Monday, 17.05.2021

Peter R. Martin: Historical Vocabulary of Addiction

 

Trauma

 

        According to the current electronic version of the Oxford English Dictionary (OED), the noun trauma is derived from the Latin traumaticus via the Greek τραυματικός, meaning “of or pertaining to a wound or wounds” and  τραῦμα-ματ-, meaning “wound,” appearing in the 16th century French as traumatique.  In fact, the adjectival form appeared in the English language before the noun trauma (Blount 1656): “Traumatick, belonging to wounds or to the cure of wounds, vulnerary.”  The relevant OED definition for traumatic is: “Of, pertaining to, or caused by a wound, abrasion, or external injury...” An example of the word trauma appeared in the 1684 book A physical dictionary; in which all the terms relating either to anatomy, chirurgery, pharmacy, or chymistry…written by Steven Blankaart (1650–1704), a Dutch physician, iatrochemist and entomologist, who proved the existence of a capillary system, as had been suggested by Leonardo da Vinci (1684): “Trauma,... a Wound from an external Cause.”  The OED definition of trauma as used in this quotation is: “A wound, or external bodily injury in general; also the condition caused by this; traumatism.” 

        Whereas initial understanding of trauma was as an external and physical injury, the meaning has expanded to include an internal and, metaphorically, an emotional wound.  The definition of trauma as used in addiction came from neurology/psychiatry: “A psychic injury, especially one caused by emotional shock the memory of which is repressed and remains unhealed; an internal injury, especially to the brain, which may result in a behavioural disorder of organic origin. Also, the state or condition so caused.”  An example of this sense of the word, as first used in the English language, is by William James (1842–1910), American philosopher and psychologist, who discussed the article Ueber den psychischen Mechanismus hysterischer Phanomen in Psychological Review (James 1894).  This article appeared the preceding year in a German neurology journal, written by Josef Breuer (1842–1925), a distinguished Viennese physician, and his protégé, Sigmund Freud (1856–1939), then a neurologist; these two colleagues had combined forces to lay the foundation of the discipline of psychoanalysis (“talk cure”).  Interestingly enough, in the previous pages of this same issue of Psychological Review is James’ summary of a series of articles written originally by Pierre Janet (1859–1947), a pioneering French psychologist, physician, philosopher and psychotherapist in the field of dissociation and traumatic memory who studied under Jean-Martin Charcot in the Pitié-Salpêtrière Hospital in Paris — Etat mental des hysteriques: les stigmates mentaux; Etat mental des hysteriques: Les accidents mentaux; L'amnesie continue — which are referenced below, as follows:

        “Hysteria is a disease of the hypnotic stratum," wrote Mr. F. W. H. Myers [Frederic William Henry Myers (1843–1901) was a poet, classicist and philologist whose ideas about a "subliminal self" were influential in his time, but have not been accepted by the scientific community] many years ago, and this important paper is a comment on his dictum and an independent corroboration of Janet's above [pp. 195-199]. The distinguished Viennese neurologists who sign it stumbled accidentally on cures which enable them not only to give a general formula for the disease, but a general method for its treatment. Hysteria for them starts always from a shock, and is a 'disease of the memory.' Certain reminiscences of the shock fall into the subliminal consciousness, where they can only be discovered in ' hypnoid' states. If left there, they act as permanent 'psychic traumata' thorns in the spirit, so to speak. The cure is to draw them out in hypnotism, let them produce all their emotional effects, however violent, and work themselves off. They make then (apparently) a new connection with the principal consciousness, whose breach is thus restored, and the sufferer gets well.”

        The OED definition of traumatic is: “Of, pertaining to, or caused by a psychic wound or emotional shock, especially leading to or causing behavioural disturbance.” This sense of the word was first used in the 1889 English translation of Clinical Lectures on Diseases of the Nervous System by Jean-Martin Charcot (1825–1893), a French neurologist and professor of anatomical pathology, known for his work on hypnosis and hysteria and considered “the founder of modern neurology”: “The existence of traumatic psychosis [Fr. psychose traumatique] adds still more to the gravity of the prognosis.”  That leaders in medicine, neurology and psychiatry almost simultaneously conceptualized a role of emotional trauma in clinical medicine underlines the breath of presentation of trauma-related conditions.  The frequent association of trauma with addiction points to one way in which coping with the associated emotional suffering can occur.            

        Despite the introduction of psychic underpinnings for disease, the word trauma has retained its concrete meaning, namely a physical wound.  This point is illustrated by a quote from A Text-book of Psychiatry (Henderson and Gillespie 1927): “Trauma may produce mental symptoms in one of two ways.  Either it causes structural injury to the brain, or it causes emotional disturbances... In the first instance the mental reaction is of the organic type… in the second the result is usually a psychoneurosis.”  This quotation embodied the broadly-based viewpoint of David Kennedy Henderson (1884–1965), a Scottish physician and psychiatrist who served as president of the Royal College of Physicians of Edinburgh and represented the influential Scottish tradition of organic psychiatry and psychological medicine combined with social psychiatry (Cameron 1965). 

