Samuel Gershon’s comments on Ronald Pies’ “Do antipsychotics thin the brain?”
Journal of Clinical Psychopharmacology 2018; 38 (3): 167- 9.
This is a thoughtful and carefully presented paper and, in my view,poses a question that has been asked many times and put aside. In the 1970-80s Earl Usdin,one of the administrators at the USNational Institute of Mental Health (NIMH),funded some studies in primatesfocussing on this question.He died (1984) during this project and I do not remember seeing any publicationsabout his work.I thought that so many years after the introduction of these drugs in massive amounts we should have more information about this phenomenon.
This question has been present as a shadow for the past 70 years.It has come back to haunt us many times with the appearance of pathological neurological effects, such as Parkinson’s Syndrome, which we went ahead and medicated with antiparkinsonianmedication, but often continued with the offending antipsychotic agent. I am sure some clinicians did scratch their head and question, subtly, is this going to be OK? We also saw acute dystonic reactions, akathisia, brain malignant syndrome and the drastic tardive dyskinesia. So, we were all aware that the brain was having a bad time every now and again.
I myself had these thoughts repeatedly and kept on asking people about this as possible hidden damage to the brain and its functions. Most people shook it off and felt symptoms were being treated by these anticholinergic drugs.
So, now we have some additional urgency becausemany people are proposing early treatment intervention for children and adolescents with the real concern being,for example, can you make a reliable diagnosis of, say Bipolar Disorder, in young children and adolescents and then expose them to compounds like these over which still hangs this unresolved question of “thin brain”?
These questions bring us back again and again to diagnostic questions about some of our psychiatric disorders. Manic depressive disorder as a diagnostic issue can be difficult and complex in the adult, but in a developing teenager or adolescent the alterations over time in this age group can present a changing picture and thus the introduction of medication at one phase may have to be revised and with it the “medication plan” whichoffers the introduction of several different medications to this still developing individual.
Another diagnostic label that can cause questions is schizoaffective disorder;the label almost invites the presentation of multiple medications at the outset. The practicalities of clinical care raise another common practice that is: if treatment A is either not effective or only minimally so and then often drug B is added to A this practice of poly pharmacy becomes more common in busy out-patient care. Thus, multiple drug exposures are more common and obviously the possibility of increased neurotoxicity.
It appears that the question posed by Pies’ report really forces us to go back to base to address some of the fundamental issues left behind on the aggressive needs of clinical practice.
I am the fortunate recipient of Psychiatric Times and in this year’s May Supplementthere are several papers relevant to this issue:
1. “Subthreshold bipolarity, low-dose lithium and non-drug options for complex depressions”by James Phelps
2.“Not bipolar, but not unipolar either”; and
3. “Diagnosis - or lithium anyway”
I believe Barry Blackwell would be able to describe this sort of thinking and practice. It is a reflection of the unused ability of our current diagnostic labels, as in DSM 5 of the American Psychiatric Association,and the random use of medications to fit this unfit table animal. In my view, these practices all need be considered as an urgent need for answering the questions raised by the “Thin Brain”paper.
October 25, 2018