Effective Treatment for Anxiety Attacks

Panic Away Ebook

The author of the Panic Away program, Barry began his research studying books on psychology, but he was not so happy with what he found there. The method described promise to teach people to get rid of the panic attacks and anxiety permanently, but they just teach methods for managing it. Panic Away provides a number of specific applications of the 21-7 Technique that relates to everyday life like how to deal with panic attacks while driving, leaving home, anxiety caused by the fear of flying and the fear of public speaking. If you have the fear of public speaking, fear of driving, or encounter panic disorders due to leaving your home than you may especially be fond of the segment dedicated to applying the One Move method to these particular problems. This Panic away technique is said to successfully fight the general anxiety disorder. Read more here...

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Types of Anxiety Disorders

The fourth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) describes 11 different anxiety disorders. Each of these is listed in Table 1, along with their most important defining features. Although other psychological problems may be associated with extreme fear or anxiety (e.g., eating disorders are associated with a fear of gaining weight), only the conditions listed in Table 1 are officially classified as anxiety disorders in the DSM-IV.

Neuroimaging of Fear Anxiety

1999) and vocalizations (Phillips et al., 1998), as well as in response to aversive pictures (Garrett and Maddock, 2001), and in human adaptations of animal paradigms of conditioned fear (LaBar et al., 1995 Morris et al., 1998 Whalen et al., 1998), to aversive auditory, olfactory and gustatory stimuli (Zald, 2003), and to exposure to procaine and inhalation of CO2 (Ketter et al., 1996 Brannan et al., 2001). These combined findings suggest a general role for the amygdala in the automatic, preconscious early detection of threat and danger in the environment, and possibly in triggering the experience of fear anxiety. Interestingly, amygdalar responses to fearful faces are increased in childhood and adolescence (Killgore et al., 2001) and in childhood anxiety and in posttraumatic stress disorder (PTSD) patients (Thomas et al., 2001 Hull, 2002). 2001), providing further evidence that processing of cognitive explicit components of emotional stimuli is carried out by the prefrontal neocortex...

Benzodiazepines GABA and Neurosteroids

Endogenous or exogenously ingested benzodiazepines may also play a role in the etiology of acute and chronic hepatic encephalopathy. In the past several years, dozens of basic science and clinical reports have appeared implicating these substances which enhance the inhibitory GABA-ergic tone. The gut flora has been postulated to contribute benzodiazepine ligand activity, which fits well with the general theory regarding the functional failure of hepatic clearance.37 Indeed, animal models of acute liver failure have demonstrated increased benzodiazepine receptor agonist activity.38 Clinical studies in patients with fulminant liver failure have documented an increase in benzodiazepine receptor ligands with enhanced GABA-ergic tone in all stages of encephalopathy.29,39 Increased densities of brain peripheral-type benzodiazepine receptors, and elevated levels of neurosteroids, have also been reported in animal models of acute liver failure.40,41 It is suggested that ammonia-induced...

Opioids Ketamine and Benzodiazepines

Opioids are not thought generally to have neuroprotective properties but they do blunt stress-induced responses. Ketamine is an NMDA antagonist and has been shown to be protective in animal models of ischaemia.51 While the benzodiazepines decrease cerebral blood flow and cerebral metabolic rate, these effects are less impressive than with the intravenous anaesthetic agents. Despite occasional reports of neuroprotective benefit,52 these drugs are not generally thought to be useful neuroprotective agents.

Basic Models Of The Etiology Of Panic Disorder Neurophysiological Models

Parabrachial Nucleus

Several lines of evidence suggest a neurophysiological basis for panic disorder, including genetic studies. The illness's medication responsiveness (discussed in the treatment section below) has been interpreted to imply a neurophysiological etiology. Evidence for a genetic basis for panic disorder has also been derived from studies of twins that demonstrate a higher rate of concordance for panic in monozygotic than dizygotic twins (Torgersen, 1983, Kendler et al., 1993 Skre et al., 1993). Neurophysiological models of the etiology of panic disorder have developed primarily from animal models of brain functioning and studies of substances that provoke panic. The interpretation of these data by different theorists in developing models for panic will be described below. Neuroimaging studies are expected to be an increasingly important source of data. and heart rate), and periaqueductal gray region (defensive behaviors). In fact, data from animal models suggest that stimulation of the...

Treatment of poststroke anxiety disorder

Post Huddle Stroke Forms

The first treatment study of generalized anxiety disorder (GAD) following stroke was based on a merged analysis of results from previous treatment studies conducted by our research group (Kimura and Robinson 2003). These previous treatment studies included poststroke depression (Lipsey et al. 1984), pathological laughing and crying (Robinson et al. 1993) and a comparison of nortriptyline and fluoxetine for poststroke depression (Robinson et al. 2000). From the total of 106 patients in these three double-blind studies, 27 patients had a diagnosis of GAD as Among the 27 patients with GAD, 13 patients were assigned nortriptyline and 14 patients were assigned to placebo. Analysis of variance (ANOVA) of baseline Hamilton anxiety (Ham-A) and Hamilton depression (Ham-D) scores with two factors (factor one, treatment versus placebo, factor two, study population) showed no significant active versus placebo effects or treatment by study population effects. There were no significant differences...

The role of anxiety in sexual dysfunction

Anxiety played a significant role in early psychody-namic formulations of sexual dysfunction and later became the foundation for the etiologic concepts of sex therapy established by Masters and Johnson 3 and Kaplan 4 . Kaplan believed that sexually related anxiety became the final common pathway through which multiple negative influences led to sexual dysfunction. More recent studies have suggested that it may not be the subjective role of anxiety, per se, that causes and maintains sexual dysfunction but rather the manner in which anxiety affects an individual's ability to focus on, and process sexual stimuli. Barlow 5 has offered a theoretical model explaining why anxiety may operate differentially in men with and without erectile dysfunction. His model emphasizes the role of cognitive interference in male arousal. In general, what appears to distinguish functional from dysfunctional responding is a difference in selective attention and dis-tractibility. What sex therapists consider...

Effect of Tranquilizers on the Reward or Punishment Centers

Administration of a tranquilizer, such as chlorpro-mazine, usually inhibits both the reward and the punishment centers, thereby decreasing the affective reactivity of the animal. Therefore, it is presumed that tranquilizers function in psychotic states by suppressing many of the important behavioral areas of the hypothalamus and its associated regions of the limbic brain.

Aggressive patients had more anterior hemisphere lesions greater depressive and anxiety symptoms but less cognitive

In addition to confirming many of the findings from our first study of aggression in patients with stroke, in our second study, the patients were participating in our treatment study of poststroke depression (see Chapter 23). Response to antide-pressant medication was therefore evaluated in the 23 initially aggressive patients who entered this 12-week treatment trial. Among the active treatment patients, six were treated with fluoxetine titrated from 10 mg day up to 40 mg day. Four were treated with nortriptyline titrated from 25 to 100 mg day and 13 received placebo. Patients given active antidepressant medication during the 12-week treatment trial were not significantly different from the placebo patients in background characteristics, psychometric measures of severity of depression or anxiety or the prevalence of major depression or generalized anxiety disorder prior to treatment. The active treated patients had aggression scores of 2.0 0.87 SD at baseline and 0.2 0.45 SD at 3...

Managing Anxiety and Panic

If you've ruled out thyrotoxicosis, and do not require a beta-blocker, talk therapy (specifically, cognitive behavioral therapy), discussed earlier, is an excellent way to manage anxiety and panic. This style of therapy can teach you to anticipate the situations and bodily sensations that are associated with panic attacks having this awareness can actually help to control the attacks. There are also a number of mental exercises that can help to control hyperventilating or fearful thoughts that could heighten the panic in the throes of an attack. For instance, by replacing the thought I'm going to faint with I'm just hyperventilating I can handle this, panic attacks can be calmed before fear takes over and the symptoms worsen. Your doctor may also prescribe antidepressants or tranquilizers, depending on how severe your anxiety and panic are and whether they are affecting your ability to function normally. We cannot devote space to the huge variety of agents available, but you can refer...

Anxiety Panic Disorder and Thyroid Disease

We discuss both generalized anxiety disorder (GAD) and panic attacks in Chapter 4, because they are commonly confused with, or aggravated by, thyrotoxicosis. In that chapter, we also discuss the hormone system in the body called the adrenergic system, which releases adrenaline (also known as epinephrine) and noradrenaline (norepi-nephrine). Normally, these hormones are released in a fight or flight response when you are scared, shocked, or highly excited. It is also these hormones that trigger panic attacks, causing your heart to race, profuse sweating, and all the other symptoms described in Chapter 4. We also discussed in Chapter 4 the concept of beta-andrenergic receptors, which make the heart beat faster and also make you more prone to panic and anxiety. When you're thyrotoxic, the numbers of beta-adrenergic receptors increase in your body's cells. This makes you much more sensitive to the effects of your own adrenaline, and predisposes people ordinarily able to cope with various...

