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Anxiety, normal

Normally, dietary tyramine is broken down in the gastrointestinal tract by MAO and is not absorbed. In the presence of MAOI, however, all of its potent sympathomimetic actions are seen. Other side effects of MAOI include excessive CNS stimulation, orthostatic hypotension, weight gain, and in rare cases hepatotoxicity. Because the monoamine oxidase inhibitors exhibit greater toxicity, yet no greater therapeutic response than other, newer agents, clinical use has been markedly curtailed. The primary use for MAOIs is in the treatment of atypical depressions, eg, those associated with increased appetite, phobic anxiety, hypersomnolence, and fatigues, but not melancholia (2). [Pg.466]

Anxiety is a normal reaction. Pathological anxiety interferes with daily-life activities and may be accompanied by autonomic symptoms (chest pain, dyspnoea and palpitations). Severe forms include phobic anxiety and panic disorder. [Pg.201]

The expected outcomes for the patient depend on the type and severity of the seizure but may include an optimal response to tiierapy (control of seizure), management of common adverse drug reactions (includes minimizing injury and maintaining normal oral mucous membranes), reduction in anxiety, and an understanding of and compliance with the prescribed therapeutic regimen. [Pg.259]

However, lorazepam and oxazepam are relatively safe for older adults when given in normal dosages. Buspirone (BuSpar) also is a safe choice for older adults with anxiety because it does not cause excessive sedation, and the risk of falling is not as great. Before bus-pirone therapy is begun, benzodiazepines and sedatives and hypnotics are gradually withdrawn. Buspirone, unlike most of the benzodiazepines, must be taken regularly and is not effective on an as-needed basis. [Pg.279]

Managing Anxiety and Body image Disturbance The parents, and sometimes the children, may be concerned about the success or possible failure of treatment with GH. The child is provided with the opportunity to share fears, concerns, or anger. The nurse acknowledges these feeling as normal and corrects any misconceptions the child or parents may have concerning treatment. Time is allowed for the parents and children to ask questions not only before therapy is started but also during the months of treatment. [Pg.515]

Ciraulo DA, Jaffe JH Tricyclic antidepressants in the treatment of depression associated with alcoholism. Clin Psychopharmacol 1 146—150, 1981 Ciraulo DA, Nace E Benzodiazepine treatment of anxiety or insomnia in substance abuse patients. Am J Addict 9 276—284, 2000 Ciraulo DA, Barnhill JG, Jaffe JH, et al Intravenous pharmacokinetics of 2-hydroxy-imipramine in alcoholics and normal controls. J StudAlcohol 51 366-372, 1990 Ciraulo DA, Knapp CM, LoCastro J, et al A benzodiazepine mood effect scale reliability and validity determined for alcohol-dependent subjects and adults with a parental history of alcoholism. Am J Drug Alcohol Abuse 27 339—347, 2001 Collins MA Tetrahydropapaveroline in Parkinson s disease and alcoholism a look back in honor of Merton Sandler. Neurotoxicology 25 117-120, 2004 COMBINE Study Research Group Testing combined pharmacotherapies and behavioral interventions in alcohol dependence rationale and methods. Alcohol Clin Exp Res 27 1107-1122, 2003a... [Pg.43]

Anxiety is a normal part of mental life and plays a crucial role in human psychological development and other forms of learning. Although systematic studies are lacking, suppression of normal levels of anxiety could impair the development of adaptive coping mechanisms. On the other hand, disabling anxiety impairs adaptation as well and is associated with significant morbidity and mortality. [Pg.137]

Finally, the peptide can induce anxiety and panic in normal and anxious volunteers. Some synthetic CCK-B receptor antagonists are chemically similar to the benzodiazepine anxiolytics. Again, the clinical role of CCK manipulation in anxiety remains to be resolved. [Pg.261]

