previous or current psychiatric conditions requiring medication or ECT. Some of these methodological problems were addressed in a study b y Vuilleumier and collea gues in 2001 (Vuilleumier et al 2001). SPECT studies were performed on seven right-handed patients with strictly unilateral loss of motor function (with or without associated sensory loss) who had no other psychiatric or medical conditions. Scans were repeated in a subset of patients, once their symptoms had resolved allowing them to act as their own controls (Vuilleumier et al 2001). This study was also unique in using controlled stimulation with passive vibration rather than actual movements to activate the sensorimotor cortex. Vibration is known to activate motor and sensory cortical areas via proprioceptive pathways (Seitz and Roland 1992). The authors argue that this may reduce confounding due to ambiguity of instructions, strategy, degree of effort, and “conflict reaction” seen when patients are asked to perform voluntary movements. The data obtained were analysed using both statistical parametric mapping and region-of- interest segmentation, comparing activation in 20 pre- defined anatomical regions. Both methods of analysis showed reduced blood flow in the contralateral thalamus, caudate, and putamen during passive vibration when patients were symptomatic compared with when their symptoms had resolved (Vuilleumier et al 2001). They also found that lower Table 2 Functional imaging studies of conversion disorder Neurobiology of conversion disorder activation in the contralateral caudate was a predictor of poor recovery. The authors comment that the basal ganglia and thalamus are strategically placed in neuronal circuits to modulate sensory and motor signals and thus may affect conscious sensory processing or willed action. This theory is supported by the observational studies of brain-injured patients with conversion disorder described above (Eames 1992), and is consistent with the proposed role of cortical– subcortical circuits in volition (Spence and Frith 1999). The caudate nucleus has direct limbic inputs from the amygdala and orbitofrontal cortex, suggesting a possible link with previous reports of increased orbitofrontal activation in conversion symptoms (Vuilleumier et al 2001). The authors hypothesize that emotional stressors act via limbic inputs from the orbitofrontal cortex and amygdala to modulate basal ganglia–thalamocortical circuits, leading to a selective deficit of willed action (Vuilleumier et al 2001). More recently, functional magnetic resonance imaging (fMRI) has been used to study the Blood Oxygenation Level Dependent (BOLD) response to sensory stimulation in four patients with nondermatomal somatosensory deficits (Mailis-Gagnon et al 2003). These patients met diagnostic criteria for conversion disorder but also had chronic pain in the affected limbs. Unperceived stimuli applied to the affected limb were associated with a different pattern of BOLD response to both innocuous and noxious stimuli, 5 7 4 5 2 Imaging modality SPECT PET Patients’ symptoms N Control condition L hemiparesis and 1 hemisensory loss L hemiparesis 1 Same patient when recovered Unaffected side Paradigm Stimulation of L median nerve Attempting to move SPECT Astasia–abasia Contralateral hemisphere Resting Perfusion changes associated with conversion symptoms ↑ R frontal cortex ↓ R parietal cortex ↓ R premotor and primary sensorimotor cortex ↑ R anterior cingulate cortex and R orbitofrontal cortex ↓ L temporal and parietal cortex Hemiparesis +/– sensory loss Nondermatomal somatosensory deficits Visual loss L arm weakness Same patients Passive vibration ↓ contralateral thalamus and striatum when recovered stimulation Unaffected limb Innocuous and ↑ rostral anterior cingulate cortex noxious stimulation ↓ thalamus, anterior cingulated (posterior region), ventrolateral prefrontal cortex, anterior insula Healthy controls Visual stimulation ↓ visual cortex ↑ L inferior frontal, L insula, L striatum, thalami, midbrain, L posterior cingulate Healthy controls Movement of joystick ↓ L DLPFC Authors Tiihonen et al 1995 Marshall et al 1997 Yazici and Kostakoglu 1998 Vuilleumier et al 2001 Mailis-Gagnon fMRI et al 2003 SPECT Werring et al 2004 Spence et al 2000 fMRI PET Abbreviations: DLPFC, dorsolateral prefrontal cortex; fMRI, functional magnetic resonance imaging; L, left; PET, positron emission tomography; SPECT, single-photon emission computed tomography; R, right. Neuropsychiatric Disease and Treatment 2006:2(1) 17