chap 13- anxiety disorders Flashcards

1
Q

egyptian perspective on psychopathology

A
  • Writings describe disordered states of concentration and attention
  • Emotional distress associated with the heart or mind.
  • Somatic treatments typically included applying bodily fluids while reciting magic spells
  • Hallucinogens may have been used as part of healing rituals.
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2
Q

Native american perspectives on psychopathology

A

Ancient scriptures contain descriptions of depression and anxiety states
Mental disorders reflected abstract metaphysical entities, supernatural agents, sorcery or witchcraft
Causes included inappropriate diet; disrespect towards the gods, teachers or others; mental shock due to excessive fear or joy; and faulty bodily activity
Treatments using herbs and ointments, charms and prayers, moral or emotional persuasion, and shocking the person

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3
Q

chinese perspectives on psychopathology

A

Described symptoms, mechanisms and therapies for mental illness, emphasizing connections between bodily organs and emotions
Conditions were thought to comprise five stages or elements and imbalance between Yin and Yang
Mental disorders were treated mainly under by herbs, acupuncture or emotional therapy

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4
Q

hippocrates perspectives on psychopathology

A

Moved away from the superstitious beliefs surrounding mental illness and towards a medical perspective Studied pathology of the brain and suggested that mental illness stemmed from imbalances in the body. Imbalances were in the four essential fluids: blood, phlegm, yellow bile, and black bile which produce unique personalities of individuals

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5
Q

galen perspective on psychopathology

A

Agreed with the notion that an imbalance of the four bodily fluids could cause mental illness
Also considered psychogenic explanations for mental illness allowing for the experience of psychological stress as a potential cause of abnormality.

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6
Q

phillipe pineal

A

was a French physician instrumental in developing more humane approaches to the custody and care of psychiatric patients, referred to today as moral therapy. He also made contributions to the classification of mental disorders and has been described by some as “the father of modern psychiatry”. [He may have described a case providing the first evidence for the existence of what later became known as dementia praecox or schizophrenia although Emil Kraepelin is generally accredited with its first conceptualization.]

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7
Q

pineal perspective on psychopathology

A

French physician instrumental in the development of a more humane psychological approach( a.k.a. the moral therapy) to the care of psychiatric patients

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8
Q

diagnosis of mental disorders: emil kraepelin

A

Began to study psychiatric disorders as a disease processes

Focused on three features
	1.  Signs of disease presented
	2.  Course of the disease
	3.  Outcome Distinguished two major mental illnesses
	1.  Dementia praecox (DP)
		- early age of onset
		- progressive deterioration of intellect
	2.  Depressive psychosis
		- later onset
		- remissions and relapses
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9
Q

emil kraepelin

A

was a German psychiatrist who has been called the founder of modern scientific psychiatry, psychopharmacology, and psychiatric genetics.
Kraepelin began to study psychiatric disorders as disease processes caused by biological and genetic malfunction.

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10
Q

eugene bleuler

A

Objected to term DP because the onset occurred in some adults and because in some cases there was remission of the disorder

Thought DP described a group of related illnesses characterized by disorder of thought rather than intellect

Proposed that the thought disorder reflected a “splitting” of the cognitive side of personality from affective side; i.e., a splitting of the mind or schizophrenia.

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11
Q

inclusionary diagnosis of psychological disorders

A
  • The Number of Symptoms and Signs
    • Duration of Symptoms and Signs
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12
Q

exclusionary diagnosis of psychological disorders

A
  • the condition can not be attributed to
    some physical medical disorder
    or another mental disorder
    • can not be due to substance use
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13
Q

world health organization medical classification versus DSM

A

Differs from DSM-V in…
- Includes all disorders: medical and mental health
- International classification, easy to translate between countries
- Available in several different languages (DSM-V only in English)

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14
Q

world health organization

A

maintains several internationally classifications designed to facilitate the comparison of health-related data within and across populations and over time as well as the compilation of nationally consistent data

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15
Q

prevalence of serious mental illness among u.s adults

A

The overall rate is just over 4%. Women are affected more than men and young adults more than older adults. The prevalence of serious mental illness seems to be consistently inconsistent across races.

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16
Q

genetic component of behavioral/mental disorders

A

Concordance for disease phenotypes among monozygotic twins (MZ) and dizygotic twins (DZ) for some behavioral disorders. The proband is the family member through which the family was initially discovered and explored.

