Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine were evaluated. Verapamil (10-80 mg/kg), diltiazem (20-120 mg/kg) and nicardipine (20-160 mg/kg), when administered subcutaneously, produced a dose-dependent reduction in forepaw tremor and weight loss during the abstinence reaction; jumping was also reduced by all three drugs, although the effect was not statistically significant in the case of nicardipine. By contrast, the calcium agonist Bay K 8644 (0.5-2 mg/kg, SC) increased forepaw tremor and weight loss, although this latter effect did not reach statistical significance. The effects of the calcium channel active drugs on the rotarod test were also explored, no correlation appearing with the results observed in abstinence (except for the jumping response), which suggests that the withdrawal results are not influenced by motor incoordination or unspecific CNS depression. These findings suggest that L-type calcium channels probably play an important role in withdrawal after acute morphine dependence. Taken together with other observations in chronic models, these results show that calcium channels are similarly involved in morphine abstinence after acute and chronic dependence, in contrast to the differences in the content and uptake of neuronal calcium induced by morphine under both conditions.
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PMID:Differential effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine. 171 13

Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. Twenty-seven patients suffered from marked akinesia and rigidity (AR-type) and 18 patients from predominant resting tremor (T-type). Dementia, depression, and psychosis occurred in 26, 18, and 18 patients, respectively. Neuronal counts were performed in defined areas of the medial and lateral substantia nigra (SNM, SNL), locus ceruleus (LC), and dorsal raphe nucleus (DRN). The AR-type (compared with the T-type) showed higher neuronal loss of LC, SNL, SNM, and more severe gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in substantia nigra. Demented PD patients showed more intense cortical Alzheimer lesions and higher neuronal depletion in the SNM, whereas PD subjects with moderate or marked dementia differed from mildly or not demented ones only in the higher degree of cortical Alzheimer lesions. More severe neuronal cell loss of DRN was observed in PD patients with depression. Occurrence of psychosis was not associated with any pathologic feature. Our findings indicate that some major clinical features of PD are related to distinct neuropathologic lesions.
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PMID:The neuropathologic basis of different clinical subgroups of Parkinson's disease. 174 81

A woman in her late 40s with a 5 year history of anxiety was treated with relaxation training and cognitive restructuring. Her anxiety was manifested by facial twitching, hand fidgeting, vocal tremor, loss of self-esteem, and depression. Therapy seemed to reduce motor symptoms and improve her self-esteem, confidence, and mood. Six months after the start of therapy the client was found to have Meige's Disease. Following treatment with botulinum toxin, motor symptoms disappeared. This case highlights the need for psychotherapists to be more aware of neurological and medical problems which may mimic psychological ones.
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PMID:Meige's disease misdiagnosed as anxiety disorder. 180 56

Sertraline is slowly absorbed after oral administration, with peak plasma concentrations at 6-8 h. Plasma concentrations are linearly related to dose. The elimination half-life is about 32 h; metabolism is by demethylation to an inactive metabolite. Once-daily dosing is recommended, with steady state being reached after about 7 days. The kinetics of sertraline in the elderly and in patients with renal impairment are similar to those in young healthy female volunteers. In young male volunteers, peak plasma concentrations were lower, and elimination half-life shorter, than in elderly men or both groups of women. Nevertheless, no reduction in dosage is recommended for these groups. Sertraline is highly active in animal models of depression, and administration of the drug to healthy human beings causes a selective, dose-related inhibition of 5-hydroxytryptamine (5-HT) uptake into blood platelets. Single doses of sertraline in volunteers caused changes in the quantitative pharmaco-electroencephalogram suggesting antidepressant and anxiolytic actions, with sedative potential evident only at doses of 200 mg or more. Sertraline does not impair psychomotor performance, including simulated car driving, and overall seems neither stimulating nor sedating: an increase in critical flicker fusion threshold suggests a slight alerting effect, whereas subjective tests indicate an increase in perceived sedation at doses of 100 mg or more. No potentiation of the effects of ethanol has been noted in either young or elderly subjects. No adverse effects on the electrocardiogram, blood pressure, or systolic time intervals have been detected, and sertraline lacks anticholinergic action. These studies imply a low probability of adverse central nervous and cardiovascular effects. Sertraline is probably a weak inducer of hepatic microsomal enzyme activity. Sertraline does not affect the clearance of lithium but there may be a pharmacodynamic interaction which leads to increased tremor when the drugs are given together. No clinically relevant effects were noted in the interaction studies with digoxin, atenolol and diazepam. The pharmacokinetics and pharmacodynamics of sertraline are generally favourable. However, caution is needed when sertraline is given to patients receiving lithium or drugs with a low therapeutic ratio, such as corticosteroids, oral hypoglycaemic agents, and warfarin.
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PMID:Clinical implications of the pharmacology of sertraline. 180 26

