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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the relationship between suicidality, agitation, panic attacks, and the thyrotropin-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH), and tested the hypothesis that panic would account for the association between a reduced TSH response and the other conditions. Twenty-seven euthyroid primary unipolar depressed inpatient women received a TRH test and systematic psychiatric assessment. Panic attacks were insufficient to explain the link between the TSH response and suicidal intent, lethality, and agitation; each condition was independently associated with a lower TSH response. In an additive fashion, copresence of conditions further reduced TSH response. The symptom constellation of panic, agitation, and suicidality in depression may correlate with the greatest reduction in TSH response.
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PMID:Panic, suicide, and agitation: independent correlates of the TSH response to TRH in depression. 826 37

Suicide has been associated traditionally with major depression, alcoholism, and schizophrenia and in the past several years with alcoholism and comorbid depression. More recently, however, panic disorder has been linked with suicide attempts, and the importance of severe anxiety symptoms (panic attacks, psychic anxiety, and agitation) as possible predictors of suicide risk in patients with major affective disorder has been studied. The author discusses data sets from three such studies: (1) the Clinical Studies of the National Institute of Mental Health Collaborative Program on the Psychobiology of Depression, (2) a study on 17-hydroxycorticosteroid concentrations in inpatients with major affective disorder, and (3) a study on inpatient suicides. The author concludes by suggesting that anxiety, which is readily treatable, may in fact be one of the most clinically important symptoms in depressive disorders.
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PMID:Suicide risk factors in depressive disorders and in panic disorder. 154 56

The effects of oral administration of caffeine (10 mg/kg) on behavioral ratings, somatic symptoms, blood pressure and plasma levels of 3-methoxy-4-hydroxyphenethyleneglycol (MHPG) and cortisol were determined in 17 healthy subjects and 21 patients meeting DSM-III criteria for agoraphobia with panic attacks or panic disorder. Caffeine produced significantly greater increases in subject-rated anxiety, nervousness, fear, nausea, palpitations, restlessness, and tremors in the patients compared with healthy subjects. In the patients, but not the healthy subjects, these symptoms were significantly correlated with plasma caffeine levels. Seventy-one percent of the patients reported that the behavioral effects of caffeine were similar to those experienced during panic attacks. Caffeine did not alter plasma MHPG levels in either the healthy subjects or patients. Caffeine increased plasma cortisol levels equally in the patient and healthy groups. Because caffeine is an adenosine receptor antagonist, these results suggest that some panic disorder patients may have abnormalities in neuronal systems involving adenosine. Patients with anxiety disorders may benefit by avoiding caffeine-containing foods and beverages.
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PMID:Increased anxiogenic effects of caffeine in panic disorders. 298 30

In this article we report on the reliable production of several features of panic attacks following subcutaneous administration of sodium lactate to nonhuman primates. Unrestrained monkeys were evaluated by an observer without knowledge of the subjects' treatment with either sodium lactate or a dextrose control solution. The lactate produced temporally circumscribed episodes of agitation, wariness, and motor responses, normally elicited under stressful or threatening conditions. In an initial pharmacological intervention, we found that pretreatment with imipramine blocked the response to lactate. The further development of this model offers promise for the systematic examination of etiological factors in susceptibility to lactate induction of panic attacks, the physiological basis of the response, and new modes of treatment of panic disorder.
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PMID:A nonhuman primate model of panic disorder. 336 17

Of a group of 288 depressed female inpatients, 43 (15%) had secondary panic attacks. Compared to other depressives, the subgroup with panic attacks had significantly higher frequencies of anorexia, weight loss, gastrointestinal disturbances, hypochondriasis, and psychomotor agitation, and significantly lower frequencies of melancholic symptoms, including loss of interest in usual activities, guilt feelings, delusional thinking, psychomotor retardation, and orientation or memory impairment. Patients with panic attacks were less likely to have a depressed parent and were more likely to be described as having been nervous, worrisome, sensitive, and sexually dysfunctional before the onset of depression. Phenomenologically, they resembled "anxious depressives" as described by other authors.
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PMID:Depressed women with panic attacks. 646 19

Yohimbine, an alpha 2-adrenergic receptor antagonist that increases noradrenergic function, was administered to 20 healthy subjects and 39 drug-free patients with agoraphobia and panic attacks. Following drug administration, changes in plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), BP, pulse rate, and subjective ratings of feelings and somatic symptoms were examined during a four-hour period. Yohimbine produced significantly greater increases in patient-rated anxiety, nervousness, palpitations, hot and cold flashes, restlessness, tremors, piloerection, and sitting systolic BP in the total patient group compared with healthy subjects. There were significant correlations between the yohimbine-induced rise in plasma MHPG level and patient-rated anxiety and nervousness and the frequency of reported panic attacks. Patients experiencing frequent panic attacks (greater than 2.5 per week) had a significantly greater plasma MHPG response to yohimbine than the healthy subjects and patients having less frequent panic attacks. These observations support a hypothesis of increased sensitivity to augmented noradrenergic function in anxiety states associated with panic, and they suggest that impaired presynaptic noradrenergic neuronal regulation may exist in patients with frequent panic attacks.
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PMID:Noradrenergic function in panic anxiety. Effects of yohimbine in healthy subjects and patients with agoraphobia and panic disorder. 674 77

