Psychoneuroimmunology

From Wikipedia, the free encyclopedia

Psychoneuroimmunology (PNI), also referred to as psychoendoneuroimmunology (PENI) or psychoneuroendocrinoimmunology (PNEI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body. PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.

The main interests of PNI are the interactions between the nervous and immune systems and the relationships between mental processes and health. PNI studies, among other things, the physiological functioning of the neuroimmune system in health and disease; disorders of the neuroimmune system (autoimmune diseases; hypersensitivities; immune deficiency); and the physical, chemical and physiological characteristics of the components of the neuroimmune system in vitro, in situ, and in vivo.

History

Interest in the relationship between psychiatric syndromes or symptoms and immune function has been a consistent theme since the beginning of modern medicine.

Claude Bernard, the father of modern physiology, with his pupils

Claude Bernard, a French physiologist of the Muséum national d'Histoire naturelle, formulated the concept of the milieu interieur in the mid-1800s. In 1865, Bernard described the perturbation of this internal state: "... there are protective functions of organic elements holding living materials in reserve and maintaining without interruption humidity, heat and other conditions indispensable to vital activity. Sickness and death are only a dislocation or perturbation of that mechanism" (Bernard, 1865). Walter Cannon, a professor of physiology at Harvard University coined the commonly used term, homeostasis, in his book The Wisdom of the Body, 1932, from the Greek word homoios, meaning similar, and stasis, meaning position. In his work with animals, Cannon observed that any change of emotional state in the beast, such as anxiety, distress, or rage, was accompanied by total cessation of movements of the stomach (Bodily Changes in Pain, Hunger, Fear and Rage, 1915). These studies looked into the relationship between the effects of emotions and perceptions on the autonomic nervous system, namely the sympathetic and parasympathetic responses that initiated the recognition of the freeze, fight or flight response. His findings were published from time to time in professional journals, then summed up in book form in The Mechanical Factors of Digestion, published in 1911.

Bust of Hans Selye at Selye János University, Komárno, Slovakia

Hans Selye, a student of Johns Hopkins University and McGill University, and a researcher at Université de Montréal, experimented with animals by putting them under different physical and mental adverse conditions and noted that under these difficult conditions the body consistently adapted to heal and recover. Several years of experimentation that formed the empiric foundation of Selye's concept of the General Adaptation Syndrome. This syndrome consists of an enlargement of the adrenal gland, atrophy of the thymus, spleen, and other lymphoid tissue, and gastric ulcerations.

Selye describes three stages of adaptation, including an initial brief alarm reaction, followed by a prolonged period of resistance, and a terminal stage of exhaustion and death. This foundational work led to a rich line of research on the biological functioning of glucocorticoids.^[3]

Mid-20th century studies of psychiatric patients reported immune alterations in psychotic individuals, including lower numbers of lymphocytes^[4][5] and poorer antibody response to pertussis vaccination, compared with nonpsychiatric control subjects.^[6] In 1964, George F. Solomon, from the University of California in Los Angeles, and his research team coined the term "psychoimmunology" and published a landmark paper: "Emotions, immunity, and disease: a speculative theoretical integration."^[7]

Origins

In 1975, Robert Ader and Nicholas Cohen, at the University of Rochester, advanced PNI with their demonstration of classic conditioning of immune function, and they subsequently coined the term "psychoneuroimmunology".^[8][9] Ader was investigating how long conditioned responses (in the sense of Pavlov's conditioning of dogs to drool when they heard a bell ring) might last in laboratory rats. To condition the rats, he used a combination^{[clarification needed]} of saccharin-laced water (the conditioned stimulus) and the drug Cytoxan, which unconditionally induces nausea and taste aversion and suppression of immune function. Ader was surprised to discover that after conditioning, just feeding the rats saccharin-laced water was associated with the death of some animals and he proposed that they had been immunosuppressed after receiving the conditioned stimulus. Ader (a psychologist) and Cohen (an immunologist) directly tested this hypothesis by deliberately immunizing conditioned and unconditioned animals, exposing these and other control groups to the conditioned taste stimulus, and then measuring the amount of antibody produced. The highly reproducible results revealed that conditioned rats exposed to the conditioned stimulus were indeed immuno suppressed. In other words, a signal via the nervous system (taste) was affecting immune function. This was one of the first scientific experiments that demonstrated that the nervous system can affect the immune system.

In the 1970s, Hugo Besedovsky, Adriana del Rey and Ernst Sorkin, working in Switzerland, reported multi-directional immune-neuro-endocrine interactions, since they show that not only the brain can influence immune processes but also the immune response itself can affect the brain and neuroendocrine mechanisms. They found that the immune responses to innocuous antigens triggers an increase in the activity of hypothalamic neurons^[10][11] and hormonal and autonomic nerve responses that are relevant for immunoregulation and are integrated at brain levels (see review^[12]). On these bases, they proposed that the immune system acts as a sensorial receptor organ that, besides its peripheral effects, can communicate to the brain and associated neuro-endocrine structures its state of activity.^[11] These investigators also identified products from immune cells, later characterized as cytokines, that mediate this immune-brain communication^[13] (more references in ^[12]).

In 1981, David L. Felten, then working at the Indiana University School of Medicine, discovered a network of nerves leading to blood vessels as well as cells of the immune system. The researcher, along with his team, also found nerves in the thymus and spleen terminating near clusters of lymphocytes, macrophages, and mast cells, all of which help control immune function. This discovery provided one of the first indications of how neuro-immune interaction occurs.

Ader, Cohen, and Felten went on to edit the groundbreaking book Psychoneuroimmunology in 1981, which laid out the underlying premise that the brain and immune system represent a single, integrated system of defense.

