Abnormal cerebral activation in conversion disorder


REPORT FROM THE AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING, PHILADELPHIA PA, APRIL 26-MAY 3, 2014 – Conversion disorder, or the development of neurological symptoms originating in psychological factors, has undergone a shift in recent years, with neurologists playing a larger role in what was once the exclusive domain of psychiatrists.

When characterized as hysterical neurosis, the emphasis was on the psychogenic basis of symptoms. However, in the current iteration of the Diagnostic and Statistical Manual (DSM-5), the importance of changes in the functioning of the nervous system has been underlined. Thus, Conversion Disorder may also be considered as a Functional Neurological Symptom Disorder in DSM-V, and a critical component of diagnosis is a neurological exam that excludes organic signs and identifies positive signs of a functional disorder. One challenge, however, is that there are numerous clinical signs for functional neurological symptoms, but few of these have been validated (for a systematic review see Daum et al. J Neurol Neurosurg Psychiatry 2014;85:180-190).

A number of functional neuroimaging studies (EEG, fMRI, SPECT, PET) have examined the possible neuroanatomical correlates of conversion symptoms. Most recently, a Canadian fMRI study has investigated 10 female patients (mean age 41 years) with unilateral sensory conversion disorder (Burke et al. AAN 2014; abstract P2.158). Three of 10 patients had clinical depression (with one diagnosed with comorbid PTSD). Subjects received a series of  vibrotactile stimuli (4 seconds followed by a 26-second rest period, repeated 10 times). Overall, 10 areas showed significantly greater activation when stimulation was applied to the anesthetic compared to the contralateral sensate area. The areas were categorized as the limbic cortex (right insula, right anterior cingulate), the cortico-striato-thalamic loop (right superior frontal gyrus, right and left middle frontal gyri, right caudate, right ventral-anterior thalamus) and the attentional centres (right inferior parietal lobule, right and left angular gyri). In contrast to limbic activation, there was a noteworthy reduction in sensory cortex activity. Thus, sensory conversion symptoms appeared to be associated with specific patterns of abnormal cerebral activation that implicated emotional and attentional processing.

It has been suggested that abnormalities in attentional processing may exclude sensory symptoms from consciousness. However, Vuilleumier has downplayed this view, noting that affective or stress-related factors may activate primitive pathways of protection and alertness that are not fully within consciousness, but which may be modulated by limbic and sensory network interactions (Vuilleumier P. Prog Brain Res 2005;150:309-329; Vuillemer et al. Brain 2001;124[Pt 6]:1077-1090).

It is important to note that symptoms of sensory and motor conversion disorder are treatable. The keys to management are a thorough neurological work-up and an appropriately non-judgmental approach with patients when discussing the diagnosis and the available therapeutic options.

Guest Reviewer: Dr. Daniel Selchen, Head of Neurology, St. Michael’s Hospital, Toronto, Canada

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