Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For phenomenological elucidation of panic attacks, 26 patients with panic attacks were requested to name the panic symptoms in order of their occurrence and specify the patterns of their abatement. Panic symptoms were found to be classifiable into three categories: early symptoms consisting of dizziness or faintness, palpitations, and sweating; intermediate symptoms dyspnea, nausea or abdominal distress, flush or chills, chest pain or discomfort, shaking, and choking; late symptoms paresthesias, fear of dying, and fear of going crazy. Panic symptoms disappeared in 61.6% irrespective of the sequence of their occurrence. Twenty-one patients were interviewed about the experience of nocturnal panic attacks, and 23.8% experienced them. These findings suggest that fear is caused by sudden physical abnormality triggered by some biological factors.
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PMID:The sequence of panic symptoms. 148 43

A review of the clinical efficacy of four structurally distinct antidepressant drugs is presented. Their antidepressant activity can be rationalised within current pharmacological hypotheses of drug action, despite markedly different effects on "in vitro" testing. Fluoxetine, a specific serotonin re-uptake inhibitor, has proven safe, effective treatment for depressive illness and may have a role to play in the treatment of obsessive-compulsive disorder and panic attacks. While it has few of the anticholinergic side effects of the tricyclic antidepressants, nausea, tremor, headache, weight loss, nervousness and sweating are side effects most frequently reported. Minaprine, a compound with weak MAO inhibiting properties and effects on serotonergic receptors, has clinical efficacy in the treatment of depression based on several comparative studies. It is claimed that minaprine lacks anticholinergic and sedative properties. Moclobemide, a specific, reversible inhibitor of MAO-A, has been extensively evaluated in depressive illness. The major advantage of this agent over other irreversible, non-specific MAO inhibitors, is the significant attenuation of the so-called "cheese effect" with doses of tyramine likely to be encountered in foodstuffs. Rolipram, a phosphodiesterase inhibitor, represents a new approach to antidepressant treatment. Limited clinical data suggest that the drug may be an effective antidepressant with few side effects. The place of these agents in therapy is yet to be established.
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PMID:New pharmacological approaches to the management of depression: from theory to clinical practice. 158 Aug 88

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosage of clomipramine hydrochloride are described, and clinical studies of the use of clomipramine in treating obsessive-compulsive disorder (OCD), other psychiatric conditions, and chronic pain are reviewed. Clomipramine hydrochloride, a tricyclic antidepressant, is a potent inhibitor of serotonin reuptake and may affect dopaminergic neurotransmission, suppress rapid eye movement sleep, produce changes in electrocardiograms, and elevate plasma prolactin. The drug is well absorbed from the gastrointestinal tract and undergoes extensive first-pass metabolism. Peak plasma concentrations occur three to four hours after a 150-mg oral dose. The mean elimination half-life is 39 hours. Some 66% of a dose is excreted in the urine, the remainder being eliminated in the feces. In clinical trials, clomipramine was significantly more effective than placebo, clorgiline, amitriptyline, imipramine, and doxepin in ameliorating the symptoms of OCD. Initial effects are seen at four weeks; improvement may continue for up to 18 weeks. Clomipramine may also be effective in treating panic attacks, phobias, depression, and chronic pain. The most common adverse effects of clomipramine are anticholinergic; others include nausea, seizures, and sexual difficulties. Interactions between clomipramine and barbiturates, haloperidol, monoamine oxidase inhibitors, and cigarette smoking have been documented. The usual initial adult dosage is 25-50 mg/day, titrated gradually to 250 mg/day if necessary. Clomipramine hydrochloride is a welcome new agent for the treatment of obsessive-compulsive disorder. Although its adverse-effect profile is like that of other tricyclic antidepressants, sexual dysfunction and seizures may be more frequent with this agent and limit its use.
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PMID:Clomipramine: an antiobsessional tricyclic antidepressant. 218 Jun 23