In 1985, research by neuropharmacologist Candace Pert, of the National Institutes of Health at Georgetown University, revealed that neuropeptide-specific receptors are present on the cell walls of both the brain and the immune system.^[14][15] The discovery that neuropeptides and neurotransmitters act directly upon the immune system shows their close association with emotions and suggests mechanisms through which emotions, from the limbic system, and immunology are deeply interdependent. Showing that the immune and endocrine systems are modulated not only by the brain but also by the central nervous system itself affected the understanding of emotions, as well as disease.

Contemporary advances in psychiatry, immunology, neurology, and other integrated disciplines of medicine has fostered enormous growth for PNI. The mechanisms underlying behaviorally induced alterations of immune function, and immune alterations inducing behavioral changes, are likely to have clinical and therapeutic implications that will not be fully appreciated until more is known about the extent of these interrelationships in normal and pathophysiological states.

The immune-brain loop

PNI research looks for the exact mechanisms by which specific neuroimmune effects are achieved. Evidence for nervous-immunological interactions exist at multiple biological levels.
The immune system and the brain communicate through signaling pathways. The brain and the immune system are the two major adaptive systems of the body. Two major pathways are involved in this cross-talk: the Hypothalamic-pituitary-adrenal axis (HPA axis), and the sympathetic nervous system (SNS), via the sympathetic-adrenal-medullary axis (SAM axis). The activation of SNS during an immune response might be aimed to localize the inflammatory response.

The body's primary stress management system is the HPA axis. The HPA axis responds to physical and mental challenge to maintain homeostasis in part by controlling the body's cortisol level. Dysregulation of the HPA axis is implicated in numerous stress-related diseases, with evidence from meta-analyses indicating that different types/duration of stressors and unique personal variables can shape the HPA response.^[16] HPA axis activity and cytokines are intrinsically intertwined: inflammatory cytokines stimulate adrenocorticotropic hormone (ACTH) and cortisol secretion, while, in turn, glucocorticoids suppress the synthesis of proinflammatory cytokines.

Molecules called pro-inflammatory cytokines, which include interleukin-1 (IL-1), Interleukin-2 (IL-2), interleukin-6 (IL-6), Interleukin-12 (IL-12), Interferon-gamma (IFN-Gamma) and tumor necrosis factor alpha (TNF-alpha) can affect brain growth as well as neuronal function. Circulating immune cells such as macrophages, as well as glial cells (microglia and astrocytes) secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders.^[17]

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis. Like the stress response, the inflammatory reaction is crucial for survival. Systemic inflammatory reaction results in stimulation of four major programs:^[18]

• the acute-phase reaction
• sickness behavior
• the pain program
• the stress response

These are mediated by the HPA axis and the SNS. Common human diseases such as allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro-inflammatory versus anti-inflammatory and T helper (Th1) versus (Th2) cytokine balance.

Recent studies show pro-inflammatory cytokine processes take place during depression, mania and bipolar disease, in addition to autoimmune hypersensitivity and chronic infections.

Chronic secretion of stress hormones, glucocorticoids (GCs) and catecholamines (CAs), as a result of disease, may reduce the effect of neurotransmitters, including serotonin^{[medical citation needed]}, norepinephrine and dopamine, or other receptors in the brain, thereby leading to the dysregulation of neurohormones. Under stimulation, norepinephrine is released from the sympathetic nerve terminals in organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released norepinephrine, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells.

Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the pituitary (negative feedback). Under certain conditions stress hormones may facilitate inflammation through induction of signaling pathways and through activation of the Corticotropin-releasing hormone.

These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health, developing into a "systemic anti-inflammatory feedback" and/or "hyperactivity" of the local pro-inflammatory factors which may contribute to the pathogenesis of disease.

This systemic or neuro-inflammation and neuroimmune activation have been shown to play a role in the etiology of a variety of neurodegenerative disorders such as Parkinson's and Alzheimer's disease, multiple sclerosis, pain, and AIDS-associated dementia. However, cytokines and chemokines also modulate central nervous system (CNS) function in the absence of overt immunological, physiological, or psychological challenges.^[19]

Psychoneuroimmunological effects

There are now sufficient data to conclude that immune modulation by psychosocial stressors and/or interventions can lead to actual health changes. Although changes related to infectious disease and wound healing have provided the strongest evidence to date, the clinical importance of immunological dysregulation is highlighted by increased risks across diverse conditions and diseases. For example, stressors can produce profound health consequences. In one epidemiological study, all-cause mortality increased in the month following a severe stressor – the death of a spouse.^[20] Theorists propose that stressful events trigger cognitive and affective responses which, in turn, induce sympathetic nervous system and endocrine changes, and these ultimately impair immune function.^[21][22] Potential health consequences are broad, but include rates of infection^[23][24] HIV progression^[25][26] cancer incidence and progression,^[20][27][28] and high rates of infant mortality.^[29][30]

Understanding stress and immune function

Stress is thought to affect immune function through emotional and/or behavioral manifestations such as anxiety, fear, tension, anger and sadness and physiological changes such as heart rate, blood pressure, and sweating. Researchers have suggested that these changes are beneficial if they are of limited duration,^[21] but when stress is chronic, the system is unable to maintain equilibrium or homeostasis; the body remains in a state of arousal, where digestion is slower to reactivate or does not reactivate properly, often resulting in indigestion. Furthermore, blood pressure stays at higher levels.^[31]

In one of the earlier PNI studies, which was published in 1960, subjects were led to believe that they had accidentally caused serious injury to a companion through misuse of explosives.^[32] Since then decades of research resulted in two large meta-analyses, which showed consistent immune dysregulation in healthy people who are experiencing stress.

