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)

A recently proposed diagnostic class, psychotic trigger reaction, is deduced from careful clinical studies of eight white men, who upon a very specific trigger stimulus committed murder or attempted to (and in one case also rape). The new class is defined as a sudden ego-alien, motiveless (at least with respect to aggression), motor-wise well organized, violent complex action without emotional concomitants. The action is evoked (not provoked) by an individually unique stimulus within a specific context reviving repeated past traumatic experience. Typically there is no (significant) loss of consciousness and practically full recall. Observed are first-time hallucinations (visual, auditory, tactile, somesthetic, but not olfactory as in temporal lobe epilepsy) and signs of imbalance in the autonomic nervous system (loss of bladder control, ejaculation, profuse sweating, nausea). Only four of these men had previous psychiatric diagnoses (and then various ones) or abnormal EEGs at some time in their lives. Variety in prior diagnoses would be consistent with a seizure-like disorder, here specifically implicating an imbalance in functioning between limbic and frontal lobe systems. Clinical tests for the latter were prevailingly indicative of dysfunctioning. A detailed clinical analysis of the violent acts within their context suggests behaviors are analogous to certain limbic system mechanisms, especially the kindling phenomenon.
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PMID:Specific stimulus-evoked violent action in psychotic trigger reaction: a seizure-like imbalance between frontal lobe and limbic systems? 649 48

A group of 90 breast cancer patients undergoing chemotherapy were assessed prospectively to estimate the prevalence of acute (post-treatment) and anticipatory emesis in the 1990s. For this purpose, two protocols of chemotherapy were analysed separately: cyclophosphamide/methotrexate/5-fluorouracil (CMF) and 5-fluorouracil/doxorubicin/cyclophosphamide (FAC). All patients were treated with antiemetic therapy, which included one corticoid plus ondansetron (in the FAC regimen), or one corticoid plus thiethylperazine (in the CMF regimen). For at least one cycle of chemotherapy 86.1% and 91.7% patients in the FAC protocol presented vomiting and nausea respectively: 11.1% had anticipatory vomiting and 30.6% had anticipatory nausea. In the CMF protocol, 79.6% had post-chemotherapy vomiting and 71.7% had post-chemotherapy nausea associated with at least one cycle. In this group, 7.4% had anticipatory vomiting and 16.6% had anticipatory nausea. A high proportion of patients suffered anticipatory anxiety in both groups (75% in FAC, 74.1% in CMF). The stimuli most frequently associated with the appearance of anticipatory emesis were olfactory stimuli and cognitive stimuli. In summary, as a result of the advances made in antiemetic control during the last decade, the severity of chemotherapy-induced emesis seems to have significantly decreased, but the prevalence of these symptoms along the course of the treatment still remains high.
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PMID:Acute and anticipatory emesis in breast cancer patients. 888 31

Individuals who report illness (e.g. nausea, headache) from common chemical odors tend to report CNS symptoms suggestive of olfactory-limbic system involvement. This study compared the resting quantitative electroencephalographic (qEEG) patterns of young adult college students reporting subjectively elevated chemical odor intolerance ratings (HICI) with those of controls reporting little or no odor intolerance (LOCI). Each group was subdivided into those with higher (HIDEP) vs. lower (LODEP) ratings of concomitant depression. Nineteen channels of EEG were recorded during a single session over four separate rest periods, respectively, following baseline, cognitive, chemical exposure and olfactory identification tests. Each recording involved two 30-s, eyes-closed, filtered room air breathing conditions: (1) nose inhalation followed by mouth exhalation and (2) mouth inhalation followed by mouth exhalation. HICI showed significantly less beta 1 (beta 1) over the temporal-central region during nose than during mouth inhalation. Over some temporal and central leads, task, DEP and CI interacted to influence beta 1 as well. For theta (theta), CI differences emerged during nose inhalation after the cognitive task at Cz, after chemical exposures at C3, Cz and C4 and after the olfactory ID task at C4. CI differences emerged during mouth breathing after the olfactory ID task at Cz, C4 and T4. The T5-T6 coronal array showed significant CI differences after chemical exposures during nose breathing and during mouth breathing after the cognitive and olfactory ID tasks. The theta findings in the HICI may be related to reports of disturbed attention in CI.
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PMID:Quantitative EEG patterns during nose versus mouth inhalation of filtered room air in young adults with and without self-reported chemical odor intolerances. 950 9