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17
Q

diathesis stress model

A

a psychological theory that attempts to explain a disorder, or its trajectory, as the result of an interaction between a pre-dispositional vulnerability and a stress caused by life experiences. The diathesis, or predisposition, interacts with the individual’s subsequent stress response. Stress is a life event or series of events that disrupts a person’s psychological equilibrium and may catalyze the development of a disorder. Thus the diathesis–stress model serves to explore how biological or genetic traits (diatheses) interact with environmental influences (stressors) to produce disorders such as depression, anxiety, or schizophrenia.
The diathesis–stress model asserts that if the combination of the predisposition and the stress exceeds a threshold, the person will develop a disorder.

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18
Q

diathesis

A

predisposition, genetic

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19
Q

stress

A

triggers disorders, both diathesis(risk) and stress must be present for diathesis-stress disorders

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20
Q

two dimensions of emotion

A

positive valence, negative valence (pleasant relaxation, joy, sadness, fear, anger)
low arousal, high arousal
- chart on slide 13

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21
Q

relationship between behavioral performance and level of arousal

A

Yerkes-Dodson Law is relevant to a discussion of emotion because arousal affects level of behavioral performance, and strong emotions or motivations involve arousal. Note the curve is an “inverted U-shaped function”. Increases in arousal increase performance up to a point after which further arousal impairs performance. Any given behavior is thought to have an optimal level of arousal to produce optimal levels of performance.

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22
Q

types of emotional responses

A

Emotions have three components: (1) overt behavior, (2) physiological changes (autonomic, endocrine, cardiovascular, respiratory, GI, immune), and (3) subjective (personal) cognitive feelings.

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23
Q

commonality of emotions in the faces of animals and people

A

Darwin in his book The Expression of the Emotions in Man and Animals (published in 1872) proposed that the chief expressive actions exhibited by man and animals are innate (inherited) and are conserved across species as part of our common evolutionary similar inheritance. For example, most mammals snarl when angry as do we. These three drawings illustrate angry facial expressions in a baboon, adult male and adolescent female. In both species an expression of anger often involves a direct gaze and a partly opened mouth with lips retracted vertically so that the teeth show.

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24
Q

james-lange theory of emotion

A

An external stimulus, such as the sight of a bear, is perceived by the sensory areas of the cerebral cortex. Through the motor cortex, responses, such as running away, are controlled. Sensations produced by the responses are fed back to the cerebral cortex, where they are perceived. The perception of bodily sensations associated with the emotional responses is what gives the peculiar quality to the emotion in James’ theory.

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25
Q

cannon-bard theory of emotion

A

changed the neuroanatomy of emotional responses. Cannon and Bard believed that external stimuli processed by the thalamus were routed to the cerebral cortex (path 2b) and to the hypothalamus (path 2a). The hypothalamus, in turn, sent messages to both bodily muscles and organs (path 3a) and the cortex (path 3b). The interactions of messages in the cortex about what the stimulus is (path 2b) and about its emotional significance (path 3b) results in the conscious experience of emotion (feelings). Emotional responses and feelings occur in parallel in this theory

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26
Q

the papez circuit theory of emotion

A

Like Cannon and Bard, Papez believed that sensory messages reaching the thalamus are directed to both the cerebral cortex and the hypothalamus; the outputs of the hypothalamus to the body control emotional responses; and outputs to the cortex give rise to emotional feelings. The paths to the cortex were called the “stream of thinking” and the ones to the hypothalamus the “stream of feeling.” Papez was considerably more specific than Cannon and Bard about how the hypothalamus communicates with the cortex and about which cortical areas are involved. He proposed a series of connections from the hypothalamus to the anterior thalamus, to the cingulate cortex (part of the evolutionarily old, medial cortex). Emotional experiences occur when the cingulate cortex integrates signals from sensory cortex (part of the evolutionarily new, lateral cortex) and the hypothalamus. Outputs from the cingulate cortex to the hippocampus and then the hypothalamus allow thoughts occurring in the cerebral cortex to control emotional responses.