In the first meta-analysis by Herbert and Cohen in 1993,^[33] they examined 38 studies of stressful events and immune function in healthy adults. They included studies of acute laboratory stressors (e.g. a speech task), short-term naturalistic stressors (e.g. medical examinations), and long-term naturalistic stressors (e.g. divorce, bereavement, caregiving, unemployment). They found consistent stress-related increases in numbers of total white blood cells, as well as decreases in the numbers of helper T cells, suppressor T cells, and cytotoxic T cells, B cells, and natural killer cells (NK). They also reported stress-related decreases in NK and T cell function, and T cell proliferative responses to phytohaemagglutinin [PHA] and concanavalin A [Con A]. These effects were consistent for short-term and long-term naturalistic stressors, but not laboratory stressors.

In the second meta-analysis by Zorrilla et al. in 2001,^[34] they replicated Herbert and Cohen's meta-analysis. Using the same study selection procedures, they analyzed 75 studies of stressors and human immunity. Naturalistic stressors were associated with increases in number of circulating neutrophils, decreases in number and percentages of total T cells and helper T cells, and decreases in percentages of natural killer cell (NK) cells and cytotoxic T cell lymphocytes. They also replicated Herbert and Cohen's finding of stress-related decreases in NKCC and T cell mitogen proliferation to phytohaemagglutinin (PHA) and concanavalin A (Con A).

More recently, there has been increasing interest in the links between interpersonal stressors and immune function. For example, marital conflict, loneliness, caring for a person with a chronic medical condition, and other forms on interpersonal stress dysregulate immune function.^[35]

Communication between the brain and immune system

• Stimulation of brain sites alters immunity (stressed animals have altered immune systems).
• Damage to brain hemispheres alters immunity (hemispheric lateralization effects).^[36]
• Immune cells produce cytokines that act on the CNS.
• Immune cells respond to signals from the CNS.

Communication between neuroendocrine and immune system

• Glucocorticoids and catecholamines influence immune cells.^[37][38]
• Endorphins from pituitary and adrenal medulla act on immune system.
• Activity of the immune system is correlated with neurochemical/neuroendocrine activity of brain cells.

Connections between glucocorticoids and immune system

• Anti-inflammatory hormones that enhance the organism's response to a stressor.
• Prevent the overreaction of the body's own defense system.
• Regulators of the immune system.
• Affect cell growth, proliferation and differentiation.
• Cause immunosuppression.
• Suppress cell adhesion, antigen presentation, chemotaxis and cytotoxicity.
• Increase apoptosis.

Corticotropin-releasing hormone (CRH)

Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.

• CRH is a major regulator of the HPA axis/stress axis.
• CRH Regulates secretion of Adrenocorticotropic hormone (ACTH).
• CRH is widely distributed in the brain and periphery
• CRH also regulates the actions of the Autonomic nervous system ANS and immune system.

Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.

• Central mediated since peripheral administration of CRH antagonist does not affect immunosuppression.

Pharmaceutical advances

Glutamate agonists, cytokine inhibitors, vanilloid-receptor agonists, catecholamine modulators, ion-channel blockers, anticonvulsants, GABA agonists (including opioids and cannabinoids), COX inhibitors, acetylcholine modulators, melatonin analogs (such as Ramelton), adenosine receptor antagonists and several miscellaneous drugs (including biologics like Passiflora edulis) are being studied for their psychoneuroimmunological effects.
For example, SSRIs, SNRIs and tricyclic antidepressants acting on serotonin, norepinephrine, dopamine and cannabinoid receptors have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory cytokine processes, specifically on the regulation of IFN-gamma and IL-10, as well as TNF-alpha and IL-6 through a psychoneuroimmunological process.^{[39][40][41][42]} Antidepressants have also been shown to suppress TH1 upregulation.^{[39][40][41][43][44]}

Tricyclic and dual serotonergic-noradrenergic reuptake inhibition by SNRIs (or SSRI-NRI combinations), have also shown analgesic properties additionally.^[45][46] According to recent evidences antidepressants also seem to exert beneficial effects in experimental autoimmune neuritis in rats by decreasing Interferon-beta (IFN-beta) release or augmenting NK activity in depressed patients.^[17]

These studies warrant investigation of antidepressants for use in both psychiatric and non-psychiatric illness and that a psychoneuroimmunological approach may be required for optimal pharmacotherapy in many diseases.^[47] Future antidepressants may be made to specifically target the immune system by either blocking the actions of pro-inflammatory cytokines or increasing the production of anti-inflammatory cytokines.^[48]

The endocannabinoid system appears to play a significant role in the mechanism of action of clinically effective and potential antidepressants and may serve as a target for drug design and discovery.^[42] The endocannabinoid-induced modulation of stress-related behaviors appears to be mediated, at least in part, through the regulation of the serotoninergic system, by which cannabinoid CB₁ receptors modulate the excitability of dorsal raphe serotonin neurons.^[49] Data suggest that the endocannabinoid system in cortical and subcortical structures is differentially altered in an animal model of depression and that the effects of chronic, unpredictable stress (CUS) on CB₁ receptor binding site density are attenuated by antidepressant treatment while those on endocannabinoid content are not.

The increase in amygdalar CB₁ receptor binding following imipramine treatment is consistent with prior studies which collectively demonstrate that several treatments which are beneficial to depression, such as electroconvulsive shock and tricyclic antidepressant treatment, increase CB₁ receptor activity in subcortical limbic structures, such as the hippocampus, amygdala and hypothalamus. And preclinical studies have demonstrated the CB₁ receptor is required for the behavioral effects of noradrenergic based antidepressants but is dispensable for the behavioral effect of serotonergic based antidepressants.^[50][51]

Extrapolating from the observations that positive emotional experiences boost the immune system, Roberts speculates that intensely positive emotional experiences —sometimes brought about during mystical experiences occasioned by psychedelic medicines—may boost the immune system powerfully. Research on salivary IgA supports this hypothesis, but experimental testing has not been done.

