Meeting of the American Psychiatric Association

Psychiatric and neuropsychological aspects of Lyme Disease

Thursday, May 18, 2002

Felice A. Tager, Ph.D., Department of Psychiatry, Columbia University, 622 West 168th Street, Box 427, New York, NY 10032; Brian A. Fallon, M.D.
Objective: This presentation will review the published literature on the psychiatric and neuropsychological aspects of Lyme disease. The goal is to help mental health clinicians by
  1. describing the psychiatric and neuropsychological symptoms typical of Lyme disease and
  2. analyzing laboratory tests that are useful in confirming or supporting the diagnosis.
All studies found through MEDLINE and PsycINFO (1970ópresent) focusing on cognitive and psychiatric aspects of Lyme disease were reviewed.

Reports from Europe and the United States suggest that psychiatric symptoms, e.g.,

may be prominent characteristics of Lyme disease. In addition, impairments in occur among adults with late-stage Lyme disease.

Patients with disseminated Lyme disease may present with psychiatric and cognitive problems including disturbances of memory, attention, mood, and sleep. Psychiatrists in areas where Lyme is endemic will be referred such patients, sometimes before the disease has been diagnosed. Clinicians need to be aware of the range of features associated with Lyme disease in order to aid in the differential diagnosis and care of these patients.

Chairperson: David R. Coursin, M.D., 6-D Hills Ave, Concord, NH 03301
Participant: Douglas B. Coursin, M.D.
EDUCATIONAL OBJECTIVES:At the conclusion of this workshop, the participant should be able to 1) identify "blaming the patient" from a perspective that is, itself, less blaming, 2) identify basic concepts of contemporary evolutionary theory, 3) apply them to an understanding of social behaviors that generate stigmatization of mental illness, 4) critically examine a grass-roots plan addressing stigmatization in our communities.
SUMMARY:"Blaming the patient" is a dynamic placing clinicians and patients at risk. We will examine its evolutionary origins, yielding insights into the maleficence it creates in all medical specialties and the stigmatization it generates toward the mentally ill.
The presentation of a patient's case of neuroborreliosis demonstrates this dynamic complicating the doctor-patient relationship. It compromises accurate self-assessment by the patient and puts blinders of suspicion on clinicians addressing her prominent symptoms without convincing findings.
Initial exercises engage group participation through the use of the Wason Card-Sorting Task to demonstrate adaptive problem-solving, the byproduct of which is the cognitive blind-spot where "blaming the Patient" hides. Later exercises will critique a plan to combat this face of stigma by organizing a nationwide coalition of psychiatrists, lawyers, legal aid agencies, law students, and psychiatric residents. The plan aims to identify and coordinate local psychiatric resources willing to provide live psychiatric testimony in cases of working people seeking compensation for mental illness. This is one of the places where stigmatization occurs right under our noses every day. Fair hearing in such cases is too often denied by "blaming the patient" and insuring availability of live psychiatric testimony is an untapped opportunity for our profession.
REFERENCES:1. Fallon BA: Lyme disease: a neuropsychiatric illness, Am J Psychiatry 1994; 151:1571-1583.
2. Barkow JH, Cosmides L, Tooby J: The Adapted Mind: Evolutionary Psychology and the Generation of Culture. New York, Oxford University Press, 1992.
2000]NR683 Thursday, May 18, 12:00 p.m.-2:00 p.m. Fluvoxamine Treatment of Hypochondriasis
Altamash I. Qureshi, M.D., Department of Psychiatry, Columbia University, 1051 Riverside Drive, #69, New York, NY 10032; Brian A. Fallon, M.D., Michael R. Liebowitz, M.D., J. Arturo Sanchez-Lacay, M.D.
Background. Because SSRIs may be a particularly effective treatment for hypochondriasis, we explored the efficacy of fluvoxamine.
Methods. 18 patients with DSM-IV hypochondriasis entered. All received placebo for 2 weeks and fluvoxamine for 10 weeks starting at 50 mg/day and increasing to 300 mg/day. Ratings included SCID-I and -II, patient-rated measures (Analog scale, Whiteley Index [IAS], MOS Short-Form 36), and physician-rated measures (CGI, HIC Severity Scale, and a modified Y-BOCS). Responder status was defined by physician-rated CGI improvement of at least "much improved". Minimum treatment required at least 6 weeks of fluvoxamine.
Results. Among the 18 patients, 4 were dropped during the 2-week placebo run-in. Among the 14 patients given active medication, 3 discontinued before week 6. Of the remaining 11 patients, 8 (72.7%) were responders. One non-responder was later identified as having Lyme disease. Detailed results from the various ratings will be presented.
Discussion. The CGI responder rate from this fluvoxamine trial (72.7% for the minimum treatment analysis and 57.1% for the intent-to-treat analysis) was comparable to the results reported previously for fluoxetine. Fluvoxamine therefore appears to be an effective treatment for hypochondriasis. A controlled trial is needed.


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