Conclusions Conversion disorders are common and cause considerable morbidity but, despite attracting ongoing controversy and theoretical interest, there has been relatively little empirical research in this field. Early neuropsychiatric studies of conversion symptoms focusing on the apparent importance of laterality and patients with brain lesions failed to produce consistent findings. Neurophysiological studies have suggested that conversion disorder results from changes in higher-order cortical processing. The development of functional neuroimaging has provided a new paradigm with which to study the neural basis of conversion, but the few studies to date have often been limited by small sample sizes and significant methodological issues, and there have been some inconsistencies in their findings. At present the evidence available suggests a broad hypothesis that frontal cortical and limbic activation associated with emotional stress may act via inhibitory basal ganglia–thalamocortical circuits to produce a deficit of conscious sensory or motor processing. Functional imaging and neurophysiological evidence to support the distinction between conversion and factitious disorders is limited. Difficulties with classification and terminology continue to hamper research in this area. The place of conversion disorder in psychiatric classification depends on its presumed unconscious psychological mechanism and so necessarily relies on clinicians’ judgments which may be subjective and difficult to validate (Broome 2004). This has led some authors to question the usefulness of a distinction between conversion and factitious disorders (Austen and Lynch 2004; Shapiro and Teasell 2004). However, we would argue that there is an important difference in phenomenology between these two disorders. Current theories of con- sciousness suggest a continuum of awareness of intentions or perceptions that may fluctuate over time (Zeman 2001). We would suggest that the functional anatomical basis of symptoms is likely to differ between patients with different levels of awareness and that this is an important area to study. To use functional imaging more effectively to understand the psychopathology of conversion disorder, we first need a clear cognitive model of the information processing deficits that underlie these symptoms. At present, our understanding of the “neural correlate of consciousness” is limited, making it harder to propose cognitive models of “unconscious” processes. Studies of the visual system have so far provided the best understanding of the neural basis of awareness. Neuropsychiatric Disease and Treatment 2006:2(1) Neurobiology of conversion disorder Blindsight and visual neglect, like hysterical blindness, are both characterized by reduced awareness of visual stimuli with preservation of some aspects of visual processing. Indeed, the one functional imaging study of hysterical blindness found activations in very similar areas to those previously reported in blindsight (Werring et al 2004). Comparisons between these syndromes may provide useful insights into relevant cognitive processes and suggest hypotheses about brain regions which may be important in conversion symptoms. Studies with larger numbers of patients and better attempts to control for confounders are needed to further test these hypotheses. Despite increasingly sophisticated study designs and imaging techniques, conceptual problems may continue to limit progress in this area. However, by beginning to understand the neurobiology of conversion disorder we may gain valuable insights into the cognitive processes involved in attention and volition and reduce some of the controversy and stigma associated with this common condition. References Andy OJ. 1973. Successful treatment of long-standing hysterical pain and visceral disturbances by unilateral anterior thalamotomy. Case report. J Neurosurg, 39:252–4. [APA] American Psychiatric Association. 1994. Diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: American Psychiatric Association. Austen S, Lynch C. 2004. Non-organic hearing loss redefined: understanding, categorizing and managing non-organic behaviour. Int J Audiol, 43:449–57. Axelrod S, Noonan M, Atanacio B. 1980. On the laterality of psychogenic somatic symptoms. J Nerv Ment Dis, 168:517–25. Briquet P. 1859. Traite clinique et therapeutique de l’Hysterie. Paris: J. B. Balliere. Broome MR. 2004. A neuroscience of hysteria? Curr Opin Psychiatry, 17:465–9. Carson AJ, Best S, Postma K, et al. 2003. The outcome of neurology outpatients with medically unexplained symptoms: a prospective cohort study. J Neurol Neurosurg Psychiatry, 74:897–900. Couprie W, Wijdicks EF, Rooijmans HG, et al. 1995. Outcome in conversion disorder: a follow up study. J Neurol Neurosurg Psychiatry, 58:750–2. Crimlisk HL, Bhatia K, Cope H, et al. 1998. Slater revisited: 6 year follow up study of patients with medically unexplained motor symptoms. BMJ, 316:582–6. Devinsky O, Mesad S, Alper K. 2001. Nondominant hemisphere lesions and conversion nonepileptic seizures. J Neuropsychiatry Clin Neurosci, 13:367–73. Drake ME Jr. 1993. Conversion hysteria and dominant hemisphere lesions. Psychosomatics, 34:524–30. Driver J, Mattingley JB 1998. Parietal neglect and visual awareness. Nat Neurosci, 1:17–22. Eames P. 1992. Hysteria following brain injury. J Neurol Neurosurg Psychiatry, 55:1046–53. Freud S, Breuer J. 1978. Studies in hysteria. Harmonsworth, UK: Penguin. 19