New system allows near-zero-power sensors to communicate data over long distances

Could make low-cost remote medical monitoring and the "internet of things" practical

September 18, 2017
Original link:  http://www.kurzweilai.net/new-system-allows-near-zero-power-sensors-to-communicate-data-over-long-distances

This low-cost, flexible epidermal medical-data patch prototype successfully transmitted information at up to 37500 bits per second across a 3,300-square-feet atrium. (credit: Dennis Wise/University of Washington)

University of Washington (UW) researchers have developed a low-cost, long-range data-communication system that could make it possible for medical sensors or billions of low-cost “internet of things” objects to connect via radio signals at long distances (up to 2.8 kilometers) and with 1000 times lower required power (9.25 microwatts in an experiment) compared to existing technologies.

“People have been talking about embedding connectivity into everyday objects … for years, but the problem is the cost and power consumption to achieve this,” said Vamsi Talla, chief technology officer of Jeeva Wireless, which plans to market the system within six months. “This is the first wireless system that can inject connectivity into any device with very minimal cost.”

The new system uses “backscatter,” which uses energy from ambient transmissions (from WiFi, for example) to power a passive sensor that encodes and scatter-reflects the signal. (This article explains how ambient backscatter, developed by UW, works.) Backscatter systems, used with RFID chips, are very low cost, but are limited in distance.

So the researchers combined backscatter with a “chirp spread spectrum” technique, used in LoRa (long-range) wireless data-communication systems.

This tiny off-the-shelf spread-spectrum receiver enables extremely-low-power cheap sensors to communicate over long distances. (credit: Dennis Wise/University of Washington)

This new system has three components: a power source (which can be WiFi or other ambient transmission sources, or cheap flexible printed batteries, with an expected bulk cost of 10 to 20 cents each) for a radio signal; cheap sensors (less than 10 cents at scale) that modulate (encode) information (contained in scattered reflections of the signal), and an inexpensive, off-the-shelf spread-spectrum receiver, located as far away as 2.8 kilometers, that decodes the sensor information.

Applications could include, for example, medical monitoring devices that wirelessly transmit information about a heart patient’s condition to doctors; sensor arrays that monitor pollution, noise, or traffic in “smart” cities; and farmers looking to measure soil temperature or moisture, who could affordably blanket an entire field to determine how to efficiently plant seeds or water.

The research team built a contact lens prototype and a flexible epidermal patch that attaches to human skin, which successfully used long-range backscatter to transmit information across a 3300-square-foot building.

The research, which was partially funded by the National Science Foundation, is detailed in an open-access paper presented Sept. 13, 2017 at UbiComp 2017. More information: longrange@cs.washington.edu.

UW (University of Washington) | UW team shatters long-range communication barrier for devices that consume almost no power

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Abstract of LoRa Backscatter: Enabling The Vision of Ubiquitous Connectivity

The vision of embedding connectivity into billions of everyday objects runs into the reality of existing communication technologies — there is no existing wireless technology that can provide reliable and long-range communication at tens of microwatts of power as well as cost less than a dime. While backscatter is low-power and low-cost, it is known to be limited to short ranges. This paper overturns this conventional wisdom about backscatter and presents the first wide-area backscatter system. Our design can successfully backscatter from any location between an RF source and receiver, separated by 475 m, while being compatible with commodity LoRa hardware. Further, when our backscatter device is co-located with the RF source, the receiver can be as far as 2.8 km away. We deploy our system in a 4,800 ft2 (446 m2) house spread across three floors, a 13,024 ft2 (1210 m2) office area covering 41 rooms, as well as a one-acre (4046 m2) vegetable farm and show that we can achieve reliable coverage, using only a single RF source and receiver. We also build a contact lens prototype as well as a flexible epidermal patch device attached to the human skin. We show that these devices can reliably backscatter data across a 3,328 ft2 (309 m2) room. Finally, we present a design sketch of a LoRa backscatter IC that shows that it costs less than a dime at scale and consumes only 9.25 &mgr;W of power, which is more than 1000x lower power than LoRa radio chipsets.

References:

• Vamsi Talla, Mehrdad Hessar, Bryce Kellogg, Ali Najafi, Joshua R. Smith and Shyamnath Gollakota. 2017. LoRa Backscatter: Enabling The Vision of Ubiquitous Connectivity. Proc. ACM Interact. Mob. Wearable Ubiquitous Technol. 1, 3, Article 105 (September 2017), 24 pages. DOI: 10.1145/3130970 (open access)

Psychological trauma

From Wikipedia, the free encyclopedia

 

Psychological trauma is a type of damage to the mind that occurs as a result of a severely distressing event. Trauma is often the result of an overwhelming amount of stress that exceeds one's ability to cope, or integrate the emotions involved with that experience. A traumatic event involves one's experience, or repeating events of being overwhelmed that can be precipitated in weeks, years, or even decades as the person struggles to cope with the immediate circumstances, eventually leading to serious, long-term negative consequences.

However, trauma differs between individuals, according to their subjective experiences. People will react to similar events differently. In other words, not all people who experience a potentially traumatic event will actually become psychologically traumatized.^[2] However, it is possible to develop posttraumatic stress disorder (PTSD) after being exposed to a potentially traumatic event.^[3] This discrepancy in risk rate can be attributed to protective factors some individuals may have that enable them to cope with trauma; they are related to temperamental and environmental factors. Some examples are mild exposure to stress early in life,^[4] resilience characteristics, and active seeking of help.^[5]

Definition

DSM-IV-TR defines trauma as direct personal experience of an event that involves actual or threatened death or serious injury; threat to one's physical integrity, witnessing an event that involves the above experience, learning about unexpected or violent death, serious harm, or threat of death, or injury experienced by a family member or close associate. Memories associated with trauma are implicit, pre-verbal and cannot be recalled, but can be triggered by stimuli from the in vivo environment. The person's response to aversive details of traumatic event involve intense fear, helplessness or horror. In children it is manifested as disorganized or agitative behaviors.^[6]

