Neurologists' understanding and management of conversion disorder

Abstract

BackgroundConversion disorder is largely managed by neurologists, for whom it presents great challenges to understanding and management. This study aimed to quantify these challenges, examining how neurologists understand conversion disorder, and what they tell their patients.MethodsA postal survey of all consultant neurologists in the UK registered with the Association of British Neurologists.Results349 of 591 practising consultant neurologists completed the survey. They saw conversion disorder commonly. While they endorsed psychological models for conversion, they diagnosed it according to features of the clinical presentation, most importantly inconsistency and abnormal illness behaviour. Most of the respondents saw feigning as entangled with conversion disorder, with a minority seeing one as a variant of the other. They were quite willing to discuss psychological factors as long as the patient was receptive but were generally unwilling to discuss feigning even though they saw it as their responsibility. Those who favoured models in terms of feigning were older, while younger, female neurologists preferred psychological models, believed conversion would one day be understood neurologically and found communicating with their conversion patients easier than it had been in the past.DiscussionNeurologists accept psychological models for conversion disorder but do not employ them in their diagnosis; they do not see conversion as clearly different from feigning. This may be changing as younger, female neurologists endorse psychological views more clearly and find it easier to discuss with their patients.

MELAS syndrome mimicking somatoform disorder

“…Not only the physicians, but also the patient, failed to seek further investigation, which could be considered as 'belle indifference' and might have contributed to the later misdiagnosis of somatoform disorder. The diagnostic categories of somatoform disorders are being radically reviewed for the DSM-V [7] to make them more reliable [6,[8][9][10][11][12], as there is currently a great heterogeneity in how physicians identify and manage this patient population [13]. Current descriptive features such as the symptoms' relatedness to psychological factors [14] and the presence of 'la belle indifference' [15] have been challenged based on systematic reviews and should be weighted accordingly in the diagnostic process.…”

Conversion disorder: A systematic review of current terminology

“…The absence of the views of psychiatrists is lamentable, though perhaps understandable given their perceived absence from the diagnostic process (25,26). Nevertheless, Conversion…”

What do neurologists think about conversion disorder?

“…3 Given that 89% of patients with the 'classical phenotype' (including walking onset before the age of age 15 months) and motor conduction velocities of 15-35 m/s had CMT1A, the authors propose initial test ing only for PMP22 duplication in these cases. In patients with severely slowed motor conduction velocity (<15 m/s), the authors sug gest beginning by testing for the PMP22 duplication or mutation in MPZ, although delayed walking is characteristic of patients with MPZ mutation.…”

“…The paper by Saporta et al also con tributes to the accurate determination of genetic testing hit rates and methods for tar geted testing, with positive results ranging between 80% for PMP22 and 13% for MFN2. 3 Further more, the authors designed useful diag nostic algorithms starting from pheno typic data and physiology, which further improved their ability to predict an accurate genetic diagnosis. Molecular diagnosis and classification of CMT may be orient ed from a simple flow chart, as illustrated in Figure 1.…”

“…3 Genetic testing for CMT4 or ARCMT2 should be guided by the genetic epidemiology of each region, as discussed above. Although current clas sification of intermediate CMT (DICMT) includes three subtypes, DICMT1A (unknown muta tion), DICMTB (DNM2 mutation) and DICMTC (YARS muta tion), 4 I entirely agree with Saporta et al that mutations in GJB1 or MPZ are the most common causes of intermediate CMT 3 and, therefore, appear as such in Figure 1.…”