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27
Q

MacLean’s visceral brain (limbic system) theory of emotion

A

Paul MacLean developed the idea that the brain is really three brains-in-one, a “triune brain”. The brain initially was composed of the reptilian brain, and then the paleomammalian brain (i.e., limbic system) and the neomammalian brain (neocortex) were sequentially added to the forebrain in the course of evolution.
In this model, emotional experience results from the integration of internal and external sensations. The centerpiece of the limbic system was the hippocampus (shown as a sea horse). It was believed to receive inputs from the external world (sight, smell, hearing, touch, taste) as well as from the internal or visceral environment. The pyramidal cells of the hippocampus (black triangle inside the sea horse) were viewed as the emotional keyboard.

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28
Q

originators and popularizers of the concept of stress

A

Schematic representation of progressive changes in stress concept. Original application of term began with Cannon, who spoke of “great emotional stress” or “stress of the moment.” For Cannon, aversive physical and emotional stimuli disrupting homeostasis were responded to with generalized sympathetic nervous system activation. Selye first used stress and later stressor to indicate types of stimuli that gave rise to general adaptation syndrome (GAS). Selye was interested in both adrenal mineralocorticoids and glucocorticoids. However, glucocorticoids moved to the fore of investigation probably because the role of the brain and pituitary in the control of glucocorticoid release were recognized before other neural-related mechanisms were understood to be involved in the control of aldosterone secretion. Selye’s work led investigators to attend to the ACTH-glucocorticoid response as the primary focus in response to stressors and as primary index of stages of GAS.

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29
Q

clarification of stress-related terms

A
  • Stress broadly viewed as a process, concept, hypothetical construct or intervening variable
  • Stressor = a physical, physiological, pathophysiological or psychological stimulus (a challenge) that induces a stress response in an individual (e.g., painful stimulus, a drug, hormone or cytokine that produces a stress response
  • Stress Response = the physiological, behavioral and/or cognitive response to a stressor
  • The stress response may be either adaptive or non-adaptive
    *note how vague the notion of stress can be, basic to the concept is that stress implies something that is somehow damaging to the organism or is psychologically aversive. it arises from pain, for example, but also from drugs or hormones, or an extreme emotional situation
30
Q

selye’s general adaptation syndrome (GAS)

A

1: AlarmUpon perceiving a stressor, the body reacts with a “fight-or-flight” response and the sympathetic nervous system is stimulated as the body’s resources are mobilized to meet the threat or danger.
2: ResistanceThe body resists and compensates as the parasympathetic nervous system attempts to return many physiological functions to normal levels while body focuses resources against the stressor and remains on alert.
3: ExhaustionIf the stressor or stressors continue beyond the body’s capacity, the resources become exhausted and the body is susceptible to disease and death.
* the presentation of a second stressor can produce a more precipitous decline into exhaustion and death

31
Q

autonomic and endocrine effects of chronic stress

A

The most immediate response has the brain signaling the sympathetic nervous system and the adrenal glands to release epinephrine and norepinephrine. Then, the hypothalamus and pituitary activate another part of the adrenals, releasing cortisol. This is followed by the nervous system initiating behavioral responses like alertness, focus, reduction of pain receptors and the inhibition of reproductive behaviors and desires. The sympathetic nervous system then kicks in to increase the heart rate, blood pressure and release glucose to help fight or get out of danger as it redirects blood flow to the heart, muscles and brain, away from the gastrointestinal tract and digestive processes. To accommodate these demands there is a vast increase in energy production and utilization of nutrients and fluids in the body. Once the stressful situation has passed, the brain signals the responses to be “turned off” and finally recovery and relaxation allow the body to re-establish balance in all systems, replacing lost nutrients and eliminating waste products accumulated during the process.

32
Q

role of glucocorticoids and mineralocorticoids in the stress response

A

for many the HPA has been the definition of stress, in the 1960s it was discovered that angiotensin II released aldosterone and that activation of the SNS released renin
- glucocorticoids: antiphlogistic
- mineralocorticoids: prophologistic

33
Q

john mason

A

the role of emotional factors and multiple hormones in stress
-International leader and theoretician in the field ofstress research
- Emphasized the interplay between human emotions and the endocrine system
- He was one of the field’s most prominent voices speaking out against the reigning model of stress promoted by Hans Selye.
- He noticed that Selye repeatedly referred to emotional factors as “mere nervous stimuli,“ downplaying the role of the psychology and cognition.
- His own experiments with both animal and human subjects, suggested these “mere” stimuli were highly significant, and that psychological and emotional state of the subjects were important factors.

