the mirror. Indian J Psychiatry 2013;55:103-5

How to cite this URL:
Sathyanarayana Rao T S, Andrade C. Screening for disease, psychological testing, and psychotherapy Looking behind the mirror. Indian J Psychiatry [serial online] 2013 [cited 2014 Sep 1];55:103-5. Available from: http://www.indianjpsychiatry.org/text.asp?2013/55/2/103/111446


In this issue of the Journal, Berger [1] presents his personal viewpoint on matters related to screening for future disease in the population, use of psychological tests for clinical purposes, and the limitations of psychotherapy as a clinical intervention. All the issues raised are important, and in this editorial we consider additional theoretical and practical matters that arise from the points that he makes.


   Screening for Future Disease Top


Berger [1] describes the results in New York of screening for Krabbe disease, an inborn error of metabolism. Only 24 babies tested positive out of about a million tested. Of these, 4 developed clinical features of the disease. Two of the 4 children died (one, of treatment complications) and the other 2 showed poor outcomes despite treatment. Parents of the children who tested positive were emotionally traumatized by the test results. So, was the screening cost-effective and did it serve the purpose? It appears not.

Screening for disease in the population should serve a purpose. [2] For example, the use of mammograms or cervical smears can identify breast or cervical cancer sufficiently early for intervention to increase life expectancy. Or, a negative test for Huntington's disease in a family member of an affected patient can offer immense relief whereas a positive test, while generating stress, would at least allow the individual the opportunity to plan for his future.

Leave alone the risk of future disease, screening for early disease in medical contexts is itself not without controversy. Take women's health, for example. Benefits as well as harms have been described in relation to breast cancer screening; [3] this is because no screening instrument is perfect, and false negatives and false positives (especially the latter, because they are more common) result in unnecessary interventions that are emotionally and physically damaging. A crude estimate obtained from available data suggests that, for every case of breast cancer mortality prevented, approximately, three women would have been unnecessarily identified and treated. [3] Whereas, the outcome would be good for the one life saved, it would be traumatic for the remaining 3 women. With regard to men's health, prostate specific antigen screening has resulted in similar difficulties: There is no consensus that screening has improved survival, and there is no consensus on even whether or not screening should be performed. [4]

Unfortunately, there are no screening tests in psychiatry that reliably predict future disease. Indeed, the presence of the APOE epsilon 4 allele increases the risk of Alzheimer's disease, [5] but the sensitivity, specificity, positive predictive value, and negative predictive value of this biological marker are too poor for screening for this allele to be of practical value. [6] The same holds true for genes such as neuregulin, [7] presenilin, [8] dysbindin, [9] DISC1, [10] COMT, [11] and others that have been found to be associated with schizophrenia. The situation is no different for other psychiatric conditions. At the moment, therefore, there does not seem to be hope for effective screening for future disease in psychiatry.


   The use of Psychological Testing for Diagnosis Top


Berger describes the emergence of depression with suicidal ideation in an 8-year-old son of a woman with a history of major depression; neither family dynamics nor school issues could explain the child's depression. On the one hand, the positive family history notwithstanding, it is uncommon for clinical depression to emerge in one so young; so, a case might be made for psychological testing and probing for hidden sources of stress. On the other hand, given the apparent severity of the phenomenology in the child and the atheoretical nature of the current diagnostic systems (which dictate diagnosis based on phenomenology alone), surely immediate intervention was indicated, even if only of a psychological nature.

Psychological tests do not have the same reliability and validity as medical tests. Clinical interventions, whether psychological or psychopharmacological, have been validated against clinical diagnoses, not psychological test results. Therefore, if a clinical intervention is indicated, psychological testing, at best, would assist or guide but would not determine the need for or the nature of clinical intervention.

Having said so, some caveats are necessary. One is that there is a risk of emergent suicidal ideation when antidepressant drugs are used in depressed children and adolescents. [12] The other is that fluoxetine is the only antidepressant with a safety-efficacy profile that has resulted in approval for use in the treatment of pediatric depression. [13] Neither of these caveats emerged in Berger's [1] viewpoint; happily, the therapeutic trial with low-dose escitalopram proved successful.

