stress physiology and psychology and its associated disorders in psychiatry

1. NEUROBIOLOGY OF STRESS
Presented by Dr. Karrar husain
Moderator Dr. Piyush P. Singh

2. • Stress is defined as an internal state which can be caused by
physical demands on body(disease condition, exercise,
extreme of temperatures etc) or by environmental and social
situations which are evaluated as potentially harmful,
uncontrallable, or exceeding our resource for coping.
Introduction to psychology morgan and king
• The physical, environmental and social cause of stress state
are termed as stressors.
• Stress arises when individuals perceive that they cannot
adequately cope with the demands being made on them or
with threats to their well-being.” ..Lazarus, R.S. (1966).

3. • According to Seyle…….physiological response of the body to
external stressors.
• Cox (1975) considers that stress involves external stimuli, the
physiological response to these stimuli, and psychological
processes that mediate between stimulus and response. The
psychological processes involve differences between
individuals in their perception of the environmental demands
and their own capacity to cope with them.

4. • Stress is a physical, mental, or emotional factor that causes
bodily or mental tension. Stresses can be external (from the
environment, psychological, or social situations) or internal
(illness, or from a medical procedure)…. Medical dictionary
• A hallmark of the stress response is the activation of the ANS
and HPA axis
• The organism needs the normal stress hormone response to
survive, and inadequate or excessive adrenocortical and
autonomic function is deleterious for health and survival.

5. • Human beings are prone to prolonged periods of elevated
activity of the same systems which help us survive more acute
challenges.
• This prolonged elevation may be due to anxiety; to constant
exposure to adverse environments, and interpersonal conflict;
and to changes in life-style and health-related behaviors that
result from being under chronic stress.
• Brain - key organ of the stress response because it determines
what is threatening and, therefore stressful and also controls
the behavioral and physiological responses to potentially
stressful experiences

6. HISTORY
• For centuries, physicians and patients have made the
association between adverse life events and illness.
• The links between emotion and sudden cardiac death have
been repeatedly noted in sources as diverse as the Bible,
anthropology, and clinical experience.
• William Harvey in the 17th century and William Osler in the
19th century frequently alluded to the relationship between
adverse life events and illness onset.
• Many contemporary cultures regard illness as the outcome of
being out of balance with the environment.

7. • The term stress was coined by Hans Selye (1907 to 1982), who
observed that many highly diverse ways of perturbing the
organism resulted in common physiological responses.
• Selye invoked the adrenocortical system as the crucial
responder to stressful stimulation.
• He observed that any novelty or perturbation of the system
was associated with an elevation of adrenocortical activity.

8. • Walter Cannon (1871 to 1945): Cannon methodically
investigated the other great pathway of stressful responses,
the sympathetic nervous system.
• Cannon also focused on more immediate or short-term
responses to stressors.

9. Stress versus coping
• Coping is expending conscious effort to solve personal and
interpersonal problems, and seeking to master, minimize or
tolerate stress or conflict. The effectiveness of the coping
efforts depend on the type of stress and/or conflict, the
particular individual, and the circumstances.
• Richard Rahe et al. in 1974 suggested a model model of life
stress, coping, and response.

11. Stress response

12. A systems model of the human stress response

13. Stressor Events
• The stimulus for the stress response
• Psychosocial stressors and biogenic stressors.
• Psychosocial stressor  real or imagined environmental
events that “set the stage” for the elicitation of the stress
response. They must work through cognitive appraisal
mechanics.
• Biogenic stressors - Such stimuli bypass the higher cognitive
appraisal mechanisms and work directly on affective and
neurological triggering nuclei. eg Ginseng, Ginkgo biloba,
Amphetamine, Caffeine, Nicotine.

14. Cognitive–Affective Domain
• Cognitive appraisal refers to the process of cognitive
interpretation, that is, the meanings that we assign to the
world as it unfolds before us.
• Affective integration refers to the blending and coloring of felt
emotion into the cognitive interpretation.
• The resultant cognitive–affective complex represents how the
stressors are ultimately perceived.
• In effect, this critical integrated perception represents the
determination of whether psychosocial stimuli become
psychosocial stressors or not.