All preclinical animal models of anxiety involve exposing animals (usually rats or mice) to environmental stimuli that disrupt their normal pattern of behaviour (Table 19.2). Obviously, it can never be confirmed that animals are actually experiencing the equivalent of human anxiety and so the validity of all preclinical models rests largely on confirming that the change in behaviour is prevented by drugs that have established anti-anxiety effects in humans. [Pg.396]

Most of these models evaluate the effects of drugs on the behaviour of animals when they are exposed to a novel environment. Novelty normally reduces animals exploratory activity but established anti-anxiety drugs consistently increase exploration of, and approaches to, the novel stimulus and reduce the neophobic ( avoidance ) reaction. There are several examples of tests based on this principle (Table 19.2) but two that are widely used are the plus-maze and the social interaction tests. [Pg.397]

Inadequate activity of an endogenous ligand which is a benzodiazepine receptor agonist and suppresses anxiety. In this case, the administration of the antagonist, fiumazenil, should induce anxiety in normal subjects and exacerbate anxiety in anxious patients. [Pg.410]

Dysfunction of the GABAa receptor complex such that the effects of all benzodiazepine receptor ligands are shifted in the direction of inverse agonism. In this case, fiumazenil (which normally has zero efficacy) should induce anxiety in anxious patients but have no effects in healthy subjects because they have normal receptors. [Pg.410]

Figure 19.8 A schematic representation of the GABAa receptor shift hypothesis. This proposes that patients with panic disorder have dysfunctional GABAa receptors such that the actions of drugs that behave as antagonists in normal subjects are expressed as inverse agonism in panic patients. It is unlikely that this theory extends to generalised anxiety disorder (GAD), for which benzodiazepine agonists are highly effective treatments, but it could explain why these drugs are relatively ineffective at treating panic disorder. (Based on Nutt et al. 1990)... Figure 19.8 A schematic representation of the GABAa receptor shift hypothesis. This proposes that patients with panic disorder have dysfunctional GABAa receptors such that the actions of drugs that behave as antagonists in normal subjects are expressed as inverse agonism in panic patients. It is unlikely that this theory extends to generalised anxiety disorder (GAD), for which benzodiazepine agonists are highly effective treatments, but it could explain why these drugs are relatively ineffective at treating panic disorder. (Based on Nutt et al. 1990)...
Anxiety is a normal response to stressful or fearful circumstances. Most people experience some degree of anxiety in reaction to stressful situations, such as final exams or giving a speech. This allows an individual to adapt to or manage the stressful/threatening situation. Anxiety symptoms generally... [Pg.605]

Evaluate patients for symptom improvement frequently (e.g., weekly) during the first 4 weeks of therapy. The goal is to alleviate panic attacks and reduce anticipatory anxiety and phobic avoidance with resumption of normal activities. Alter the therapy of patients who do not achieve a significant reduction in panic symptoms after 6 to 8 weeks of an adequate dose of antidepressant or 3 weeks of a benzodiazepine. Regularly evaluate patients for adverse effects, and educate them about appropriate expectations of drug therapy. [Pg.616]

A classic example of a medicinal plant of Asia and the Pacific with GABAergic properties is Piper methysticum Forst. (Kava, British Pharmaceutical Codex, 1934), or kava-kava, the rhizomes of which have been used since a very early period of time by Polynesians to allay anxiety and reduce fatigue. Kava has been marketed in Europe to treat sleep disorders and anxiety. The beverage normally induces a form of euphoria, described as a happy state of complete comfort and peace, with ease of conversation... [Pg.102]

A 36-year-old male has been experiencing intense pressure to be more productive at work. This has resulted in his becoming extremely anxious, which makes it very dif ficult for him to function effectively. He wishes to keep his job. Physical examination and blood chemistries are normal. He is given diazepam, which diminishes his anxiety and allows him to concentrate on his work. What is the mechanism of action of diazepam ... [Pg.153]

Rodriguez, G., Cogorno, P., Gris, A. et al. Regional cerebral blood flow and anxiety a correlation study in neuro-logically normal patients. /. Cereb. Blood Flow Metab, 9 410-416,1989. [Pg.908]


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