With regard to Berger's [1] view on the differential diagnosis and possible accompaniments of a popular diagnosis of Asperger's disorder, some acknowledgement is necessary that Asperger's syndrome not amounting to a disorder may be far more common than realized, and that autistic traits are probably continuously distributed in the population. [14]


   Psychotherapy: The Other Side of the Story Top


In his viewpoint, Berger [1] implies that psychotherapy has not been measured by the same yardstick as antidepressants, that psychotherapy has not been validated in patients with vegetative symptoms, a strong family history, and a chronic course, and that psychotherapy has not been tested with remission as the primary outcome. He adds that the very validation of psychotherapy as an effective treatment is flawed because psychotherapy trials cannot be blinded and effectively placebo-controlled. When psychotherapy trials are required to meet quality standards, the efficacy of even Cognitive behavior therapy (CBT) interventions disappear or diminish in impressiveness. [15] Psychotherapy trials therefore do not merit classification as high quality evidence.

These are valid criticisms. We carry the arguments a few steps further. To start with, recruitment of patients into psychotherapy trials is inherently biased. This is because patients who obviously will not respond to psychotherapy (such as those with catatonic or psychotic symptoms), those who are more likely to respond to antidepressants (such as those with very severe depression), and those at high risk (such as those who are suicidal) will not be recruited into psychotherapy trials; in fact, such patients would not be considered suitable for psychotherapy in ordinary practice, either. Thus, entry of patients into psychotherapy in everyday practice, and into psychotherapy trials, as well, is biased because only good prognosis patients are selected. This is a luxury that is unavailable to those who need to prescribe antidepressant medications.

An additional biasing factor at the time of recruitment is that the informed consent process will ensure that only patients who are favorably inclined to psychotherapy will be recruited. Those who are unwilling to subject themselves to the rigor of therapy and those with negative attitudes towards talking cures will select themselves out. This is an important consideration because patients cannot be blinded to the intervention that they are receiving in psychotherapy studies, and so favorable attitudes will enhance the placebo effect (Andrade, 2012). Similar concerns apply to other unblindable interventions, as well, including yoga, meditation, and exercise. [16],[17],[18],[19]

A fair trial of antidepressants versus psychotherapy would require both treatments to be delivered without blinding, and patients to enter the trial in equipoise; that is, with selection for comparable attitudes towards psychotherapy and medication. Unfortunately, fair trials of such a nature are not conducted. In fact, when medication is contrasted with psychotherapy, there is a placebo-controlled arm for medication but no control for psychotherapy; [20] this contrast is obviously prejudiced against medication.

An additional consideration is that there are a large number of factors that enhance the placebo response rate in antidepressant clinical trials, diminishing the separation between drug and placebo and hence diminishing the effect size and increasing the numbers needed to treat statistic. In contrast, with untreated or waitlisted controls in psychotherapy trials, few or no placebo mechanisms exist, and this amplifies the effect size and decreases the Number needed to treat (NNT) value for psychotherapy. Effect size and NNT, therefore, cannot be validly compared between antidepressant and psychotherapy trials. [19]

A matter that is hardly ever discussed is that whereas antidepressants are the same no matter who prescribes the drug, psychotherapy is an unstandardized procedure that depends heavily on therapist, client, environmental, and interactional variables. There is no assurance that even a manual-driven format of CBT will be equally effective in every therapist's hands. The difficulty in the standardization of treatment that is well-known in the context of herbal medicine [21] probably applies with equal force in psychotherapeutic contexts.

Other limitations of psychotherapeutic interventions with particular reference to developing countries have been well discussed elsewhere, [12] and are not repeated here.

On a parting note, the suggestion that negative thoughts are only symptoms and not the cause of depression [1] would, however, unjustifiably invalidate decades of careful observation that faulty patterns of thinking and behavior trigger feedback loops that sustain and amplify depressed mood; therefore, cognitive and behavioral interventions are definitely necessary, in indicated circumstances, to break the vicious cycle as well as initiate healthy cognitions and behavior that can reduce stress and sustain healthy mood.

Finally, if the reader is puzzled by the title of this editorial, we wish to conclude with the reflection that, on subjects such as those that we have discussed, people tend to see what is already in their eyes. We have chosen to look at what lies behind the mirror; that is, what the glass conceals.