34
Q

evolution of the concept of stress

A

Schematic representation of progressive changes in stress concept. Original application of term began with Cannon, who spoke of “great emotional stress” or “stress of the moment.” For Cannon, aversive physical and emotional stimuli disrupting homeostasis were responded to with generalized sympathetic nervous system activation. Selye first used stress and later stressor to indicate types of stimuli that gave rise to general adaptation syndrome (GAS). Selye attended to ACTH-glucocorticoid response as primary focus in response to stressor and as primary index of stages of GAS. Mason’s broader endocrinological characterization of response to stressors provided insights into psychological dimension common to effective stressors and to varied and graded nature of responses in different endocrine systems. A contemporary view of the stress concept requires recognition of complexity of functional interrelationships between behavioral, hormonal, and physiological systems. These interactions vary as function of time, intensity, and nature of stressor.

35
Q

categories of stressors and their related mechanisms

A

Physiological
- painful or tissue damaging
- involves innate mechanisms
- brainstem and limbic system involvement
Psychosocial (psychological)
- perceived to be detrimental to the physical
or psychological integrity of an individual
- cognitive mechanisms usually involved
- major involvement of cortical and limbic regions

36
Q

resilience to and coping with stressors

A
  • Individuals differ in their stress response to a given stressor (resilience)
  • This difference may be due to either a genetic predisposition, current physiological state or adaptive physiological or psychological coping mechanisms
37
Q

allostasis and allostatic load

A

concepts invoked to explain how the body deals with stress and stressors, to help explain differences in resilience.
When the body undergoes chronic stress it adapts by changing, both physiologically and behaviorally. There is increased output from some systems and likely decreased output from others. But this comes at a cost: the wear and tear on the body caused by these changes.
- ideas evolved from concepts of homeostasis and stress
- P.S sterling and J. Eyer were the originators of the concept but it was popularized by Bruce McEwen

38
Q

allostasis

A

maintaining stability through change; the active process of maintaining a physiological function in the face of a challenge by old control systems adjusting level of function or “new” systems being activated.
- bruce mcewen

39
Q

allostatic load

A

wear and tear on the body that results from repeated or sustained activation of processes that maintain homeostasis

40
Q

pathologies associated with chronic stress

A

Hypertension
Fatigue
Myopathy
Diabetes
Peptic ulcers
Psychosocial dwarfism
Impotence; anovulation; loss of libido
Impaired disease resistance; cancer
Accelerated neural degeneration during aging

41
Q

the defense response

A

The neural and neurochemical basis of the stress response.
The hypothalamus is a critical neural region involved in the defense response.
Ranson and Hess placed electrodes in the hypothalamus and applied stimulation. Hess found that stimulating different parts of the hypothalamus produced characteristic reactions that appeared to correspond to specific emotional states. For example, stimulation of the LH caused autonomic and somatic responses consistent with anger: increased blood pressure, raising of the body hair, pupillary constriction, etc. These studies lead to the view that the hypothalamus can facilitate the coordination of peripheral emotional responses.

Thus, behavioral and autonomic responses are integrated by the hypothalamus. The cardiovascular responses are important here.

42
Q

behavioral defense response

A

Piloerection
Hissing
Halloween Posture

43
Q

cardiovascular defense response

A
  • increase in Cardiac Output (increased HR)
  • increased Blood Pressure
  • increased Skeletal Muscle Blood Flow
  • decreased Renal Blood Flow
  • decreased Mesenteric Blood Flow
44
Q

natural and brain stimulation-induced defense response

A

The neural and neurochemical basis of the stress response.
The hypothalamus is a critical neural region involved in the defense response.
Ranson and Hess placed electrodes in the hypothalamus and applied stimulation. Hess found that stimulating different parts of the hypothalamus produced characteristic reactions that appeared to correspond to specific emotional states. For example, stimulation of the LH caused autonomic and somatic responses consistent with anger: increased blood pressure, raising of the body hair, pupillary constriction, etc. These studies lead to the view that the hypothalamus can facilitate the coordination of peripheral emotional responses.

Thus, behavioral and autonomic responses are integrated by the hypothalamus. The cardiovascular responses are important here.

45
Q

the cardiovascular defense response

A

The outflow of information affecting the relevance of vasoconstrictors/dilators is coordinated by the CNS.

