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)

Sinemet (a combination of levodopa with carbidopa, a dopa-decarboxylase inhibitor) has replaced levodopa for early treatment of parkinsonism. The blocking of the systemic uptake of dopamine has eliminated the previous complications of nausea, vomiting, and cardiac and respiratory arrhythmias; pyridoxine need not now be avoided. However, the earlier appearance of abnormal involuntary movements, hallucinations, occasional psychosis, and a dopa-resistant state limits treatment efficacy. In all-over experience the combination drug offers the best relief for rigidity and akinesia. It has improved the quality of life and reduced mortality by one half. The greatest benefits appear in the first 3 years; then complications set in. The relation of complications to dosage is now better understood, and the ratio of dopa-decarboxylase inhibitor to levodopa inhibitor to levodopa of 1:4 is better than the previous 1:10. Levodopa with or without dopa decarboxylase is not a cure for parkinsonism. Some agonist drugs (bromocryptine, lisuride) are showing promise in the testing stage. The evolving knowledge about neurotransmitters and peptide messengers offers hope for the growing number of patients with parkinsonism.
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PMID:Sinemet and the treatment of Parkinsonism. 701 95

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

The withdrawal of heterocyclic antidepressants and antipsychotic agents can produce nausea, emesis, anorexia, diarrhoea, rhinorrhoea, diaphoresis, myalgias, paraesthesias, anxiety, agitation, restlessness and insomnia. The withdrawal of monoamine oxidase (MAO) inhibitors may result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, cognitive impairment, delirium, suicidality and delusions of persecution. The withdrawal of antipsychotic agents may give rise to symptoms preceding the onset of psychosis. These potential harbingers of relapse include anxiety, agitation, restlessness and insomnia. The withdrawal phenomena reviewed are usually prevented by gradually reducing the total daily dosage of the pertinent drug. Antimuscarinic agents often alleviate the distress produced by the withdrawal of tricyclic antidepressants and antipsychotic agents. MAO inhibitor withdrawal syndromes may constitute medical emergencies. The prevention of the evolution of a MAO inhibitor withdrawal-precipitated syndrome is a high priority.
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PMID:Withdrawal phenomena associated with antidepressant and antipsychotic agents. 791 78

Over a 3-year period, 15 patients with severe hyponatremia were referred to our emergency room from a nearby psychiatric institution. This article reports on 36 episodes of symptomatic hyponatremia in those 15 patients. All but two of the patients were receiving antipsychotic medications; one patient was taking a nonsteroidal anti-inflammatory drug, and one patient was taking an oral hypoglycemic agent. Thirteen patients were chronic schizophrenics, one had a bipolar depressive disorder with psychotic features, and one patient had no psychiatric disorder. Patients presented with seizures, change in mental status, and vegetative symptoms (nausea, vomiting, and diarrhea) associated with hyponatremia and water intoxication. Exacerbation of the patients' underlying illness, psychogenic polydipsia, compulsive smoking, alcoholic cirrhosis, drug abuse, and neuroleptic and other medications are thought to be the major causes of acute hyponatremia in these patients.
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PMID:Symptomatic hyponatremia associated with psychosis, medications, and smoking. 809 75

A neuropsychiatric and -psychological update of the crime "profile" and "signature" is a necessary addition to the traditional sociopsychological model likely to miss limbic system dysfunctioning. Thus, occurrence of a brief (c. 20 minutes) limbic seizure has been proposed based on behaviors of 12 white male homicidal loners, who showed a dozen symptoms and signs: Limbic Psychotic Trigger Reaction. Readily overlooked can be (a) a transient psychosis (hallucinations and/or delusions), (b) autonomic hyperactivation (e.g., loss of bladder control, nausea, ejaculation), (c) motiveless, out-of-character, unplanned, and well-remembered homicidal acts, (d) committed with a flat affect (not emotionally or impulsively provoked), (e) typically involving a stranger who happened to provide an objectively harmless and only subjectively important stimulus. (f) Such an individualized stimulus triggered the memory revival of mild to moderate but repeatedly experienced hurts. Such a specific sequence of events implicates the specific mechanism of limbic seizure, "kindling," which does not necessarily involve motor convulsions. Repetition of such limbic episodes with "criminal acts" is conceivable under specific circumstances including cases in which the triggering stimulus is associated with pleasurable delusions (e.g., of grandiose power or wealth) or constitutes a specific aspect of a basic drive motive. For example, eating or sexual activities might be planned but degenerate into a limbic episode with a specific core symptomatology.
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PMID:Neuropsychiatric update of the crime "profile" and "signature" in single or serial homicides: rule out limbic psychotic trigger reaction. 830 91

The levels of N-acetyl-beta-glucosaminidase (NAG) in urine from 35 patients with bipolar affective disorder were compared with scores for the 90 items (symptoms) of the Symptom Checklist (SCL-90). There were significant negative correlations between NAG levels and 23 of the SCL-90 variables (symptoms). These symptoms could be grouped into the following categories: anxiety, unusual or psychotic thinking, suicidal thinking, dysphoria, irritability, nausea, headaches, memory problems, and loss of interest. Serotonin abnormalities may play a role in the production of many of these symptoms. The hypothesis that NAG could be a marker for a serotonin activity is discussed.
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PMID:Association of levels of N-acetyl-beta-glucosaminidase with specific psychiatric symptoms in bipolar patients. 834 66