This paper has three parts: local anaesthetic adverse effects, haemorrhage control and altered immune response. Primary emphasis is placed on the problems with anaesthetics since their use is widespread. Every day, nearly 2 million injections of local anaesthetic are given in dental practice. From 2.5 to 10 per cent of patients experience adverse reactions. This adverse effect rate is 10 times higher than that in medicine for the same drugs. Allergic, toxic, idiosyncratic and psychogenic effects are discussed. New data on the role of local anaesthetic agents, vasoconstrictors and preservatives is presented. In addition, the problem of anaesthetic failure (occurring in over 10 per cent of patients) is explained. Treatment (drug and psychological) for anaesthetic related emergencies such as panic attacks, shortness of breath, palpitations and nausea is recommended. Prevention and treatment of haemorrhage is explained. Medical and dental conditions may increase clotting time (e.g., systemic disease or local factors such as granulation tissue). Preventive strategies are outlined and laboratory tests discussed. Emphasis should be placed on the use of local anaesthetics with vasoconstrictors, haemostatic agents and pressure. The final aspect of the paper discussed new data on problems for dentists arising with patients who have altered immune function. In particular AIDS is discussed from the point of view of protection of the dentist and dental treatment for the patient.
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PMID:Local anaesthetic adverse effects and other emergency problems in general dental practice. 294 76

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

Despite much recent research, there is still little systematic information about the phenomenology of panic attacks, and their possible causes remain obscure. We investigated panic attacks in the natural environment using an event sampling approach. Twenty-seven panic attack patients and 19 matched normal controls kept panic attack and self-exposure diaries for 6 days and wore an ambulatory heart rate/physical activity recorder for 3 days. Patients reported 175 attacks, generally of moderate severity. The most frequent symptoms were palpitations, dizziness/lightheadedness, dyspnea, nausea, sweating, and chest pain/discomfort. The results did not support the classification of panic attacks recently proposed by Sheehan and Sheehan, which requires three symptoms as a cutoff for panic attacks. Panic attacks classified by the patients as situational (i.e., occurring in feared situations) were more severe and occurred in situational contexts different from spontaneous attacks, but were otherwise phenomenologically similar. Heart rates did not change during spontaneous attacks and were only mildly elevated during situational attacks or during the 15 minutes preceding these attacks. These heart rate changes were interpretable as effects of anxiety, although physical activity showed a similar pattern of changes. Some normal control subjects reported on the panic diary primarily situational anxiety episodes that were phenomenologically similar to, albeit less severe than, the patients' episodes. Panic patients may sometimes fail to perceive environmental triggers for their attacks because many attacks classified as spontaneous occurred in classical "phobic" situations. Furthermore, the comparison of concurrent diary and retrospective interview and questionnaire descriptions showed that panic patients have a tendency toward retrospective exaggeration. Implications for the assessment, definition, and classification of panic attacks are discussed.
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PMID:Panic attacks in the natural environment. 365 82

Physiological dependence on benzodiazepines is accompanied by a withdrawal syndrome which is typically characterized by sleep disturbance, irritability, increased tension and anxiety, panic attacks, hand tremor, sweating, difficulty in concentration, dry wretching and nausea, some weight loss, palpitations, headache, muscular pain and stiffness and a host of perceptual changes. Instances are also reported within the high-dosage category of more serious developments such as seizures and psychotic reactions. Withdrawal from normal dosage benzodiazepine treatment can result in a number of symptomatic patterns. The most common is a short-lived "rebound" anxiety and insomnia, coming on within 1-4 days of discontinuation, depending on the half-life of the particular drug. The second pattern is the full-blown withdrawal syndrome, usually lasting 10-14 days; finally, a third pattern may represent the return of anxiety symptoms which then persist until some form of treatment is instituted. Physiological dependence on benzodiazepines can occur following prolonged treatment with therapeutic doses, but it is not clear what proportion of patients are likely to experience a withdrawal syndrome. It is also unknown to what extent the risk of physiological dependence is dependent upon a minimum duration of exposure or dosage of these drugs. Withdrawal phenomena appear to be more severe following withdrawal from high doses or short-acting benzodiazepines. Dependence on alcohol or other sedatives may increase the risk of benzodiazepine dependence, but it has proved difficult to demonstrate unequivocally differences in the relative abuse potential of individual benzodiazepines.
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PMID:The benzodiazepine withdrawal syndrome. 784 56

