Neural Correlates of Recall of Life Events in Conversion Disorder

Section of Cognitive Neuropsychiatry, Institute of Psychiatry, King's College London, London, England.
JAMA Psychiatry (Impact Factor: 12.01). 11/2013; 71(1). DOI: 10.1001/jamapsychiatry.2013.2842
Source: PubMed

ABSTRACT IMPORTANCE Freud argued that in conversion disorder (CD) the affect attached to stressful memories is "repressed" and "converted" into physical symptoms, although this has never been subject to scientific study to our knowledge. OBJECTIVE To examine the neural correlates of recall of life events judged to be of causal significance in CD. DESIGN, SETTING, AND PARTICIPANTS Case-control study. Academic research setting among 12 patients with motor CD and 13 healthy control subjects. MAIN OUTCOMES AND MEASURES Stressful life events were assessed using the Life Events and Difficulties Schedule and rated by a blinded panel for their likelihood to cause CD based on the threat posed and the extent to which subsequent illness might allow escape from some of their consequences (termed escape). Recall of those events (escape condition) was compared with recall of equally threatening control events from the same epoch (severe condition) in a functional magnetic resonance imaging task. RESULTS Relative to controls, patients showed significantly increased left dorsolateral prefrontal cortex and decreased left hippocampus activity during the escape vs severe condition, accompanied by increased right supplementary motor area and temporoparietal junction activity. Relative to controls, patients failed to activate the right inferior frontal cortex during both conditions, and connectivity between amygdala and motor areas (supplementary motor area and cerebellum) was enhanced. CONCLUSIONS AND RELEVANCE These data offer support for the notion that the way adverse events are processed cognitively can be associated with physical symptoms in CD. Abnormal emotion (dorsolateral prefrontal cortex and right inferior frontal cortex) and memory control (hippocampus) are associated with alterations in symptom-related motor planning and body schema (supplementary motor area and temporoparietal junction).

Download full-text


Available from: Owen Gareth O'Daly, Jan 16, 2014
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Previous functional neuroimaging studies investigating the neuroanatomy of conversion disorder have yielded inconsistent results that may be attributed to small sample sizes and disparate methodologies. The objective of this study was to better define the functional neuroanatomical correlates of conversion disorder. Methods Ten subjects meeting clinical criteria for unilateral sensory conversion disorder underwent fMRI during which a vibrotactile stimulus was applied to anesthetic and sensate areas. A block design was used with 4 s of stimulation followed by 26 s of rest, the pattern repeated 10 times. Event-related group averages of the BOLD response were compared between conditions. Results All subjects were right-handed females, with a mean age of 41. Group analyses revealed 10 areas that had significantly greater activation (p < .05) when stimulation was applied to the anesthetic body part compared to the contralateral sensate mirror region. They included right paralimbic cortices (anterior cingulate cortex and insula), right temporoparietal junction (angular gyrus and inferior parietal lobule), bilateral dorsolateral prefrontal cortex (middle frontal gyri), right orbital frontal cortex (superior frontal gyrus), right caudate, right ventral-anterior thalamus and left angular gyrus. There was a trend for activation of the somatosensory cortex contralateral to the anesthetic region to be decreased relative to the sensate side. Conclusions Sensory conversion symptoms are associated with a pattern of abnormal cerebral activation comprising neural networks implicated in emotional processing and sensory integration. Further study of the roles and potential interplay of these networks may provide a basis for an underlying psychobiological mechanism of conversion disorder.
    12/2014; 6. DOI:10.1016/j.nicl.2014.09.016
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Previous neuroimaging studies link both alcohol use disorder (AUD) and early adversity to neurobiological differences in the adult brain. However, the association between AUD and childhood adversity and effects on the developing adolescent brain are less clear, due in part to the confound of psychiatric comorbidity. Here we examine early life adversity and its association with brain volume in a unique sample of 116 South African adolescents (aged 12-16) with AUD but without psychiatric comorbidity. Participants were 58 adolescents with DSM-IV alcohol dependence and with no other psychiatric comorbidities, and 58 age-, gender- and protocol-matched light/non-drinking controls (HC). Assessments included the Childhood Trauma Questionnaire (CTQ). MR images were acquired on a 3T Siemens Magnetom Allegra scanner. Volumes of global and regional structures were estimated using SPM8 Voxel Based Morphometry (VBM), with analysis of covariance (ANCOVA) and regression analyses. In whole brain ANCOVA analyses, a main effect of group when examining the AUD effect after covarying out CTQ was observed on brain volume in bilateral superior temporal gyrus. Subsequent regression analyses to examine how childhood trauma scores are linked to brain volumes in the total cohort revealed a negative correlation in the left hippocampus and right precentral gyrus. Furthermore, bilateral (but most significantly left) hippocampal volume was negatively associated with sub-scores on the CTQ in the total cohort. These findings support our view that some alterations found in brain volumes in studies of adolescent AUD may reflect the impact of confounding factors such as psychiatric comorbidity rather than the effects of alcohol per se. In particular, early life adversity may influence the developing adolescent brain in specific brain regions, such as the hippocampus.
    Metabolic Brain Disease 02/2014; 29(2). DOI:10.1007/s11011-014-9489-4 · 2.40 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: There are multiple definitions of stress. For this review, as a reference point, we will use the concept of acute emotional/psychosocial stress ("stress"). The presence of acute stress has been reported to have a significant effect on seizure control, with several studies showing patients with seizure disorders being able to predict with reasonable accuracy seizure occurrence within the following hours or days. However, neuroimaging investigations of the pathophysiological mechanisms underlying stress reactivity (e.g., hypothalamic-pituitary-adrenal (HPA) axis activation) in humans, in general, and in patients with seizure disorders, in particular, are scarce. The reasons for this are multiple and likely include difficulty with designing appropriate probes that test various aspects of stress response, obtaining approval for studies that induce stress in patients who are prone to having stress-induced seizures, difficulties with assessing the physiological response to stress inside the scanner (e.g., heart rate, respiratory rate, oxygenation, cortisol levels, and galvanic skin responses), participant identification, and choice of epilepsy syndrome for investigation. With the recent explosion of neuroimaging literature focusing on correlating stress of various types and levels with cortical activations in healthy and diseased populations, it is incumbent upon us to examine the available neuroimaging data in patients with seizure disorders in order to identify the existing gaps and the needs/directions for future investigations. This approach is consistent with the goals of several of the 2014 Benchmarks for Epilepsy Research for the National Institute of Neurological Disorders and Stroke and the American Epilepsy Society.
    Epilepsy & Behavior 04/2014; 35C:19-25. DOI:10.1016/j.yebeh.2014.03.023 · 2.06 Impact Factor
Show more