This denial of behaviour can be seen as a way to overcome anxiety and helplessness brought on by the stressful event that often precedes the syndrome.These aetiological debates focus on the main symptom of Ganser syndrome and its importance in its diagnosis. Approximate answers are prominent in the Ganser syndrome literature, causing concern in those who believe that this is a relatively simple symptom to feign.Ganser syndrome was regarded as an Adjustment Reaction of Adult Life in the DSM-II and later was moved under the category of Factitious Disorder with Psychological Symptoms in the DSM-III. Ganser syndrome can also be found under the Dissociative Disorder Not Otherwise Specified (DDNOS) section of the DSM-IV-TR, however it is not listed in the DSM-5, which got rid of the DDNOS section and replaced it with Other Specified Dissociative Disorder (OSDD) and Unspecified Dissociative Disorder (USDD). Despite this, the International Classification of Diseases has Ganser syndrome listed under dissociative disorders. See also
Paraphasia

References
Further reading
Schutzman, Mady (2003). "Being Approximate: The Ganser Syndrome and Beyond" (PDF). Journal of Medical Humanities. 24 (1/2): 147–158. doi:10.1023/A:1021318118143. S2CID 141323730. Retrieved 14 December 2010. == External links ==
Opioids and especially benzodiazepines also increase the risk of potentially lethal respiratory depression.Strong inhibitors of the liver enzyme CYP3A4, such as ketoconazole, moderately increase buprenorphine concentrations; CYP3A4 inducers can theoretically decrease concentrations of buprenorphine. Pharmacology
Mechanism of action
Buprenorphine binds strongly to opioid receptors and acts as a pain-reducing medication in the central nervous system (CNS). It binds to the μ-opioid receptor with high affinity, which produces the analgesic effects in the CNS. It is a partial μ-opioid receptor agonist and a weak κ-opioid receptor antagonist. As the dose of buprenorphine increases, its analgesic effects reach a plateau, and then it starts to act like an antagonist. As a partial agonist, buprenorphine binds and activates the opioid receptors, but has only partia  efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy. It is thus well-suited to treat opioid dependence, as it produces milder effects on the opioid receptor with lower dependence and habit-forming potential. Naloxone is a pure opioid antagonist that competes with opioid molecules in the CNS and prevents them from binding to the opioid receptors. Naloxones binding affinity is highest for the μ-opioid receptor, then the δ-opioid receptor, and lowest for the κ-opioid receptor. Naloxone has poor bioavailability, and is rapidly inactivated following oral administration. When injected, it exerts its full effects. The principle behind its function as a deterrent is as follows: when taken sublingually as prescribed, buprenorphines effects at the opioid receptor dominate, while naloxones effects are negligible due to the low oral absorption.