Psychoeducation involves counseling regarding the disorder, reassurance, and emphasis on DPDR as a perceptual disturbance rather than a true physical experience. Clinical pharmacotherapy research continues to explore a number of possible options, including selective serotonin reuptake inhibitors (SSRI), benzodiazepines, stimulants and opioid antagonists (ex: naltrexone). Cognitive behavioral therapy
An open study of cognitive behavioral therapy has aimed to help patients reinterpret their symptoms in a nonthreatening way, leading to an improvement on several standardized measures. A standardized treatment for DPD based on cognitive behavioral principles was published in the Netherlands in 2011. Medications
Neither antidepressants nor antipsychotics have been found to be useful; additionally, antipsychotics can worsen symptoms of depersonalisation. Tentative evidence supports use of naloxone and naltrexone, as well as gabapentin.A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.Modafinil used alone has been reported to be effective in a subgroup of individuals with depersonalization disorder (those who have attentional impairments, under-arousal and hypersomnia). However, clinical trials have not been conducted. Repetitive transcranial magnetic stimulation (rTMS)
Some studies have found repetitive transcranial magnetic stimulation (rTMS) to be helpful. One study examined 12 patients with DPD that were treated with right temporoparietal junction (TPJ) rTMS and found that 50% showed improvement after three weeks of treatment. Five of the participants received an additional three weeks of treatment and reported overall a 68% improvement in their symptoms. Treating patients with rTMS specifically at the TPJ may be an alternative treatment.
A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as a result of the inactivity of the AChE enzyme, which normally breaks down acetylcholine. Symptoms and diagnosis
As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils). This crisis may be masked by the concomitant use of atropine along with cholinesterase inhibitor medication in order to prevent side effects. Flaccid paralysis resulting from cholinergic crisis can be distinguished from myasthenia gravis by the use of the drug edrophonium (Tensilon), as it only worsens the paralysis caused by cholinergic crisis but strengthens the muscle response in the case of myasthenia gravis. (Edrophonium is a cholinesterase inhibitor, hence increases the concentration of acetylcholine present).