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)

Forty-four Parkinson patients (19 patients of the rigid-akinetic type, 13, of the rigid-akinetic-tremor type, and 12, of the tremor type) were included in a study in order to analyse correlations of the expression of the motor symptoms tremor, rigidity, akinesia, with other clinical parameters, computertomographic aspect of brain atrophy and psychometrically assessed cognitive parameters. Rigidity and akinesia are significantly positively correlated with the severity of motor dysability, stage of the disease, and brain atrophy, as is akinesia with a history of pharmacotoxic psychosis. Tremor is significantly negatively correlated with motor dysability, stage of the disease, and history of pharmacotoxic psychosis. Akinesia is correlated with visuomotor dysfunction (tested with Bender Gestalt Test) and rigidity with the depression score (Zung scale). The tremor type is favorable, the rigid-akinetic type unfavorable with respect to motor disability and psychosis.
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PMID:Prognostic implications of the motor symptoms of Parkinson's disease with respect to clinical, computertomographic and psychometric parameters. 378 47

Muscular rigidity was induced by reserpine (10 mg/kg) in rats and the tonic activity of the gastrocnemius muscle was recorded in the electromyogram. Systemic administration of lisuride, an ergoline, resulted in a dose-dependent depression of rigidity. To examine the spinal cord as a site of action for lisuride to depress reserpine-induced rigidity, a method for the chronic catheterization of the lumbar spinal subarachnoid space was used, which allowed the administration of drugs to reserpinized, intact rats without anaesthesia. Lisuride injected into the lumbar spinal subarachnoid space resulted in a longlasting depression of rigidity. These results suggest that the spinal cord is an important site of action of lisuride.
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PMID:Depression of reserpine-induced muscular rigidity in rats after administration of lisuride into the spinal subarachnoid space. 689 83

Muscular rigidity was induced in rats by reserpine (10 mg/kg) and the tonic activity of the gastrocnemic muscle was recorded in the electromyogram. Systemic administration of lisuride, an ergoline, resulted in a dose-dependent depression of rigidity. To examine the site of action of lisuride, we injected lisuride into the striatum, the ventricular space, and the spinal subarachnoid space of intact reserpinized rats. Lisuride is effective if injected into either the striatum or the spinal subarachnoid space, the spinal effect being more pronounced. These results suggest that the spinal cord is an important site of action of lisuride.
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PMID:Action of lisuride on reserpine-induced muscular rigidity in rats after local application into the striatum, ventricular space or the spinal subarachnoid space. 720 24

Dexmedetomidine is a new alpha 2 adrenergic agonist anaesthetic adjuvant. In animal studies, dexmedetomidine produced muscle flaccidity and prevented opioid-induced muscle rigidity, apparently via a central mechanism. The effect of dexmedetomidine on the neuromuscular junction or on non-depolarizing neuromuscular block during anaesthesia has not been reported. We have studied in the anaesthesized rat, the effects of dexmedetomidine on vecuronium-induced twitch depression. Wistar rats (n = 35) were anaesthetized and their lungs ventilated to maintain normocapnia. An infusion of vecuronium of 2.3 (SEM 0.1) micrograms kg-1 min-1 produced a stable twitch height (T1) depression of the tibial nerve of 53 (2)% of control in all groups. Rats were allocated randomly to receive either saline or dexmedetomidine 10, 30 or 100 micrograms kg-1 i.v. and T1 height was measured continuously for 60 min. Dexmedetomidine did not significantly affect T1 height during the first 30 min of infusion. At later times there were minor differences between groups. With cessation of the infusion of vecuronium, T1 height recovered rapidly to normal in all groups. These data suggest that the neuromuscular blocking properties of dexmedetomidine are unlikely to be produced by action at the neuromuscular junction.
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PMID:Dexmedetomidine does not modify the neuromuscular blocking action of vecuronium in the anaesthetized rat. 773 68