Depression and Anxiety

If you look at the list of symptoms that comprise hypothyroidism (see Chapter 3) and thyrotoxicosis (see Chapter 4), many of them overlap and collide with symptoms of depression and anxiety. This chapter discusses ways to cope with and manage depression and anxiety, often a consequence of untreated hypothyroidism or thyrotoxicosis. It's important to understand that depression is a vast topic, and there are many different types of depression. For the purposes of this chapter, we'll be limiting the discussion to the most common type of depression frequently associated with hypothyroidism. Known in clinical circles as either major depression or unipolar depression, this form is characterized by one low or flat mood. This is distinct from bipolar depression, characterized by two moods a high(er) mood and a low(er) mood, which typically cycle. A few symptoms of bipolar depression can sometimes be confused with thyrotoxicosis, but as discussed in Chapters 4 and 6, the exhaustion that...

Longterm Outcome Of Treatment Trials For Panic Disorder

Patients with panic disorder are a highly symptomatic, help-seeking group who tend toward recurrent exacerbations of symptoms (Pollack and Otto 1997 Pollack and Marzol, 2000 Faravelli et al., 1995). It is therefore important to gauge not only the effectiveness of treatments over the short term but to ascertain their effectiveness over longer follow-up intervals. Useful data with regard to long-term outcome, however, has been limited thus far in the literature. In a review of follow-up studies to date, Milrod et al. (1996) found that most did not monitor concurrent nonstudy treatments (e.g., untracked medication use in CBT studies or ongoing psychotherapies in medication studies) either during study treatment or during follow-up intervals. The authors concluded that there was limited evidence that patients responding to short-term treatments maintained their gains if they did not receive further treatment. Bakker et al. (1998) conducted a meta-analysis of studies that had information...

Psychodynamic Psychotherapy for Panic Disorder

Systematic study of psychodynamic treatments for panic disorder is in its infancy. As described above, a significant minority of patients fail to respond to the more extensively empirically tested treatments, and many patients experience residual symptoms after pharmacological and cognitive-behavior treatments (Nagy et al., 1989 Noyes et al., 1989, 1991 Pollack et al., 1993 Barlow et al., 2000). Thus, attention to psychodynamic issues may potentially provide further improvement for some patients. Milrod and Shear (1991) found 35 cases in the literature with DSM-III-R panic disorder who were successfully treated with psychodynamic psychotherapy or psychoanalysis alone. Since then, other successful psychodynamic treatments for patients with panic disorder have been reported (Milrod, 1995 Stern, 1995 Renik, 1995 Busch et al., 1996 Milrod et al., 1996). Clinical reports cannot substitute for controlled clinical trials. Nonetheless, these reports suggest...

Treatment Of Panic Disorder

Medications, including tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, and benzodiazepines, as well as cognitive-behavioral therapy (CBT) have demonstrated efficacy for treatment of panic disorder in multiple double-blind, placebo-controlled studies. Common concerns have also surfaced in some of these studies (Nagy et al., 1989 Noyes et al., 1989 1991 Pollack et al., 1993 Barlow et al., 2000). Because of the narrower definition of panic disorder that was used prior to 1994 (Shear and Maser, 1994), very few panic studies to date have assessed broader quality of life aspects of treatment response. Many patients have persistent, though frequently less intense, symptoms that may cause persistent morbidity and functional impairment following completion of treatment (Nagy et al., 1989 Noyes et al., 1991 Pollack et al., 1993). For example, in the most recent large-scale, multicenter, highly controlled outcome study of patients with panic...

Psychodynamic Model of Panic Disorder

In the psychodynamic model of panic disorder, anxiety symptoms are believed to be triggered by unconscious fantasies and impulses that are experienced by the individual as unacceptable, and threaten to break through into consciousness. The anxiety also represents the failure of defense mechanisms to adequately protect against the emergence of these wishes in undisguised form. In addition, the physical symptoms of panic, as well as many other aspects of life, are a result of compromise formations (Freud, 1895b) between wishes that are unacceptable and defenses against these very wishes. As described below, unconscious fears of loss, separation, and conflicts about autonomy are important elements underlying panic attacks. Angry fantasies triggered by fantasies of being controlled by others, or unprotected by loved ones, represent an additional threat to attachment that can trigger panic. Panic attacks in part represent partial expressions of these wishes by easing the danger of...

Separation Distressanxiety

Distress resulting from separation from an attachment figure has been accepted as an attribute of normal infant development since the early part of this century (Bowlby, 1973 Freud, 1909 1955). Bowlby interpreted the distress that infants displayed to maternal separation as reflecting their anxiety at being left alone. Indeed, he saw fear of being left alone as the root cause of generalized human anxiety (Bowlby, 1973). In normal development, distress due to separation appears between the ages of 7 and 12 months and peaks around 15 to 18 months of age. This inverted U-shaped curve to the onset, peak, and diminution of distress to separation has been found across various cultures Although normative changes in distress to separation find it diminishing around 18 to 24 months of age, instances of continued distress response to separation from mothers have been described in the child clinical literature. These instances were described under the heading of separation anxiety. Freud (1895...

Relationship of anxiety to outcome

For many years clinicians have recognized the importance of anxiety disorder as well as depression in patients following stroke (Schwartzman 1976). The spectrum of anxiety disorders includes panic disorder, generalized anxiety disorder (GAD), obsessive compulsive disorder (OCD) and phobic disorders. There have been anecdotal reports of panic disorder (Maricle et al. 1991) and OCD occurring in patients with stroke. These are relatively rare conditions arising from ischemic brain injury. Our research investigations have not systematically examined patients for panic disorder or OCD. We have, however, systematically examined patients for GAD. Although this has not been a major area of investigation for other researchers, there are a number of reports of the presentation, diagnosis, and clinical and pathological correlates of poststroke anxiety disorder (Burvill et al. 1995 Astrom 1996). In contrast to the relatively large number of studies which have examined the relationship between the...

Diagnosis of anxiety disorders

As with depressive disorders, the gold standard for the diagnosis of anxiety disorders is a structured or semistructured mental status examination which is applied to the diagnostic criteria of DSM-IV or ICD-10. Although cases of phobic disorder, panic disorder, and obsessive compulsive disorder, have been reported following stroke or brain injury (House 1987 Burvill et al. 1995 Max et al. 2002). The majority of investigators have focused on the more chronic disorder of GAD associated with stroke. As we showed in Section I of this chapter, all of the symptoms of GAD except perhaps decreased energy are significantly more frequent in patients with anxiety compared to those without anxiety. Several investigators have examined the utility of screening instruments for the identification of GAD. Schramke et al. (1998) examined patients with right and left hemisphere stroke for anxiety and depressive symptoms using the Center for Epidemiological studies depression scale (CESD), Beck Anxiety...

Specificity of anxiety symptoms

In order to examine the frequency of anxiety symptoms and their specificity for anxiety disorder, patients with acute stroke were grouped according to whether they did or did not express anxiety or worry. As I discussed in Chapter 7 entitled, Phenomenology and the specificity of depressive symptoms, among patients with acute stroke, it is not obvious how one should assess the specificity of symptoms used for the diagnosis of anxiety disorder. If one uses the diagnostic criteria to define the study group, it becomes circular reasoning since the anxious patients are defined by the very criteria that are being assessed for specificity. On the other hand, if one groups patients based on the presence of anxiety or any other single symptom, the group would include patients who do not have the full syndrome of generalized anxiety disorder (GAD) but merely one or two symptoms. The criteria we have chosen is the second method which includes all patients who acknowledge the presence of anxiety...

Does Da Play A Causal Role In The Induction Of Stress Andor Anxiety States

The ability of environmental and pharmacological stressors to increase rates of DA neurotransmission within PFC suggests the possibility that PFC DA may provide a unique and critical contribution to the induction of anxiety and or stress states (for review, see Horger & Roth, 1996). Consistent with this hypothesis is the suppression of PFC DA neurotransmission by anxiolytic benzodiazepines. However, there are a few important additional observations that call into question either the extent to which the actions of DA within PFC in stress are truly unique or, more important, the extent to which PFC DA plays a causal role in the induction of stress-related behavioral states. First, the qualitative effects of stressors and anxiogenics are not necessarily unique to DA A similar activation of PFC projecting noradrenergic efferents by stressors is observed, and benzodiazepines also suppress PFC noradrenergic neurotransmission (Finlay et al., 1995). Thus, an argument can be made

Panic Disorder Epidemiology and Course

Panic Disorder (PD) (with and without agoraphobia) is a debilitating condition with a lifetime prevalence of approximately 1.5 (American Psychiatric Association ApA , 1994). Studies have demonstrated that this prevalence rate is relatively consistent throughout the world. Approximately twice as many women as men suffer from PD. Although PD typically first strikes between late adolescence and the mid-30s, it can also begin in childhood or in later life. Although data on the course of PD are lacking, PD appears to be a chronic condition that waxes and wanes in severity. Consequences of PD include feelings of poor physical and emotional health, impaired social functioning, financial dependency, and increased use of health and hospital emergency services.

