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Munchausen syndrome presenting as hemophilia: a convenient and economical "steal" of disease and treatment.

Munchausen's syndrome and Munchausen's syndrome by proxy (MSBP) can cause many conditions, including bleeding problems, seizures, failure to thrive and others. We report here an unusual case in which a mother presented to the hospital for her hemophiliac son's failure to thrive, subsequently for her own self-inflected mutilating wounds, and finally for self-induced simulation of her son's hemophiliac bleeding and arthritic complications.

Adult↗
PubMed2018

Midface toddler excoriation syndrome (MiTES) can be caused by autosomal recessive biallelic mutations in a gene for congenital insensitivity to pain, PRDM12.

BACKGROUND: Midface toddler excoriation syndrome (MiTES) is a condition recently reported in three unrelated children. Habitual scratching from the first year of life inflicted deep, chronic, scarring wounds around the nose and eyes. One child had a mild neurological deficit but there was no other evidence of insensitivity to pain. Bilateral distribution and localization to the midface distinguish MiTES from other causes of self-inflicted skin damage such as trigeminal trophic syndrome. An earlier study of five siblings from a consanguineous Irish family, with lesions corresponding to MiTES plus other sensory deficits, showed homozygous mutations in a gene for hereditary sensory and autonomic neuropathy type VIII (HSAN8), PRDM12. OBJECTIVES: To study further cases of MiTES, including analysis of PRDM12. METHODS: We describe five further children, from four families, with facial lesions typical of MiTES, in whom mutation analysis of PRDM12 was carried out. RESULTS: Homozygous or compound heterozygous pathogenic expansions of the PRDM12 polyalanine tract were found in four of five affected individuals, in three families. CONCLUSIONS: Our finding of autosomal recessive mutations in PRDM12 in four of five patients with MiTES extends the phenotypic spectrum of PRDM12 mutations, which usually cause HSAN8, characterized by mutilating self-inflicted wounds of the extremities, lips and tongue. By contrast, MiTES shows severe midfacial lesions with little if any evidence of generalized pain insensitivity. The condition is probably genetically heterogeneous, and other congenital insensitivity to pain and HSAN genes such as SCN11A may be implicated. This new understanding of the nature of MiTES, which can masquerade as factitious disease, will facilitate appropriate management.

Alleles↗
PubMed2002

Clinical and electrophysiological expression of deafferentation pain alleviated by dorsal root entry zone lesions in rats.

OBJECT: The aims of this study were to construct an animal model of deafferentation of the spinal cord by brachial plexus avulsion and to analyze the effects of subsequent dorsal root entry zone (DREZ) lesions in this model. To this end, the authors measured the clinical and electrophysiological effects of total deafferentation of the cervical dorsal horn in rats and evaluated the clinical efficacy of cervical DREZ lesioning. METHODS: Forty-three Sprague-Dawley rats were subjected to total deafferentation of the right cervical dorsal horn by performing a posterior rhizotomy from C-5 to T-1. The clinical effects of this deafferentation, namely self-directed mutilations consisting of scraping and/or ulceration of the forelimb skin or even autotomy of some forelimb digits, were then evaluated. As soon as some of these clinical signs of pain appeared, the authors performed a microsurgical DREZ rhizotomy ([MDR], microincision along the deafferented DREZ and dorsal horn). Before and after MDR, single-unit recordings were obtained in the deafferented dorsal horn and in the contralateral (healthy) side. The mean frequency of spontaneous discharge from the deafferented dorsal horn neurons was significantly higher than that from the healthy side (36.4 Hz compared with 17.9 Hz, p = 0.03). After deafferentation, 81.4% of the rats developed clinical signs corresponding to pain following posterior rhizotomy. Among these animals, scraping was observed in 85.7% of cases, ulceration (associated with edema) in 37.1%, and autotomy in 8.5%. These signs appeared a mean 5.7 weeks (range 1-12 weeks) after deafferentation. Thirteen rats benefited from an MDR; nine (69%) experienced a complete cure, that is, a total resolution of scraping or ulceration (a mean 4.6 weeks after MDR). In contrast, only one of 11 sham-operated animals showed signs of spontaneous recovery (p = 0.01). CONCLUSIONS: These results emphasize the role of the spinal dorsal horn in the genesis of deafferentation pain and suggest that dorsal horn deafferentation by cervical posterior rhizotomy in the rat provides a reliable model of chronic pain due to brachial plexus avulsion and its suppression by MDR.

Animals↗