Parkinson's disease is a progressive neurodegenerative condition of unknown cause and with no known cure. The diagnosis is based on clinical findings of rest tremor, muscle rigidity, bradykinesia, and gait instability. Over 40% of patients develop a dementia syndrome that is largely distinct from Alzheimer's disease. Depression is common, also occurring in more than 40% of patients with PD. Careful evaluation in necessary to help distinguish Parkinson's disease from secondary causes of parkinsonism. Carbidopa/levodopa, dopamine agonists, and monoamine oxidase type B inhibitors are the mainstays of treatment. Anticholinergics and other agents may also be useful. Pharmacologic treatment must be carefully titrated to control symptoms and to avoid side effects. In advanced disease, dose-related dyskinesias, end-of-dose wearing-off effect, and unpredictable sudden motor fluctuations become very disabling and difficult to manage.
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PMID:Parkinson's disease: making the diagnosis, selecting drug therapies. 792 45

Antidepressant drugs are among the most commonly encountered causes of self-poisoning. These drugs include tricyclics, tetracyclics, bicyclics and monocyclics, as well as monoamine oxidase (MAO) inhibitors and selective serotonin reuptake inhibitors (SSRIs). Of these, the tricyclic antidepressants (TCAs) are generally more toxic in overdose, with major toxicity usually manifesting within the first 6 hours after overdose. Various studies indicate that patients at risk of toxicity from TCA overdose may be identified by neurological, cardiovascular and electrocardiography status, together with a quantitative estimate of the plasma drug concentration. While there are various methods available for such chemical estimations, the most satisfactory appears to be fluorescence polarisation immunoassay which gives rapid quantitative results for a variety of TCAs. The selective MAO-A inhibitor antidepressants and the SSRIs are relatively nontoxic when taken alone. However, overdoses of combinations of MAO inhibitors and either SSRIs or TCAs with serotonin reuptake blocking activity may result in a serotonin syndrome with a severe or fatal outcome. Features of this syndrome include hyperpyrexia, disseminated intravascular coagulation, convulsions, coma and muscle rigidity, which may not develop until 6 to 12 hours after overdose. While quantitative chemical identification of these drugs following overdose is helpful in confirming the diagnosis, it is not mandatory. The increasing use of MAO-A inhibitors and SSRIs in the treatment of depression suggests that careful clinical observation is required when combination overdoses are suspected.
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PMID:Antidepressant toxicity and the need for identification and concentration monitoring in overdose. 852 78

Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine-MAOI interaction that resulted in the serotonin syndrome in a 23-y-old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1/2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120/67 mm Hg, heart rate 127/min, respiratory rate 28/min, and temperature 97 F. After 180 mg of diazepam i.v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non-immune thrombocytopenia which resolved. The patient's maximal temperature was 101.2 F and his CPK remained < 500 units/L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.
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PMID:Serotonin syndrome from venlafaxine-tranylcypromine interaction. 888 41

Several fentanyl analogs (Bagley et al., 1989, J. Med. Chem. 32, 663) were compared to fentanyl and morphine for their effects on respiratory depression as determined by arterial blood gas (pH, pCO2 and pO2) measurements. Fentanyl (0.1 mg/kg), morphine (10 mg/kg), #16 (1-phenethyl-4-[N-(pyridin-2-yl)-N-(methoxymethylcarbonyl)amino] piperidine, 1 mg/kg), #17 (1-phenethyl-4-[N-(pyridin-2-yl) -N-(2-furoyl)amino]piperidine, 0.5 mg/kg) and #29 (1-phenethyl-4-[N- (pyrimidin-2-yl)-N-(methoxy-methylcarbonyl) amino]piperidine, 10 mg/kg) produced significant respiratory depression in rats. Pretreatment with the mu1-opioid receptor selective antagonist, naloxonazine (10 mg/kg), blocked the respiratory effect of fentanyl and its analogs, but not that of morphine. The results suggest that the mu1-opioid receptor plays an important role in the respiratory effects of fentanyl and its analogs. Hence, the mechanism of fentanyl-induced respiratory depression appears to be distinct from that produced by morphine. The most likely explanation for this difference is the possible contribution of muscle rigidity and catalepsy to the observed changes in blood gas parameters caused by the fentanyl analogs, while the respiratory depression of morphine, measured by these same parameters, appears to be independent of its effect on muscle rigidity.
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PMID:Evidence for mu1-opioid receptor involvement in fentanyl-mediated respiratory depression. 889 2

