In an fMRI study of DPD patients, emotionally aversive scenes activated the right ventral prefrontal cortex. Participants demonstrated a reduced neural response in emotion-sensitive regions, as well as an increased response in regions associated with emotional regulation. In a similar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as did healthy controls. In a test of skin conductance responses to unpleasant stimuli, the subjects showed a selective inhibitory mechanism on emotional processing.Studies are beginning to show that the temporoparietal junction has a role in multisensory integration, embodiment, and self-other distinction. Several studies analyzing brain MRI findings from DPDR patients found decreased cortical thickness in the right middle temporal gyrus, reduction in grey matter volume in the right caudate, thalamus, and occipital gyri, as well as lower white matter integrity in the left temporal and right temporoparietal regions. However, no structural changes in the amygdala were observed.A PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as in areas responsible for an integrated body schema.One study examining EEG readings found frontal alpha wave overactivation and increased theta activity waves in the temporal region of the left hemisphere. It is unclear whether genetics plays a role; however, there are many neurochemical and hormonal changes in individuals with depersonalization disorder. DPDR may be associated with dysregulation of the hypothalamic-pituitary-adrenal axis, the area of the brain involved in the "fight-or-flight" response. Patients demonstrate abnormal cortisol levels and basal activity.
Gangliosidosis contains different types of lipid storage disorders caused by the accumulation of lipids known as gangliosides. There are two distinct genetic causes of the disease. Both are autosomal recessive and affect males and females equally. Types
GM1 gangliosidoses - GM1
GM2 gangliosidoses - GM2

See also
Sphingolipidoses#Overview

References


== External links ==