There is also the Dissociative Disorders Interview Schedule (DDSI), which lacks substantive clarity for differential diagnostics.Peritraumatic dissociation is measured through the Peritraumatic Dissociative Scale. Etiology
Neurobiological mechanism
Preliminary research suggests that dissociation-inducing events, drugs like ketamine, and seizures generate slow rhythmic activity (1–3 Hz) in layer 5 neurons of the posteromedial cortex in humans (retrosplenial cortex in mice). These slow oscillations disconnect other brain regions from interacting with the posteromedial cortex, which may explain the overall experience of dissociation. Trauma
Dissociation has been described as one of a constellation of symptoms experienced by some victims of multiple forms of childhood trauma, including physical, psychological, and sexual abuse. This is supported by studies which suggest that dissociation is correlated with a history of trauma.Dissociation appears to have a high specificity and a low sensitivity to having a self-reported history of trauma, which means that dissociation is much more common among those who are traumatized, yet at the same time there are many people who have suffered from trauma but who do not show dissociative symptoms.Adult dissociation when combined with a history of child abuse and otherwise interpersonal violence-related posttraumatic stress disorder has been shown to contribute to disturbances in parenting behavior, such as exposure of young children to violent media. Such behavior may contribute to cycles of familial violence and trauma.Symptoms of dissociation resulting from trauma may include depersonalization, psychological numbing, disengagement, or amnesia regarding the events of the abuse.
FASPS is the first disorder to link known core clock genes directly with human circadian sleep disorders. As the PER2 mutation is not exclusively responsible for causing FASPS, current research has continued to evaluate cases in order to identify new mutations that contribute to the disorder. Mechanisms (Per2 and CK1)
Two years after reporting the finding of FASPS, Ptáčeks and Fus groups published results of genetic sequencing analysis on a family with FASPS. They genetically mapped the FASPS locus to chromosome 2q where very little human genome sequencing was then available. Thus, they identified and sequenced all the genes in the critical interval. One of these was Period2 (Per2) which is a mammalian gene sufficient for the maintenance of circadian rhythms. Sequencing of the hPer2 gene (h denoting a human strain, as opposed to Drosophila or mouse strains) revealed a serine-to-glycine point mutation in the Casein Kinase I (CK1) binding domain of the hPER2 protein that resulted in hypophosphorylation of hPER2 in vitro. The hypophosphorylation of hPER2 disrupts the transcription-translation (negative) feedback loop (TTFL) required for regulating the stable production of hPER2 protein. In a wildtype individual, Per2 mRNA is transcribed and translated to form a PER2 protein. Large concentrations of PER2 protein inhibits further transcription of Per2 mRNA. CK1 regulates PER2 levels by binding to a CK1 binding site on the protein, allowing for phosphorylation which marks the protein for degradation, reducing protein levels. Once proteins become phosphorylated, PER2 levels decrease again, and Per2 mRNA transcription can resume.