Other Anxiety Disorders Definitions

The DSM-IV diagnostic system includes the following anxiety disorders separation anxiety disorder, panic disorder, agoraphobia, specific phobias, social phobia, obsessive-compulsive disorder, and generalized anxiety disorders, as well as the previously considered posttraumatic stress disorder and acute stress disorder (see Ref. 164 for review). Separation anxiety disorder is defined by excessive and developmentally inappropriate anxiety about separation from parents or other primary attachment figures. Typically less common in adolescents than younger children, a relationship between separation anxiety disorder and adolescent SUD has not been established. Panic disorder and agoraphobia are rare in adolescent samples. Specific phobias are relatively common but probably not a factor in SUD development. Social phobia is nearly as common in adolescent as in adult samples and may influence SUD development and course. Obsessive-compulsive disorder often begins during adolescence, but a...

Possible Mechanisms for Blunted GH Secretion to GH Secretagogues in Anxiety and Mood Disorders

Blunted GH responses to GH secretagogues, such as cloni-dine, desipramine, the insulin tolerance test, and others, were thought to detect down-regulation of postsynaptic alpha-2 receptors following excessive central noradrenaline (NA) activity in major depressive disorder (Coplan et al., 1995 Siever et al., 1982). That GH responses are blunted in response to both clonidine and growth hormone releasing factor (GRF) in Panic Disorder (PD) refuted the view that reduced GH response to clonidine simply reflects a specific alpha-2 abnormality. Uhde, Tancer, and Rubinow (1992) have reviewed the possible site(s) where blunting of GH may occur. These include (1) reduced availability of pituitary GH stores secondary to reduced synthesis or excessive secretion (this option seems unlikely as GH responses to the dopamine agonist, apomorphine, are exaggerated in PD) (2) overall hypersecretion of GH with secondary inhibition of GH secretion to secretory stimuli (3) an abnormally enhanced negative...

Characterization of GABAa Receptor Functional Modifications by Various Anxiolytic Drugs Acting on the BZ Recognition

There is considerable interest in the availability of an effective GABAa receptor-acting anxiolytic drug that will not share the problems of presently available medications. These problems are tolerance, dependence liability, and several inconvenient side effects such as sedation, induction of recent memory deficit, barbiturate or ethanol potentiation, and ataxia. The high-affinity binding site for BZs located in GABAA receptors has specific structural features. One consists of a binding pocket formed by the contiguity of an a subunit (not present in a6 and with low intrinsic activity in a5) with a g2 or g3 subunit (which is not expressed by a g1 subunit). These requirements should predict which GABAA receptors are susceptible to positive allosteric modulation by ligands to the BZ recognition sites, that is subunit isomerism and sequence. Unfortunately, we do not have suitable methods to fulfill either task. It is presently believed that BZs amplify the actions of GABAby facilitating...

Studies of Cerebral Metabolism and Blood Flow in Anxiety Disorders

A dysfunctional cortico-striato-thalamo-cortical circuitry may play an important role in this disorder (Rauch and Baxter, 1998 Rauch et al., 1998). According to this model, the primary pathology afflicts subcortical structures (striatum thalamus), which leads to inefficient gating and results in hyperactivity within the orbito-frontal cortex and also within the anterior cingu-late cortex. Compulsions are conceptualized as repetitive behaviors that are ultimately performed in order to recruit the inefficient striatum to achieve thalamic gating and hence to neutralize the unwanted thoughts and anxiety. PET and SPECT studies have consistently indicated that patients with OCD exhibit increased regional brain activity within orbitofrontal and anterior cingulate cortex, in comparison with normal control subjects (Baxter et al., 1988 Machlin et al., 1991 Nordahl et al., 1989 Rubin et al., 1992 Swedo et al., 1992). Observed differences in regional activity...

Response To Hyperventilation

Hyperventilation is a method of activating the EEG. It may bring out focal or generalized slowing in cases of structural disease or of more diffuse encephalopathy disorders. It also can bring out interictal epileptic discharges or trigger more overt symptomatic seizures. It should not be performed in the very elderly patient or in someone suspected of having any intracranial mass lesions or a recent transient ischemic event stroke. In the adult population, it is normal to hyperventilate the patient for 3 to 5 min. The technician usually tries to, at minimum, double the base breathing rate, and to have the subject exhale more deeply than usual. This act causes the subject to exhale excessive amounts of CO2 and become hypocapnic. The hypocapnia causes mild cerebral vessel vasoconstriction and, hence, mild cerebral hypoxia. The hypoxia and the hypocapnia together potentially can produce changes that may signal a disorder. One additional variable that must be considered is the blood...

Restlessness and Anxiety

The typical person with Graves' disease is chronically restless, to the point where he or she cannot sit still for a minute, and is terribly anxious and worried. As discussed in Chapter 4, this is partly because of the increased sensitivity to adrenergic hormones (adrenaline and related hormones) that comes with thyrotoxicosis. There is often a distinct tremor of the hands, also resulting from the adrenaline sensitivity. In Chapter 4, we discussed how thyrotoxicosis has many crossover symptoms with generalized anxiety disorder and panic disorder. The restlessness and anxiety may dramatically interfere with your ability to relate to others or to perform normally in your workplace.

Anxiolytics Tranquilizers

Many illnesses are accompanied by anxiety, a worried state during which a syndrome characterized by feelings of helplessness, despair, dark premonitions, and asthenia begins to develop. It can be accompanied by headaches, increased perspiration, nausea, tachycardia, dry mouth, etc. A state of anxiety can originate from neurological reasons, and can also be of a somatopsychic nature, which is associated with pathological development in diseases of the cardiovascular system, neoplasms, hypertonia, and diseases of the gastrointestinal tract. Drugs used for relieving anxiety, stress, worry, and fear that do not detract attention from or affect psychomotor activity of the patient are called anxiolytics or tranquilizers. Most of them have sedative and hypnotic action, and in high doses their effects are in many ways similar to barbiturate action. However, the primary advantage of this group over barbiturates lies in their significantly increased value in terms of the ratio of sedative...

Treatment of Anxiety Disorders

Anxiety disorders are among the most treatable of psychological problems. Most individuals who receive appropriate treatment experience a significant reduction in symptoms. For Substance-Induced Anxiety Disorders and Anxiety Disorders Due to a General Medical Condition, the focus is generally on reducing the substance use or on treating the medical condition that is causing the problem. However, for the other anxiety disorders, evidence-based treatments include medications, cognitive-behavioral therapy (CBT), or a combination of these approaches. The selective serotonin reuptake inhibitors (SSRIs), such as paroxetine, fluoxetine, and sertraline, have been shown to be useful for treating most of the anxiety disorders. Other antidepressants (e.g., venlavaxine, imipramine) are also useful for particular anxiety disorders. Anxiolytic medications (especially the benzodiazepines, such as alprazolam and diazepam) are also effective for reducing anxiety, although they are usually prescribed...

Demographic Features of the Anxiety Disorders

Anxiety disorders can occur across a wide range of cultures, ages, sexes, and income levels. In most cases, anxiety disorders are more common in women than in men. The more frequent occurrence in women is most pronounced for Panic Disorder with Agoraphobia and certain specific phobias (particularly animals and storms). For other anxiety disorders, such as Social Anxiety Disorder, blood and needle phobias, and Obsessive-Compulsive Disorder (OCD), the differences between men and women are smaller. The typical onset of anxiety disorders varies, with some tending to begin in early childhood (e.g., animal phobias), others beginning, on average, during the teen years (e.g., Social Anxiety Disorder, OCD), and others tending to begin in early adulthood (e.g., Panic Disorder).

Benzodiazepines

Long-acting drugs such as diazepam should be avoided because of the risk of sedation, but clonazepam and temazepam are useful. They consolidate stage 2 NREM sleep and reduce sleep-stage transitions and arousals from sleep, but only partially relieve the movements through their muscle relaxant effect. The patient therefore obtains more benefit than the partner. They are best if the condition is mild, and especially when

Anxiety Disorders

There is no evidence that HIV infection alone results in neurobiological changes increasing the prevalence of anxiety. However, symptoms of anxiety have had a significantly greater prevalence in HIV-positive men with major depression and or adjustment disorders than in a comparable sample of HIVnegative controls. There was also a significant increase in prevalence of adjustment disorder with anxiety in the HIV-positive population over a control group of high-risk patients (121). In this same study, the rates of generalized anxiety disorder (GAD) were relatively low. This is consistent with the low rate of GAD seen in the general population and the large spread of prevalence rates 0 -28 seen in studies of the chronically ill (122). When coping styles are examined, it is quite clear that feelings of a loss of mastery or control over one's life is an important predictor of anxiety associated with an adjustment disorder in the chronically ill (123,124). The powerful emotional response...

State Anxiety

Almost everybody has experienced anxiety at some time in life, including persons with high blood pressure as well as those with normal blood pressure. Imagine the various sensations you experience if you are asked by a teacher to report to the class the basic conclusions from an article you were supposed to have read but did not. This experience of anxiety is comprised of a number of cognitive manifestations, including catastrophic thinking, anticipation of danger, and sensing doom, accompanied by a full array of physiological symptoms associated with sympathetic and somatic nervous system arousal, including increased heart rate, sweating, shortness of breath, muscle tension, and disturbances of the gastrointestinal system. The discomfort associated with the experience of these cognitive and somatic symptoms of anxiety often leads to behavioral escape or avoidance responses (for example, I feel ill and need to go home). Although anxiety is a normal emotion to experience in situations...

