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Psychiatry (Edgemont) 2007;4(12): 22-24
Regarding Objectivity of Psychiatric Diagnoses
Dear Editor:
Dr. Ronald Pies’s commentary in the October issue of Psychiatry 2007 addresses an important issue [Pies R. How objective are psychiatric diagnoses? Guess again. Psychiatry 2007;4(10):18–22]. I have shared his concern that the stigmatization of psychiatrists and psychiatric patients is not helped by the frequent off-handed derision of the value of our diagnoses. And I too believe that much of this is coming from within our profession. Just today, a psychiatric colleague of the psychoanalytic persuasion explained to me that he thought our diagnoses are not as objective as those in the rest of medicine because “there is only one common psychiatric diagnosis where we actually know the etiology: PTSD.” Of course, I couldn’t agree that diagnostic objectivity is directly related to understanding the pathophysiology.
Unfortunately, though, Dr. Pies’s commentary is not persuasive. The one piece of research that Dr. Pies cites to support his argument involves two psychiatrists using the Structured Clinic Interview for DSM-III-R with the same patients and achieving an impressively high interrater reliability for diagnosis. But structured clinical interviews come into use because they entail adequate interrater reliability! Hence his argument is essentially circular.
I was pleased and surprised by reading of the studies that show unimpressive interrater reliability for many nonpsychiatric illnesses. But, to make our case, there needs to be something more robust supporting a psychiatrist’s day-to-day diagnostic consistency.
With regards,
Bennett Cohen, MD
Brooklyn, New York
Author Response
I appreciate Dr. Cohen’s thoughtful reading of my editorial and the opportunity to clarify some aspects of my argument. Essentially, I argue that when properly carried out, psychiatric diagnostic procedures can yield agreement between observers (“interrater reliability”) comparable to that obtained in several other medical specialties. (As Michael First, MD, has pointed out, “reliability” is properly predicated of diagnostic procedures, not diagnoses).[1] I further argue that, to the extent our diagnostic procedures produce good inter-rater reliability (high kappa scores) and to the extent that they entail careful empirical observation, psychiatric diagnosis partakes of “objectivity.” My commentary touched only briefly on the more complicated issue of validity in psychiatric diagnosis—an aspect of objectivity I will address in a follow-up article.
Dr. Cohen finds that my argument is essentially “circular” because the study I cited[2] utilized the Structured Clinic Interview for Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Dr. Cohen opines that “structured clinical interviews come into use because they entail adequate interrater reliability…” implying (as I understand Dr. Cohen) that this somehow stacks the deck in favor of producing high rates of agreement between observers who utilize structured interviews. In my view, however, a full understanding of structured clinical interviews does not support this conclusion.
Instruments such as the SCID merely ensure that questions astute clinicians usually ask (“Are you hearing any unusual voices in your head?” “Are you feeling blue or sad?” etc.) are asked in a standardized way and without unintentional omission. Structured interviews do not preordain high levels of interrater agreement, though they may facilitate reliability. The actual “kappa” derived from two structured interviews of the same patient is never known in advance. Indeed, the outcome depends crucially on factors such as the training of the observers and their ability to detect nonverbal cues. As Nassir Ghaemi, MD, puts it, “Structured interviews give us the possibility of reliability, which then needs to be demonstrated between interviewers, but [structured interviews] do not simply ensure reliability between any and all interviewers.”[3] [italics added].
To be sure, as Dr. Ghaemi notes, “…it is indeed circular logic to define [an] illness as one with a declining course and then to use course data to validate it.”(italics added).[4] But interrater reliability is not meant to carry the burden of validating a diagnosis. It is, at most, a prelude to validation. Before we can go out into the field and validate the “reality” of a putative disease, we must first agree on what signs and symptoms define the ideal or prototype of the disease.[4]
Of course, interrater reliability among psychiatric clinicians is not always good, particularly when researchers apply DSM-based criteria to diagnoses proffered by clinicians who may choose not to use DSM criteria.[3] Reliability of psychiatric diagnostic procedures may also drop when nonclinicians are doing the “observing,” as in door-to-door epidemiologic studies.[5] With regard to “naturalistic” data, however, there is reason to be more optimistic. For example, in one study,[6] the reliability of diagnostic procedures by psychiatric residents in the emergency room was assessed by comparing their diagnoses with the inpatient discharge diagnoses of the same patients [N=190]. In both settings, diagnoses were based on DSM-III-R criteria, but structured diagnostic instruments were not used. There was moderate to excellent concordance for major depression, schizophrenic disorders, bipolar disorder, and substance abuse/dependence disorders, with kappa values ranging from 0.64 for major depression to 0.87 for substance abuse and dependence disorders.
Finally, I heartily concur with Dr. Cohen on the need for removing the stigma associated with psychiatric patients, their diagnoses, and their clinicians. I believe this process begins by making the case that psychiatric diagnosis, properly performed, can be as “objective” as diagnosis in other medical specialties.
References
1. First M. Personal communication. October 31, 2007.
2. Ruskin PE, Reed S, Kumar R et al. Reliability and acceptability of psychiatric diagnosis via telecommunication and audiovisual technology. Psychiatr Serv 1998;49:1086–8.