        Recognition of the effects of trauma on humans, not surprisingly, occurred first in the military where both “structural injury to the brain” and “emotional disturbances” are very possible during active service and must be entertained in the differential diagnosis.  The American physician Jacob Mendes Da Costa (1833–1900) described a condition of the circulatory system that now bears his name in 300 cases he examined in the military hospital in Philadelphia during the American Civil War (1871):

        “In this paper I propose to consider a form of cardiac malady common among soldiers, but the study of which is equally interesting to the civil practitioner… I noticed cases of a peculiar form of functional disorder of the heart, to which I gave the name of irritable heart…

        “The general clinical history of many of the cases was this: -- A man who had been for some months or longer in active service, would be seized with diarrhea, annoying, yet not severe enough to keep him out of the field; or, attacked with diarrhea or fever, he rejoined, after a short stay in hospital, his command, and again underwent the exertions of a solidier’s life.  He soon noticed that he could not bear them as formerly; he got out of breath, could not keep up with his comrades, his accoutrements oppressed him, and all this though he appeared well and healthy.  Seeking advice from the surgeon of the regiment, it was decided that he was unfit for duty, and he was sent to a hospital, where his persistently quick acting heart confirmed his story, though he looked like a man in sound condition.  Any digestive disturbances which might have existed gradually passed away, but the irritability of the heart remained, and only very slowly did the excited organ return to its natural condition.  Or it failed to do so, notwithstanding the use of remedies which control the circulation: thus the case might go on for a long time, and the patient, after having been the round of hospitals, would be discharged, or, as unfit for active duty, placed in the Invalid Corps.

        “This may be stated to be a general summary of a considerable number of cases.  But there were many others originating more suddenly, or without previous digestive disorder, presenting also marked disturbance or irregularity of the circulation, and having also the pain in the cardiac region well developed.”

        Da Costa described a range of symptoms that seem only tenuously linked to the cardiovascular system and he documents the particular beneficial effects of rest and, additionally, of some pharmacological agents, including digitalis, belladonna, laudanum, opium and cannabis.  For opium he writes, “This was rather incidentally tested while prescribing for diarrhoea or some other affection in which it was indicated, than used persistently for the irritable heart; for in the long continuance of the treatment required there would have been great risk of making the patient an opium eater.” This last point underlines Da Costa’s awareness of the susceptibility of the stressed individual to a drug that, on one hand, relieves suffering, but on the other, is highly addictive.  This astute observation foreshadows a major theme — the relationship between the chronic consequences of the experience of trauma and the development of addiction via self-medication.

        Attempts to elucidate the pathophysiology of Da Costa’s syndrome made some progress when the cardiovascular symptoms were conceptualized in terms of dysfunction of the autonomic nervous system, “neurocirculatory asthenia” or as an “effort syndrome” (Piersol 1925).  It was not until Paul Wood (1907–1962), “the greatest British cardiologist of his time,” concluded the Goulstonian Lectures to the Royal College of Physicians of London that the perspective shifted beyond the cardiovascular system and the clinical manifestations were interpreted as a consequence, rather than the cause of the syndrome (1941): “The symptoms and signs of Da Costa's syndrome more closely resemble those of emotion, especially fear, than those of effort in the normal subject. The mechanism of the somatic manifestations depends upon central stimulation, not upon hypersensitivity of the peripheral autonomic gear. This central stimulus is emotional, and is commonly the result of fear.”

        Nonetheless, even at the end of the Second World War, Friedman (1945) acknowledged that an etiopathogenic conundrum still existed:

        “…whereas most internists have consistently stressed the psychic factors in this disease, they have not succeeded in integrating the latter in any exact, physiologic manner with the actual emergence of cardiovascular symptoms and signs in the same patient.  Likewise, the psychiatrists have not succeeded in elucidating the pathogenesis of cardiovascular manifestations in patients suffering from an obvious anxiety neurosis.  There exists, then, a physiologic or neurologic void between the psychic and cardiovascular phases of neurocirculatory asthenia which has not been probed sufficiently by either the internist or by the psychiatrist.  Until this void is explored, however, it will be impossible to understand those processes set loose in a person subject to anxiety, which express themselves in trembling, perspiration, flushing, dyspnea, palpitation, and precordial pain.”

        Friedman’s conclusion (1945) placed the problem, for the first time, in the correct organ system of the body:  “Evidence was obtained which suggested that the excitation of the sympathetic nervous system, preceding or associated in a causal fashion with the cardiovascular manifestations of neurocirculatory asthenia, resulted from hypothalamic discharge.”