15. • Appraisal is a function of any existing biological predispositions,
personality patterns, learning history, and available coping
resources. Once appraisal is made, efferent impulses project so as
to potentiate the stimulation of two major effector systems:
1. Impulses project back to the limbic system, especially the
hippocampus , for the experience of stimulus-specific felt emotion
and the potential to trigger visceral effector mechanisms.
2. Impulses similarly project to the areas of the neocortex concerned
with neuromuscular behavior where, through pyramidal and
extrapyramidal systems, muscle tone (tension) is increased and the
intention to act can be potentially translated to actual overt motor
activity.

16. • Psychosocial stimuli, once perceived, excite nonspecific
arousal and cognitive appraisal mechanisms. If the appraisal
of the stimulus is ultimately one of threat, challenge, or
aversion, then emotional arousal will likely result.
• In most individuals, activation of the limbic centers for
emotional arousal leads to expression of the felt emotion in
the form of visceral activation and neuromuscular activity
• Thus, in the final analysis, it can be seen that physiological
reactions to psychosocial stimuli result from the cognitive
interpretations and emotional reactions to those stimuli, not
the stimuli themselves.

17. Neurological Triggering Mechanisms
• The next step in the model is the neurological triggering
mechanisms consisting of the locus ceruleus (LC), limbic
system, and hypothalamic efferent triggering complex (consist of
the LC, the hippocampus, the septal–hippocampal–amygdaloid complexes, and the
anterior and posterior hypothalamic nuclei).
• These structures give rise to the multiaxial stress response.
• These centers even seem capable of establishing an
endogenously determined neurological tone that is
potentially self-perpetuating

19. The Stress Response
• three physiological pathways
(1) the neural axes,
(2) the neuroendocrine axis, and
(3) the endocrine axes.

20. The Neural Axes
• Three neural axes comprise the neural stress response:
(1) the sympathetic nervous system,
(2) the parasympathetic nervous system, and,
(3) the neuromuscular nervous system.
• These neural pathways are the first of all stress response axes
to become activated during stress arousal.

21. • Following the complex neocortical and limbic integrations that
occur in the interpretation of a stimulus as “threatening,”
neural impulses descend to the posterior hypothalamus (in
the case of a sympathetic activation) and the anterior
hypothalamus (in the case of a parasympathetic activation).
• From here, neural pathways descend from the anterior
hypothalamus through the cranial and sacral spinal cord
regions and then innervate the end organs.

22. • The effects of neural activation via the sympathetic system are
those of generalized arousal within the end an “ergotropic”
response.
• The effects of activation via the parasympathetic system are
inhibition, slowing, and “restorative” functions—a
“trophotropic” response.
• The most common form of neural autonomic stress
responsiveness in human beings is in the form of the
ergotropic response simultaneous trophotropic responses
have been observed in human beings as well

24. • Skeletal muscular is also a prime target for immediate
activation during stress and emotional arousal.
• Such activation, if excessive, may lead to a host of
neuromuscular dysfunctions as well as increased limbic
excitation and therefore heightened emotional arousal.

25. The Neuroendocrine Axis
• Result in The “Fight-or-Flight” Response
• The “ fight-or- flight” response is thought to be a mobilization
of the body to prepare for muscular activity in response to a
perceived threat. This mechanism allows the organism either
to fight or to flee from the perceived threat.
• Dorsomedial amygdalar complex  lateral and posterior
hypothalamic regions thoracic spinal cord celiac ganglion
 adrenal medulla.

26. • Upon neural stimulation, the adrenal medulla releases the
medullary catecholamines. The effect of these medullary
catecholamines is an increase in generalized adrenergic
somatic activity in human beings.
• The effect, therefore, is functionally identical to that of direct
sympathetic innervation , except that the medullary
catecholamines require a 20 to 30 second delay of onset for
measurable effects and display a tenfold increase in effect
duration .

