This view of reality could not continue, in Fairbairns theory, if the four captives were able to access the fear, terror and, indeed, rage assumed to be held in their Antilibidinal Ego-Rejecting Object structures. The depth of their fear and rage at being abused, would clash with their split-off, opposite view of the hidden “goodness” in the captors. As mentioned, the splitting defense allows the user to see others as if they are two different people. This offers a second possible reason that the terrifying memories of events remain dissociated (in the Antilibidinal Ego-Rejecting Object structures in the unconscious). If one or more of the captives were able to experience these feelings directly (including the impotent rage), during the six days when they were held captive in the presence of the captors, they might have been killed for being disruptive and threatening. This ultimate terror, of being killed for experiencing the fear/rage and humiliation that is assumed to have been dissociated into the unconscious, may be the motivation that promotes the libidinal egos view of the two captors to continue, and simultaneously avoiding the enormously toxic memories of their six days in captivity. Thus, Fairbairns model offers a sound psychological explanation for attachment to abusers (Celani, 1995). Possible evolutionary explanations
Evolutionarily speaking, research evidence exists to support the genuine scientific nature of Stockholm syndrome. Responses similar to those in human captives have been detected in some reptiles and mammals, primates in particular.
Abuse of loxapine has been reported.The inhaled formulation of loxapine carries a low risk for a type of airway adverse reaction called bronchospasm that is not thought to occur when loxapine is taken by mouth. Pharmacology
Mechanism of action
Some authors say loxapine is a "mid-potency" typical antipsychotic. However, unlike most other typical antipsychotics, it has significant potency at the 5HT2A receptor (6.6 nM), which is similar to atypical antipsychotics like clozapine (5.35 nM). The higher likelihood of EPS with loxapine, compared to clozapine, may be due to its higher affinity for the D2 receptor compared to clozapine, which has one of the lowest binding affinities at the D2 receptor of any antipsychotic. Pharmacokinetics
Loxapine is metabolized to amoxapine, as well as its 8-hydroxy metabolite (8-hydroxyloxapine). Amoxapine is further metabolized to its 8-hydroxy metabolite (8-hydroxyamoxapine), which is also found in the blood of people taking loxapine. At steady-state after taking loxapine by mouth, the relative amounts of loxapine and its metabolites in the blood is as follows: 8-hydroxyloxapine > 8-hydroxyamoxapine > loxapine.The pharmacokinetics of loxapine change depending on how it is given. Intramuscular injections of loxapine lead to higher blood levels and area under the curve of loxapine than when it is taken by mouth. Chemistry
Loxapine is a dibenzoxazepine and is structurally very similar to clozapine, an atypical antipsychotic. References
External links
"Loxapine". Drug Information Portal. U.S. National Library of Medicine.