Letters to the Editor
Factitious Anemia and Magnetic Resonance Imaging Abnormalities
Little is known about the causes and pathophysiology of factitious disorders. Several authors have proposed the possibility of preexisting organic cerebral lesions. Frontotemporal cerebral atrophy (1), marked hyperperfusion of the right hemithalamus (2), cerebral palsy (3), or areas of high signal in periventricular white matter in both hemispheres in T2-weighted magnetic resonance imaging (MRI) (4) have been respectively found in 4 patients who displayed Munchausen syndrome. We report a case of factitious anemia with MRI abnormalities, similar to those described by Fenelon and others (4).
Ms O, a 35-year-old unmarried woman, was admitted to our psychiatric department after a suicide attempt. At psychiatric examination, Ms O did not fulfill DSM-IV criteria for any psychotic or affective disorder, and the suicide attempt rapidly appeared to be a response to perceived rejection. Throughout her hospitalization, Mrs O exhibited irritability, suggestibility, and poor insight.
A review of her medical record indicated a psychiatric history of factitious anemia that began at age 15 years and included many explorations and hospitalizations for 13 years. At age 28 years, she complained of transitory neurological symptoms, such as visual disturbances, paresthesia, and dizziness. Even so, the successive neurological examinations and complementary examinations (cerebrospinal fluid analysis, central visual field, and auditory, visual, and somatosensory-evoked potentials) were normal. The MRI of the brain, however, showed areas of high signal in periventricular white matter in both hemispheres in the T2-weighted sequence. These abnormalities, although not specific, first suggested the possibility of multiple sclerosis. Nevertheless, the normality of the different neurological examinations and the performed explorations did not favour this diagnosis.
To our knowledge, this is the first report of MRI abnormalities in a patient with a factitious anemia. The first question raised is the link between the neurological symptoms and the MRI abnormalities. Although the diagnosis of multiple sclerosis cannot be invalidated, the absence of other objective neurological abnormalities does not support it. In this context, the subjective neurological complaints reported by the patient are consistent with the hypothesis of a neurological factitious disorder. The second remaining question is whether the MRI abnormalities that were found played a role in the development of factitious anemia.
This report raises an interesting question about cerebral lesions in the occurrence of pathomimia. To illuminate this association, we suggest further investigation to increase our understanding of the pathophysiology of factitious disorders.
1. Babe KS Jr, Peterson AM, Loosen PT, Geracioti TD Jr. The pathogenesis of Munchausen syndrome. A review and case report. Gen Hosp Psychiatry 1992;14:273–6.
2. Mountz JM, Parker PE, Liu HG, Bentley TW, Lill DW, Deutsch G. Tc-99m HMPAO brain SPECT scanning in Munchausen syndrome. J Psychiatry Neurosci 1996;21:49–52.
3. Diefenbacher A, Heim G. Neuropsychiatric aspects in Munchausen’s syndrome. Gen Hosp Psychiatry 1997;19:281–5.
4. Fenelon G, Mahieux F, Roullet E, Guillard A. Munchausen’s syndrome and abnormalities on magnetic resonance imaging of the brain. BMJ 1991;302:996–7.
Jérémie Aouillé, MD
Frédéric Rouillon, MD
Frédéric Limosin, MD, PhD