28. Endocrine Axes
• The most chronic and prolonged somatic responses to stress
are the result of the endocrine axes.
• Four endocrine axes associated with the stress response:
1. The adrenal cortical axis.
2. The somatotropic axis.
3. The thyroid axis.
4. The posterior pituitary axis.
• These axes require greater intensity stimulation to activate

29. The Adrenal Cortical Axis
• The septal–hippocampal complex  the median eminence
of the hypothalamus  release CRF into the hypothalamic–
hypophyseal portal system.
• The CRF acts on anterior pituitary  release ACTH in the
systemic circulation.
• At the same time, the precursor to the various endogenous
analgesic opioids (endorphins) is released. This precursor
substance, beta lipotropin, yields the proliferation of
endogenous opioids during human stress.

30. • ACTH act upon the adrenal cortex to release the
glucocorticoids cortisol and corticosterone into the systemic
circulation.

32. • ACTH  zona glomerulosa to secrete the mineralocorticoids
aldosterone and deoxycorticosterone into the systemic
circulation.
• Aldosterone  absorption of Na and Cl by the renal tubules
and a decrease in their excretion by the salivary glands, sweat
glands, and gastrointestinal tract  fluid retention.
• Others- Aldosterone may increase glycogen deposits in the
liver and decrease circulating eosinophils.

33. • (HPAC) Activation of this system in the aggregate has been
associate with the helplessness/hopelessness depression
syndrome, passivity, the perception of no control,
immunosuppression, and gastrointestinal symptomatology.
Behaviorally, the HPAC system appears to be activated when
active coping is not possible; thus, it has been called the
“passive coping” system.
• Considering the HPAC system with respect to the SAM:
1. Effort without distress → activation of the SAM system.
2. Distress without effort → activation of the HPAC system.
3. Effort with distress → activation of both SAM and HPAC.

34. The Somatotropic Axis
• The septal–hippocampal complex  the median eminence
of the hypothalamus  release somatotropin-releasing factor
(SRF) stimulates the anterior pituitary.
• The anterior pituitary responds to the SRF by releasing growth
hormone.
• The role of growth hormone in stress is somewhat less clearly
understood.

35. The Thyroid Axis
• Median eminence of the hypothalamus release thyrotropin-
releasing factor (TRF)  anterior pituitary  TSH.
• TSH stimulates the thyroid gland to release : triiodothyronine
(T3) and thyroxine (T4).
• In humans, psychosocial stimuli have generally led to an
increase in thyroidal activity.
• Thyroid hormones increases general metabolism, heart rate,
heart contractility, peripheral vascular resistance, and the
sensitivity of some tissues to catecholamines.

36. The Posterior Pituitary Axis
• The posterior pituitary (neurohypophysis) receives neural
impulses from the supraoptic nuclei of the hypothalamus.
Stimulation from these nuclei results in the release of the
hormones vasopressin and oxytocin into the systemic
circulation.
• ADH result in water retention.
• Oxytocin, the other major hormone found in the posterior
pituitary axis. Its role in the human stress response is
currently unclear but may be involved in psychogenic labor
contractions and premature birth, as well as the stress
response, particularly for women

37. others
• Various investigations have shown that both luteinizing
hormone, and testosterone have been shown to be
responsive to the presentation of various stressors.
• The hormone prolactin has clearly shown responsiveness to
psychosocial stimulation as well.

39. The “General Adaptation Syndrome”
• Hans Seyle ( 1956 ) proposed an integrative model for the
stress response, known as the “General Adaptation
Syndrome” (GAS).
• The GAS is a tri-phasic phenomenon. The first phase Selye
refers to as the“alarm” phase, representing a generalized
somatic shock, or “call to arms” of the body’s defense
mechanisms.
• The second phase is called the “stage of resistance,” in which
there is a dramatic reduction in most alarm stage processes
and the body fights to reestablish and maintain homeostasis.
• Stages 1 and 2 can be repeated throughout one’s life.