Pavlovian conditioning may contribute to some cases of multiple chemical sensitivity (MCS). On the basis of the conditioning analysis, environmental stimuli (especially olfactory cues) present at the time of a toxicant overdose become associated with the toxicant and elicit aversive conditional responses. Similar associations have been reported in patients receiving chemotherapy, and the literature on such 'pretreatment nausea' in cancer patients is relevant to understanding the role of conditioning in MCS. Evaluation of the contribution of conditioning to MCS has been complicated by confounding interpretations that emphasize conditional responses with interpretations which emphasize the psychiatric status of the patient. Appreciation of the contribution of Pavlovian conditioning to MCS will lead to a better understanding of this complex disorder.
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PMID:Multiple chemical sensitivity as a conditional response. 1041 84

The use of a self-administered noxious agent to suppress deviant sexual arousal is the focus of this paper. A recommended procedure for the use of olfactory aversion is described. Data from two publications by the author, wherein different noxious agents had been used, are presented and discussed. Several explanations for the mechanism of effect in olfactory aversion have been offered. Two of these, one using a nausea-producing agent and one using a pain-producing agent are described. The procedure using the pain-producing agent is the simplest to implement, the least ambiguous, and offers the least cumbersome explanation for the behavioral effect observed in olfactory aversion. However, a conditioning explanation is probably too simple. Several examples of cognitive mediation in conditioning procedures are presented and discussed.
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PMID:Olfactory aversion: notes on procedure, with speculations on its mechanism of effect. 1288 25

Immunosuppression during pregnancy makes the mother vulnerable to pathogens. Because meat is the principal source of ingestible pathogens, pregnancy raises the costs of meat eating. Natural selection has crafted a mechanism involving changes in nausea susceptibility and olfactory perception that reduces meat consumption during pregnancy. Evidence is presented showing that the luteal phase is marked by both immunosuppression and changes in nausea susceptibility and olfaction; meat consumption may be reduced during this period, suggesting a mechanism similar to pregnancy sickness. Constraints on compensatory increases in meat consumption outside of the luteal phase explain why women eat less meat than men. Meat is the principal target of acquired aversions. Women possess more aversions than men, suggesting that prophylactic mechanisms sometimes result in longstanding dietary changes. Reproductive immunosuppression explains many aspects of dietary behavior and sheds light on factors that may have contributed to gender-based divisions of labor during hominid evolution.
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PMID:Luteal phase immunosuppression and meat eating. 1191 97

