The population worldwide is ageing at a rapid pace and so
are forensic detainees with severe psychiatric illnesses, including
schizophrenia (SCZ) and schizophrenia-like disorders (SLDs). Forensic
institutions throughout the world house patients with severe psychiatric
illness and history of criminal violations. The primary objective of this study
is to explore novel therapies for Schizophrenia-dementia patients in forensic
settings. Improved medical care,
hygiene, psychiatric treatment, and nutrition led to an unmatched longevity in
this population, which previously lived, on average, 15 to 20 years shorter
than the public at large. On the other hand, longevity has contributed to an
increased prevalence of age-related diseases, including neurodegenerative disorders,
which complicate clinical management, increasing healthcare expenditures.
Forensic institutions, originally intended for the treatment of younger
individuals, are ill-equipped for the growing number of older offenders.
Moreover, as antipsychotic drugs became available in 1950s and 1960s, we are
observing the first generation of forensic detainees who have aged on
dopamine-blocking agents. Although the consequences of long-term treatment with
these agents are unclear, schizophrenia-associated gray matter loss may
contribute to the development of early dementia. Taken together, increased
lifespan and the subsequent cognitive deficit observed in long-term forensic
institutions raise questions and dilemmas unencountered by the previous
generations of clinicians. These include: does the presence of neurocognitive
dysfunction justify antipsychotic dose reduction or discontinuation despite a
life-long history of schizophrenia and violent behavior? Should neurolipidomic
interventions become the standard of care in elderly individuals with lifelong
schizophrenia and dementia? Can patients with schizophrenia and dementia meet
the Dusky standard to stand trial? Should neurocognitive disorders in the
elderly with lifelong schizophrenia be treated differently than age-related
neurodegeneration? In this article, we hypothesize that gray matter loss is the
core symptom of schizophrenia which leads to dementia. We hypothesize further
that strategies to delay or stop gray matter depletion would not only improve
schizophrenia-sustained recovery, but also avert the development of major
neurocognitive disorders in people living with schizophrenia. Based on this
hypothesis, we suggest the utilization of both receptor-dependent and
independent therapeutics for chronic psychosis. While acute psychosis responds
very well to antipsychotic drugs, chronic psychotic illnesses are much more
refractory to these agents. Over the past decades, psychopharmacology has
focused excessively on the receptor-dependent actions of antipsychotic drugs
and put much less emphasis on the receptor-independent ones, such as
antimicrobial and anticancer actions.
Author(s) Details:
Adonis Sfera,
Paton State Hospital, 3102 Highland Ave, Patton, CA 92369, USA,
School of Behavioral Health, Loma Linda University, 11139 Anderson St., Loma
Linda, CA 92350, USA and Department of Psychiatry, University of California,
Riverside 900 University Ave, Riverside, CA 92521, USA.
Luminita
Andronescu,
Paton
State Hospital, 3102 Highland Ave, Patton, CA 92369, USA.
William G. Britt,
Department of Psychiatry, School of Medicine, Loma Linda University,
Loma Linda, CA 92350, USA.
Kiera x Kiera Himsl,
Paton State Hospital, 3102 Highland Ave, Patton, CA 92369, USA.
Carolina Klein,
California
Department of State Hospitals, Sacramento, CA 95814, USA.
Leah
Rahman,
Department
of Neuroscience, University of Oregon, 1585 E 13th Ave, Eugene, OR 97403, USA.
Zisis Kozlakidis,
International Agency for Research on Cancer, 69366 Lyon Cedex,
France.
Please see the link here: https://stm.bookpi.org/RUDHR-V4/article/view/13757
