Illustration
of an ATOMS microchip localized within the gastrointestinal tract (not
to scale; a prototype measures just 0.7 cubic millimeters). The
microchip contains a magnetic field sensor, integrated antennas, a
wireless powering device, and a circuit that adjusts its radio frequency
signal based on the magnetic field strength and wirelessly relays the
chip’s precise location. (credit: Ella Marushchenko/Caltech)
Caltech researchers have developed a “Fantastic Voyage” style
prototype microchip that could one day be used in “smart pills” to
diagnose and treat diseases when inserted into the human body.
Called ATOMS (addressable transmitters operated as magnetic spins),
the microchips could one day monitor a patient’s gastrointestinal
tract, blood, or brain, measuring factors that indicate a patient’s
health — such as pH, temperature, pressure, and sugar concentrations —
with sub-millimeter localization and relay that information to doctors.
Or the devices could even be instructed to release drugs at precise
locations.
An open access paper describing the new device appears in the September issue of the journal Nature Biomedical Engineering. The lead author is Manuel Monge, who now works at Elon Musk’s new Neuralink company.
The
ATOMS microchips, proven to work in tests with mice, mimic the way
nuclear spins in atoms in the body resonate to magnetic fields in a
magnetic resonance imaging (MRI) machine and can be precisely identified
and localized within the body. Similarly, the ATOMS devices resonate at
different frequencies depending on where they are in a magnetic field.
(credit: Manuel Monge et al./ Nature Biomedical Engineering)
Abstract of Localization of Microscale Devices In Vivo using Addressable Transmitters Operated as Magnetic Spins
The function of miniature wireless medical devices, such as capsule
endoscopes, biosensors and drug-delivery systems, depends critically on
their location inside the body. However, existing electromagnetic,
acoustic and imaging-based methods for localizing and communicating with
such devices suffer from limitations arising from physical tissue
properties or from the performance of the imaging modality. Here, we
embody the principles of nuclear magnetic resonance in a silicon
integrated-circuit approach for microscale device localization.
Analogous to the behaviour of nuclear spins, the engineered miniaturized
radio frequency transmitters encode their location in space by shifting
their output frequency in proportion to the local magnetic field;
applied field gradients thus allow each device to be located precisely
from its signal’s frequency. The devices are integrated in circuits
smaller than 0.7 mm3 and manufactured through a standard
complementary-metal-oxide-semiconductor process, and are capable of
sub-millimetre localization in vitro and in vivo. The technology is
inherently robust to tissue properties, scalable to multiple devices,
and suitable for the development of microscale devices to monitor and
treat disease.
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.
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 neuropharmacologistCandace 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.
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]
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 stresshormones, 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]
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.
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 subcorticallimbic 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.
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
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.
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]
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]
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.