Evolution of the human fear-circuitry and acute sociogenic pseudoneurological symptoms: the Neolithic balanced-polymorphism hypothesis.
In light of the increasing threat of large-scale massacres such as terrorism against non-combatants (civilians), more attention is warranted not only to posttraumatic stress disorder (PTSD) but also to acute sociogenic pseudoneurological ("conversion") symptoms, especially epidemic sociogenic symptoms. We posit that conversion disorders are etiologically related to specific evolutionary pressures (inescapable threats to life) in the late stage of the human environment of evolutionary adaptedness (EEA). Bracha et al. have recently argued that from the neuroevolutionary perspective, medically unexplained efferent vasovagal syncope and medically unexplained craniofacial musculoskeletal pain in young otherwise healthy individuals, may be taxonomized as stress and fear-circuitry disorders. In the present article, we extend neuroevolutionary perspectives to acute pseudoneurological sociogenic ("conversive") symptoms: psychogenic non-epileptic attacks ("pseudoseizures"), epidemic sociogenic disorders (DSM-IV-TR Epidemic "Hysteria"), conversive motor deficits (pseudo-paralysis and pseudo-cerebellar symptoms), and psychogenic blindness. We hypothesize that these perplexing pseudoneurological stress-triggered symptoms, which constitute psychopathology in extant humans, are traceable to allele-variant polymorphisms which spread during the Neolithic EEA. During Neolithic warfare, conversive symptoms may have increased the survival odds for some non-combatants by visually (i.e., "non-verbally") signaling to predatory conspecifics that one does not present a danger. This is consistent with the age and sex pattern of conversive disorders. Testable and falsifiable predictions are presented; e.g., at the genome-transcriptome interface, one of the major oligogenic loci involved in conversive spectrum disorders may carry a developmentally sensitive allele in a stable polymorphism (balanced polymorphism) in which the gene expression mechanism is gradually suppressed by pleiotropic androgens especially dehydroxyepiandrosterone sulfate (DHEA-S). Taxonomic implications for the much-needed rapprochement between the forthcoming Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition (DSM-V) and the International Classification of Diseases (ICD) are discussed.
Bracha
H Stefan
HS
National Center for Posttraumatic Stress Disorder, Department of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga Medical Center, 1132 Bishop St. #307, Honolulu, HI 96813, USA. h.bracha@med.va.gov
Yoshioka
Dawn T
DT
Masukawa
Nicole K
NK
Stockman
Deborah J J
DJ
D000483:Alleles; D000728:Androgens / Q000502:physiology; D000883:Anthropology; D005075:Biological Evolution; D001794:Blood Pressure; D003291:Conversion Disorder / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology*; D005239:Fear / Q000502:physiology*; D015870:Gene Expression / Q000235:genetics; D006801:Humans; D009415:Nerve Net / Q000502:physiology*; D010163:Paleontology; D011110:Polymorphism, Genetic / Q000235:genetics*; D011569:Psychiatric Status Rating Scales; D011582:Psychological Theory; D011965:Receptors, Glucocorticoid / Q000502:physiology; D018161:Receptors, Mineralocorticoid / Q000502:physiology; D012931:Social Environment; D013575:Syncope / Q000235:genetics* / Q000503:physiopathology*; D009626:Terminology as Topic; D014857:Warfare
D000728:Androgens; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid