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)

Anesthetic doses of fentanyl (46 +/- 1.3 micrograms/kg) and oxygen (group I) were compared to a moderate dose of fentanyl (3 to 4.7 micrograms/kg; mean = 3.54 +/- 0.1 micrograms/kg) + etomidate (0.4 mg/kg) intravenously (IV) (group II) during the anesthetic induction-endotracheal intubation sequence to evaluate hemodynamic changes and the incidence of side effects in 23 New York Heart Association class III and IV patients. Chest wall rigidity only occurred in group I (27%), and pain on injection (8%) and myoclonus (25%) only in group II. Patients in group I experienced transient, small increases in central venous pressure (immediately after induction) and mean pulmonary artery pressure (after tracheal intubation). Patients in group II had small, transient decreases in heart rate, mean arterial blood pressure and cardiac index after induction which returned to baseline levels immediately after tracheal intubation. The data indicate that a modest dose of fentanyl with etomidate is similar to a large (anesthetic) dose of fentanyl in terms of avoiding cardiovascular depression and preventing hemodynamic stimulation during and following the induction-tracheal intubation sequence. Our findings also demonstrate that these doses of fentanyl before etomidate decrease but do not eliminate side effects of etomidate. The results suggest that a modest dose of fentanyl followed by etomidate may be an attractive alternative to high doses of fentanyl in patients with limited cardiovascular reserve, especially when prolonged postoperative respiratory depression secondary to high doses of an opioid is undesirable.
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PMID:Induction of anesthesia with fentanyl or fentanyl plus etomidate in high-risk patients. 297 66

The baboon Papio papio develops a nonepileptic myoclonus 20 to 30 min after i.m. benzodiazepine injection. It is characterized by bilateral jerks involving mainly the neck and the trunk, by the absence of any correlative EEG paroxysmal discharge, and by its facilitation during movement or agitation. This myoclonus resembles the intention myoclonus of human patients as seen, for example, after anoxia. We found in experiments on 10 adolescent baboons that atropine alone induced the myoclonus for several hours, that physostigmine completely antagonized the benzodiazepine-induced as well as the atropine-induced myoclonus, and that the peripherally acting cholinergic antagonist, methyl-QNB, and agonist prostigmine had no action on the myoclonus, suggesting that the benzodiazepine-induced myoclonus in this species depends on a strong depression of the central cholinergic system by benzodiazepine. The benzodiazepine-induced myoclonus was mediated by benzodiazepine receptors as it was blocked by the specific benzodiazepine receptor antagonist, Ro 15-1788, which did not block atropine-induced myoclonus; latency to myoclonus after benzodiazepine was longer than after atropine. These facts suggest that benzodiazepines, by an as yet unknown mechanism, induce a depression of the cholinergic system which in turn leads to the development of myoclonus. Finally, the benzodiazepine-induced myoclonus of the baboon can be considered as a good model for testing drugs that act on the muscarinic cholinergic system and also for testing benzodiazepine-acetylcholine interactions.
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PMID:Stimulus-sensitive myoclonus of the baboon Papio papio: pharmacological studies reveal interactions between benzodiazepines and the central cholinergic system. 307 7

Aluminum has been proposed as the causative agent in dialysis encephalopathy syndrome. We prospectively assessed whether other, less severe, neuropsychologic abnormalities were also associated with aluminum. A total of 16 patients receiving chronic dialytic therapy were studied. The deferoxamine infusion test (DIT) was used to assess total body aluminum burden. Neurologic function was evaluated by quantitative measures of asterixis, myoclonus, motor strength, and sensation. Cognitive function was assessed by measures of dementia, memory, language, and depression. There were four patients with a positive DIT (greater than 125 micrograms/L increment in serum aluminum) that was associated with an increase in the number of neurologic abnormalities observed, as well as an increase in severity of myoclonus, asterixis, and lower extremity weakness. Patients with a positive DIT also showed significant impairment in memory; however, no differences were noted on tests of dementia, depression, or language. There was no significant correlation between sex, age, presence of diabetes, mode of dialysis, years of chronic renal failure, years of dialysis or years of aluminum ingestion and any neurologic or neurobehavioral measurement, serum aluminum level, or DIT. These changes may represent early aluminum-associated neurologic dysfunction.
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PMID:Relationship of aluminum to neurocognitive dysfunction in chronic dialysis patients. 317 74

The most predictable electroencephalographic sleep changes of major depression are a shortened first NREM sleep period, a prolonged first REM period (with increased density of rapid eye movements), sleep continuity disturbance, and diminished slow wave sleep (with shifting of delta activity from the first to the second NREM sleep period). The more rapid appearance of the first REM sleep period occurs in relation to sleep onset but not apparently in relation to clock time. The changes occurring in the first NREM-REM cycle of the night appear to be relatively specific to major (particularly endogenous) depression. Depressed men appear to have diminished nocturnal penile tumescence compared with healthy controls, but depressed patients generally do not have a higher incidence of sleep apnea or nocturnal myoclonus. The sleep physiologic changes of depression appear to persist into clinical remission, suggesting that they are trait-like. Published studies appear to support the conclusion that there is a close link between the regulation of sleep and the regulation of mood in affective illness.
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PMID:Sleep and affective disorders. A minireview. 333 19

The authors present a case of a 62-year-old woman who was hospitalized with severe medical problems that included congestive heart failure secondary to mitral stenosis and atrial fibrillation, coronary artery disease, chronic renal failure, and a recent history of a right cerebral lacunar infarction. She also had a 2-year history of anxiety and depression, manifested in the hospital by frequent crying spells, sleeplessness, and ruminating about her illnesses. The patient received buspirone 5 mg three times a day for her anxiety and depression. Approximately 12 hours after her first dose, she developed dramatic myoclonus, dystonias, and akathisia. She was given 25 mg of intramuscular diphenhydramine and 1 mg of intramuscular benztropine mesylate, which resulted in little relief; however, 1 mg clonazepam caused both the myoclonic jerks and dystonias to resolve completely.
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PMID:Acute generalized myoclonus following buspirone administration. 337 31

The development of direct serotonin agonists, selective inhibitors of serotonin uptake, serotonin receptor antagonists, and other drugs affecting serotonergic function has aided the study of physiologic functions of brain serotonin neurons in laboratory animals and the recognition and classification of serotonin receptor subtypes. Agents of these types are real or potential drugs for the treatment of psychiatric disorders (e.g., depression) and other disorders such as overeating, alcoholism, myoclonus, and chronic pain. In addition, the agents may permit assessment of the functional state of brain serotonin receptors in humans.
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PMID:Pharmacologic modification of serotonergic function: drugs for the study and treatment of psychiatric and other disorders. 351 85

Dementias which are either reversible or avoidable are discussed in the light of the literature. The frequency is between 6 and 32%. The most important etiological groups are immunological vasculopathies, hyperlipidemia, some types of encephalitis and, mainly, progressive dementia of the insane, benign tumors and in particular meningioma, low pressure hydrocephalus, intoxications due to drugs, industrial products and alcohol, metabolic disturbances, encephalopathy in dialysed patients, ileo-jejunal-bypass encephalopathy and encephalopathy due to neoplasms. Dementias are also seen in endocrinological disturbances and particularly in hypothyroidism. Vitamin B12 and folate deficiency, as well as epilepsy, may be causes of dementia. Depression may mimic a state of dementia. Some features of reversible dementias are listed, including in particular the somewhat more rapid onset, the younger age of patients, and accompanying neurological symptoms such as headache, gait disturbances, ataxia, polyneuropathy, myoclonus or epileptic fits.
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PMID:[Reversible and preventable dementias]. 361 87

Myoclonic movements have been observed in depressed patients receiving therapeutic doses of clomipramine. Such movements, which appear in states of deep muscular relaxation such as sleep, do not appear to have any repercussion in the outcome of the depression and are reversible following withdrawal of the drug. In this study the plasma levels of clomipramine and desmethylclomipramine were determined and their possible relationship with myoclonus studied. No statistically significant relationships were found.
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PMID:Myoclonic movements as a side-effect of treatment with therapeutic doses of clomipramine. 369 73

Bicuculline methiodide (0.5-3 nmol) and picrotoxin (0.5-4 nmol) were injected uni- or bilaterally into the rat amygdala and the resulting behavioural, electroencephalographic and morphological alterations were studied. In rats treated unilaterally with lowest doses of either bicuculline or picrotoxin (0.5 and 1 nmol) increase in the locomotor activity, occasional myoclonus of the hindlimbs and wet dog shakes were observed. At doses of 2-3 nmol, both gamma-aminobutyrate antagonists produced a sequence of repetitively occurring behavioural alterations including limbic gustatory automatisms, tremor and myoclonus of the forelimbs, head nodding and rearing, that developed over 15-30 min and built up progressively into the recurrent motor limbic seizures lasting for 1-6 h. In animals injected bilaterally with either bicuculline (0.5-3 nmol) or picrotoxin (0.5-3 nmol) motor limbic seizures rapidly developed into the status epilepticus lasting for several hours. Bicuculline and picrotoxin produced both ictal and interictal epileptiform activity in the electroencephalogram. A spectrum of electroencephalographic changes consisted of high voltage fast activity, slow and fast voltage spiking, paraoxysmal bursts and periods of postictal depression. The earliest electrographic alterations appeared in the amygdala and then rapidly spread to cortical areas. Electrographic seizures started 1-10 min after unilateral injections of large doses of bicuculline and pictrotoxin (2-4 nmol). Ictal periods lasted for 1-2 min, recurred every 5-10 min and were followed by periods of depression of the electrographic activity. Bilateral injections of large doses of both gamma-aminobutyrate antagonists (2-3 nmol) resulted in the status epilepticus. Morphological examination of frontal forebrain sections with light microscopy revealed a widespread damage to the amygdala, olfactory cortex, substantia nigra, thalamus, hippocampus and neocortex. Pretreatment of animals with diazepam prevented the build-up of convulsive activity and brain damage produced by bicuculline or picrotoxin. Muscimol retarded the appearance and shortened the duration of convulsive activity, but did not alter the sequence and intensity of seizures. The results indicate that gamma-aminobutyrate antagonists, bicuculline and picrotoxin when directly applied to the amygdala can elicit in rats motor limbic seizures, epileptic changes in the electroencephalogram indicative of repetitive limbic seizures, and status epilepticus accompanied by seizure-related brain damage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Injections of picrotoxin and bicuculline into the amygdaloid complex of the rat: an electroencephalographic, behavioural and morphological analysis. 397 84

From the results obtained with the experimental series CORASIN (fast compression with He-N2-O2), a method of compression has been developed for the baboon (Papio papio) to dive deeper than 600 m. This method utilizes an exponential compression profile with stages of 40 min every 100 m and with the introduction of N2 before each stage from 200 m onward to maintain a concentration of 5.5%. Between 0 and 800 m, this procedure did not produce myoclonus or epileptic seizures; tremor appeared beyond 400 m (578 +/- 109 m) but remained slight. If N2 was not introduced, the tremor appeared earlier (266 +/- 52 m) and became severe; between 600 and 800 m, muscular hypertonus, myoclonus, and muscular cramps occurred. The modifications of the electroencephalogram were slight; the increase in slow activity did not exceed 300% with or without N2. Beyond 800 m, the compression procedure with N2 injections revealed new phenomena. There was a general depression of EEG activity starting at 800 m; from 1,000 m and deeper, there were periods of motor disturbances (hypertonus, spasms, and shaking), palpebral clonus, and eye movements associated with peak EEG activities localized in the posterior region of the skull that sometimes evolved toward an epileptic seizure localized in this region. These symptoms differed from the classical description of high-pressure nervous syndrome, which comprises an increase in tremor followed by convulsions. These differences may perhaps be linked to our compression procedure using N2 injection, to the effect of the pressure itself, or to a combination of the two.
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PMID:HPNS of baboons during helium-nitrogen-oxygen slow exponential compressions. 646 4


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