There is considerable evidence that antidepressants, particularly serotonin uptake inhibitors, are effective in the treatment of panic disorder (PD). Monoamine oxidase inhibitors (MAOI) may also have beneficial effects in PD. In this study 30 patients with PD with or without agoraphobia (DSM-III-R) were treated with the selective and reversible MAO-A inhibitor brofaromine (150 mg daily) in a 12-week double-blind placebo controlled design. A clinical relevant improvement was found in more than 70% of the patients treated with brofaromine, whereas no significant improvement was observed on placebo. After an increase in anxiety in the first week, a clinically relevant improvement in anxiety symptoms was found, followed by a subsequent reduction in agoraphobic avoidance in patients treated with brofaromine. A similar improvement was observed on distress scores related to panic attacks, although there was no significant reduction in the number of panic attacks. The most prominent side-effects were middle sleep disturbance and nausea. No increase in blood pressure was observed. During a follow-up period of another 12 weeks a further improvement was found in patients treated with brofaromine.
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PMID:MAO inhibitors in panic disorder: clinical effects of treatment with brofaromine. A double blind placebo controlled study. 787 Oct 61

Panic attack symptomatology was investigated in 212 panic disorder patients (60 men, 152 women) using the Panic Attack Questionnaire, Feelings of helplessness and thoughts of escape had the highest mean severity ratings, but are not currently listed in the DSM-III-R. The DSM-III-R symptoms labeled choking or smothering sensations, paresthesias, nausea, and chest pain had low severity ratings. Evidence was obtained for a three-factor model of panic symptomatology consisting of dizziness-related symptoms, cardiorespiratory distress, and cognitive factors. These results provide only limited support for the current DSM-III-R symptom structure, and support the notion that panic disorder is a heterogeneous condition.
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PMID:The symptom structure of panic attacks. 799 26

This review attempts to critically assess the evidence regarding the relationship between the specificity of antidepressants in modulating different neurotransmitter systems and their therapeutic activity. Evidence from experimental and clinical studies suggests that all antidepressants and electroconvulsive shock therapy produce qualitatively similar adaptive changes in serotonergic, adrenergic, and possibly GABAergic and dopaminergic transmission following chronic treatment. Such adaptational changes parallel the onset of the therapeutic response. The relationship between the pharmacokinetics and the therapeutic efficacy and safety of the serotonin selective reuptake inhibitors (SSRIs) is considered with particular attention to fluoxetine, fluvoxamine, sertraline, and paroxetine. The primary difference between these drugs lies in their half-lives; fluoxetine and its major active metabolite norfluoxetine have a combined half-life exceeding 7 days. All the SSRIs are well tolerated with a low incidence of life-threatening side effects. Nausea and, rarely, vomiting occur quite frequently as a consequence of increased serotonergic activity in the gastrointestinal tract and possibly via central 5-HT3 receptors. The safety and prolonged efficacy of the SSRIs render them particularly beneficial for the long-term treatment of the depressed patient. Evidence is provided that, in order to prevent relapse, depressed patients should be maintained on continuous antidepressant therapy for at least 1 year, and at the same dose as that required to treat the acute phase of the illness. The review concludes with a brief summary of the therapeutic use of the SSRIs in the treatment of panic attack, obsessive compulsive disorder, and bulimia with a brief comment on the different subtypes of serotonin receptors that may be involved.
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PMID:The comparative pharmacology of new antidepressants. 825 4


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