Promethazine hydrochloride is a drug used for the management of allergic conditions, motion sickness and nausea, and as a sedative to (treat psychiatric disorders. This drug was nominated for testing by the Food and Drug Administration because of its widespread use in human medicine and because of lack of data on its potential carcinogenicity. Oral administration is the most common route of human exposure. Toxicology and carcinogenicity studies were conducted by administering promethazine hydrochloride (>99% pure) in distilled water by gavage to groups of male and female F344/N rats and B6C3F1 mice for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, in cultured Chinese hamster ovary cells, and in Drosophila melanogaster. 16-DAY STUDY IN RATS: Groups of five male and five female rats received 0, 18.5, 55.5, 166.5, 500, or 1,500 mg promethazine hydrochloride/kg body weight once daily, 5 days per week for a total of 12 doses in a 16-day period. All rats receiving 1,500 mg/kg, four males and four females receiving 500 mg/kg, and one male and one female receiving 166.5 mg/kg died during the study. No deaths occurred in the remaining dose groups. Final mean body weights of rats receiving 166.5 mg/kg were significantly lower (12% to 25%) than those of the controls. Clinical findings included decreased activity, ocular discharge, and labored breathing in males and females receiving 166.5, 500, and 1,500 mg/kg as well as tremors in females receiving 166.5 and 500 mg/kg. There were dose-related increases in the absolute and relative liver weights of rats. Focal suppurative inflammation occurred in the nose of some male and female rats receiving 55 or 166.5 mg/kg and in the trachea of some male and female rats receiving 166.5 mg/kg. 16-DAY STUDY IN MICE: Groups of five male and five female mice received 0, 18.8, 37.5, 75, 150, or 300 mg promethazine hydrochloride/kg body weight once daily, 5 days per week for a total of 12 doses in a 16-day period. Two females receiving 75 mg/kg, one male and one female receiving 150 mg/kg, and four females receiving 300 mg/kg died during the study. No deaths occurred in the remaining dose groups. Final mean body weights of mice receiving promethazine hydrochloride were similar to those of the controls. However, in male and female controls, the final mean body weights were 11% to 12% lower than the initial mean body weights. Clinical findings occurred as early as the first day of the study and included decreased activity in male and female mice receiving 150 and 300 mg/kg. Tremors occurred in one male and five females in the 300 mg/kg group on day 1 and in one male in the 150 mg/kg group and five males and one female in the 300 mg/kg group on day 2. Absolute and relative liver weights of male mice receiving 75, 150, or 300 mg/kg were significantly greater than those of the controls. No chemical related lesions were present in male or female mice. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats received 0, 3.7, 11.1, 33.3, 100, or 300 mg promethazine hydrochloride/kg body weight once daily, 5 days per week for 13 weeks. One female receiving 100 mg/kg and six males and nine females receiving 300 mg/kg died during the study. No deaths occurred in the remaining dose groups. Final mean body weights of male rats receiving 100 or 300 mg/kg were significantly lower (19% to 22%) than those of the controls. Mean body weight gain of females receiving 100 mg/kg was significantly lower (14%) than that of the controls. Clinical findings in rats included hunched posture and labored breathing. Absolute and relative liver weights of males receiving 11.1, 33.3, 100, or 300 mg/kg and females receiving 33.3 or 100 mg/kg were significantly greater than those of the controls. Focal suppurative inflammation of the nose and trachea occurred with an increased incidence in rats receiving 100 and 300 mg/kg. A dose-related increased incidence of vacuolar degeneration of the nasal olfactory epithelium occurred in male and female rats that received 11.1, 33.3, or urred in male and female rats that received 11.1, 33.3, or 100 mg/kg. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice received 0, 5, 15, 45, 135, or 405 mg promethazine hydrochloride/kg body weight once daily, 5 days per week for 13 weeks. One control female, one female receiving 5 mg/kg, two females receiving 45 mg/kg, four females receiving 135 mg/kg, and all mice receiving 405 mg/kg died during the study. No deaths occurred in the remaining dose group. Final mean body weights of mice receiving 135 mg/kg were significantly lower (8% to 9%) than those of the controls. Clinical findings of toxicity included labored breathing and decreased activity in one 135 mg/kg female. Absolute and relative liver weights increased in a dose-related trend in both sexes. No chemical-related lesions were observed in mice. 2-YEAR STUDY IN RATS: Based on mortality and body weight differences observed at higher levels, doses of promethazine hydrochloride selected for the 2-year study in rats were 0, 8.3, 16.6, and 33.3 mg/kg. Groups of 60 male or 60 female rats were administered promethazine hydrochloride in deionized water by gavage once daily, 5 days per week for up to 103 weeks. Up to ten male and ten female rats per dose group were evaluated at 15 months. Survival, Body Weights, and Clinical Findings: There was a significant dose-related decrease in survival of rats. The survival rates in the 16.6 and 33.3 mg/kg male groups and in the 33.3 mg/kg female group were significantly lower than those of the controls. The final mean body weight of male rats receiving 33.3 mg/kg promethazine hydrochloride was 10% lower than that of the controls. Final mean body weights of female rats in the 16.6 and 33.3 mg/kg groups were 9% and 11% lower than that of the controls, respectively. No chemical-related clinical findings were noted in any dose group. Significant increases in the absolute and relative liver weights of mid- and high-dose female rats and the relative liver weights of mid- and high-dose male rats were observed at the 15-month interim evaluation. There were no biologically significant differences in the hematology or clinical chemistry parameters measured at 15 months. Pathology Findings: No neoplasms that could be attributed to promethazine hydrochloride administration were found in male or female rats. Several neoplasms occurred with a significantly decreased incidence in rats receiving promethazine hydrochloride. These included adrenal medullary pheochromocytoma (benign or malignant) and pituitary gland adenoma in the 33.3 mg/kg males and uterine stromal polyp in the 33.3 mg/kg females. The decreased incidences of adrenal medullary pheochromocytoma were chemical related. The decreased incidences of pituitary gland adenoma and uterine stromal polyp may have been related to chemical administration. Diffuse fatty change of the liver of male rats increased with dose and was attributed to chemical administration. 2-YEAR STUDY IN MICE: Based on mortality and body weight differences observed at higher levels, the doses of promethazine hydrochloride selected for the 2-year study were 0, 11.25, 22.5, and 45 mg/kg for male mice and 0, 3.75, 7.5, and 15 mg/kg for female mice. Groups of 60 male or 60 female mice were administered promethazine hydrochloride in deionized water by gavage once daily, 5 days per week for up to 103 weeks. Up to 10 male and 10 female mice per dose group were evaluated at 15 months. Survival, Body Weights, and Clinical Findings: Survival of mice receiving promethazine hydrochloride was similar to that of the controls. Mean body weights of mice were within 7% of those of the controls throughout the study. There were no chemical-related clinical findings in male or female mice. There were no differences in hematology or clinical chemistry parameters measured at 15 months that were attributed to the administration of promethazine hydrochloride. Pathology Findings: There were no neoplasms or nonneoplastic lesions that were attributed to the administration of promethazine hydrochloride. GENETIC TOXICOLOGY: Promethazine hydrochloride did not induce gene mutations in Salmonella typhimurium strains TA97, TA98, TA100, TA1535, or TA1537, or a significant increase in chromosomal aberrations in cultured Chinese hamster ovary cells; both of these tests were conducted with and without exogenous metabolic activation (S9). A small dose-related increase in sister chromatid exchanges was observed in cultured Chinese hamster ovary cells in the presence of S9; this response was considered to be equivocal. No increase in sister chromatid exchanges was observed in the absence of S9. Promethazine hydrochloride did not induce sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster administered the chemical by feeding or injection. CONCLUSIONS: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of promethazine hydrochloride in male or female F344/N rats receiving 8.3, 16.6, or 33.3 mg/kg. There was no evidence of carcinogenic activity of promethazine hydrochloride in male B6C3F1 mice receiving 11.25, 22.5, or 45 mg/kg. There was no evidence of carcinogenic activity of promethazine hydrochloride in female B6C3F1 mice receiving 3.75, 7.5, or 15 mg/kg. The decrease in the incidences of adrenal medullary pheochromocytoma in male rats was considered to be related to promethazine hydrochloride administration. The decrease in the incidences of pituitary gland adenoma in male rats and uterine stromal polyp in female rats may have been related to promethazine administration. Synonyms: Phenothiazine,10-(2-(dimethylamino)propyl)-,monochlorohydrate; 10H-phenothiazine-10-ethanamine;10-(2-dimethylamino-2-methylethyl)phenothiazine hydrochloride; N-(2 -dimethylamino-2 -methyl)ethylphenothiazine hydrochloride Trade names: Diprazi; Kinetosin; Phenergan; Phenergan hydrochloride; Promine; Pipolfen; Plletia; Prorex; Promantine; Pyrethia; Romergan hydrochlonde
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PMID:NTP Toxicology and Carcinogenesis Studies of Promethazine Hydrochloride (CAS No. 58-33-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1261 86

