NEUROBIOLOGY OF STRESS

Presented by Dr. Karrar husain

Moderator Dr. Piyush P. Singh

• 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).

• According to Seyle…….physiological response of the body toexternal stressors.

• Cox (1975) considers that stress involves external stimuli, thephysiological response to these stimuli, and psychologicalprocesses that mediate between stimulus and response. Thepsychological processes involve differences betweenindividuals in their perception of the environmental demandsand their own capacity to cope with them.

• 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.

• 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

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.

• 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.

• 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.

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.

Stress response

A systems model of the human stress response

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.

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.

• 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.

• 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.

Neurological Triggering Mechanisms

• The next step in the model is the neurological triggeringmechanisms consisting of the locus ceruleus (LC), limbicsystem, 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 anendogenously determined neurological tone that ispotentially self-perpetuating

The Stress Response

• three physiological pathways

(1) the neural axes,

(2) the neuroendocrine axis, and

(3) the endocrine axes.

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.

• 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.

• The effects of neural activation via the sympathetic system arethose of generalized arousal within the end an “ergotropic”response.

• The effects of activation via the parasympathetic system areinhibition, slowing, and “restorative” functions—a“trophotropic” response.

• The most common form of neural autonomic stressresponsiveness in human beings is in the form of theergotropic response simultaneous trophotropic responseshave been observed in human beings as well

• 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.

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.

• Upon neural stimulation, the adrenal medulla releases the medullary catecholamines. The effect of these medullarycatecholamines 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 medullarycatecholamines require a 20 to 30 second delay of onset for measurable effects and display a tenfold increase in effect duration .

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

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.

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

• ACTH zona glomerulosa to secrete the mineralocorticoidsaldosterone 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.

• (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.

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.

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.

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

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.

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 Selyerefers 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.

• 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

• 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

Target-Organ Activation

• The term target-organ activation refers to the phenomenon inwhich the neural, neuroendocrine, and endocrineconstituents of the stress response (1) activate, (2) increase or(3) inhibit normal activation, or (4) catabolize some organsystem in the human body.

• Potential target-organ systems the CVS, the GIS, the skin, theimmune system, the brain and its mental status

• Result in various clinical signs and symptoms.

• 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.

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

• 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.

• 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).

• when coping is successful, extraordinary target organactivation is reduced or eliminated and homeostasis isreestablished.

• If coping strategies are unsuccessful, target-organ activation ismaintained and the chances of target-organ disease areincreased.

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;

• 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;

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;

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

• 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).

Clinical Implications of Psychoneuroimmunologyand 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

• HIV : Immune system decline and HIV replication areparticularly rapid in patients living under chronic stress.

• Rheumatoid Arthritis : recent data suggest that stressfulevents, particularly those of an interpersonal nature, provokesymptoms of disease, such as greater pain and functionallimitations, and disease progression.

• Cancer : Experimental studies acute stress leads todecreases in NK cell function and facilitates the metastaticspread of NK-sensitive tumors. There are some observationsof a higher rate of survival in cancer who have receivedpsychological interventions.

STRESS AND PSYCHIATRIC ILLNESS

• In the early to mid-1800s, a school of thought emerged, led byPhilippe Pinel (1745 to 1826) of the Salpetriere in Paris andAmariah Brigham (1798 to 1849) in America, that theexpression of mental illness was affected by life circumstancesand, more broadly, by societal factors.

• This orientation held that an individual's response to stress ismodified by a number of intrinsic factors and extrinsic factors.The model incorporated individual temperamental andexperiential characteristics, such as potential vulnerabilityfactors, stressful life events as initiating or exacerbatingfactors, and a variety of support networks as potentiallymodifying factors for the occurrence of mental illness.

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.

• Preliminary evidence suggests that polymorphisms within the catechol-O-methyltransferase and brain-derived neurotrophicfactor genes may interact with psychosocial stress in the development of psychosis.

Schizophr Bull (2008) 34 (6): 1095-1105.

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.

• In the development of major mood disorders, chronicstressors (e.g., unemployment, difficult marriage) play a moreimportant role than specific, acute stressors. However,accumulation of stressful negative life events is the strongestpredisposing factor.

• The higher level and, probably, the different nature of socialstressors in individuals living in urban communities may beamong the main sources accounting for their higherpsychiatric morbidity.

• There is a fundamental similarity between theneuroendocrine effects of stress on humans and theneuroendocrine abnormalities in major depression ieoveractivity of the HPA axis, as inferred by increased plasmacortisol and ACTH levels.

• Challenge studies with CRH that have demonstrated reducedACTH responses to CRH in depressed patients compared tocontrol subjects suggest that chronic CRH secretion (withcompensatory downregulation of CRH receptors at thepituitary level) is an important feature of major depression.

• A functional polymorphism in the promoter region of theserotonin transporter (5-HT T) gene was found to moderatethe influence of stressful life events on depression. Individualswith one or two copies of the short allele of the 5-HT Tpromoter polymorphism exhibited more depressivesymptoms, diagnosable depression, and suicidality in relationto stressful life events than individuals homozygous for thelong 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

• serotonin transporter promoter polymorphism (5-HTTLPR)moderates the relationship between stress and depression,with the less functional allele associated with increased stresssensitivity. (The principal function of the serotonin transporter is to remove

serotonin from the synapse, returning it to the presynaptic neuron where theneurotransmitter can be degraded or rereleased at a later time. A polymorphism inthe promoter region of the serotonin transporter gene (5-HTTLPR) has been foundto affect the transcription rate of the gene, with the short (s) alleletranscriptionally less efficient than the alternate long (l) allele)

Arch Gen Psychiatry. 2011;68(5):444-454

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.

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).

• 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.

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

Thank you

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

Management of stress

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

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.

• 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.

• CBT approaches to stress management have three major aims:

(1) to help individuals become more aware oftheir own cognitive appraisals of stressful events,

(2) to educate individuals about how their appraisals of stressfulevents can influence negative emotional and behavioralresponses and to help them reconceptualize their abilities toalter these appraisals, and

(3) to teach individuals how to develop and maintain the use of avariety of effective cognitive and behavioral stressmanagement skills

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.

• 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.

• RELAXATION TRAINING: Relaxation skills can be very helpfulin managing stress.

• When individuals learn to relax, their overall muscle tensionis reduced, as is their overall level of autonomic arousal.

• Individuals who are able to relax are also more likely to beable to think more rationally and restructure negativecognitions when faced with stressful events.

• Finally, relaxation skills may be helpful in reducingmaladaptive behavior patterns.

• 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.

• 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.

• 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.