This study compared the efficacy, tolerability, and safety of fluvoxamine, imipramine, and placebo in the treatment of panic disorder with or without agoraphobia. Fifty-four outpatients participated in the randomized, double-blind trial as part of a multicenter trial. After meeting inclusion criteria and completing screening requirements (e.g., laboratory testing, electrocardiogram, physical examination), patients were entered in a single-blind placebo washout phase. They were then randomized to either fluvoxamine, imipramine, or placebo. Measurements completed at each visit included the number and severity of panic attacks per week, the Sheehan Panic and Anticipatory Anxiety Scale, and the Clinical Global Impressions, and others. Results show that fluvoxamine is more effective than placebo and as effective as imipramine in reducing spontaneous panic attacks in moderate to severe panic disorder. However, starting doses of fluvoxamine and imipramine should be low to minimize untoward side effects (such as insomnia and agitation) and maintain compliance.
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PMID:A double-blind placebo-controlled trial comparing fluvoxamine and imipramine in the treatment of panic disorder with or without agoraphobia. 892 63

Severe anxiety can disrupt neurohumoral metabolism and lead to agitation and brain failure, which may result in delirium. Predisposing factors include cerebral vascular or endocrine insufficiency, cardiopulmonary decompensation, poor tissue perfusion, multiple medications, and sleep-wake cycle disruption; the stressful ICU environment puts patients especially at risk. Stress-induced noradrenergic hyperactivity can precipitate panic attacks; dopaminergic hyperactivity can lead to delirium (marked by paranoid delusions, visual or auditory hallucinations, and psychomotor agitation). The underlying cause of anxiety must be identified to guide appropriate therapy.
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PMID:Understanding the neurohumoral causes of anxiety in the ICU. Clinical consequences include agitation, brain failure, delirium. 1015 Jul 60

It has been found that while over 90% of people who commit suicide have a psychiatric illness at the time, over 50% are under active psychiatric or mental health care. How can suicide risk be detected and preventive treatment provided? Both communication of suicidal ideation or intent and prior suicide attempts have been shown to be risk factors, which should be assessed in patients with psychiatric illness. Research shows that suicidal ideation is often not communicated to professionals or is denied by patients just prior to suicide and, when present, is often useful not as an immediate risk factor, but as a chronic risk factor. Suicide attempts predict a 10-30% occurrence of suicide over 10 years, but often do not indicate immediate risk. Recent research has shown that impulsiveness and severe anxiety, panic attacks, and agitation comorbid with depression are often immediate suicide risk factors that are potentially modifiable if recognized and treated urgently with effective medications and watchful support.
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PMID:Treating impulsivity and anxiety in the suicidal patient. 1141 Nov 93

Low and medium potency benzodiazepines were initially introduced for the treatment of insomnia and anxiety. Their therapeutic actions as anxiolytics, sedative hypnotics, anticonvulsants, and muscle relaxants (with their low toxicity) have led to their use as first-line treatments, and they have become one of the most prescribed classes of drugs. Novel therapeutic uses of benzodiazepines were discovered with the introduction of the high-potency benzodiazepines (e.g., alprazolam, clonazepam, and lorazepam). They were found to be effective in treating panic disorder and panic attacks with or without agoraphobia, as add-on therapy to selective serotonin reuptake inhibitors in the treatment of obsessive-compulsive disorder and panic disorders, and as adjunctive therapy in treating patients with acute mania or acute agitation. High-potency benzodiazepines have replaced low and medium potency benzodiazepines in all benzodiazepine clinical indications due to their greater therapeutic effects and rapid onset of action. Differences in distribution, elimination half-life, and rate of absorption are important considerations when choosing a high-potency benzodiazepine. Typically, a benzodiazepine with long distribution and elimination half-lives is preferred. A maximum dose of 2 mg/day of any of the high-potency benzodiazepines when given for more than 1 week is recommended. Although as a class benzodiazepines act rapidly and are well tolerated, their use presents clinical issues such as dependence, rebound anxiety, memory impairment, and discontinuation syndrome.
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PMID:Issues in the clinical use of benzodiazepines: potency, withdrawal, and rebound. 1507 12


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