40. • Eventually the “adaptive energy,” that is, the adaptive
mechanisms in the second stage, may become depleted. At
this point, the body enters the third and final stage,
• the “stage of exhaustion,” which, when applied to a target
organ, is indicative of the exhaustion of that organ, and the
symptoms of disease and dysfunction become manifest.
• When the final stage is applied to the entire body, life itself
may be in jeopardy

43. • Most immediate response to a stressful stimulus occurs via
the direct neural innervations of end organs.
• The intermediate stress effects are due to the neuroendocrine
“ fight-or- flight” axis. Its effects range from intermediate to
chronic in duration.
• The endocrine axes are the final pathways to react to stressful
stimuli ,a higher intensity stimulus is needed to activate this
axis.
• The GAS provides an additional schema to extend the
endocrine response axis in the adaptation of the organism to
the presence of a chronic stressor

45. Target-Organ Activation
• The term target-organ activation refers to the phenomenon in
which the neural, neuroendocrine, and endocrine
constituents of the stress response (1) activate, (2) increase or
(3) inhibit normal activation, or (4) catabolize some organ
system in the human body.
• Potential target-organ systems the CVS, the GIS, the skin, the
immune system, the brain and its mental status
• Result in various clinical signs and symptoms.

46. • Target-organ activation and subsequent signs and symptoms
of disease may affect the patient’s cognitive–affective
behavior and, therefore, further neurological triggering and
continued stress response activity.
• In some cases (e.g., agoraphobic patients, obsessive patients,
and hysteria-prone patients), a hypersensitive awareness to
target-organ symptoms can create a self-sustaining
pathogenic feedback loop.

49. Coping
• Coping is defined as: efforts, both action-oriented and
intrapsychic, to manage environmental and internal demands,
and conflicts among them, which exceed a person’s resources.
• Coping can occur prior to a stressful confrontation, in which
case it is called anticipatory coping, as well as in reaction to a
present or past confrontation with harm.
• More recently, coping has been defined as “constantly
changing cognitive and behavioral efforts to manage specific
demands that are appraised as taxing or exceeding the
resources of the person

50. • Coping may be thought of as environmental or cognitive
tactics designed to attenuate the stress response.
• The present model views coping as residing subsequent to the
physiological stress response and target-organ activation.
• Thus, coping is seen as an attempt to reestablish homeostasis.

51. • Adaptive or maladaptive.
• Adaptive coping strategies reduce stress while at the same
time promoting long-term health (e.g., exercise, relaxation,
proper nutrition).
• Maladaptive coping strategies, on the other hand, do indeed
reduce stress in the short term but serve to erode health in
the long term (alcohol/drug abuse, cigarette smoking,
interpersonal withdrawal).

52. • when coping is successful, extraordinary target organ
activation is reduced or eliminated and homeostasis is
reestablished.
• If coping strategies are unsuccessful, target-organ activation is
maintained and the chances of target-organ disease are
increased.

54. Structural changes of brain
(animal studies)
The Hippocampus
• Certain types of acute stress and many chronic stressors
suppress neurogenesis or cell survival in the dentate gyrus.
• CA3 pyramidal cells undergo a reversible remodeling of their
dendrites in chronic stress.
• chronic stress causes retraction and simplification of dendrites
in the CA3 region of the hippocampus.
Physiology and Neurobiology of Stress and Adaptation:
Central Role of the Brain.. Physiol Rev 87: 873–904, 2007;

55. • These structural changes are mediated by adrenal steroids it
also involves interactions with neurochemical systems in the
hippocampus, including serotonin, endogenous opioids,
calcium currents, GABA-benzodiazepine receptors, and
excitatory amino acids.
• Structural changes cause impairments in memory and
learning. The effects of chronic stress on both morphology
and learning disappeared within 1–2 wk after cessation of the
stress suggesting that it serves an adaptive function and does
not constitute “damage.
Physiology and Neurobiology of Stress and Adaptation: Central Role
of the Brain.. Physiol Rev 87: 873–904, 2007;