The present study was designed to examine withdrawal from a therapeutic, non abused drug, haloperidol. Rats were trained to discriminate the anxiogenic compound pentylenetetrazol (PTZ) from water in a two lever, food reinforced, drug discrimination procedure. Dose effect curves were then determined for PTZ and the antipsychotic drug, haloperidol (0.1-1 mg/kg). Haloperidol did not substitute for PTZ, even at a dose that decreased rates of responding to approximately 15% of control values. Rats were then treated chronically with either 1 or 2 mg/kg/day haloperidol while training was suspended. After 5 days of chronic haloperidol 4/6 animals in the 1 mg/kg/day group and 5/7 in the 2 mg/kg/day group chose the PTZ lever when tested 24-48 hours after the last haloperidol injection. Haloperidol, 1 or 2 mg/kg, did not reverse PTZ-lever responding. After an additional 5 days of chronic haloperidol, 3/6 rats in the 1 mg/kg/day group and 5/7 rats in the 2 mg/kg/day group responded on the PTZ lever 24 hours after the last injection, and this was reversed with the anxiolytic, chlordiazepoxide (3.2-5.6 mg/kg). The current findings indicate that there is an anxiogenic component to withdrawal from haloperidol. In psychotic patients, abrupt discontinuation of haloperidol results in nausea, vomiting and sweating, as well as a "relapse into psychosis" characterized by anxiety, depression and internal chaos (1). Interestingly, the authors caution that the so-called relapse into psychosis may simply be a sign of withdrawal. The current findings support their view and suggest that abrupt discontinuation of psychoactive therapeutic agents may result in anxiety.
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PMID:Withdrawal from chronic haloperidol substitutes for the pentylenetetrazol discriminative stimulus. 846 31

102 patients were divided into 3 groups: epileptics, psychotics and epileptics with psychotic symptoms. All had long been monitored for a number of clinical and laboratory parameters. Though different in many respects, all share states of sudden dysphoria, cacophoria, panic anxiety, horror, and EEG (stereo-EEG, too) signs of epileptic or other gross anomalies, often correlated to those affective disorders. Attacks of dysphoria, epilepsy, and psychosis come spontaneously and in response to biological (hypoglycemia, sleep deprivation, alcohol, menses) or psychosocial stimulation (agitation, quarrels, fear of redundancy, psychic trauma). These states (attacks, dysphoria, "neurotic" or even psychotic episodes) often provoke one another. -Calling this syndrome epileptosis, we believe its mechanism is due to lesions of the limbic and brainstem modulation systems. At the start of the process there is an epileptic focus in the amygdalo-hippocampal complex (AHC) which in itself can trigger simple or complex partial paroxysm but also-by means of electric stimulation of the AHC-states of dysphoria, anxiety, and psychotic hallucinations. Besides, a form of pathological learning develops in premorbid "hypersensitive" personality which can be put down to associative learning and to Overton's phenomenon of "state-dependent retention of learned responses". This may give rise to mutual stimulation where epileptic focal activity in AHC can provoke dysphoria while an external psychosocial situation can trigger epileptic activity there, too (AHC). Since there need not always be mydriasis (though other vegetative signs such as tachycardia, tachypnoea, nausea, blush and others are frequent) or unconsciousness, and some psychomotor manifestations may be out of the ordinary, and scalp EEG may be normal, such patients are often regarded as "hysterics" or malingerers.
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PMID:"Epileptosis"--a syndrome or useless speculation? 871 19

When treating patients with psychoses, clinicians must often consider changing their treatment from one antipsychotic agent to another. The transition may be necessary because the patient experiences serious side effects or because the existing therapy no longer controls the patient's symptoms. A principal problem in changing antipsychotic agents is the potential for withdrawal symptoms resulting from discontinuation of the existing therapy. These syndromes can manifest as reemergence or worsening of psychosis, rebound or unmasked dyskinesia, and cholinergic-rebound symptoms. Withdrawal signs and symptoms may include insomnia, nausea, vomiting, anxiety, and agitation. When switching a patient to the new antipsychotic agent risperidone, the clinician can keep withdrawal symptoms to a minimum by considering the patient's clinical history and current status. For some patients, abrupt withdrawal of the current antipsychotic may be possible. For others, the dose of the previous medication must be gradually reduced before risperidone is initiated. In many cases, the transition is best made by overlapping the existing therapy and risperidone.
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PMID:Changing antipsychotic medication: guidelines on the transition to treatment with risperidone. The Consensus Study Group on Risperidone Dosing. 887 89

Following the conduct of a 28-day inpatient bioequivalence study of clozapine in schizophrenia patients, withdrawal effects after abrupt discontinuation from clozapine were assessed. Thirty patients who met DSM-III-R criteria for schizophrenia, residual type, or schizophrenia in remission were enrolled in the study. Patients were evaluated for symptoms of withdrawal effects for 7 days after clozapine 200 mg/day was abruptly withdrawn. Of 28 patients who completed the study, 11 had no withdrawal symptoms; 12 had mild withdrawal adverse events of agitation, headache, or nausea; four patients experienced moderate withdrawal adverse events of nausea, vomiting, or diarrhea; and one patient experienced a rapid-onset psychotic episode requiring hospitalization. Cholinergic rebound is a likely explanation for the mild to moderate withdrawal symptoms and is easily treated with an anticholinergic agent. Mesolimbic supersensitivity, as well as specific properties of clozapine, are discussed as likely causes for rapidonset psychosis. Our findings are consistent with previous reports of withdrawal reactions associated with clozapine, further reminding clinicians to monitor patients closely following abrupt discontinuation of clozapine.
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PMID:Cholinergic rebound and rapid onset psychosis following abrupt clozapine withdrawal. 893 13


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