OUR CONCEPTUALLY-DRIVEN PAPERS THAT MAY BE RELEVANT TO THE RESEARCH AGENDA FOR DSM-V

2005-07-24T13:00:00.000-10:00

.1.
Bracha HS, Yoshioka DT, Masukawa MK, Stockman DJ: Evolution of the Human Fear-Circuitry and Acute Sociogenic Pseudo-Neurological Symptoms: The Neolithic Balanced-Polymorphism Hypothesis. The Journal of Affective Disorders August 2005
In light of the increasing threat of large-scale man-made disasters, such as terrorism against non-combatants (civilians), more attention is warranted not only to PTSD but also to acute sociogenic pseudo-neurological (“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). We 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-induced fear-circuitry disorders. In the present article, we extend neuroevolutionary perspectives to acute sociogenic pseudo-neurological (“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 pseudo-neurological stress-induced symptoms, which are considered psychopathological in extant humans, are traceable to genetic polymorphisms encoded 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 be a developmentally sensitive allele in a stable/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 DSM-V and the ICD are discussed.

.2.
Bracha HS. Freeze, flight, fight, fright, faint: adaptationist perspectives on the acute stress response spectrum. CNS Spectr 2004 Sep, 9:679-85
PAPER IS ONLINE FULL TEXT IN CNSSPECTRUMS.COM
This article reviews the existing evolutionary perspectives on the acute stress response habitual faintness and blood-injection-injury type-specific phobia (BIITS phobia). In this article, an alternative evolutionary perspective, based on recent advances in evolutionary psychology, is proposed. Specifically, that fear-induced faintness (eg, fainting following the sight of a syringe, blood, or following a trivial skin injury) is a distinct Homo sapiens-specific extreme-stress survival response to an inescapable threat. The article suggests that faintness evolved in response to middle paleolithic intra-group and inter-group violence (of con-specifics) rather than as a pan-mammalian defense response, as is presently assumed. Based on recent literature, freeze, flight, fight, fright, faint provides a more complete description of the human acute stress response sequence than current descriptions. Faintness, one of three primary physiological reactions involved in BIITS phobia, is extremely rare in other phobias. Since heritability estimates are higher for faintness than for fears or phobias, the author suggests that trait-faintness may be a useful complement to trait-anxiety as an endophenotype in research on the human fear circuitry. Some implications for the forthcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition as well as for clinical, health services, and transcriptomic research are briefly discussed.

.3.
Bracha HS, Bracha AS, Williams AE, Ralston TC, Matsukawa JM: The human fear-circuitry and fear-induced fainting in healthy individuals--the paleolithic-threat hypothesis. Clin Auton Res 2005 Jun, 15:238-41The Paleolithic-Threat hypothesis reviewed here posits that habitual efferent fainting can be traced back to fear-induced allelic polymorphisms that were selected into some genomes of anatomically, mitochondrially, and neurally modern humans (Homo sapiens sapiens) in the Mid-Paleolithic because of the survival advantage they conferred during periods of inescapable threat. We posit that during Mid-Paleolithic warfare an encounter with "a stranger holding a sharp object" was consistently associated with threat to life. A heritable hardwired or firm-wired (prepotentiated) predisposition to abruptly increase vagal tone and collapse flaccidly rather than freeze or attempt to flee or fight in response to an approaching sharp object, a minor injury, or the sight of blood, may have evolved as an alternative stress-induced fear-circuitry response. Such a stable (balanced) polymorphism for the hemodynamically "paradoxical" flaccid-immobility in response to these stimuli may have increased some non-combatants' chances of survival. This is consistent with the unusual age and sex pattern of fear-induced fainting. The Paleolithic-Threat hypothesis also predicts a link to various hypo-androgenic states (e. g. low dehydroxy-epiandrosterone-sulfate. We offer five predictions testable via epidemiological, clinical, and ethological/ primatological methods. The Paleolithic-Threat hypothesis has implications for research in the aftermath of man-made disasters, such as terrorism against civilians, a traumatic event in which this hypothesis predicts epidemics of fear-induced fainting.

.4.
Bracha HS, Ralston TC, Williams AE, Yamashita JM, Bracha AS: The clenching-grinding spectrum and fear circuitry disorders: clinical insights from the neuroscience/paleoanthropology interface. CNS Spectr 2005 Apr, 10:311-8
PAPER IS ONLINE FULL TEXT IN CNSSPECTRUMS.COM
This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8 percent of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching-induced palpable masseter tenderness may be examples of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).

.5.
Bracha HS. Neuro-evolutionary factors in the etiology of fear-circuitry-related traits: Current perspectives, falsifiable predictions and the “Time-Depth Principle” (in press) Progress in Neuro-Psychopharmacology & Biological Psychiatry, (2005).

.6.
Bracha HS, Ralston TC, Matsukawa JM, Williams AE, Bracha AS. Does "fight or flight" need updating? Psychosomatics 2004 Sep-Oct, 45:448-9

EVOUTIONARY NEUROPSYCHIATRY AND DSM-V FEAR-CIRCUITRY DISORDERS

OUR CONCEPTUALLY-DRIVEN PAPERS THAT MAY BE RELEVANT TO THE RESEARCH AGENDA FOR DSM-V