56. Prefrontal Cortex and Amygdala
• Acute and repeated stress caused dendritic shortening in
medial prefrontal cortex but produced dendritic growth in
neurons in amygdala.
• Remodeling in PFC result in impairment in attention, extinction
of a fear.
• In amygdala it result in enhances amygdala-dependent
unlearned fear and fear conditioning.
• Chronic stress also increases aggression and produce anxiety.
Physiology and Neurobiology of Stress and Adaptation: Central
Role of the Brain.. Physiol Rev 87: 873–904, 2007;

57. Stress and immune response
• The immune system is regulated by neural input from sensory,
sympathetic and parasympathetic nerves, as well as by
circulating hormones, of which the glucocorticoids are among
the most prominent
• Brief or mild stressors may actually enhance acquired
immunity
• Lymphocytes, monocytes and NK cells are all reduced in
number in blood and increased in number in tissues, such as
the skin, as a result of acute stress

58. • Chronic stress  decrements in memory T cell responses to
latent virus antigens and to vaccines, in terms of antigen-
induced T-cell proliferation and T-cell–mediated killing of
virally transformed B lymphocytes.
• Chronic stress over 3–5 weeks produces a suppression of the
DTH response (DTH is the standard test of in vivo cell-
mediated immunity).

59. Clinical Implications of Psychoneuroimmunology
and the Cytokine Brain Link
• Increasing evidence suggests that abnormalities in cytokine
expression and regulation that occur during stress might
exacerbate the course of many chronic diseases.
• Cardiovascular Disease-psychological and physical stressors
increase both release of proinflammatory cytokines and
expression of adhesion molecules that tether and bind
immune cells to the vascular endothelium atherosclerosis
• Infectious Disease Risk : individuals reporting more
psychological stress have both a higher incidence and a greater
severity of certain infectious illnesses, such as Epstein-Barr
virus infections and the common cold

60. • HIV : Immune system decline and HIV replication are
particularly rapid in patients living under chronic stress.
• Rheumatoid Arthritis : recent data suggest that stressful
events, particularly those of an interpersonal nature, provoke
symptoms of disease, such as greater pain and functional
limitations, and disease progression.
• Cancer : Experimental studies  acute stress leads to
decreases in NK cell function and facilitates the metastatic
spread of NK-sensitive tumors. There are some observations
of a higher rate of survival in cancer who have received
psychological interventions.

61. STRESS AND PSYCHIATRIC ILLNESS
• In the early to mid-1800s, a school of thought emerged, led by
Philippe Pinel (1745 to 1826) of the Salpetriere in Paris and
Amariah Brigham (1798 to 1849) in America, that the
expression of mental illness was affected by life circumstances
and, more broadly, by societal factors.
• This orientation held that an individual's response to stress is
modified by a number of intrinsic factors and extrinsic factors.
The model incorporated individual temperamental and
experiential characteristics, such as potential vulnerability
factors, stressful life events as initiating or exacerbating
factors, and a variety of support networks as potentially
modifying factors for the occurrence of mental illness.

62. Stress and Psychotic Disorders
• Adverse life events and stressful social and familial milieu play
an important role in determining the course of illness in
general and episodes of relapse in particular.
• Chronic interpersonal stress, usually studied in the context of
the family, has been shown to be an important risk factor for
relapse in schizophrenia.
• Individuals with schizophrenia residing in homes with high
expressed emotion tend to relapse at twice the rate of those
who live in families with low expressed emotion.

63. • Preliminary evidence suggests that polymorphisms within the
catechol-O-methyltransferase and brain-derived neurotrophic
factor genes may interact with psychosocial stress in the
development of psychosis.
Schizophr Bull (2008) 34 (6): 1095-1105.

64. Affective Disorders
• Social stressors, in general, have been well recognized as risk
factors for mood disorders.
• However, different kinds of social stressors (i.e., childhood vs.
adulthood events, acute vs. chronic stressors, positive vs.
negative life events) can play different roles in the
predisposition and precipitation of depressive or manic
disorders.
• In the case of major depression and bipolar disorder, the
association of acute stressors and the onset of illness become
progressively weaker with the increasing number of previous
episodes.