46
Q

the defense response as an inducer of chronic hypertension

A
  • hypothalamic stimulation producing the defense response and chronic hypertension
  • about 50 years ago, Folkow hypothesized that sustained or repeated activation of the defense response predisposes towards developing chronic hypertension
47
Q

the conditioned emotional response (CER)

A

The rat is first exposed to the sound alone. It orients towards the sound, but after several occurrences, the sound is ignored. Next, the sound and the brief, relatively mild shock occur together several times. Later, the sound, when presented alone, will elicit conditioned fear responses. The sound, by association with the shock, has become a learned trigger of fear responses. This is similar to what goes on in humans when they are exposed to dangers or trauma. The stimuli associated with the danger or trauma become learned triggers that unleash emotional reactions in us. Studies of fear conditioning in rats can thus reveal important aspects of the way human emotional (fear) learning occurs.

48
Q

neural pathways mediating the cardiovascular and the behavioral components of the defense response

A

Thalamo-amygdala pathways mediating learned fear responses in the rat. Schematic drawing of a sagittal section through the rat brain illustrating pathways essential for conditioned changes in autonomic activity (i.e., increases in arterial pressure) (A) and emotional behavior (i.e., “freezing”) (B) in response to a simple acoustic stimulus. The autonomic and behavioral response pathways overlap through the auditory system and amygdala. Different efferent projections of the amygdala, however, mediate the autonomic and behavioral responses. AMY = amygdala; CG = central gray; CS = conditioned stimulus; IC – inferior colliculus; MG = medial geniculate; LH = lateral hypothalamus; RVL = rostral ventrolateral medulla.

49
Q

stress pathways and the control of glucocorticoids

A

Stimuli associated with danger activate the amygdala. By way of pathways from the amygdala to the paraventricular nucleus of the hypothalamus (PVN Hypo), corticotrophin-releasing factor (CRF) is sent to the pituitary gland, which, in turn, releases adrenocorticotrophic hormone (ACTH) into the bloodstream. ACTH then acts on the adrenal cortex, causing it to release steroid hormones (CORT) into the bloodstream. CORT freely travels from the blood into the brain, where it binds to specialized receptors on neurons in regions of the hippocampus and amygdala, as well as other regions. Through the hippocampus, CORT inhibits the further release of CRF from the PVN. However, as long as the emotional stimulus is present, the amygdala will attempt to cause PVN to release CRF. The balance between the excitatory input (+) from the amygdala and inhibitory inputs (-) from the hippocampus to PVN determines how much CRF, ACTH, and ultimately CORT will be released.

50
Q

the amygdala and fear

A

The amygdala receives inputs from a wide range of levels of cognitive processing. By way of inputs from sensory areas of the thalamus, the emotional functions of the amygdala can be triggered by low level stimulus features, whereas inputs from cortical sensory processing systems (especially the late stages of processing in these systems) allow more complex aspects of stimulus processing (objects and events) to activate the amygdala. Inputs from the hippocampus play an important role in setting the emotional context. In addition, the hippocampus and related areas of the cortex (including the rhinal or transitional cortical areas) are involved in the formation and retrieval of explicit memories, and inputs to the amygdala from these areas may allow emotions to be triggered by such memories. The medial prefrontal cortex has been implicated in the process known as extinction, whereby the ability of conditioned fear stimuli to elicit conditioned fear responses is weakened by repeated exposure to the conditioned stimulus without the unconditioned stimulus. Inputs to the amygdala from the medial prefrontal cortex appear to contribute to this process. By knowing which cortical areas project to the amygdala, and knowing the functions in which those areas participate, predictions can be made about how those functions might contribute to fear reactions. Anatomy can, in other words, illuminate psychology.

51
Q

putative CRF pathways

A

Major CRF-immunoreactive cell groups and fibers are shown by black dots and lines, respectively. Pathways are separated into those that project to brain areas expressing relatively high densities of (a) CRF1 or (b) CRF2 receptor mRNA.

Main Points:
- CRF is synthesized in the hypothalamus and secreted to control ACTH release from the adrenal.
- In addition, it is also present in brain pathways and releases nuclei with the CNS as a neurotransmitter.

52
Q

the physiological effects of CRF

A

In addition to its well known effects on ACTH and glucocorticoid secretion by the pituitary-adrenocortical system, CRF also acts within the CNS to influence various autonomic functions. This results in heightened epinephrine (EPI) secretion by the adrenal medulla, increased sympathetic noradrenergic (NE) activity in the heart, kidney, and certain vascular beds, and reduced parasympathetic cholinergic (ACh) outflow to the heart.

53
Q

effects of amygdala lesions on the CRF enhancement of the startle response

A

shows the mean change in startle (relative a 15 min preinfusion baseline) after intraventricular infusion of 1 g corticotropin-releasing factor (CRF) or artificial cerebrospinal fluid (ACSF) in sham lesioned animals or animals with bilateral lesions of the central nucleus of the amygdala.

54
Q

key role for GABA in controlling activity of the amygdala

A

it is the one place where benzodiazepines bind to produce anxiolytic effects.
By infusing drugs directly into the amygdala, research indicates that benzodiazepines inhibit anxiety by increasing GABA transmission and that benzodiazepine antagonists increase anxiety by decreasing GABA transmission.

Details:
Schematic diagram of principal connections within the central, basolateral and lateral amygdaloid nuclei based on in vitro electrophysiological recording and anatomical data. For simplicity, many other connections, notably subcortical projections, are not included.

55
Q

anxiety

A

Unpleasant state of inner turmoil
Accompanied by nervous behavior
– pacing (increased locomotor activity)
– somatic complaints
– rumination
- emotion characterized by an unpleasant state of inner turmoil, often accompanied by” nervous” behaviour such as pacing back and forth, somatic complaints, and rumination. It is the subjectively unpleasant feelings of dread over anticipated events, such as the feeling of imminent death. Anxiety is not the same as fear, which is a response to a real or perceived immediate threat, whereas anxiety involves the expectation of future threat. Anxiety is a feeling of uneasiness and worry.

56
Q

animal models of anxiety

A

Passive or active avoidance of light
Open field behavior
Conditioned defensive burying
Elevated-plus maze
Response suppression
- Unconditioned behaviors (e.g., licking)
- Conditioned behaviors (e.g., operant conditioning)No single behavioral test can be used as a measure of all possible signs (and symptoms).
Thus, multiple tests must be employed to analyze the therapeutic benefits of drugs for different symptoms.

Here are some examples of animal models of anxiety that have validity for assessing some aspects of anxiety.
- The light/dark (LD) test is a measure of anxiety-like behavior based on an approach/avoidance conflict between the drive to explore novel areas and an aversion to brightly lit, open spaces.
- The Defensive Burying Test involves the intrusion of a new aversive object into a familiar environment that triggers the burying reflex. This is thought to be a measure of “anxiety” in the rat. The tube elicits bursts of air that rats don’t like (i.e., “air jet” stress).

57
Q

elevated plus maze

A

This aspect of anxiety is expressed by the animal spending more time in the enclosed arms. The EPM is used to screen anxiolytic and anxiogenic compounds and as a general research tool in neurobiological anxiety research such as PTSD and Traumatic Brain Injury.

58
Q

operant chamber and a cumulative recorder

A

The idea behind conditioned suppression of a response is that the animal is placed into a conflict situation in which it must “choose” between two behaviors that cannot be done simultaneously.
First, the rat is trained to press a lever for reward, like food. After this training, a predictor stimulus is presented that sometimes signals the arrival of an aversive stimulus, such as a mild shock to the feet.
The predictor stimulus causes the animal to have a fear response involving “freezing” or “crouching” behavior. Freezing behavior is incompatible with bar pressing behavior.
Thus, presentation of the predictor stimulus for shock suppresses the lever pressing for food. The rat is in conflict: does it resume bar pressing for food because it is hungry, or does it freeze and crouch as it anticipates the possibility of shock?

59
Q

regression analysis of drug potency in conflict test

A

This figure shows the strength of the validity of using the conditioned suppression test for predicting clinical efficacy of anxiety reducing drugs.
The effective dose in rat conflict testing is plotted against the average daily clinical dose for people prescribed anxiolytic drugs.

60
Q

a three component model of anxiety

A

A three-component model of anxiety hypothesizes that stress induces a cyclic interaction of bodily response, ineffective behavior and upsetting thoughts. Stressors may be perceived as a threat, which initiates portions of the anxiety responses. Each of the three components influence the others, potentially escalating the overall damaging effect of anxiety. For other individuals, the stressor may be perceived as a challenge, which engages more constructive behavior. Individual differences based on genetic traits and early experience may make some people more or less vulnerable to stressors.

61
Q

anxiety disorders

A

Separation anxiety disorder, selective mutism, specific phobia, social phobia, panic disorder, agoraphobia, generalized anxiety disorder

62
Q

obsessive compulsive disorders

A

OCD, body dysmorphic disorder, hoarding disorder, trichotillomania

63
Q

trauma and stressor related disorders

A

PTSD, acute stress disorder, adjustment disorder, reactive attachment disorder

64
Q

generalized anxiety disorder

A
  • excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance)
  • the individual finds it difficult to control the worry
  • the anxiety and worry are associated with three or more of the following six symptoms
    -note: only one item required in children
    • restlessness, feeling keyed up or on edge
    • being easily fatigued
    • irritability
    • difficulty concentrating or mind going blank
    • muscle tension
    • sleep disturbance
  • the anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other areas of functioning
  • the disturbance is not attritubale to the physiological effects of a substance or another medical condition
  • the disturbance is not better explained by another medical disorder
65
Q

post-traumatic stress disorder

A
  • PTSD is a disorder that develops in some people who have seen or lived through a shocking, frightening, or dangerous event
    • Could also be indirect, learning that a relative or close friend was exposed to trauma
    • Or, repeated, extreme indirect exposure to aversive details of an event, usually in the course of professional duties (e.g., first responders, collecting body parts, professionals repeatedly exposed to details of child abuse). Does not include non-professional exposure through media, television, or pictures
  • Not every traumatized person develops ongoing (chronic) or even short-term (acute) PTSD
  • Symptoms usually begin early, within 3 months of the traumatic incident, but sometimes they begin years afterward
    To be diagnosed with PTSD, an adult must have all of the following for at least 1 month:
    At least one re-experiencing symptom
    e.g., Nightmares, flashbacks
    At least one avoidance symptom
    e.g., persistent, effortful avoidance of distressing trauma-related stimuli
    At least two arousal and reactivity symptoms
    e.g., problems concentrating, sleep disturbance
    At least two cognition and mood symptoms
    e.g., feeling alienated from others, constricted affect, anhedonia
66
Q

a neural model of PTSD

A

The important point here is the central role of the amygdala.
The amygdala mediates the acquisition and expression of conditioned fear and the enhancement of emotional memory, whereas the cortex (vmPFC) mediates the extinction of conditioned fear and the volitional regulation of negative emotion.
It has been theorized that the vmPFC exerts inhibition on the amygdala, and that a defect in this inhibition could account for the symptoms of PTSD.

67
Q

drugs used to treat various anxiety disorders

A

benzodiazepines - valium, xanax
tricyclic antidepressants - tofrantil, aventil
monoamine oxidase inhibitors - nardil, parnate
selective serotonin reuptake inhibitors - prozac, zoloft, paxil
busprinone - buspar

68
Q

tricyclic antidepressants

A

have been widely used as a treatment for anxiety. They enhance both serotonin and norepinephrine at the receptor. Tricyclics are especially useful when treating anxiety in people with co-occurring anxiety disorders and depression.

69
Q

benzodiazepines

A

enhance the effect of the GABA at the GABAA receptor resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety) effects

70
Q

monoamine oxidase inhibitors

A

block the actions of monoamine oxidase enzymes which break down neurotransmitters such as dopamine, norepinephrine, and serotonin in the brain. Low levels of these three neurotransmitters have been linked with depression and anxiety. Monoamine oxidase inhibitors (MAOIs) usually are not the first medicines given for anxiety, because they have serious side effects when combined with certain foods and/or medicines. They are usually given to people who have anxiety and who did not get better with other antidepressants.

71
Q

busprinone

A

an anxiolytic psychotropic drug. It is primarily used to treat GAD . Unlike most anxiolytics, buspirone pharmacology is not related to benzodiazepines or barbiturates and does not have a large risk of physical dependence and withdrawal symptom. GAD = Generalized Anxiety Disorder; PTSD = Posttraumatic Stress Syndrome; OCD = Obsessive Compulsive Disorder

72
Q

exposure therapy

A
  • Gold standard treatment in which an individual
    is exposed gradually to their specific phobia or fear,
    and learns that it is not threatening
    • e.g., if someone is afraid of spiders, begin with thinking about spiders, then look at pictures of spiders, moving
      up to holding a spider