Munchausen by Proxy and Malingering by Proxy

Munchausen by Proxy and Malingering by Proxy

Letters ventilation/perfusion scan. An ultrasound investigation did not reveal thrombi in the lower extremities. Because Mr. A had no apparent risk fa...

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Letters ventilation/perfusion scan. An ultrasound investigation did not reveal thrombi in the lower extremities. Because Mr. A had no apparent risk factors for pulmonary emboli, a workup for potential causes was performed. A series of biochemical markers for hypercoagulable states, including homocysteine, antithrombin III, protein C, protein S, anticardiolipin antibody, lupus anticoagulant, factor V Leiden mutation, and prothrombin gene mutation G20210A, were obtained. All values were found to be normal, with the exception of a slightly decreased protein S value (66%; reference range⳱70%– 140%). The possibility of colonic malignancy was investigated by means of a colonoscopy, which revealed a single benign polyp. A CT of the abdomen and pelvis revealed two small hypodense areas in the liver, which were subsequently found to be consistent with benign hemangiomata per ultrasound; no other abnormalities were found. Prostate-specific antigen was found to be 1.6 ng/ml (normal⳱0–4.0 ng/ml). Blood and urine cultures were negative. Mr. A was treated with intravenous heparin and supportive oxygen therapy. His oxygenation status improved over the next 5–7 days, and he was transitioned from heparin-based anticoagulation to coumadin and discharged to the psychiatric service for treatment of his behavioral decompensation. Discussion This scenario illustrates the case of a patient with multiple pulmonary emboli without any recognized risk factors other than the patient’s profound inactivity and subsequent venous stasis. His hypercoagulability panel did reveal a slightly decreased protein S value, which is often seen as an artifact of elevated factor VIII. (In this paPsychosomatics 45:4, July-August 2004

tient, the value was 225% [reference range⳱50%–200%], which is an acute phase reactant and was likely elevated secondary to this patient’s multiple pulmonary emboli.6) This is supported by the patient’s elevated fibrinogen (812 mg/dl; reference range⳱150–400 mg/ dl), another acute phase reactant. A convalescent serum level was not available for comparison since the patient was placed on long-term coumadin therapy. No malignancy was found with either age-appropriate testing or with additional examination of the abdomen and pelvis with a CT scan. We submit that the patient’s severely maladaptive behavioral pattern was the principal factor predisposing him to the formation of a deep-venous thrombus and ultimately to a pulmonary embolus. There is increasing epidemiological evidence that depressive disorder is an independent risk factor for coronary artery disease,1,2 and recent studies have demonstrated that platelets in depressed patients are hyperaggregable.3,4 In addition, it has been shown that catatonia is a risk factor the development of pulmonary emboli.7,8 However, to our knowledge, there have been no large-scale reports describing the development of pulmonary emboli in noncatatonic but severely anhedonic patients. This case, combined with the evolving view of depression as a systemic illness involving hematological pathology3,4 and the high prevalence of this disease, suggests that a systematic study of the incidence of pulmonary emboli in depressed patients would have clinical impact. Furthermore, for patients such as the one described here, aggressive intervention to reverse the anhedonic state should be implemented to prevent life-threatening complications. In refractory cases, prophylactic use of heparin or heparinoids may be useful.

Daniel A. Llano, M.D., Ph.D. Robert S. Abernethy III, M.D. Boston, Mass. References

1. Musselman D, Evans D, Nemeroff C: The relationship of depression to cardiovascular disease: epidemiology, biology and treatment. Arch Gen Psychiatry 1998; 55:580–592 2. Glassman A, Shapiro P: Depression and the course of coronary artery disease. Am J Psychiatry 1998; 155:4–11 3. Lederbogen F, Gilles M, Maras A, Hamann B, Colla M, Heuser I, Dueschle M: Increased platelet aggregability in major depression? Psychiatry Res 2001; 102:255–261 4. Musselman DL, Tomer A, Manatunga AK, Knight BT, Porter MR, Kasey S, Marzee U, Harker LA, Nemeroff CB: Exaggerated platelet reactivity in major depression. Am J Psychiatry 1996; 153:1313–1317 5. Arnone D, Hansen L, Davies G: Pulmonary embolism and severe depression. Am J Psychiatry 2002; 159:873–874 6. Van Cott EM, Laposata M: Laboratory evaluation of hypercoagulable states. Hematology/Oncology Clin North Am 1998; 12:1141–1166 7. McCall WV, Mann SC, Shelp FE, Caroff SN: Fatal pulmonary embolism in the catatonic syndrome: two case reports and a literature review. J Clin Psychiatry 1995; 56:21–25 8. Regestein QR, Alpert JS, Reich P: Sudden catatonic stupor with disastrous outcome. JAMA 1977; 238:618–620