Trauma can be caused by a wide variety of events, but there are a few common aspects. There is frequently a violation of the person's familiar ideas about the world and their human rights, putting the person in a state of extreme confusion and insecurity. This is seen when institutions depended upon for survival violate, humiliate, betray, or cause major losses or separations instead of evoking aspects like deserve, special, safe, new and freedom.^[7]

Psychologically traumatic experiences often involve physical trauma that threatens one's survival and sense of security.^[8] Typical causes and dangers of psychological trauma include harassment, embarrassment, abandonment, abusive relationships, rejection, co-dependence, physical assault, sexual abuse, partner battery, employment discrimination, police brutality, judicial corruption and misconduct, bullying, paternalism, domestic violence, indoctrination, being the victim of an alcoholic parent, the threat or the witnessing of violence (particularly in childhood), life-threatening medical conditions, and medication-induced trauma.^[9] Catastrophic natural disasters such as earthquakes and volcanic eruptions, large scale transportation accidents, house or domestic fire, motor vehicle accident, mass interpersonal violence like war, terrorist attacks or other mass tortures like sex trafficking, being taken as a hostage or kidnapped can also cause psychological trauma. Long-term exposure to situations such as extreme poverty or milder forms of abuse, such as verbal abuse, exist independently of physical trauma but still generate psychological trauma.

Some theories suggest childhood trauma can increase one's risk for mental disorders including posttraumatic stress disorder (PTSD),^[10] depression, and substance abuse. Childhood adversity is associated with neuroticism during adulthood.^[11] Parts of the brain in a growing child are developing in a sequential and hierarchical order, from least complex to most complex. The brain's neurons are designed to change in response to the constant external signals and stimulation, receiving and storing new information. This allows the brain to continually respond to its surroundings and promote survival. Our five main sensory signals contribute to the developing brain structure and its function.^[12] Infants and children begin to create internal representations of their external environment, and in particular, key attachment relationships, shortly after birth. Violent and victimized attachment figures impact infants' and young children's internal representations.^[13] The more frequent a specific pattern of brain neurons is activated, the more permanent the internal representation associated with the pattern becomes.^[14] This causes sensitization in the brain towards the specific neural network. Because of this sensitization, the neural pattern can be activated by decreasingly less external stimuli. Childhood abuse tends to have the most complications with long-term effects out of all forms of trauma because it occurs during the most sensitive and critical stages of psychological development.^[5] It could also lead to violent behavior, possibly as extreme as serial murder. For example, Hickey's Trauma-Control Model suggests that "childhood trauma for serial murderers may serve as a triggering mechanism resulting in an individual's inability to cope with the stress of certain events."^[15]

Often psychodynamic aspects of trauma are overlooked even by health professionals: "If clinicians fail to look through a trauma lens and to conceptualize client problems as related possibly to current or past trauma, they may fail to see that trauma victims, young and old, organize much of their lives around repetitive patterns of reliving and warding off traumatic memories, reminders, and affects."^[16]

Symptoms

People who go through these types of extremely traumatic experiences often have certain symptoms and problems afterward. The severity of these symptoms depends on the person, the type of trauma involved, and the emotional support they receive from others. Reactions to and symptoms of trauma can be wide and varied, and differ in severity from person to person. A traumatized individual may experience one or several of them.^[17]

After a traumatic experience, a person may re-experience the trauma mentally and physically, hence trauma reminders, also called triggers, can be uncomfortable and even painful. It can damage people’s sense of safety, self, self-efficacy, as well as the ability to regulate emotions and navigate relationships. They may turn to psychoactive substances including alcohol to try to escape or dampen the feelings. These triggers cause flashbacks, which are dissociative experiences where the person feels as though the events are reoccurring. They can range from distracting to complete dissociation or loss of awareness of the current context. Re-experiencing symptoms are a sign that the body and mind are actively struggling to cope with the traumatic experience.

Triggers and cues act as reminders of the trauma, and can cause anxiety and other associated emotions. Often the person can be completely unaware of what these triggers are. In many cases this may lead a person suffering from traumatic disorders to engage in disruptive or self-destructive coping mechanisms, often without being fully aware of the nature or causes of their own actions. Panic attacks are an example of a psychosomatic response to such emotional triggers.

Consequently, intense feelings of anger may frequently surface, sometimes in inappropriate or unexpected situations, as danger may always seem to be present, as much as it is actually present and experienced from past events. Upsetting memories such as images, thoughts, or flashbacks may haunt the person, and nightmares may be frequent.^[18] Insomnia may occur as lurking fears and insecurity keep the person vigilant and on the lookout for danger, both day and night. Trauma doesn't only cause changes in one's daily functions but could also lead to morphological changes. Such epigenetic changes can be passed on to the next generation, thus making genetics one of the components of psychological trauma. However, some people are born with or later develop protective factors such as genetics and sex that help lower their risk of psychological trauma.^[19]

The person may not remember what actually happened, while emotions experienced during the trauma may be re-experienced without the person understanding why (see Repressed memory). This can lead to the traumatic events being constantly experienced as if they were happening in the present, preventing the subject from gaining perspective on the experience. This can produce a pattern of prolonged periods of acute arousal punctuated by periods of physical and mental exhaustion. This can lead to mental health disorders like acute stress and anxiety disorder, traumatic grief, undifferentiated somatoform disorder, conversion disorders, brief psychotic disorder, borderline personality disorder, adjustment disorder, etc.^[20]

In time, emotional exhaustion may set in, leading to distraction, and clear thinking may be difficult or impossible. Emotional detachment, as well as dissociation or "numbing out", can frequently occur. Dissociating from the painful emotion includes numbing all emotion, and the person may seem emotionally flat, preoccupied, distant, or cold. Dissociation includes depersonalisation disorder, dissociative amnesia, dissociative fugue, dissociative identity disorder, etc. Exposure to and re-experiencing trauma can cause neurophysiological changes like slowed myelination, abnormalities in synaptic pruning, shrinking of the hippocampus, cognitive and affective impairment. This is significant in brain scan studies done regarding higher order function assessment with children and youth who were in vulnerable environments.