Anxiety Introduction

One of the best definitions of anxiety, put forth over fifteen years ago by Kandel (1983), remains highly apt and appropriate today Anxiety is a normal inborn response either to threat to one's person, attitudes, or self-esteem or to the absence of people or objects that assure and signify safety (p. 1277). Anxiety is an emotion and state of mind characterized by aversive cognitive (apprehensive expectation of negative experience or consequences), physiologic (autonomic hyper-arousal with multiple somatic symptoms), and behavioral (hypervigilance, avoidance, paralysis of action) components. Its relationship to fear states in animals is ambiguous. Fear is an adaptive response to a clear-cut, external threat anxiety is excessive or inappropriate in relation to the stimulus and often extends well beyond the provoking situation (i.e., the cognitive aspect of anxious anticipation and uncertainty about the future). This distinction may simply reflect the highly complex and more developed...

Panic attacks

Panic attacks are commoner in adolescents and young adults and two to three times more frequent in females than in males. They occur during wakefulness, usually in the morning but also in sleep, particularly during the first third of the night and usually at the time of NREM sleep transition from stage 2 to 3 or 3 to 4. They are not associated with dreams and the patient awakens fully, often with a sensation of intense fear, choking, breathlessness, palpitations, tremor and hyperarousal which prevents subsequent sleep. There is no tendency towards aggression or violence, but recall of the fear experienced during the event is retained. Panic attacks may lead to a fear of falling asleep.

Anxiety

Lactating rats show an attenuated elevation in stress hormone in response to white noise compared to virgins. Infusion of oxytocin in virgin rats also dampens the elevation of stress hormones in response to stress, suggesting that the increased oxytocin released during lactation may be acting to buffer the individual from environmental stressors. Oxytocin also has anxi-olytic effects in behavioral assays of anxiety, such as the elevated plus maze.

Fear and Anxiety

Learning of all kinds, including early life experiences, shapes the way animals and humans respond to stressful and fear-arousing events. Different situations arouse motivation of fear and anxiety for different species and for different individual prior experiences. Stimuli associated with pain come to evoke fear, such that fear occurs when painful stimulation is anticipated. In humans, painful events are often symbolic and not merely physical, such as fear of failure (Atkinson, 1964). Sigmund Freud postulated that human neurosis has its roots in anxiety. Clinical, field, and laboratory findings have demonstrated that defensive motivations like fear and anxiety are likely to lead to behaviors that interfere with effective task performance and creative problem solving. Task-oriented anxiety can be beneficial when the individual exerts effort toward task mastery, but self-oriented anxiety is likely to engender thoughts that indicate preoccupation with self-worth or personal safety,...

Directed Neurological Examination Overview

The examination of the patient with altered consciousness begins by ensuring that the patient's vital signs and basic biochemistry are adequate to support brain function. It is essential to ensure that blood pressure, respiration, and oxygen saturation are adequate and that the patient is not hypoglycemic or thiamine deficient before proceeding with the examination outlined later. In many situations (e.g., emergency departments), naloxone is also administered at this point to reverse any putative effects of opiates. The empirical use of flumazenil to antagonize potential benzodiazepine intoxication as a routine measure is controversial because of the risk of provoking seizures or status epilepticus, especially in patients with mixed benzodiazepine and cyclic antidepressant overdoses.

Association Between Glucocorticoid Regulation and Psychopathology

Several lines of research support the association between glucocorticoid regulation and psychiatric disorders (Hols-boer, 1989 Tsigos & Chrousos, 1994). Both physical and psychological stressors have been shown to be temporally related to psychiatric illness. Because glucocorticoids are intricately linked to the neurobiology of stress, alterations in glucocorticoid levels and or activity are expected in association with psychiatric conditions. Indeed, altered HPA function has been shown in a variety of psychiatric disorders, including depression, Anxiety Disorders, Substance Abuse, Anorexia Nervosa, and Schizophrenia. Pharmacological studies indicate that glucocorticoids directly modulate neurotransmitter function and behavioral systems, as well as the activity of psychotropic agents. Moreover, there is evidence that glucocorticoids exert genomic effects in the brain and regulate transcription of many genes, including those that code for behaviorally active neuropeptides....

AMPA Receptors as Pharmacotherapeutic Sites

AMPA receptors are widespread in the brain, including most regions of the cerebral cortex, hippocampus, amygdala, thalamus, hypothalamus, brain stem, and spinal cord. The regional variations in expression of the subunits, splice variants, and editing efficiency are apparent and are probably involved in local and global network function. AMPA receptors are being studied as potential therapeutic targets in diseases such as Alzheimer's disease, cerebrovascular disease (preventive and poststroke), epilepsy, schizophrenia, neural trauma, and other conditions involving cognitive impairments. Such promise has been raised by the successes reported for AMPA agonists (AMPAmimetics or AMPAkines) to enhance maze learning in age-associated memory impairment in mice and for antagonists (blockers) to prevent the spread of necrosis in ischemic events. Agonists (such as CX516 and aniracetam) and antagonists of varying specificity for AMPA receptor variants are being studied, with goals of safer and...

Affective Disorder Syndromes

The differential diagnosis of depression includes primary psychiatric syndromes other than major depression such as behaviors associated with schizophrenia, generalized anxiety disorder, and obsessive-compulsive neuroses. Medical and neurological disorders either associated with or mimicking depression include malignancy, infections, medications (steroids, reserpine, levodopa, benzodiazepines, propranolol, anticholinesterases), endocrinological dysfunction (Cushing's disease, hypothyroidism, apathetic hyperthyroidism, diabetes), pernicious anemia, and electrolyte and nutritional disorders (inappropriate secretion of antidiuretic hormone, hyponatremia, hypokalemia, hypercalcemia). Depression is also associated with multiple sclerosis, Parkinson's disease, head trauma, stroke (particularly of the left frontal lobe), and Huntington's disease. Interictal changes in temporal lobe epilepsy may mimic depression, particularly with right-sided epileptic foci. Patients with diencephalic and...

Functions Of Diagnostics

Still, these ideas are open territory for further developments. A classic psychosis can be generated by imbalancing glutamate activity in the brain with the phencyclidine hallucinogens. Thus, it is still generally agreed that schizophrenia is closely linked to imbalanced activities of certain brain dopamine systems, in concert with various other neurochemistries (Carlsson et al., 2001) and that anxiety is intimately related to the activity of GABA along FEAR systems (Chapter 16).

Clinical Pharmacokinetics of SSRIs

Citalopram,1 fluoxetine,2,3 fluvoxamine,4 paroxetine5 and sertraline6 are the five antidepressants which are known as selective serotonin reuptake inhibitors (SSRIs) (Fig. 2.1). Their clinical efficacy, good tolerance and safety have been demonstrated in many studies7,8 and some of them may also be prescribed successfully for the treatment of obsessive compulsive disorder, bulimia or panic attacks. Despite their common pharmacological properties, the SSRIs differ in their metabolism by cytochrome P450 and in their interaction profile with other drugs which are also substrates of this enzyme system. Sensitive and selective (including stereoselective) methods, using high performance liquid chromatography or gas chromatography, have been introduced for their quantitative analysis in blood samples.9 These have enabled studies of their pharmacokinetics as well as investigations of the relationship between plasma concentration and clinical efficacy. This review summarizes our present...

Directed Neurological Examination

The first goal of the neurological examination of memory is to ascertain that memory impairment is not secondary either to a specific perceptual, motor, or cognitive disability or to a broad impairment of mental status. This goal can be accomplished by performing a mental status assessment and brief bedside tests of orientation, receptive and expressive language, and visual constructional abilities. Confusional states can be evaluated both informally, while the patient tells his or her history, by noting confusion or incoherence in thinking, anxiety level, and inconsistencies and inaccuracies about dates and symptoms, and formally by asking about the present day, date, place, and year. Further memory assessment should be undertaken only if a patient's level and content of consciousness and attention are determined to be unimpaired. One widely used standardized mental status test is the mini mental status examination (MMSE). 31

Methodological Concerns

Another important difficulty in the neuroimaging of human emotions arises from the wide discrepancy in experimental situations, mood induction paradigms, emotional tasks, and instructions employed. While some studies have been carefully designed to address a specific domain of emotional processing (emotion recognition, subjective feeling or affect, emotion expression), others have used a combination of these. Importantly, studies of affect (e.g., anxiety and sadness) have generally been biased toward cognitive processing of the emotion-inducing materials (perceptual, mnemonic, visual imagery tasks), resulting in widespread activations of cortical structures probably involved in the nonaffective components of the emotional task. Only a few studies have imaged the induced affect after the initial affect-induction phase, when the subjective

Legitimate Masculinity

Me there are several connections to be made between the increased knowledge about and control over sperm and the cultural anxiety men experience in contemporary societies. To offset these masculinity-lite or sperm-lite texts, I offer here a more nuanced and complicated account of masculinity in the postfeminist era.

Beta And Gamma Rhythms

Three main types of beta rhythms are commonly observed in the scalp EEG of human adult subjects (1) a fronto-central beta rhythm that can be blocked by contralateral movement or tactile stimulation, (2) a diffused beta rhythm without specific reactivity, and (3) a posterior beta rhythm that can be blocked by visual activity, similar to the occipital alpha rhythm (Kuhlo, 1976). An increase in beta rhythm has been reported in neuropsychiatric patients, but Kuhlo (1976) concluded that no adequate evidence exists at present of any relationship between normal or excessive beta activity and psychiatric disorders. Apro-nounced increase in beta-frequency EEG was found with drugs that enhance gamma-aminobutyric acid-A(GABA-A) receptor functions, including sedative doses of barbiturates and benzodiazepines (Kozelka & Pedley, 1990) and the anesthetic propofol. Neural circuitry that involves GABAergic interneurons in the cortex is probably responsible for the generation of the drug-induced...

Interaction Transactional Theories and Research

Lazurus and Folkman (1984) proposed a transactional theory of stress that has received considerable attention over the years. According to their perspective, it was not the initial stressor per se that was critical in linking stress to disease, but the individual's response to the stressor that determined whether a cyclic stress reaction developed. Focusing upon the acute cognitive stress response system, Lazurus suggested that three types of cognitive appraisal occurred in determining the magnitude of the stress reaction primary appraisal, secondary appraisal, and reappraisal. Primary appraisal focused upon the degree to which a person detected a stressor as being harmful (leading to potential injury or illness), threatening (causing anxiety, fear, or damage to self-esteem), or challenging (leading to potential gain or growth). According to Lazurus, individuals determined whether a stimulus was irrelevant, benign-positive, or stressful only stimuli appraised as stressful elicited...

General Management Goals

Treatment of patients with anosmia due to sensorineural problems is challenging. Although there are a few advocates of zinc and vitamin therapies, sound empirical evidence of their efficacy is lacking. In patients in whom olfactory loss has been present for a long period of time and can be attributed to neural damage within the olfactory neuroepithelium, prognosis is poor, and no treatment is possible. Nevertheless, simply providing such patients with accurate information about their disorder, establishing objectively the degree and nature of the deficit, and ruling out the possibility of a serious disorder as the cause of the problem can diminish anxiety and may be very therapeutic. Because half of elderly persons with permanent olfactory loss are at or above the fiftieth percentile of their norm group, these individuals can be informed that while their olfactory function is below what it used to be, they still are outperforming most of their peers. This knowledge is extremely...

A Fear System in the Brain

Several distinct systems for anxious trepidation may exist in the brain. One FEAR circuit that courses parallel to the RAGE circuit has been extensively studied. When artificially aroused, this circuit promotes freezing and hiding at low levels of arousal and flight during more intense arousal. We can be confident that other animals experience negative affect when this circuit is aroused, since they avoid environmental contexts in which such brain stimulation has been experienced in the past. Humans stimulated at homologous brain sites are commonly engulfed by intense anxiety. If it turns out to be that there is much less variability across species in the subcortical FEAR systems of the brain that helps generate anxiety than in the cognitive structures that regulate such feelings, then it follows that the study of the FEAR system in animals constitutes an excellent strategy for coming to terms with the affective nature of fear in humans. This system as well as other variants of...

Other Drugs And Depression

Use of sedatives, including benzodiazepines, has been linked to depression (187,188), although few empirical studies of this relationship exist (189). A positive correlation between prewithdrawal depressive symptoms and sedative-withdrawal symptom severity has been reported (190), as has the presence of depressive symptoms in withdrawal as a predictor of withdrawal failure (191). In a prospective study involving 82 alcohol- or benzodiazepine-dependent subjects undergoing detoxification, Charney et al. (192) found that the benzodiazepine-dependent subjects had a worse outcome in terms of abstinence at 3 months but not at 6 months.

Separation Distress PANIC and Social Bonding Affiliative Love Systems of the Brain

One of the most distinct outputs of this care-soliciting system, quite easy to study in animal models, is crying or emission of separation calls when socially separated from caretakers. Based on the possibility that precipitous arousal of this circuitry, which courses between the PAG and more rostral brain areas (preoptic, septal, bed-nucleus of the stria terminalis, and anterior cingulate cortex) via medial thalamic corridors, may contribute to panic attacks, this system was originally designated the PANIC system (Panksepp, 1982). This and several other working hypotheses await empirical evaluation (Chapter 12).

Mechanisms of action

The benzodiazepines do not have any direct action on neurological function, but enhance the effects of GABA. Benzodiazepines interact especially with GABAa rather than GABAb receptors. They bind to the macromolecular GABA receptor complex close to the GABA binding site and increase its affinity for GABA (Fig. 4.1). This leads to opening of the chloride channels and hyperpolarization of the post-synaptic membrane with inhibition of neuronal activity. Subtypes of the benzodiazepine receptors (e.g. BZ1, omega-1 BZ2, omega-2) have been identified but their significance is uncertain. BZ1 receptors may mediate sedation and BZ2 cognition, memory and psychomotor function. They also increase the affinity of the barbiturate and alcohol receptors for these compounds, and potentiate the effects of these drugs. The action of benzodiazepines on the GABA receptor complex is most marked in the hypothalamus, thalamus and limbic system, and the inhibition of these regions underlies the sedative and...

Effects on wakefulness

The sedative effect of benzodiazepines impairs motor skills, attention, memory and judgement, and if severe may lead to confusion and incoordination. The risk of accidents, including road traffic accidents, is increased, particularly in those who take alcohol as well. Accidents, such as falls, may also occur during the night if the subject becomes confused and leaves the bed.

Problems with use

These, and addiction to barbiturates, are more frequently a problem than with benzodiazepines. Withdrawal of barbiturates leads to REM sleep rebound and rebound insomnia. The barbiturates have a lower toxic therapeutic ratio than benzodiazepines and much more frequently cause death when an overdose is taken.

Indications in sleep disorders

Barbiturates are rarely used nowadays because of their disadvantages relative to the benzodiazepines and related drugs. Their only place is for short-term treatment if benzodiazepines and other modern hypnotics cannot be tolerated or are ineffective, as well as in those patients who have been taking barbiturates regularly for many years without any side-effects. When barbiturate treatment is initiated it should be restricted to 2 weeks because of the risk of tolerance and dependence developing.

Case Study 1 Deliriuma Common Disorder Of Attentional Function And Working Memory

Delirium may be the most commonplace disturbance of consciousness encountered by psychiatric clinicians, as well as by other physicians, and is virtually ubiquitous on medical services in general hospitals. Its quite commonplace nature contrasts with a curious neglect within both clinical neuroscience and consciousness studies of the disorder, as relatively little attention has been paid to understanding the underlying neural and neurodynamic foundations for delirium and confusional states. Delirium is most classically associated with toxic-metabolic disturbances of a wide variety, or neuro-modulatory disruptions secondary to psychotropic medicines, often superimposed upon and degrading a baseline dementia of the Alzheimer's type. In terms of neuromodula-tory disruptions, it is most typically associated with the effect of anticholinergics, but it is also commonly seen in dopamine precursor loading, from the effects of opiates, and from gamma-aminobutyric acid (GABA) agonist effects of...

Convulsants That Decrease Inhibition

Benzodiazepine receptor tors for the predominant brain inhibitory neurotransmitter, g-aminobutyric acid (GABA). More potent antagonists, such as bicuculline and the ion channel-blocker picrotoxin, are now more typically used. Seizures and epileptiform discharge can also be elicited by blocking the synthesis or release of GABA. In addition, substances active at modulatory sites on GABA receptors can also exert convulsant activity, such as inverse agonists of the benzodiazepine receptor.

Course Of Bipolar Disorder With

Strakowski and colleagues (29) found that substance abuse was independently (because of noncompliance) associated with lower syndromic recovery rates. Weiss and colleagues (49) studied the patterns of medication compliance, and reasons given for noncompliance, among 45 patients with bipolar disorder and SUD. The authors found that patients who were prescribed both lithium and valproate were significantly more likely to report full compliance with valproate than with lithium. Side effects were the most common reason for lithium noncompliance, but were not cited as a reason for valproate noncompliance. Another finding was that patients prescribed benzodiazepines, neuroleptics, and tricyclic antidepressants used more medication than prescribed. With this study, the authors conclude that valproate may have greater acceptability than lithium among patients with bipolar disorder and SUD.

The SSRI Withdrawal Discontinuation Syndrome

Many, if not all, drugs that cause adaptive receptor changes on chronic administration are liable to be associated with symptoms if the drug is abruptly discontinued. Withdrawal symptoms are well documented for TCAs and related compounds,1-8 MAOIs,6 trazodone9 and the serotonin (5-hydroxytryptamine, 5-HT) noradrenaline reuptake inhibitor (SNRI), venlafaxine,10 and it is not surprising that similar symptoms can occur on cessation of long-term treatment with SSRIs. The question of whether the emergence of a withdrawal reaction on drug discontinuation is evidence of drug dependence, as defined for therapeutic dose benzodiazepine dependence, is discussed by Medawar.11

Theoretical Framework For Understanding Stress Responsive Systems

On some level, we all have an intuitive understanding of stress as a psychological concept. Most people would define stress as a sense of internal pressure, nervous tension, anxiety, strain, or even a state of constant worry. While these terms are perfectly accurate and sufficient for communicating about stress in a colloquial setting, they are insufficient when we try to operationalize stress in a scientific manner. Indeed, scientists have argued for the better part of the last century about what would be an appropriate scientific definition for the term stress. In 1946, Hans Selye published a seminal paper describing a nonspecific biological response to physical stressors (Selye, 1946). His approach was based on the observation that the bodily consequences of physical trauma were independent of the nature of the precipitating insult. His ultimate synthesis was encapsulated as the general adaptation syndrome (GAS), which remains one of the guiding theories for stress research today....

Extrahypothalamic CRH Systems

Of whether these fears are learned or innate, exposure to stimuli that elicit such fear will ultimately lead to activation of stress responsive systems. Common experimental paradigms used to examine the neural substrates of learned and innate fears (i.e., the anticipation of aversive events) include contextual and cue-elicited fear conditioning in the rat and exposure to predator cues such as fox feces and feline odors. The interesting point to be made here is that the anticipation of aversive events leads to mobilization of stress responsive systems. However, when sustained anticipation occurs over a prolonged period of time, the resources necessary for effective coping with such stressors eventually become depleted, and deleterious health consequences are likely to ensue. Indeed, the ultimate cost to the individual of prolonged negative anticipation has been conceptualized as allostatic load (McEwen, 2000 Schulkin et al., 1994). Thus, it is advantageous to look toward animal models...

Integrative Role For Brain Cytokines

Many of these behavioral changes observed following immune stimulation are mediated by central production of the proinflammatory cytokine interleukin-1 (IL-1). Central administration of IL-1 produces fever, hyperalgesia (Watkins et al., 1994), induces slow-wave sleep (Opp and Krueger, 1991), reduces food and water intake (Kent et al., 1996), alters peripheral immune function (Sullivan et al., 1997), increases plasma ACTH and glucocorticoids (Dunn, 1995), reduces social interaction (Kent et al., 1992), and decreases some measures of anxiety (Montkowski et al., 1997). Many of the behavioral changes produced by icv administration of IL-1 can be blocked or attenuated by prior icv administration of IL-1 receptor antagonist (IL-1ra) (Opp and Krueger, 1991 Kent et al., 1996). Thus, central production of IL-1 appears to be a critical component of host defense against peripheral infection and subsequent recovery.

Management of Withdrawal

Although the mechanisms of the withdrawal reaction from SSRIs require further explanation, it is clear from clinical evidence that the symptoms can be minimized or avoided by slow tapering of dosage. The principles are similar to those recommended for benzodiazepine withdrawal.35 Schatzberg et al16 suggest that paroxetine should be reduced by 5 mg week, and tapering of the shorter half-life SSRIs, especially fluvoxamine and paroxetine, may have to continue for several months. The longer elimination half-life of fluoxetine and norfluoxetine to some extent protects against withdrawal symptoms, but nevertheless reactions can occur even from fluoxetine in some patients.36 If withdrawal symptoms from any of the SSRIs occur, Lejoyeux et al10 recommend that the dosage of the drug should be temporarily increased and then tapered again at a slower rate. Although it might appear rational, it is not always possible to substitute one SSRI for another Lane (1996)13 quotes the case of a patient who...

The Acute Affective Stress Response

Affective variables associated with the stress-hypertension relation include an array of acute emotional responses to environmental stressors. Although positive emotions like happiness or joy could serve as potential acute affective stress responses associated with hypertension, research in this area has typically focused on emotions that constitute negative affect, mainly anxiety and anger. In this regard, not all emotions have received equal attention. In order to examine more closely the role of acute anxiety or anger responses in connection with the stress-hypertension relation, it is more important to measure short-term affective states that occur in response to situational or environmental stressors than the more enduring anxiety and anger traits. In Spielberger, Gorsuch, and Lushene's (1970) terminology, acute stress responses are best assessed using measures of state affect (responding how anxious or angry you feel right now), and the more enduring characteristics of affect...

Pharmacology of the Motor System

The lower motor neuron uses acetylcholine as its neurotransmitter. The internuncial pool of neurons in the spinal cord are all inhibitory neurons that use the amino acid neurotransmitters gamma-aminobutyric acid (GABA) and glycine. Whereas glutamate is the most important excitatory neurotransmitter in the brain as well as the motor system, GABA is the most widely distributed and major chemical neurotransmitter used in the inhibitory systems. Some output neurons in the basal ganglia and cerebellum use GABA as their transmitter, but most GABA is contained and utilized by local circuit inhibitory interneurons including the internuncial pool in the spinal cord. GABA is synthesized from glutamate by the enzyme glutamic acid decarboxylase (GAD) and is catabolized by the enzyme GABA-transaminase (GABA-t). Drugs that inhibit GABA-t such as some newly developed antiepileptic drugs increase the concentrations of GABA and inhibitory tone. Drugs can also act as agonists at GABA receptors....

Factors that Promote and Impair Sleep

It is well known that satisfying basic bodily needs, from hunger to sexual urgency, promote sleepiness. Conversely, all kinds of emotional distress tend to reduce sleep onset and quality. This effect is very prominent in the difficulty that depressed individuals commonly experience in falling asleep and sustaining sleep, and also in the disrupted sleep patterns found in various anxiety disorders, mania, and schizophrenia (Kryger et al., 2000). It is well known that physical exertion during the day tends to increase SWS, while mental and emotional exertions, as long as they are not too extreme, tend to increase REM (Panksepp, 1998). Traditional Benzodiazepine (BZ) Hypnotics Anxiolytic Benzodiazepines Used as Hypnotics (off-label) Clonazepam CID 0.5 mg FDA AMDD 4 mg divided (for anxiety conditions) Lorazepam CID 1 mg FDA AMDD 6 mg divided (for anxiety conditions) Alprazolam CID 0.25 mg FDA AMDD 4 mg divided (for anxiety conditions)

Sleep Problems and Remedies from Ambien to Zolpidem

Objectively measured sleep problems allow clinicians to provide pharmacological assistance that has been standardized in clinical populations (Kryger et al., 2000). The enormous amount of drug development in this area attests to the prevalence of sleep problems in our society. Although there is no space to detail this massive literature, the list of effective sleep aids now on the market is lengthy, and far exceeds the list of those agents approved by the Food and Drug Administration (FDA) (Table 4.1). This is because all the benzodiazepine (BZ) receptor agonists can serve as sleeping aids, but the approved ones are typically the shorter-acting agents such as triazolam (Halcion) for individuals simply having difficulty falling asleep. The longer-acting agents can sustain sleep, but are more likely to have sedative carryover effects into the morning (Mitler, 2000). Considering the antistress effects of a good night's sleep for all forms of mental distress, the search for more specific...

Interaction of Serotonergic Pathways with Reward Systems

There appears to be little information on the interactions between opioids and serotonergic systems46 but benzodiazepines and alcohol are thought to exert their anxiolytic effects at least partly by decreasing serotonergic activity in critical pathways via GABA enhancement.50

Efficacy Research on Psychotherapy

Anxiety and Stress Generalized Anxiety Disorder Geriatric anxiety and depression Obsessive-Compulsive Disorder Panic Disorder Posttraumatic Stress Disorder Public speaking anxiety Social Anxiety Disorder (Social Phobia) Specific Phobia Benzodiazepine withdrawal Psychotherapies are not efficacious for all conditions (for example, interpersonal psychotherapy (IPT) has been shown to be ineffective in two studies with opiate abusers). However, for several disorders, psychotherapies have been shown to be as effective as psychotropic interventions (e.g., cognitive-behavioral therapy CBT for Panic Disorder, CBT and IPT for Bulimia Nervosa). For other disorders, psychotherapy is an invaluable adjunct to medication (e.g., bipolar disorder, Schizophrenia). Anxiety Disorders. A considerable body of evidence has shown that CBT is as effective as, or more effective than, medications in the treatment of the full range of anxiety disorders (cf. Nathan & Gorman, 1998, for a comprehensive review),...

Summary of Measures of State Affect as Mediators of the Stress Hypertension Relation

Measures of state affect, both anger and anxiety, often are confounded by the novelty of the experimental situation. If differences in state affect are detected between hypertensive and normotensive participants, it is unknown whether the changes in affect are occurring in response to stressful stimuli used in the study or whether they represent study participants' responses to the novelty of the experimental situation. Certainly, if you volunteered for a study and found yourself in a strange laboratory environment for the first time, there is a possibility that even basal levels of state affect measured upon arrival to the laboratory would not reflect the levels of state affect that you were experiencing earlier in the day. Therefore, to truly examine acute state affective responses to standard laboratory stressors, it becomes crucial to calculate the difference between measures of affect obtained during a rest period and those obtained immediately following stress presentation. This...

Substance Abuse and Personality Disorders in the General Population

Psychiatric disorders studied included the Axis I disorders of mania, schizophrenia, somatization, anorexia, affective disorders, and anxiety disorders and the Axis II disorder ASPD. Of all the psychiatric diagnoses investigated, the highest comorbidity rate observed was between alcoholism and ASPD. In the general population, male alcoholics were four times more likely to have a diagnosis of ASPD than nonalcoholics, and female alcoholics were 12 times more likely to be diagnosed with ASPD then nonalcoholic females. In 1997, Kessler and colleagues (5) examined the lifetime co-occurrence of alcohol use disorders and other psychiatric disorders among a nationally representative household sample. They found that persons with alcohol dependence had higher rates of comorbidity with ASPD than with Axis I Anxiety or Affective disorders. In both of these studies, ASPD was the only personality disorder investigated along with selected Axis I disorders. Thus, a comprehensive picture...

What Leads To Disordered Personality

The promise of measuring dimensions of personality disorder symptoms leads to the possibility of linking those measures to physiological substrates. As succinctly stated by Jang and Vernon (2001) The definition of the phenotype remains the most important prerequisite for successful genetic studies (p. 177). In other words, investigators can most easily link protein expression mechanisms to phenotypes that are internally coherent, distinct from other phenotypes, and stable across measurement attempts. Because some personality traits show desirable psychometric qualities of validity and reliability and describe key features of personality disorders, they may provide ideal endophenotypes for linkage to genetic and intermediate physiological mechanisms (Jang and Vernon, 2001). Investigations of the relationship between genetic polymorphisms and personality traits provide fertile ground for inquiry. For instance, mice genetically engineered to lack serotonin 1a receptors show increased...

Existential Psychology

Given all this, why would anyone characteristically avoid choosing the future The reason is that choosing the future brings with it ontological anxiety, or fear of uncertainty and failure. One cannot be sure whether what transpires will be pleasurable, effective, successful, or what one hoped for. If what happens is positive, that will further your self-esteem, but if it is negative, you will have no one to blame but yourself. Needless to say, the most authentic way of life is regularly to choose the future, despite the ontological anxiety this brings. To do this well, one needs existential courage, or the recognition and acceptance that growth and development is not only a vibrant but also a painful experience. Existential courage has been operationalized as hardiness, which is a motivational set of attitudes comprising the three Cs of challenge, commitment, and control. Persons strong in challenge see change as normal and something to be learned from rather than a threat to be...

Summary of Cognitive Measures as Mediators of the Stress Hypertension Relation

Given findings from studies examining hypertensive patients' cognitive appraisals of emotion-laden information and painful stimuli, it could be hypothesized that hypertension is associated with an overall tendency to minimize sensitivity to a broad range of environmental stimuli. Nykli'cek et al. (2001) tested this hypothesis by exposing a group of hypertensive patients and normotensive controls to a painful electric current stimulus as well as a variety of stressful laboratory tasks. Findings revealed that hypertensive women, in contrast to normoten-sive women, exhibited diminished pain sensitivity to the electric current in addition to lower pre-task ratings of state anxiety and less negative appraisal associated with watching a stressful film segment. Pain sensitivity measures were positively correlated with ratings of negative task appraisals, providing some support for this hypothesis. However, these findings were observed only among women, and only with appraisal ratings of the...

Female Sexual Arousal Disorder

Female sexual arousal disorder (FSAD) is operationalized as the difficulty in reaching and maintaining vaginal lubrication or genital swelling until the completion of the sexual activity (ApA, 2000). Recently, theorists have argued that diagnosis of FSAD should consider not only the physiological dimension of sexual arousal (i.e., lubrication) but the psychological experience as well. Women of all ages may experience difficulty lubricating, although it tends to be more of a problem in later life, typically after menopause. Female sexual arousal disorder is generally assessed and treated in conjunction with female orgasmic disorder or HSDD. To date, there are no validated treatments that focus exclusively on treating female arousal problems, although a number of pharmacological agents for enhancing vaginal engorgement and lubrication are currently under investigation. Techniques are often employed to help the patient become aware of her anxiety or her sexual turn-off thoughts,...

Orgasm Disorders Female Orgasmic Disorder

Female orgasmic disorder (FOD) is defined in the DSM-IV (ApA, 2000) as the delay or absence of orgasm following a normal sexual excitement phase. The cognitive-behavioral treatment approach has received the greatest amount of empirical support for treating FOD. Reported success rates range between 88 and 90 . This therapy technique aims at reducing anxiety-producing thoughts associated with sexual activities and increasing positive behavioral experiences. The treatment is moderately short, averaging 10 to 20 sessions. The major treatment components include sensate focus, directed masturbation, and systematic de-sensitization. Sensate focus involves exchanging physical caresses, moving from nonsexual to increasingly sexual touching of one another's body over an assigned period of time. Directed masturbation involves a series of at-home exercises that begin with visual and tactile total body exploration and move toward increased genital stimulation with the eventual optional use of a...

Characteristics of Affected Individuals

Approximately 95 of affected males have mild to profound MR and some form of communication disorder. Affected males have particular difficulty with processing and short-term memory of serial information. Auditory memory and reception are poor. General language development is delayed relative to intelligence, and specific problems such as perseverations, repetitions, echolalia, cluttered speech, and dysfluencies are often shown. Many fully affected males show an apparently unique complex of behaviors, including stereotypies, particularly hand flapping, gaze aversion, avoidance of touch, hyperactivity, inatten-tiveness, aggression, and anxiety (Meyer & Batshaw, 2002).

Agedependent Variants

Posterior slow waves of youth, also called youth waves, posterior fused transients, and sail waves, are triangular, 2- to 4-Hz waveforms that coexist with other waking background rhythms (Fig. 10). They commonly form a complex that consists of the slow delta component with superimposed and following faster rhythms of the waking background rhythm, hence the term fused. They are best seen over the posterior head regions in waking. These waves are occasionally asymmetric. These waveforms behave just like normal waking background rhythms in that they block with eye opening, increase with hyperventilation, and disappear in drowsiness. Youth waves usually appear between the ages of 8 to 20 yr, maximally in early adolescence. Hyperventilation-induced slowing refers to a build-up of diffuse theta and delta activities in response to hyperventilation for several minutes during the EEG. This build-up may be abrupt or gradual and is often rhythmic and of high amplitude (up to 500 V) it should...

Aging Stress and Mental Disorders

The present cohort of older persons has lower rates of major depression, substance abuse, and some other mental disorders than younger cohorts. Older persons are at increased risk for a number of mental disorders, including the dementias (of which Alzheimer's disease is most common) and subsyndromal depressive and anxiety disorders. Future projections suggest we will see increased prevalence of late-life mental disorders when the baby boom cohort reaches advanced age. Mental disorder in older adults is distinct in that it is often comorbid with multiple physical disorders and complicating social factors. Older persons are often taking multiple medications and seeing multiple health care providers. These changes mean that mental health or behavioral health services should be carefully coordinated with medical and social services, ideally through multidisciplinary teams.

Neurotransmitter Imaging of the Serotoninergic System

The serotoninergic system is thought to be critically involved in a large number, if not the majority, of psychiatric illnesses. The most important and well studied of these is major depressive disorder (MDD). However, the serotonin system is also considered important in schizophrenia, anxiety and phobias, obsessive-compulsive disorder, eating disorders, sleep, and numerous other psychiatric conditions. Serotonin and Anxiety. Serotonin 5-HT1A receptors are thought to play a role in modulating anxiety. Lately, there has been a report of an inverse correlation between 5-HT1A receptor BP and anxiety in healthy subjects (Tauscher et al., 2001a), but thus far there are no published reports on in vivo 5-HT1A binding in anxiety disorders.

Physical disruption stress failure

Component of the surfactant pool relative to the less active small aggregate (SA) component. Although stretch of type 2 cells in vitro and a modest degree of hyperventilation stimulate surfactant production,70 more injurious ventilatory strategies of high tidal volume and low PEEP lead to a reduced pool of functional surfactant and a decreased LA SA ratio, particularly in injured lungs.71 Large cyclical alterations in the alveolar surface area and the presence of serum proteins in the airspace may be responsible for these changes.

Imaging of Other Neurotransmitter Systems

The GABAergic system is thought to play a central role in mediating the effects of alcohol. This is substantiated by the finding that besides binding sites for gamma-aminobutyric acid (GABA) and benzodiazepines, the GABAa receptor also contains a binding site for alcohol. Direct measurements using PET and 11C flumazenil, an inverse agonist at the GABAa receptor, have found a reduction in the concentration of these receptors in the medial frontal lobes and cingulate gyrus of alcoholic subjects and the cerebellum of patients with alcoholic cerebellar degeneration (Gilman et al., 1996). Baxter LR, Jr, Schwartz JM, Mazziotta JC, et al. (1988). Cerebral glucose metabolic rates in nondepressed patients with obsessive-compulsive disorder. Am J Psychiatry 145 1560-1563. Baxter LR, Jr, Schwartz JM, Bergman KS, et al. (1992). Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Arch Gen Psychiatry 49 681-689. Benkelfat C, Nordahl TE,...

Growth Hormone [gh Somatotropin

The release of GH by the pituitary gland is regulated by many of the monoamine and neuropeptide systems, also involved in mood and anxiety regulation, acting through the hypothalamus. The release of GH, by either a provocative stimulus or a spontaneous release as part of a physiological process (e.g., sleep) has therefore been viewed as a potential window into CNS trophic function. The neuroscientific challenge remains to wholly integrate frontolimbic dysfunction, which current technology are increasingly well equipped to detect, with previously documented hypothalamic-pituitary dysfunction, which, to date, is most readily apparent with psychoneuroendocrine evaluation.