Milnacipran is a new antidepressant which inhibits equipotently the reuptake of serotonin and noradrenaline both in vitro and in vivo with no effect on dopamine reuptake. Microdialysis studies have shown increased extracellular levels of both serotonin and noradrenaline after acute administration. Milnacipran is devoid of interactions at any known neurotransmitter receptor. In particular, and unlike tricyclic antidepressants (TCAs), it has no activity at noradrenergic, muscarinic or histaminergic receptors. Contrary to TCAs, chronic administration of milnacipran does not modify beta-adrenoceptor binding or second messenger function. Milnacipran is active on various animal models of depression such as the forced swimming test in the mouse, learned helplessness in the rat and the olfactory bulbectomized rat model. Milnacipran has a high bioavailability, low plasma protein binding, and is largely eliminated in the urine as the parent drug or as a glucuronide. These features suggest that interactions with other drugs given concurrently are unlikely. Studies in patients with liver dysfunction and in the elderly suggest that dose adjustment is not necessary. In patients with renal impairment, decreased elimination of milnacipran is correlated to the degree of renal impairment allowing an easy dosage adjustment. An intermediate half-life of approximately 8 h is compatible with twice-daily administration. Clinical studies comparing milnacipran, placebo and other antidepressants provide evidence of its efficacy in moderate to severe depression in both hospitalized and outpatient settings. Meta-analyses of the original data of controlled trials comparing milnacipran with imipramine or selective serotonin reuptake inhibitors (SSRIs) show that milnacipran provides antidepressant efficacy similar to that of TCAs and significantly superior to that of SSRIs. An analysis of a database of over 3300 patients shows that both the general and cardiovascular tolerability of milnacipran are superior to those of TCAs with notably less cholinergic side effects. The tolerance of milnacipran was comparable to that of SSRIs with a higher incidence of dysuria with milnacipran but a higher frequency of nausea and anxiety with the SSRIs. Milnacipran represents an interesting new therapeutic option in depression, being as well tolerated as the SSRIs but offering clinical efficacy similar to the TCAs.
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PMID:Milnacipran, a new specific serotonin and noradrenaline reuptake inhibitor. 1498 77