The efficacy and safety of remifentanil and alfentanil for patients undergoing major abdominal surgery were compared. Premedicated patients received a loading dose of remifentanil (1.0 microgram.kg-1; n = 116) and a continuous infusion of 0.5 microgram.kg-1.min-1, or a loading dose of alfentanil (25 micrograms.kg-1; n = 118) and a continuous infusion of 1.0 microgram.kg-1.min-1. Propofol was administered (10 mg every 10 s) until loss of consciousness. Patients' lungs were ventilated with 66% nitrous oxide and 0.5% (end-tidal) isoflurane in oxygen. The study drug infusion rate was reduced by 50% 5 min after intubation. Alfentanil was discontinued 15 min before the end of surgery, whereas remifentanil was continued in the immediate postoperative period at a reduced dose. Responses to intubation (28%) and skin incision (17%) occurred approximately twice as often in the alfentanil group (15% and 8%; p = 0.014 and p = 0.037, respectively). More patients receiving alfentanil had one or more responses to surgery (72% vs. 57%; p = 0.016). The time to spontaneous respiration, adequate respiration, response to verbal command and time to recovery room discharge were similar. However, owing to decreased variability, the time to extubation was shorter with remifentanil than with alfentanil (p = 0.048). There was a similar overall incidence of adverse events in both groups, 82% and 75% of patients, respectively. Adverse events associated with remifentanil were rapidly controlled by dose reductions. The incidence of intra-operative hypotension and bradycardia was higher in the remifentanil group (p < or = 0.033). An initial remifentanil infusion rate of 0.1 microgram.kg-1.min-1 titrated to individual need provided postoperative pain relief in the presence of adequate respiration in 71% of patients. When using remifentanil in the immediate postoperative setting, rapid administration of bolus doses and infusion rate increases resulted in a relatively high incidence of muscle rigidity, respiratory depression and apnoea. Changing the postoperative regimen to avoid rapid changes in remifentanil blood concentration resulted in more effective analgesia and dramatically reduced the incidence of adverse events during this period. In patients undergoing major abdominal surgery, remifentanil appears to offer superior intra-operative haemodynamic stability during stressful surgical events compared with alfentanil without compromising recovery from anaesthesia. Remifentanil can be administered as a postoperative analgesic agent at a starting dose of 0.1 microgram-.kg-1.min-1; however, it should only be used in the presence of adequate supervision and monitoring of the patient. Administration of bolus doses is not recommended in this setting.
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PMID:A comparison of remifentanil and alfentanil in patients undergoing major abdominal surgery. 961 18

This study explored the diagnostic specificity of the Munich Personality Test (MPT) in major depression, comparing its scores between patients with major depression, patients with panic disorder and control subjects. One of the 6 dimensions of the MPT, Rigidity, had been developed based on Tellenbach's description of depressive personality, and it was expected that especially this personality dimension would demonstrate a good facility for describing a specific personality feature of major depression. Comparisons were made in 2 ways: ignoring the effects of current depression and anxiety on the personality scorings; and partialling out these effects. Results of the 2 analyses differed radically. Scores on Rigidity and isolation Tendency were significantly different between groups, even after the effects of current depression and anxiety were partialled out. The multiple comparison procedure revealed that the depressive patients were differentiated from both the panic patients and the controls only in the dimension of Rigidity. The results of this study suggest that the Rigidity dimension of MPT may have a strong capability for describing the specific personality feature of depressive patients, and that the MPT may be quite useful for studies, particularly prospective ones, investigating premorbid personality of depression.
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PMID:Evaluating the diagnostic specificity of the Munich Personality Test dimensions in major depression. 918 89


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