3. Ghaemi SN. Personal communication. October 31, 2007.
4. Ghaemi SN. The Concepts of Psychiatry. Baltimore, MD: Johns Hopkins University Press, 2003.
5. Anthony JC, Folstein M, Romanoski AJ, et al. Comparison of the lay Diagnostic Interview Schedule and a standardized psychiatric diagnosis. Experience in eastern Baltimore. Arch Gen Psychiatry 1985;42:667–75.
6. Warner MD, Peabody CA. Reliability of diagnoses made by psychiatric residents in a general emergency department. Psychiatr Serv 1995;46(12):1284–6.
With regards,
Ronald Pies, MD
Professor of Psychiatry, SUNY Upstate Medical University, Syracuse, New York; and Clinical Professor of Psychiatry, Tufts USM, Boston, Massachusetts
Varenicline and Alzheimer’s Disease
Dear Editor:
Cholinergic treatments, such as donepezil, and glutamatergic medicine, such as memantine, frequently show partial efficacy in the treatment of Alzheimer’s disease and mild cognitive impairment (MCI), whether prescribed alone or in combination.[1] Cholinergic and glutamatergic pathways may not be the only deficient neuropsychiatric systems in Alzheimer’s disease. Serotonergic, dopaminergic, noradrenergic, and other pathways also may be dysfunctional in Alzheimer’s and MCI.
Nicotine enhances memory by its effect on specific nicotinic cholinergic receptors.[2] In addition, nicotine has antianxiety and antidepressant properties, possibly due to associative pathways between nicotinic cholinergic and noncholinergic specialty neurons, such as GABA, 5-hydroxy-tryptamine, dopamine, and norepinephrine.[3] Nicotine also improves learning and attention.[4]
Varenicline behaves like nicotine and is the new selective alpha4beta2 nicotinic cholinergic receptor partial agonist used to treat nicotine dependence, which may also improve attention and learning.[5] A case of Alzheimer’s that responded to the addition of varenicline is reported here.
Case report. Ms. A, a 72-year-old Caucasian woman, was referred by her son in June, 2006, for obsessive worrying, anxiety, depression, and mildly impaired memory. She met DSM-IV-TR criteria for cyclothymic disorder but not dementia. Her previous physician prescribed venlafaxine and donepezil for her mood disorder and MCI, respectively. Venlafaxine was raised to 300mg daily, gabapentin was started and eventually raised to 2,000mg daily, and donepezil was discontinued in favor of memantine 5mg, eventually raised to 20mg daily. She became euthymic and her MCI improved slightly for about 10 months, at which time Ms. A began setting two extra place settings for dinner every late afternoon, acting defensive, showing signs of irritability, and significant memory impairment, especially in the evening. She met DSM-IV-TR criteria for Alzheimer’s disease, and varenicline 1mg was started at 3pm daily. Ms. A’s husband was instructed to have his wife eat a low-acid snack with an eight-ounce glassful of water before taking the medicine. She resumed setting the correct two dinner settings within a few days; her memory and mood improved considerably; and she no longer met criteria for Alzheimer’s. In addition, she downgraded to MCI for two weeks with no side effects reported. Her level of functioning continued to improve during the treatment month that followed; she spontaneously resumed processing the household laundry, a practice she had abandoned for more than two years. Ms. A’s memory remained much improved after three months of treatment with varenicline.
Although the placebo effect is negligible, a therapeutic link between varenicline and Alzheimer’s cannot be established with certainty in this case. This case report does suggest that the new nicotinic cholinergic partial agonist varenicline was useful in this individual and may be useful in the management of the memory deficits associated with Alzheimer’s disease. Further investigation is warranted using larger numbers of subjects at various stations along the MCI-Alzheimer’s continuum. Varenicline may be a novel treatment for the cognitive deficits associated with Alzheimer’s, other types of dementia, and MCI. Additional clinical trials using varenicline may also help us better understand the currently unsolved neuropsychiatric maze underlying Alzheimer’s and MCI.
References
1. Grossberg GT Rationale for combination therapy with galantamine and memantine in Alzheimer’s disease. J Clin Pharmacol 2006 Jul;46(7 Suppl 1):17S–26S
2. Mansvelder HD, van Aerde KI, Couey JJ, Brussaard AB. Nicotinic modulation of neuronal networks: from receptors to cognition. Psychopharmacology (Berl). 2006;184(3–4):292–305
3. Rosecrans JA. The biobehavioral effects of nicotine: Interaction with brain neurochemical systems. In: Cocores JA (ed). The Clinical Management of Nicotine Dependence. New York, NY: Springer-Verlag,1991:53–65
4. Levin ED Nicotinic effects on cognitive function: Behavioral characterization, pharmacological specification, and anatomic localization. Psychopharmacology 2006;184(3–4):523–39
5. Cocores JA. Varenicline and Adult ADHD. J Neuropsychiatry Clin Neurosci Accepted 7/23/2007.
With regards,
James A. Cocores, MD
Nutritional Neuropsychiatry
Southcoast Psychotherapy and Education Associates
Boca Raton, Florida