The novel tricyclic antidepressant drug tianeptine had an antidepressant-like effect on a rat model of depression based on the deficit in open field activity observed on the day after 2 h restraint. Thus, when tianeptine (10 mg/kg IP) was given 2 h after the end of the restraint to either untreated rats or to animals previously given 10 mg/kg of the drug per day for 13 days, then the deficit was opposed. Tianeptine, given acutely but not chronically, moderately enhanced the 5-HT1C receptor-dependent hypolocomotor effect of m-chlorophenylpiperazine (mCPP) but did not alter other 5-HT1 receptor subtype-dependent behaviour. Acute but not chronic tianeptine also decreased 5-HT2 receptor-dependent body shakes induced by 5-hydroxytryptophan. Shakes induced by the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2 aminopropane (DOI) were unaffected. The results are discussed in relation to the possible mechanism of antidepressant action of tianeptine.
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PMID:Effects of tianeptine on stress-induced behavioural deficits and 5-HT dependent behaviour. 183 9

A total of 240 patients of Parkinson's disease (PD) were studied (125 male, 115 female). The age of onset was 60.0 +/- 9.9 years(Y) (mean +/- S.D.) (range 30-87). A 0-4 rating score was applied on each of 6 major symptoms: i.e. tremor, rigidity, bradykinesia, gait, activities of daily living and fluctuation with maximum score of 24. According to the Hoehn and Yahr's stages, there were 44 cases in stage I, 141 in stage II, 31 in stage III, 19 in stage IV and 5 in stage V. Fluctuation in symptoms occurred in 42.9%, dyskinesia in 7.1%, psychosis in 9.6%, depression in 4.6%, and dementia in 2.9%. The mean duration of PD was 4.9 +/- 4.5 Y with 40% 5 years or longer. Significantly longer duration of PD was seen in the patients suffering from fluctuation (6.7 +/- 4.7 Y), dyskinesia (10.7 +/- 6.7 Y) and psychosis (9.4 +/- 6.5 Y). The mean duration of L-dopa treatment was 4.1 +/- 3.4 Y. The patients showing fluctuation (6.2 +/- 4.0 Y) or dyskinesia (7.6 +/- 4.7 Y) had significantly longer duration of L-dopa treatment. The mean daily dose of L-dopa was 370 +/- 203 mg. The patients with fluctuation (430 +/- 187 mg) or dyskinesia (545 +/- 265 mg) received significantly higher dose of L-dopa. Dementia tended to occur in the patients having later age of onset of PD (71.2 +/- 11.2 Y). The symptom score was significantly worse in those with fluctuation, dyskinesia, psychosis and dementia. It was well correlated with the Hoehn and Yahr's staging system.
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PMID:Abbreviated rating score for Parkinson's disease. 184 38

Butorphanol tartrate (Stadol; Anaquest, Madison, WI/Bristol-Meyers Squibb, Evansville, IN) is an analgesic possessing mixed agonist-antagonist activity at opiate receptors. Receptor specificity has been used to limit respiratory depression, gastrointestinal side effects, and reduce the risk of dependency. Theoretically it offers an advantage over traditional opiates such as morphine and meperidine in the treatment of moderate pain. Butorphanol has been used as a preoperative sedative and analgesic, as a supplement to balanced anesthesia, and for suppression of postanesthesia shaking. Other recognized uses include obstetric analgesia during labor and relief of moderate postpartum pain. In addition, butorphanol has been used effectively for conscious sedation. Its lack of euphoric effects may be useful in emergency medicine for clinical populations prone to drug-seeking behavior. Butorphanol has been used more recently for epidural analgesia or for intravenous patient-controlled analgesia when allergies to opiates exist. Since butorphanol is not a controlled substance, its use can reduce administrative liability for abuse and can lower the number of distribution records associated with Schedule II narcotics.
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PMID:Butorphanol tartrate (stadol): a review. 184 91