Some traumatized people may feel permanently damaged when trauma symptoms do not go away and they do not believe their situation will improve. This can lead to feelings of despair, transient paranoid ideation, loss of self-esteem, profound emptiness, suicidality, and frequently depression. If important aspects of the person's self and world understanding have been violated, the person may call their own identity into question.^[17] Often despite their best efforts, traumatized parents may have difficulty assisting their child with emotion regulation, attribution of meaning, and containment of post-traumatic fear in the wake of the child's traumatization, leading to adverse consequences for the child.^[13][21] In such instances, it is in the interest of the parent(s) and child for the parent(s) to seek consultation as well as to have their child receive appropriate mental health services.

Assessment

As "trauma" adopted a more widely defined scope, traumatology as a field developed a more interdisciplinary approach. This is in part due to the field's diverse professional representation including: psychologists, medical professionals, and lawyers. As a result, findings in this field are adapted for various applications, from individual psychiatric treatments to sociological large-scale trauma management. However, novel fields require novel methodologies. While the field has adopted a number of diverse methodological approaches, many pose their own limitations in practical application.

The experience and outcomes of psychological trauma can be assessed in a number of ways.^[22] Within the context of a clinical interview, the risk for imminent danger to the self or others is important to address but is not the focus of assessment. In most cases, it will not be necessary to involve contacting emergency services (e.g., medical, psychiatric, law enforcement) to ensure the individuals safety; members of the individual's social support network are much more critical.

Understanding and accepting the psychological state an individual is in is paramount. There are many mis-conceptions of what it means for a traumatized individual to be in crisis or 'psychosis'. These are times when an individual is in inordinate amounts of pain and cannot comfort themselves, if treated humanely and respectfully they will not get to a state in which they are a danger. In these situations it is best to provide a supportive, caring environment and communicate to the individual that no matter the circumstance they will be taken seriously and not just as a sick, delusional individual. It is vital for the assessor to understand that what is going on in the traumatized persons head is valid and real. If deemed appropriate, the assessing clinician may proceed by inquiring about both the traumatic event and the outcomes experienced (e.g., posttraumatic symptoms, dissociation, substance abuse, somatic symptoms, psychotic reactions). Such inquiry occurs within the context of established rapport and is completed in an empathic, sensitive, and supportive manner. The clinician may also inquire about possible relational disturbance, such as alertness to interpersonal danger, abandonment issues, and the need for self-protection via interpersonal control. Through discussion of interpersonal relationships, the clinician is better able to assess the individual's ability to enter and sustain a clinical relationship.

During assessment, individuals may exhibit activation responses in which reminders of the traumatic event trigger sudden feelings (e.g., distress, anxiety, anger), memories, or thoughts relating to the event. Because individuals may not yet be capable of managing this distress, it is necessary to determine how the event can be discussed in such a way that will not "retraumatize" the individual. It is also important to take note of such responses, as these responses may aid the clinician in determining the intensity and severity of possible posttraumatic stress as well as the ease with which responses are triggered. Further, it is important to note the presence of possible avoidance responses. Avoidance responses may involve the absence of expected activation or emotional reactivity as well as the use of avoidance mechanisms (e.g., substance use, effortful avoidance of cues associated with the event, dissociation).

In addition to monitoring activation and avoidance responses, clinicians carefully observe the individual's strengths or difficulties with affect regulation (i.e., affect tolerance and affect modulation). Such difficulties may be evidenced by mood swings, brief yet intense depressive episodes, or self-mutilation. The information gathered through observation of affect regulation will guide the clinician's decisions regarding the individual's readiness to partake in various therapeutic activities.

Though assessment of psychological trauma may be conducted in an unstructured manner, assessment may also involve the use of a structured interview. Such interviews might include the Clinician-Administered PTSD Scale (CAPS; Blake et al., 1995), Acute Stress Disorder Interview (ASDI; Bryant, Harvey, Dang, & Sackville, 1998), Structured Interview for Disorders of Extreme Stress (SIDES; Pelcovitz et al., 1997), Structured Clinical Interview for DSM-IV Dissociative Disorders- Revised (SCID-D; Steinberg, 1994), and Brief Interview for Posttraumatic Disorders (BIPD; Briere, 1998).

Lastly, assessment of psychological trauma might include the use of self-administered psychological tests. Individuals' scores on such tests are compared to normative data in order to determine how the individual's level of functioning compares to others in a sample representative of the general population. Psychological testing might include the use of generic tests (e.g., MMPI-2, MCMI-III, SCL-90-R) to assess non-trauma-specific symptoms as well as difficulties related to personality. In addition, psychological testing might include the use of trauma-specific tests to assess posttraumatic outcomes. Such tests might include the Posttraumatic Stress Diagnostic Scale (PDS; Foa, 1995), Davidson Trauma Scale (DTS: Davidson et al., 1997), Detailed Assessment of Posttraumatic Stress (DAPS; Briere, 2001), Trauma Symptom Inventory (TSI: Briere, 1995), Trauma Symptom Checklist for Children (TSCC; Briere, 1996), Traumatic Life Events Questionnaire (TLEQ: Kubany et al., 2000), and Trauma-related Guilt Inventory (TRGI: Kubany et al., 1996).

Children are assessed through activities and therapeutic relationship, some of the activities are play genogram, sand worlds, coloring feelings, Self and Kinetic family drawing, symbol work, dramatic-puppet play, story telling, Briere's TSCC, etc.^[23]

Treatment

A number of psychotherapy approaches have been designed with the treatment of trauma in mind—EMDR, progressive counting (PC), somatic experiencing, biofeedback, Internal Family Systems Therapy, and sensorimotor psychotherapy.

