Evidence-based practice
April 10, 2005

I am following the postings on EBP with great interest (it took me time to read many of them). I would like to share some thoughts on this subject. First, evidence-based treatment/practice (EBP) must be counterbalanced with practice-based evidence (PBE). I am fully aware that many of my long-term patients (and I continue to see many persons with severe psychosis in my private practice-it is eminently worthwhile work and doable) would not emerge as recovered on standard indices of recovery in outcome studies. However, for this work we also need to include quality of life measures. For example, one of my patients can now walk wherever she wishes, take the New York City subway without obsessing that she will push someone in front of a train or bus (she is also receiving work training and has reduced her complicated polypsychopharmacological regimen).

Another can express his envious feelings towards me without running to numb painful feelings of worthlessness, helplessness, powerlessness, and envy of others with crack. One other can occasionally make emotional contact within a steady stream of grandiose and persecutory delusions which serve many functions for him, including foreclosure of emotional contact. Many never have had to return to state or community hospitals. Suicidal episodes are reduced. Several engage in meaningful volunteer work.

As to RCT (randomized control trials-the 'gold standard' of research-perhaps more suited to psychopharmacology), I side with the criticisms of Yrjö Alanen put forth in his many publications on need-adaptive treatment. See the following volume for details:

Alanen, Y. O. (1997). Schizophrenia: Its Origins and Need-Adapted Treatment. London : Karnac Books.

While in Stavanger , Norway Alanen told me that many of their patients were not exposed to neuroleptics or to high dosages due to psychotherapeutic interventions. As Luc Ciompi theorized long ago in his theory of Affect-Logic, the psychopharmacological agents, when they work, probably do so by reducing LHPA activity (limbic-hypothalamic-pituitary-adrenal axis)-as well as intracellular signal transduction (which from my way of thinking, may be more effectively modified if the essential factors generating such elevated LHPA arousal are understood and addressed within the constraints of evolutionarily conserved processes, e.g., maintaining whatever degree of emotional contact can be tolerated and 'taken in' at the present moment-working through the dual polar terrors of separation and intrusion anxieties and the hostilities such deep threats to the intactness of the self engenders-within the transferences and countertransferences emergent in a relatively safe and containing holding environment).

Brian Koehler PhD
New York University Postdoctoral Program