Munchausen by Proxy and Malingering by Proxy TO THE EDITOR: The term “Munchausen by proxy” has long referred to a form of maltreatment in which an individual in loco parentis fabricates or produces illness (physical and/or emotional-behavioral) in another to assume the vicarious sick role.1 More recently, “malingering by proxy” has been used to refer to people whose motives for such abuse or neglect are external and often tangible.2 The following case displays both phenomena in a single person. 365

Letters Case Report Ms. A, a teacher’s aide, expressed concerns about “statements” and “incidents” at home that were allegedly reported to her by a severely retarded female student. No worrisome verbalizations or events were ever detected by teachers, counselors, or others who had worked long-term with the student. Nevertheless, Ms. A individually met with teachers, a social worker, an assistant principal, a counselor, and a nurse, crying about feared abuse. Although the other personnel were unpersuaded, the aide reported suspected abuse to child protective services. The aide remained the central figure as police and child protective services thoroughly investigated the charges. The child and her family were subjected to property searches, interviews with specialists, and potential termination of parental rights. The charges were ultimately found to be totally untrue. Ms. A continued to speak of the case and her own unrequited effort to “save” the child. Once vindicated, the parents removed the child from the school. The next year, Ms. A served as an aide to an autistic boy at the school. Now pregnant, Ms. A warned others that “nothing had better happen to this baby” as a result of the boy’s behaviors. She also requested additional sick leave as a result of her prediction that the baby might be harmed in some way by the boy. For the next several weeks, she reported that the boy made inappropriate comments, touched her, and cursed her. Such behaviors had never been observed by anyone else. Soon thereafter, a co-worker heard a foot stomp on the floor and then heard the aide yelling at the boy. The aide reported that the boy had struck her in the abdomen. She filed a police report and met with and cried to the same personnel as before. Although there was never any indica366

tion of harm to the fetus, Ms. A remained at home, using others’ accrued sick leave before starting to draw worker’s compensation payments. The boy explained that the aide had poked him repeatedly whenever others were not around, verbally abused him, and told him that “your parents are going to pay for my doctor.” Prior to these events, she had told other staff members that she wished to stay at home and had hoped to sue someone to help pay her medical bills from prior surgery. Discussion In the first instance, the aide engaged in Munchausen by proxy in an effort to garner attention and concern. She also basked transiently in the accolades of child protective services workers, who originally believed she had uncovered child abuse that others had missed. In the second situation, the aide engaged in malingering by proxy by attempting to incite an autistic student into violent behavior. Failing that, she staged an unconvincing punch that led to her being able to stay at home and still receive income—from workers’ compensation and potentially from a hoped-for civil suit. According to DSM-IV-TR, malingering and factitious disorder (called “Munchausen syndrome” in its extreme form) are mutually exclusive, the goal being external in the former and internal in the latter.3 However, my experience with numerous clinical and forensic cases has repeatedly shown that individuals can have multiple motivations for their medical or emotionalbehavioral deceptions and that these diagnoses can co-exist. In a parallel way, the patient’s Munchausen by proxy and malingering by proxy appear at least serial and possibly concurrent. The case provides further support for the

concept of malingering by proxy and emphasizes the need for further attention to the possible co-existence of this behavior with Munchausen by proxy maltreatment. Marc D. Feldman, M.D. Birmingham, Ala. References

1. Meadow R: Munchausen syndrome by proxy: the hinterland of child abuse. Lancet 1977; 8033:343–345 2. Feldman MD: Playing Sick? Untangling the Web of Munchausen Syndrome, Munchausen by Proxy, Malingering, and Factitious Disorder. New York, BrunnerRoutledge, 2004 3. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC, APA, 2000, pp 513–517, 739–740

Wernicke-Korsakoff Syndrome and Galantamine TO THE EDITOR: Korsakoff’s psychosis, a chronic amnestic disorder, is defined as a severe anterograde amnesia in which memory is not transferred from short- to long-term storage.1 It is believed to be a consequence of Wernicke’s encephalopathy, a thiamine-deficient state resulting in encephalopathy, truncal ataxia, ophthalmoplegia, and mental confusion. Of those with Wernicke’s encephalopathy who survive, about three-fourths will develop Korsakoff’s psychosis.1,2 These two disorders are often described together as Wernicke-Korsakoff syndrome. Prompt administration of thiamine to patients with Wernicke’s encephalopathy can prevent or reduce the severity of Korsakoff’s psychosis and prevent the progression of deficits, although it is unlikely to reverse existing deficits in patients who already have Korsakoff’s psychosis.2 It should also be noted, however, that a study by Davis et al. found Wernicke-Korsakoff Psychosomatics 45:4, July-August 2004