There is a large body of empirical support for the use of cognitive behavioral therapy^[24][25] for the treatment of trauma-related symptoms,^[26] including posttraumatic stress disorder. Institute of Medicine guidelines identify cognitive behavioral therapies as the most effective treatments for PTSD.^[27] Two of these cognitive behavioral therapies, prolonged exposure^[28] and cognitive processing therapy,^[29] are being disseminated nationally by the Department of Veterans Affairs for the treatment of PTSD.^[30][31] Recent studies show that a combination of treatments involving dialectical behavior therapy (DBT), often used for borderline personality disorder, and exposure therapy is highly effective in treating psychological trauma.^[19] If, however, psychological trauma has caused dissociative disorders or complex PTSD, the trauma model approach (also known as phase-oriented treatment of structural dissociation) has been proven to work better than simple cognitive approach. Studies funded by pharmaceuticals have also shown that medications such as the new anti-depressants are effective when used in combination with other psychological approaches.^[32]

Trauma therapy allows processing trauma-related memories and allows growth towards more adaptive psychological functioning. It helps to develop positive coping instead of negative coping and allows the individual to integrate upsetting-distressing material (thoughts, feelings and memories) resolve internally. It also aids in growth of personal skills like resilience, ego regulation, empathy...etc.^[33]

Process' involved in trauma therapy are:

• Psychoeducation: Information dissemination and educating in vulnerabilities and adoptable coping mechanisms.
• Emotional regulation: Identifying, countering discriminating, grounding thoughts and emotions from internal construction to an external representation.
• Cognitive processing: Transforming negative perceptions and beliefs to positive ones about self, others and environment through cognitive reconsideration or re-framing.
• Trauma processing: Systematic desensitization, response activation and counter-conditioning, titrated extinction of emotional response, deconstructing disparity (emotional vs. reality state), resolution of traumatic material (state in which triggers don't produce the harmful distress and able to express relief.)
• Emotional processing: Reconstructing perceptions, beliefs and erroneous expectations like trauma-related fears are auto-activated and habituated in new life contexts, providing crisis cards with coded emotions and appropriate cognition's. (This stage is only initiated in pre-termination phase from clinical assessment & judgement of the mental health professional.)
• Experiential processing: Visualization of achieved relief state and relaxation methods.

Causative discourses

Situational trauma

Trauma can be caused by man-made, technological disasters and natural disasters,^[34] including war, abuse, violence, mechanized accidents (car, train, or plane crashes, etc.) or medical emergencies.

Responses to psychological trauma: Response to Psychological trauma can be varied based on the type of trauma, sociodemographic and background factors.^[34] There are several behavioral responses common towards stressors including the proactive, reactive, and passive responses. Proactive responses include attempts to address and correct a stressor before it has a noticeable effect on lifestyle. Reactive responses occur after the stress and possible trauma has occurred, and are aimed more at correcting or minimizing the damage of a stressful event. A passive response is often characterized by an emotional numbness or ignorance of a stressor.

Those who are able to be proactive can often overcome stressors and are more likely to be able to cope well with unexpected situations. On the other hand, those who are more reactive will often experience more noticeable effects from an unexpected stressor. In the case of those who are passive, victims of a stressful event are more likely to suffer from long-term traumatic effects and often enact no intentional coping actions. These observations may suggest that the level of trauma associated with a victim is related to such independent coping abilities.

There is also a distinction between trauma induced by recent situations and long-term trauma which may have been buried in the unconscious from past situations such as childhood abuse. Trauma is often overcome through healing; in some cases this can be achieved by recreating or revisiting the origin of the trauma under more psychologically safe circumstances, such as with a therapist.

In psychoanalysis

French neurologist Jean-Martin Charcot argued in the 1890s that psychological trauma was the origin of all instances of the mental illness known as hysteria. Charcot's "traumatic hysteria" often manifested as a paralysis that followed a physical trauma, typically years later after what Charcot described as a period of "incubation". Sigmund Freud, Charcot's student and the father of psychoanalysis, examined the concept of psychological trauma throughout his career. Jean Laplanche has given a general description of Freud's understanding of trauma, which varied significantly over the course of Freud's career: "An event in the subject's life, defined by its intensity, by the subject's incapacity to respond adequately to it and by the upheaval and long-lasting effects that it brings about in the psychical organization".^[35]
The French psychoanalyst Jacques Lacan claimed that what he called "The Real" had a traumatic quality external to symbolization. As an object of anxiety, Lacan maintained that The Real is "the essential object which isn't an object any longer, but this something faced with which all words cease and all categories fail, the object of anxiety par excellence".^[36]

Stress disorders

All psychological traumas originate from stress, a physiological response to an unpleasant stimulus. Long term stress increases the risk of poor mental health and mental disorders, which can be attributed to secretion of glucocorticoids for a long period of time. Such prolonged exposure causes many physiological dysfunctions such as the suppression of the immune system and increase in blood pressure.^[39] Not only does it affect the body physiologically, but a morphological change in the hippocampus also takes place. Studies showed that extreme stress early in life can disrupt normal development of hippocampus and impact its functions in adulthood. Studies surely show a correlation between the size of hippocampus and one's susceptibility to stress disorders.^[40] In times of war, psychological trauma has been known as shell shock or combat stress reaction. Psychological trauma may cause an acute stress reaction which may lead to posttraumatic stress disorder (PTSD). PTSD emerged as the label for this condition after the Vietnam War in which many veterans returned to their respective countries demoralized, and sometimes, addicted to psychoactive substances. The symptoms of PTSD must persist for at least a month for diagnosis. The main symptoms of PTSD consist of four main categories: Trauma (i.e. intense fear), reliving (i.e. flashbacks), avoidance behavior (i.e. emotional numbing), and hypervigilance (i.e. irritability).^[41] Research shows that about 60% of the US population reported as having experienced at least one traumatic symptom in their lives but only a small proportion actually develops PTSD. There is a correlation between the risk of PTSD and whether or not the act was inflicted deliberately by the offender.^[19] Psychological trauma is treated with therapy and, if indicated, psychotropic medications.