 
   References Top

1.Berger DM. Tests, testing, and tested: We need to critically evaluate the meaning of tests in psychiatry. Indian J Psychiatry 2013;55:200-3.  Back to cited text no. 1
  Medknow Journal  
2.Wilson JM, Jungner G. Principles and practice of screening for disease. Public Health Papers. Geneva: World Health Organization; 1968.  Back to cited text no. 2
    
3.Independent UK Panel on Breast Cancer Screening. The benefits and harms of breast cancer screening: An independent review. Lancet 2012;380:1778-86.  Back to cited text no. 3
    
4.Gomella LG, Liu XS, Trabulsi EJ, Kelly WK, Myers R, Showalter T, et al. Screening for prostate cancer: The current evidence and guidelines controversy. Can J Urol 2011;18:5875-83.  Back to cited text no. 4
    
5.Liu CC, Kanekiyo T, Xu H, Bu G. Apolipoprotein E and Alzheimer disease: Risk, mechanisms and therapy. Nat Rev Neurol 2013;9:106-18.  Back to cited text no. 5
    
6.Elias-Sonnenschein LS, Viechtbauer W, Ramakers IH, Verhey FR, Visser PJ. Predictive value of APOE-ε4 allele for progression from MCI to AD-type dementia: A meta-analysis. J Neurol Neurosurg Psychiatry 2011;82:1149-56.  Back to cited text no. 6
    
7.Rico B, Marín O. Neuregulin signaling, cortical circuitry development and schizophrenia. Curr Opin Genet Dev 2011;21:262-70.  Back to cited text no. 7
    
8.Zhang J, Chen J, Xu Q, Shen Y. Does the presenilin 2 gene predispose to schizophrenia? Schizophr Res 2009;109:121-9.  Back to cited text no. 8
    
9.Maier W, Zobel A, Kühn KU. Clinical impact of recently detected susceptibility genes for schizophrenia. Dialogues Clin Neurosci 2006;8:79-84.  Back to cited text no. 9
    
10.Sawamura N, Sawa A. Disrupted-in-schizophrenia-1 (DISC1): A key susceptibility factor for major mental illnesses. Ann N Y Acad Sci 2006;1086:126-33.  Back to cited text no. 10
    
11.Lewandowski KE. Relationship of catechol-O-methyltransferase to schizophrenia and its correlates: Evidence for associations and complex interactions. Harv Rev Psychiatry 2007;15:233-44.  Back to cited text no. 11
    
12.Andrade C, Bhakta SG, Singh NM. Controversy revisited: Selective serotonin reuptake inhibitors in paediatric depression. World J Biol Psychiatry 2006;7:251-60.  Back to cited text no. 12
    
13.Busch SH, Barry CL. Pediatric antidepressant use after the black-box warning. Health Aff (Millwood) 2009;28:724-33.  Back to cited text no. 13
    
14.Constantino JN, Todd RD. Autistic traits in the general population: A twin study. Arch Gen Psychiatry 2003;60:524-30.  Back to cited text no. 14
    
15.Lynch D, Laws KR, McKenna PJ. Cognitive behavioural therapy for major psychiatric disorder: Does it really work? A meta-analytical review of well-controlled trials. Psychol Med 2010;40:9-24.  Back to cited text no. 15
    
16.Andrade C. Yoga: Some unanswered questions. Indian J Psychiatry 1995;37:189.  Back to cited text no. 16
[PUBMED]  Medknow Journal  
17.Andrade C. Yoga: Better treatment or better placebo? Indian J Psychiatry 2002;44:83.  Back to cited text no. 17
[PUBMED]  Medknow Journal  
18.Andrade C. Transcendental meditation and components of the metabolic syndrome: Methodological issues. Arch Intern Med 2006;166:2553.  Back to cited text no. 18
    
19.Andrade C. There's more to placebo-related improvement than the placebo effect alone. J Clin Psychiatry 2012;73:1322-5.  Back to cited text no. 19
    
20.Vitiello B, Rohde P, Silva S, Wells K, Casat C, Waslick B, et al. Functioning and quality of life in the Treatment for Adolescents with Depression Study (TADS). J Am Acad Child Adolesc Psychiatry 2006;45:1419-26.  Back to cited text no. 20
    
21.Andrade C, Sudha S, Venkataraman BV. Herbal treatments for ECS-induced memory deficits: A review of research and a discussion on animal models. J ECT 2000;16:144-56.  Back to cited text no. 21
    

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Correspondence Address:
Chittaranjan Andrade
Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore - 560 029, Karnataka
India
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DOI: 10.4103/0019-5545.111446

PMID: 23825840

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