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Folie en Famille: A Case Report of Shared Delusory Parasitosis
- A. Al Siaghy, Y. Zoghbi, M. Azeem
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, p. S779
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- Article
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Introduction
Delusional parasitosis, first documented in 1946, is a rare psychiatric illness described as both a stand-alone diagnosis, as well as a secondary condition to an underlying psychiatric or medical pathology, or substance use. Interestingly, the fixed false belief of being infested has also been identified in partners of individuals with the disease, and in some cases the delusion permeated families and was thus given the name “folie en famille”.
ObjectivesTo describe the first reported case of delusional disorder, somatic type, with similar delusional symptoms in the patient’s husband, in the State of Qatar.
MethodsPatient and her husband were interviewed. Her file was reviewed for past history and medications.
Results34-year-old female with no past psychiatric history, 5 months post-partum, reported fixed beliefs of insect infestation in her baby’s skin, hers, and her husband’s, of 2 months duration. She reports a pruritic rash, and perceives proliferating insects in different life stages. The family relocated 5 times in 2 months. They bathe in vinegar several times a day to exterminate the insects. Husband mirrors her account of infestation with milder symptoms. Repeated medical investigations were insignificant. OCD, mood disorder, and other psychotic illnesses were ruled out.
ConclusionsDelusional parasitosis presents a unique therapeutic challenge to psychiatrists. It is necessary to build rapport with patients, rule out comorbidities, and conduct randomized controlled trials to evaluate the effectiveness of psychotropic drugs in its treatment. In cases of shared delusions, identifying the primary patient is crucial for treatment of all the individuals that share the delusion.
DisclosureNo significant relationships.
117 - The hereditary ataxias
- from PART XVI - DEGENERATIVE DISORDERS
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- By Puneet Opal, Department of Pediatrics and Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX, USA, Huda Y. Zoghbi, Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA
- Edited by Arthur K. Asbury, University of Pennsylvania School of Medicine, Guy M. McKhann, The Johns Hopkins University School of Medicine, W. Ian McDonald, University College London, Peter J. Goadsby, University College London, Justin C. McArthur, The Johns Hopkins University School of Medicine
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- Book:
- Diseases of the Nervous System
- Published online:
- 05 August 2016
- Print publication:
- 11 November 2002, pp 1880-1895
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Summary
The hereditary ataxias are a group of disorders characterized by motor incoordination resulting from dysfunction of the cerebellum and its connections. Although these diseases are easily recognizable due to the obvious cerebellar dysfunction, distinguishing among them is no easy matter. On the one hand, there is a great deal of clinical overlap between genetically heterogeneous diseases; on the other, the manifestations of any given genetic ataxia are protean. Today, although we as clinicians might wish to believe otherwise, we feel forced to conclude that in most instances, once a general diagnosis of hereditary ataxia has been made, determining the specific type relies more on genetic testing than on clinical criteria. Genetic testing, because of its specificity, is a powerful tool; if positive, the diagnosis is irrefutable. This might suggest that the role of the neurologist has been circumscribed, but this is really not the case. Rather, we must take on new responsibilities. Not only must we become familiar with the scientific, ethical, and statistical implications of genetic testing, but we must also learn how best to counsel our patients, an activity previously limited to geneticists in tertiary health-care centres.
The hereditary ataxias fall into two main classes. The first group of ataxias result from enzyme defects and can be either intermittent (e.g. when caused by defects in intermediary metabolism) or chronic (e.g. ataxia telangiectasia, caused by deficiency in DNA repair). These ataxias are inherited in an autosomal recessive or X-linked manner and are typically present in childhood. The second group, consisting of the progressive degenerative ataxias, do not appear to be caused by catalytic abnormalities. They can be further divided based on the mode of inheritance: the autosomal recessive ataxias, of which Friedreich's ataxia is by far the most common; the relatively large group of autosomal dominant inherited ataxias; the rare X-linked ataxias; and, finally, those resulting from defects in mitochondrial function. In this chapter we discuss the genetics of hereditary ataxias within this broad framework, focusing on the chronic degenerative ataxias and their differential diagnosis.
Ataxias resulting from specific enzyme defects: the metabolic ataxias
This heterogenous group of ataxias are best viewed as a subset of inborn errors of metabolism. The cerebellar dysfunction stems from specific enzyme defects that result in either toxic by-products or a deficiency in metabolites that affect neuronal function.
26 - Spinocerebellar ataxia type 1
- from PART VIII - DOMINANTLY INHERITED PROGRESSIVE ATAXIAS
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- By Xi Lin, Departments of Pediatrics, Neurology, Neuroscience, and Molecular and Human Genetics, Howard Hughes Medical Institute, Baylor College ofMedicine, Houston, Texas, USA, Harry T. Orr, Institute of Human Genetics, University of Minnesota, Minneapolis, USA, Huda Y. Zoghbi, Departments of Pediatrics, Neurology, Neuroscience, and Molecular and Human Genetics, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas, USA
- Edited by Mario-Ubaldo Manto, University of Brussels, Massimo Pandolfo, Université de Montréal
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- Book:
- The Cerebellum and its Disorders
- Published online:
- 06 July 2010
- Print publication:
- 15 November 2001, pp 409-418
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Summary
Introduction
Spinocerebellar ataxia type 1 (SCA1) is one of a complex group of autosomal dominant ataxias, which were first recognized as distinct from the recessive Friedreich's ataxia in 1893 by Marie. The clinicopathological presentations of these ataxias are extremely heterogeneous, with variable degrees of neurodegeneration in the cerebellum, spinal tracts, and brainstem. Thus, the classification of SCAs remained difficult and controversial until the 1990s, when the identification of distinct genes for several dominant ataxias allowed unequivocal genetic, if not clinical, differentiation (Orr and Zoghbi, 1996). SCA1 was one of the first neurogenetic diseases to be mapped to an autosome using classical linkage studies (Yakura et al., 1974; Jackson et al., 1977). The cloning of the SCA1 gene, the elucidation of a dynamic CAG trinucleotide repeat expansion as the mutational mechanism, and the establishment of cellular and animal models for this disorder have greatly advanced our understanding of the molecular and cellular mechanisms underlying SCA1 pathogenesis. These studies will undoubtedly provide the basis for developing effective therapeutics.
Clinical features
SCA1 usually strikes during the third or fourth decade of life, typically progressing over 10 to 15 years. In SCA1 families, the affected individuals in successive generations tend to have an earlier onset and more severe manifestations of the disease, a phenomenom referred to as anticipitation. Early onset in the first decade has been documented in such families (Schut, 1950; Zoghbi et al., 1988). The most salient clinical features of SCA1 include ataxia, dysarthria, and bulbar palsies. Other neurological abnormalities, such as extrapyramidal signs and peripheral neuropathy, often show extensive interfamilial and intrafamilial variability (Subramony and Vig, 1998; Zoghbi and Orr, 2000).