Other Valuable Uses for Beta Blockers

Beta-blockers are also effective medications to treat high blood pressure, prevent angina or heart attacks in people with cardiovascular disease, reduce the frequency of migraine headaches, and prevent panic attacks. This makes their appropriate use, in thyroid cancer patients, multifunctional. Sara has told me that her beta-blocker has also eliminated her panic attacks and feelings of jitteriness after eating (which she had wrongly attributed to hypoglycemia). In this context, the beta-blocker nicely balances the thyroid hormone suppression therapy (to keep TSH low) that is a mainstay of thyroid cancer treatment.

Treatment of Hypoparathyroidism Low Calcium

Thyroid cancer surgery, which entails removing the thyroid gland and enlarged lymph nodes in the neck, runs a risk of damaging the parathyroid glands near the thyroid (see Chapter 1). This would cause a low calcium level in the blood, which can be severe, resulting in muscle spasms, anxiety, and abnormal numbness or tingling sensations. Most often this is temporary, caused by bruising of the parathyroid glands during surgery that resolves on its own within a few days or weeks. But sometimes this is a permanent situation that requires lifelong treatment. Low calcium caused by one or more damaged parathyroid glands is called hypoparathyroidism. To understand the treatment for hypoparathyroidism, it's important to first explain how parathyroid glands normally function otherwise, medications used to treat hypoparathyroidism will not make sense to you.

Psychological disturbances

2 Irritability and mood disturbance including anxiety and depression. Anxiety and depression are present in more than 50 of those with chronic insomnia and may be either a cause or a result of the insomnia. A vicious cycle of insomnia and worsening anxiety and depression often develops. If insomnia persists despite treatment of depression or alcoholism or following cessation of antipsychotic drugs and schizophrenia, it is more likely that the underlying psychiatric disorder will relapse.

Management of Sexual Dysfunction

General principles of psychological management include explanation and reassurance, reduction of performance anxiety, reduction of feelings of failure and resentment, and establishment of better communication between partners when addressing relationship difficulties.112,113 This is likely to be helpful even for those patients whose sexual dysfunction is primarily drug-related. Common-sense suggests waiting for spontaneous improvement, especially in patients in the early stages of drug treatment, still recovering from depression.

Optimize sleep hygiene

It is important to treat depression and anxiety, which can both be either causes of insomnia or responses to it, before more complex aspects of management are considered. Antidepressants should only be used if features of depression are present and not as a routine treatment. Sedating tricyclic antidepressants, such as trimipramine, imipramine and doxepin, are particularly effective. Paroxetine is the most suitable of the SSRI antidepressants, several of which worsen insomnia even if it is due to depression (Table 7.6). The sedating action of mirtazapine is useful in treating insomnia. Table 7.6 Choice of benzodiazepine and related types of hypnotic.

Parental History of Hypertension

Several psychological individual difference parameters have also been shown to interact with parental history of hypertension in affecting the magnitude of behaviorally elicited cardiovascular reactivity. For example, research has shown that relations between parental history of hypertension and cardiovascular response to stress were observed among participants who inhibit anger expression, but not those who express anger openly (Holroyd and Gorkin, 1983 Vogele and Steptoe, 1993), among participants reporting heightened anxiety (Manuck et al., 1985 Miller, 1992), among individuals high on measures of de-fensiveness (Shapiro, Goldstein, and Jamner, 1995), and among persons who deny the experience and expression of emotion, particularly in association with a high need for social approval (Jorgensen, Gelling, and Kliner, 1992 Jorgensen and Houston, 1986 1988). Several of these psychological characteristics (anger inhibition, defensiveness, anxiety) have also been shown to be related to...

Gender Similarities and Differences

Two studies that examined gender-related aspects of BDD found that the clinical features of the disorder appear to be similar in men and women. One of these studies (N 188) found, however, that women were more likely than men to focus on their hips and weight, camouflage with makeup and pick their skin, and have comorbid bulimia nervosa (Phillips and Diaz 1997). In addition, the study found that men were more likely to be unmarried be preoccupied with body build, genitals, and hair thinning use a hat for camouflage and have alcohol abuse or dependence. In the other study (N 58), women were more likely to focus on their breasts and legs, check mirrors and camouflage, and have bulimia, panic disorder, and generalized anxiety disorder men were more likely to focus on their genitals, height, and excessive body hair, and have bipolar disorder (Perugi et al. 1997a).

Suggested Reading

B., Ketter, T. A., Denicoff, K. D., George, M. S., Frye, M. A., Smith, M. A., & Leverich, G. S. (1997). The kindling model Implications for the etiology and treatment of Mood Disorders. Current Review of Mood and Anxiety Disorders, 1, 113-126.

So what can be learnt from this

Research in other areas of professional-patient client communication has indicated that professionals sometimes fail to provide basic information (Eiser 1996 Weinman 1997). This was true at the time of sperm banking, including information about content (types of containers available, likelihood of producing a sample etc.) and process (where to sit, where to leave the sample etc.). These are complex areas to manage but need to be agreed in advance on an individual patient basis. Not only does this have the potential to reduce anxiety at the time but may also minimize the potential for lasting distress being generated.

Learned Helplessness

In some cases, the situation itself provides the explanation. In other cases, the person relies on a habitual way of making sense of events that occur, what is called explanatory style. Explanatory style is therefore a distal influence on helplessness and the failures of adaptation that involve helplessness. Explanatory style has been studied in its own right, and it has an array of correlates. People who explain bad events with internal, stable, and global causes show passivity poor problem-solving depression anxiety failure in academic, athletic, and vocational realms social estrangement morbidity and mortality. Explanatory style can be highly stable, sometimes over decades. The self-fulfilling nature of explanatory style and helplessness per se explains this stability. At the same time, explanatory style can and does change in response to ongoing life events. Cognitive therapy, for example, can move explanatory style in an optimistic direction.

Basic Principles and Technique

In recording the EEG, an attempt is generally made to activate abnormalities by hyperventilation for about 3 minutes, and also by photic stimulation at flash rates up to 20 Hz. Other common activating procedures include sleep during the recording procedure and sleep deprivation on the night before the examination. y

Clinical features

There may be a genetic factor or personality type which predisposes to CFS in the presence of an initiating event, which may be a viral infection such as the Epstein-Barr virus, or emotional stress. The characteristic response in CFS is a hyperarousal state with abnormalities of pituitary and other aspects of endocrine function. It may be complicated by depression and anxiety.

Craig W Berridge Rodrigo A Espana and Thomas A Stalnaker

The rise to prominence of the concept of stress within modern society is a relatively recent development, arising from scientific observations made since the early twentieth century. These studies identified two important principles. First, they identified a sensitivity of physiological systems to challenging environmental conditions. Second, later studies demonstrated a strong association between stress (and anxiety) and a wide variety of physiological, cognitive, and affective dysfunctions. Much effort been devoted to elucidating the neural mechanisms underlying stress and anxiety, and the contribution of stress-related neural circuits to cognitive and affective dysfunction. The vast majority of this work has utilized animal models and these studies have yielded substantial insight into the neurobiology of stress and anxiety. One early observation was that a robust activation of cerebral dopamine (DA) and other monoamines occurs in stress, including within the prefrontal cortex...

Male Sexual Dysfunction Male Erectile Disorder

Previous estimates of ED complaints in clinical samples have indicated that from 36 to 48 of men who present for treatment in sex clinics have a primary diagnosis of male erectile disorder (Ackerman & Carey, 1995). Current estimates of clinical prevalence are missing, and may be important in describing the change in treatment for erectile dysfunction from sex therapy to pharmacology. Physiologically-based risk factors for ED include older age, alcohol use, nicotine use, and a sedentary lifestyle (Acker-man & Carey, 1995 Tengs & Osgood, 2001). Psychological risk factors include mental disorders and acute emotional states, particularly anxiety and depression (Barlow, 1986 Masters & Johnson, 1970 Wincze & Carey, 1991). The predominant themes in the psychological treatment of erectile dysfunction are the reduction of performance anxiety and the increase of sexual stimulation, and this treatment approach is still based largely on the work of Masters and Johnson...

Male Orgasmic Disorder

Male Orgasmic Disorder, previously referred to as Inhibited Ejaculation, has received very little attention in the therapeutic literature. As initially reported by Masters and Johnson (1970), this remains a relatively rare dysfunction, and etiology remains unclear. Clinical case studies suggest a variety of psychological factors as causes, but there is virtually no empirical support for these theories (Dow, 1981 Schull & Sprenkle, 1980). Male Orgasmic Disorder can, however, result from a number of physiological conditions, such as multiple sclerosis and damage to the hypothalamus. Finally, the inability to reach orgasm may be a side effect of several medications, including anti-hypertensives sedatives and anti-anxiety, anti-depressive, and antipsychotic agents (Ban & Freyhan, 1980). Perhaps due to the ambiguity surrounding the etiology of Male Orgasmic Disorder, relatively little has appeared in the literature regarding treatment. The standard treatment strategies eliminating...

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