The term continuous post traumatic stress disorder (CTSD)^[42] was introduced into the trauma literature by Gill Straker (1987). It was originally used by South African clinicians to describe the effects of exposure to frequent, high levels of violence usually associated with civil conflict and political repression. The term is also applicable to the effects of exposure to contexts in which gang violence and crime are endemic as well as to the effects of ongoing exposure to life threats in high-risk occupations such as police, fire and emergency services.

As one of the processes of treatment, confrontation with their sources of trauma plays a crucial role. While critical incident debriefing people immediately after an event has not been shown to reduce incidence of PTSD, coming alongside people experiencing trauma in a supportive way has become standard practice.^[43]

Vicarious

Vicarious trauma affects workers being 'witnesses' to their clients' trauma. It is more likely to occur in situations where trauma related work is the norm rather than the exception. Listening with empathy to the clients generates feeling, and 'seeing oneself' in clients' trauma may compound the risk for developing trauma symptoms.^[44] May also result if we are witness to situations that happen in the course of our work (e.g. violence in the workplace, reviewing violent video tapes,^[45] etc.). Risk increases with exposure and with the absence of seeking protective factors and pre-preparation of preventive strategies.

Scientists remove one of the final barriers to making lifelike robots

3D-printable, synthetic soft muscle can mimic natural biological systems, lifting 1000 times its own weight

September 20, 2017
Original link:  http://www.kurzweilai.net/scientists-remove-one-of-the-final-barriers-to-making-lifelike-robots#!prettyPhoto

(L) The electrically actuated muscle with thin resistive wire in a rest position; (R) The muscle is expanded using only a low voltage (8V). (credit: Aslan Miriyev/Columbia Engineering)

Researchers at the Columbia Engineering Creative Machines lab have developed a 3D-printable, synthetic soft muscle that can mimic natural biological systems, lifting 1000 times its own weight. The artificial muscle is three times stronger than natural muscle and can push, pull, bend, twist, and lift weight — no external devices required.

Existing soft-actuator technologies are typically based on bulky pneumatic or hydraulic inflation of elastomer skins that expand when air or liquid is supplied to them, which require external compressors and pressure-regulating equipment.

“We’ve been making great strides toward making robot minds, but robot bodies are still primitive,” said Hod Lipson, PhD, a professor of mechanical engineering. “This is a big piece of the puzzle and, like biology, the new actuator can be shaped and reshaped a thousand ways. We’ve overcome one of the final barriers to making lifelike robots.”

The research findings are described in an open-access study published Tuesday Sept. 19, 2017 by Nature Communications.

Replicating natural motion


Inspired by living organisms, soft-material robotics hold promise for areas where robots need to contact and interact with humans, such as manufacturing and healthcare. Unlike rigid robots, soft robots can replicate natural motion — grasping and manipulation — to provide medical and other types of assistance, perform delicate tasks, or pick up soft objects.

Structure and principle of operation of the soft composite material (stereoscope image scale bar is 1 mm). Upon heating the composite to a temperature of 78.4 °C, ethanol boils and the local pressure inside the micro-bubbles grows, forcing the elastic silicone elastomer matrix to comply by expansion in order to reduce the pressure. (credit: Aslan Miriyev et al./Nature Communications)

To achieve an actuator with high stress and high strain coupled with low density, the researchers used a silicone rubber matrix with ethanol (alcohol) distributed throughout in micro-bubbles. This design combines the elastic properties and extreme volume change attributes of other material systems while also being easy to fabricate, low cost, and made of environmentally safe materials.*

The researchers next plan to use conductive (heatable) materials to replace the embedded wire, accelerate the muscle’s response time, and increase its shelf life. Long-term, they plan to involve artificial intelligence to learn to control the muscle — perhaps a final milestone towards replicating natural human motion.

* After being 3D-printed into the desired shape, the artificial muscle was electrically actuated using a thin resistive wire and low-power (8V). It was tested in a variety of robotic applications, where it showed significant expansion-contraction ability and was capable of expansion up to 900% when electrically heated to 80°C. The new material has a strain density (the amount of deformation in the direction of an applied force without damage) that is 15 times larger than natural muscle.

Columbia Engineering | Soft Materials for Soft Actuators

Roboticists show off their new advances in “soft robots” (credit: Reuters TV)

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Abstract of Soft material for soft actuators

Inspired by natural muscle, a key challenge in soft robotics is to develop self-contained electrically driven soft actuators with high strain density. Various characteristics of existing technologies, such as the high voltages required to trigger electroactive polymers ( > 1KV), low strain ( < 10%) of shape memory alloys and the need for external compressors and pressure-regulating components for hydraulic or pneumatic fluidicelastomer actuators, limit their practicality for untethered applications. Here we show a single self-contained soft robust composite material that combines the elastic properties of a polymeric matrix and the extreme volume change accompanying liquid–vapor transition. The material combines a high strain (up to 900%) and correspondingly high stress (up to 1.3 MPa) with low density (0.84 g cm⁻³). Along with its extremely low cost (about 3 cent per gram), simplicity of fabrication and environment-friendliness, these properties could enable new kinds of electrically driven entirely soft robots.

References:

• Aslan Miriyev et al. Soft Material for Soft Actuators. Nature Communications, 2017 DOI: 10.1038/10.1038/s41467-017-00685-3 (open access)