Following a 1-week, single-blind placebo washout, 150 patients were randomized to double-blind treatment with daily doses of either mianserin, 30 mg to 150 mg; amitriptyline, 60 mg to 300 mg; or placebo, 1 to 5 capsules taken at bedtime (qhs). Mianserin and amitriptyline were found to be comparable in efficacy, and both significantly more effective than placebo in the treatment of major depressive illness. Rating instruments, all of which showed significant improvement in the active drug groups over the placebo, included the 17- and 21-item Hamilton Rating Scale for Depression (HAM-D), Montgomery and Asberg Depression Rating Scale (MADRS), Self-rating Depression Scale (SDS) index, and the Clinical Global Impressions (CGI) Severity of Illness and Improvement rating scales. Furthermore, for most efficacy parameters in the efficacy-evaluable group, the earliest statistically significant difference vs. placebo could be observed at Visit 1 for the mianserin patients and at Visit 3 for the amitriptyline patients. The safety profile for mianserin was comparable with placebo with respect to laboratory values, electrocardiogram changes, vital signs, ophthalmologic evaluations, and most adverse clinical experiences. Complaints of somnolence and weight gain were comparable in the amitriptyline and mianserin groups. Mianserin was superior to amitriptyline in terms of vital signs; anticholinergic effects; and complaints of dizziness, dyspepsia, and tremor.
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PMID:A controlled study of mianserin in moderately to severely depressed outpatients. 192 59

Several classes of medications have been used to treat generalized anxiety disorders (GAD). Antidepressants are useful for chronic subpanic anxiety and anxiety associated with depression. Benzodiazepines are generally safe, but recent research suggests that the incidence of chronic abstinence syndromes may be higher than has been suspected. This class of medications is best used for circumscribed periods of time. Because buspirone has no significant interactions, it does not prevent benzodiazepine withdrawal and cannot be directly substituted for this class of medications. beta-Blockers are used when cardiovascular symptoms and tremor are prominent, for stage fright (propranolol) and possibly for social phobia (atenolol). Antihistamines have been used for elderly patients and for those with a history of substance abuse. Neuroleptics should only be prescribed for anxiety associated with psychosis, psychotic and possibly severe depression, and borderline personality disorder. Drug treatment of GAD should be used as part of a comprehensive treatment plan that includes assessment for medical illnesses that can aggravate anxiety, withdrawal of all unnecessary medications (especially CNS depressants) and caffeine, structured relaxation techniques, evaluation of the specific type of anxiety, and psychotherapy.
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PMID:Generalized anxiety disorder: new concepts and psychopharmacologic therapies. 196 48

The effects of levocabastine (R 50 547; CAS 79516-68-0) on the central nervous system were studied in comparison with those of diphenhydramine, ketotifen and azelastine. At high doses, levocabastine caused a decrease in locomotor activity, prolongation of thiopental-induced sleep, depression of acetic acid-induced writhing in mice and inhibition of active avoidance response in rats, but these adverse effects were much less potent than those seen in diphenhydramine, ketotifen and azelastine. Oxotremorine-induced tremor and salivation in mice were delayed after extremely high dosage of levocabastine; however, these were much less effective than those seen after diphenhydramine and ketotifen. Levocabastine did not affect the tonic extensor seizure induced by maximal electroshock in mice which is different from that of diphenhydramine. In EEG analysis, levocabastine at a dose of 20 mg/kg caused no significant changes in the EEG recorded from the frontal cortex, occipital cortex, hippocampus and amygdala in rats with chronic electrodes.
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PMID:Central effect of the potent long-acting H1-antihistamine levocabastine. 198 50


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