Lymphocytic hypophysitis is a rare inflammatory disease of the pituitary gland that is being increasingly recognized as a cause of hypopituitarism. This condition may be due to an autoimmune pituitary destruction which usually occurs in young women during pregnancy or in the immediate postpartum period. We describe a case of cystic pituitary mass in a thirty-eight year-old woman presenting with nausea, vomiting, cold intolerance, blurring of vision and the presence of disagreeable odors for a one-month period. She had secondary amenorrhea and galactorrhea for three months. Combined anterior pituitary stimulation test confirmed the diagnosis of hypopituitarism. Magnetic resonance imaging scan with enhancement showed a huge cystic sellar mass with suprasellar extension and thickening of the pituitary stalk. Transsphenoidal exploration was performed with preoperative diagnosis of pituitary macroadenoma with cystic necrosis. Histological examination revealed lymphocytic hypophysitis characteristic of diffuse, dense lymphocytes and plasma cells infiltration with surrounding interstitial reactive fibrosis. Postoperatively, the patient's olfactory function returned to normal but combined anterior pituitary stimulation test showed persistence of hypopituitarism with mild hyperprolactinemia. Prednisolone, thyroxine and estrogen replacements were started and clinical symptoms were much improved. In summary, we report an extremely rare case of a woman with cystic lymphocytic hypophysitis with cacosmia and hypopituitarism, confirmed by histological examination.
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PMID:A case of cystic lymphocytic hypophysitis with cacosmia and hypopituitarism. 1525 85

Olfactory abnormalities in temporal lobe epilepsy (TLE) usually involve either brief hallucinations prior to seizures or chronic impairments in odor discrimination and identification. We describe the case of a man (B.C.) with TLE with an unusual presentation, an ictus-related parosmia. B.C. reported distorted perception of odor quality and hedonics that could provoke nausea and gagging, typically at its most extreme in the week or so following a seizure. Measures of B.C.'s olfactory functioning were obtained at stages of the ictal cycle when parosmia symptoms were severe and when they had decreased. Unlike other parosmics, B.C.'s detection thresholds were always normal, and unlike others with TLE, he evidenced little impairment in identification or discrimination. Testing during a period of more severe parosmia suggested that B.C.'s experiences might be the result of hedonic changes. We argue this may be the effect of seizure activity on the amygdala, which is known to be involved in mediating emotive reactions to odors.
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PMID:Olfactory dysfunction in temporal lobe epilepsy: a case of ictus-related parosmia. 1776 59


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