        It was not until after the Vietnam War, a time of social changes in codes of behavior related to sexuality and gender roles (“Sexual Revolution”) in the 1960s, that the perspective of trauma in psychiatry progressed beyond notions of “soldier’s heart,” “shell shock,” “neurocirculatory asthenia” and “combat fatigue and neurosis.”  The focus shifted to the neurobiology of stress (Cannon 1920; Selye 1937; McEwen 2007) and inter-individual vulnerability (Meaney 2001) to the experience of stress and its toxicity to various organs, in particular, the brain and its neuroendocrine offshoots (Sapolsky 1996).  The diagnostic entity postraumatic stress disorder (PTSD) emerged in the 1970s and was subsequently included in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Third Edition (1980).  It soon became apparent that this disorder, characterized by pathological responses to stress, also affected women and occurred in civilian life — as was suggested by Da Costa (1871) but not fully appreciated for a century. 

        In the National Comorbidity Survey, the lifetime prevalence of PTSD was reported as 7.8% (5% of men and 10.4% of women) and strongly comorbid with other lifetime DSM-III-R disorders, including alcohol and drug use disorders (Kessler, Sonnega, Bromet et al. 1995).  Furthermore, PTSD was found to be the primary diagnosis if it was a comorbid condition.  In addition to effects of war in soldiers, pathological response syndromes to trauma were described in sexual assault (Burgess and Holmstrom 1974) and many other stressful experiences (Grinker and Spiegel 1945).  In particular, adverse childhood experiences were profound predictors of adult psychopathology and have become a focus of investigation (Brown and Harris 1993).   Not only do disturbing memories of the traumatic events impair functioning throughout life, but in association with re-experiencing these traumatic memories, ongoing memory dysfunctions for current events can be identified (Yehuda, Keefe, Harvey et al. 1995; Jenkins, Langlais, Delis and Cohen 1998).  In particular, the association of adverse childhood experiences and development of an addictive disorder has become firmly established (Dube, Anda, Felitti et al. 2002; Turner and Lloyd 2003).

        Stress responses leave enduring emotion-laden memory traces in the brain (Rodrigues, Schafe and LeDoux 2004).  Traumatic memories cannot be forgotten and emerge into consciousness and disrupt current functioning.  Because re-experience of the stressful events further strengthen these memory traces, they become generalized to elements of the environment (Miller 2004).  The desire to suppress re-experiencing painful memories during the day and in nightmares are compelling and individuals recognize that temporary relief can be obtained by alcohol or other drugs of abuse (Martin, Weinberg and Bealer 2007).  Repeated use of alcohol/drugs, although intitially beneficial, likely fade with time and a use disorder due to self-medication emerges and becomes recalcitrant to treatment (Derefinko, Salgado García, Talley et al. 2019).  Conceptually, evidence has emerged that vulnerability to development of PTSD is determined by an interaction between experienced stress and characteristic susceptibilities of the individual, complicated by identifiable risk for development of alcohol and drug use (Ohashi, Anderson, Bolger et al. 2019; Martin 2020).  Psychiatrists have striven to identify medications that can temper re-experiencing traumatic memories, demonstrated to be associated with over-activation of the noradrenergic system and other CNS impairments which persist indefinitely after the trauma was initially experienced (Cahill, Prins, Weber and McGaugh 1994; Raskind, Peskind, Kanter et al. 2003; Squire and Davis 1981).  Additionally, since the response to stress involves a tremendous outpouring of cortisol (Selye 1937), which is toxic to the brain and especially hippocampal regions vital for memory consolidation and emotional linkages via the amygdala to the prefrontal cortex, there has been a focus on both impairments in memory consolidation and the capacity to forget (Sapolsky 1996; Miller 2004). 

        The story comes full circle from Da Costa with identification of the brain origins of stress-induced cardiomyopathy, the so-called “broken heart syndrome” (Silva, Magalhães, Arantes et al. 2019).  Using fMRI to compare neural connectivity during the resting-state and during stressful stimulation in controls and patients recovered from this syndrome, it was found that patients displayed a reorganization of cortical and subcortical networks, including areas associated with emotional responses and autonomic regulation. This suggests that dysregulation of autonomic control at the central level plays a significant role in stress-induced cardiomyopathy.  Via neural connection between brain and heart, pychosocial stressors can be expressed in the heart.  More recent work has identified the physiologic basis of a central master driver of psychosocial stress responses in a rat model.  Kataoka, Shima, Nakajima and Nakamura (2020) provide evidence for the prominent role of a ventral part of the medial prefrontal cortex in sympathetic responses to social defeat stress. This brain region sends excitatory projections to the dorsomedial hypothalamus as a central coordinator of the psychosocial stress responses throughout the body.  This reifies emotional trauma to a degree that, heretofore, could only be imagined.

  

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January 14, 2021