With ideas like primary and secondary gain, and the posited relationship between the development of symptoms and the presence of some external stressor, conversion disorder has long been viewed as the quintessential psychological disorder. Psychosocial causes were deemed more important than cerebral causes, a theory that was bolstered by long-held, increasingly outmoded notions of a functional–organic divide. Advances in neuroscience are slowly changing this view, but the challenge is considerable given the heterogeneity of clinical expression, frequent presence of comorbidities such as anxiety and depressive disorders and the role of psychosocial stressors as putative precipitating factors and, at times, perpetuating factors.
There is a paucity of data from structural imaging of the brains of people with conversion disorder. One study showed reduced volumes of the right and left basal ganglia and right thalamus relative to people without the disorder.17
Emerging literature on the functional imaging of the brain is more informative. Sample sizes are modest (single case studies predominate), experimental paradigms differ, and participants, mostly female and young to middle-aged, vary in their presentation (sensory, motor or mixed sensory and motor symptoms). Despite these limitations, however, some consistent results are being seen.
In a study of unilateral sensory loss thought to be a conversion symptom, patients had a vibratory stimulus applied first to their sensate region, then to their anesthetic side. Data from a functional MRI study showed contralateral somatosensory activation when the stimulus was applied to the sensate region, as expected, but no such activation when the stimulus was applied to the anesthetic side ().18
Instead, the stimulus applied to the anaesthetic side activated regions in the patients’ orbitofrontal and anterior cingulate regions. Similar results, including anciliary activation in the basal ganglia, have emerged from other studies using functional MRI and single-photon emission computed tomography (SPECT) scans to investigate motor conversion symptoms.19,20
The association between conversion symptoms and activity in the orbitofrontal and cingulate regions is informative because these regions are important components of the neural networks regulating emotion and the expression of that emotion, i.e., a person’s affect.
Figure 1: Functional magnetic resonance image showing somatosensory activity evoked by stimulation in a patient with sensory conversion disorder affecting the left hand. When the patient’s left hand was stimulated, no activity was seen in the primary somatosensory (more ...)
These results suggest that patients with conversion disorder have an abnormal pattern of cerebral activation in which limbic areas (or areas richly connected to the limbic system) override the activation of the motor and sensory cortices. Precisely how this happens is unclear, but one theory holds that specific regions of the cingulate cortex may function in a mutually exclusive way. A mechanism called “reciprocal inhibition” allows each region to shut off the other during the processing of information. This is relevant to conversion disorder in that the caudal segment, responsible for willed action, may be deactivated or suppressed by the pregenual anterior cingulate cortex as it processes intense emotion.21
Patients with repressed (unwanted) emotional memories (what the DSM terms dissociative amnesia) have a functional MRI pattern of regional cerebral deactivation and ancillary activation that complements the data on conversion disorder. Neural activity in the hippocampus (a repository of memories) is suppressed by activation in a network rich in frontal (i.e., dorsolateral and ventrolateral prefrontal cortices and the anterior cingulate gyrus) connectivity.22
It is to be expected that regional brain specificity would differ between the data from functional MRI studies of patients with conversion disorder and patients with dissociative amnesia, given the differences in phenomenology. Of greater importance is that, in both conditions, the discrete neural networks involved in processing emotion and executive control can suppress regions associated with a plethora of other functions (e.g., motor, sensory, memory, vision). This bolsters the validity of the construct underpinning how atypical symptoms, irrespective of their phenotype, may arise. These explanations do not necessarily refute current psychological theories as outlined by the DSM-IV. Rather, they provide a complementary cerebral model to account for the development of symptoms using the notion of primary gain. What the imaging data cannot answer, however, is why a particular symptom manifests.
At present, functional MRI technology remains largely experimental and is not yet used in routine clinical practice. In time, this is likely to change.