65. • In the development of major mood disorders, chronic
stressors (e.g., unemployment, difficult marriage) play a more
important role than specific, acute stressors. However,
accumulation of stressful negative life events is the strongest
predisposing factor.
• The higher level and, probably, the different nature of social
stressors in individuals living in urban communities may be
among the main sources accounting for their higher
psychiatric morbidity.

66. • There is a fundamental similarity between the
neuroendocrine effects of stress on humans and the
neuroendocrine abnormalities in major depression ie
overactivity of the HPA axis, as inferred by increased plasma
cortisol and ACTH levels.
• Challenge studies with CRH that have demonstrated reduced
ACTH responses to CRH in depressed patients compared to
control subjects suggest that chronic CRH secretion (with
compensatory downregulation of CRH receptors at the
pituitary level) is an important feature of major depression.

67. • A functional polymorphism in the promoter region of the
serotonin transporter (5-HT T) gene was found to moderate
the influence of stressful life events on depression. Individuals
with one or two copies of the short allele of the 5-HT T
promoter polymorphism exhibited more depressive
symptoms, diagnosable depression, and suicidality in relation
to stressful life events than individuals homozygous for the
long allele.
Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene;
Science 18 July 2003: Vol. 301 no. 5631 pp. 386-389

68. • serotonin transporter promoter polymorphism (5-HTTLPR)
moderates the relationship between stress and depression,
with the less functional allele associated with increased stress
sensitivity. (The principal function of the serotonin transporter is to remove
serotonin from the synapse, returning it to the presynaptic neuron where the
neurotransmitter can be degraded or rereleased at a later time. A polymorphism in
the promoter region of the serotonin transporter gene (5-HTTLPR) has been found
to affect the transcription rate of the gene, with the short (s) allele
transcriptionally less efficient than the alternate long (l) allele)
Arch Gen Psychiatry. 2011;68(5):444-454

69. Anxiety Disorders
• Panic disorder frequently has its onset or recrudescence in
the context of stressful life events. In particular, there is
evidence to suggest that either interpersonal conflict or
serious illness (in a significant other) may trigger the onset of
panic disorder in susceptible individuals
• In terms of the effects of early life stressors, there is growing
evidence that certain adverse early life events, such as sexual
or physical abuse, may be risk factors for the later
development of panic disorder, particularly in women.

70. Stress and trauma related disorders
• DSM-5 recognizes the existence of a group of disorders that
are, by definition, stress-related.
• It includes PTSD, acute stress disorder, adjustment disorder,
reactive attachment disorder and disinhibited social
engagement disorder.
• Acute stress disorder has its onset after particularly traumatic
(often life-threatening) events, such as violent assault or
serious accidents, and is denoted by the presence of
prominent dissociative symptoms (e.g., derealization,
numbing).

71. • When acute stress disorder occurs after trauma, it identifies a
subset of individuals who are at several fold increased risk for
the subsequent development of PTSD (and major depression).
• Any life-threatening event, however common can be
considered sufficiently traumatic that it is capable of eliciting
PTSD.
• The neuroendocrine profile of patients with PTSD is not what
one might expect to see after chronic stress, ie it is associated
with hypocortisolism.

72. Substance use
• Stress clearly play a role in acquisition, maintenance, and
relapse with drug of abuse.
• Studies in human drug addicts have shown that drug desire
can be elicited with stressors and that this stress-induced
response predicts relapse.
• Stress-induced dopamine release in the NAc correlates
temporally with relapse to heroin seeking, and stress-induced
relapse is partially attenuated by pretreatment with
dopamine antagonists

73. Thank you

74. References
• Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
• INTRODUCTION TO PSYCHOLOGY 7th Edition ,Clifford T. Morgan richard A
king..
• Physiology and Neurobiology of Stress and Adaptation: Central Role of the
Brain.. Physiol Rev 87: 873–904, 2007;
• The Anatomy and Physiology of the Human Stress Response, G.S. Everly and
J.M. Lating, A Clinical Guide to the Treatment of the Human Stress Response,©
Springer Science+Business Media New York 2013
• The neurobiology of stress: from serendipity to clinical relevance Bruce S.
McEwen, Brain Research 886 (2000) 172–189
• DSM-5, Diagnostic and statistical manual of mental disorders, 5th edition

77. Management of stress
• Pharmacological : Short-term use of low-dose
benzodiazepines is of considerable use in helping patients
struggle with unusual stressors.

78. Cognitive-Behavioral Approaches
• Cognitive-behavioral therapy methods are increasingly used
to help individuals better manage their responses to stressful
life events. These treatment methods are based on the notion
that cognitive appraisals about stressful events and the coping
efforts related to these appraisals play a major role in
determining stress responding.
• Richard Lazarus and Susan Folkman developed a model of
stress and coping .
• According to this model, there are two types of cognitive
appraisal that are especially in mediating reactions to stress.

79. • The first, primary appraisal : refers to the way in which one
evaluates the significance or meaning of a given event.
• When events are appraised as harmful and threatening, the
individual is more likely to become anxious, depressed, and
withdrawn. However, if the same event is viewed as, then
more positive outcomes are more likely to occur.
• Secondary appraisal refers to the process of evaluating what
can be done about the stressful event.

80. • CBT approaches to stress management have three major
aims:
(1) to help individuals become more aware of
their own cognitive appraisals of stressful events,
(2) to educate individuals about how their appraisals of stressful
events can influence negative emotional and behavioral
responses and to help them reconceptualize their abilities to
alter these appraisals, and
(3) to teach individuals how to develop and maintain the use of a
variety of effective cognitive and behavioral stress
management skills

81. Stress-Management Training
• When cognitive-behavioral therapy is used for stress
management, training is provided in a wide range of stress-
management skills: self-observation, cognitive restructuring,
relaxation training, time management, and problem solving
• SELF-OBSERVATION: One of the most effective ways to help
individuals become more aware of how they respond to
problem situations is to have them keep a daily record of their
behavior. A daily diary format is often used.

82. • COGNITIVE RESTRUCTURING: A hallmark of cognitive-
behavioral therapy is its insistence that cognition plays a
central role in the stress and coping process.
• Major thrust of cognitive-behavioral therapy approaches to
stress management is on helping participants become aware
of and change their maladaptive thoughts, beliefs, and
expectations.

83. • RELAXATION TRAINING: Relaxation skills can be very helpful
in managing stress.
• When individuals learn to relax, their overall muscle tension
is reduced, as is their overall level of autonomic arousal.
• Individuals who are able to relax are also more likely to be
able to think more rationally and restructure negative
cognitions when faced with stressful events.
• Finally, relaxation skills may be helpful in reducing
maladaptive behavior patterns.

84. • TIME MANAGEMENT: A stressful event can place inordinate
demands on time. When exposure to such an event is
prolonged or is combined with exposure to other stressors, the
demands on time and energy are multiplied.
• In such circumstances, individuals often report feeling that
they have lost control of their daily schedule and that, as a
result, they have little or no time in which to attend to their
own needs.
• Time-management methods are designed to help individuals
restore a sense of balance to their lives.
• Time-management skills is designed to enhance awareness of
current patterns of time use.

85. • PROBLEM SOLVING: Problem solving is a skill that is
introduced in the later stages of stress-management training.
Problem solving involves several basic steps.
• The first is problem identification. In this step, one tries to
identify the key problematic aspects of a stressful event, such
as problematic behaviors, thoughts, feelings, and
physiological responses.
• The second step in problem solving is generating alternatives.

86. • The third step in problem solving involves evaluating the
alternatives and selecting the best solution.
• The final step of problem solving involves implementing the
solution.
• Problem-solving skills is crucial to the prevention of relapse
and maintenance of the effects of cognitive-behavioral
therapy.