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 neuromuscular block of myasthenia gravis has the characteristics of an antidepolarizing (competitive block), similar to that produced by d-tubocurarine in normal subjects: progressive decrease in muscle action potentials evoked by two or more nerve stimuli, posttetanic facilitation, posttetanic fatigue, inhibition of the depolarizing action of acetylcholine (ACh) or anticholinesterase compounds, and reversal of the block by ACh or anticholinesterase compounds. In myasthenic patients spontaneously recurring negative discharges were more difficult to locate in the end-plate zone than in normal subjects, suggesting that the number or density of functioning end plates may be reduced. The threshold dose of intra-arterial ACh that increased electrical activity was higher than in normal subjects; the duration of the increased electrical activity was briefer, and was followed by more depression of negative discharges than in normal subjects and by a greater increase in the threshold dose of ACh. These results indicate that the end-plate zone of myasthenic patients is less responsive than that of normal subjects to the excitatory action of ACh, and may be more readily desensitized by ACh. In both myasthenic patients and normal subjects the intra-arterial injection of ACh produced a prompt transient decrease in evoked potentials, attributable to depolarization of the end plates, followed by recovery (and in myasthenic patients by repair), and then by a more prolonged late decrease in evoked potentials, attributable to desensitization of the end plates to transmitter. This prompt depressant effect of ACh on evoked potentials was less in myasthenic patients than in normal subjects, and the late depressant effect of ACh was greater. In myasthenic patients the late block produced by ACh had the characteristics of an antidepolarizing (competitive) type of block, including inhibition of the depolarizing action of ACh and reversibility by ACh or neostigmine, while in normal subjects the characteristics were those of a depolarizing (noncompetitive) type of block, including little or no inhibition of the depolarizing action of ACh and lack of reversal by ACh or neostigmine. The differences between the late depressant action of ACh in myasthenic patients and normal subjects resembled differences in the effect of other depolarizing compounds, such as choline, succinylcholine, and decamethonium, and are best explained by differences in behavior of the postsynaptic receptor. The disease appears to be due to the presence of abnormal forms of receptor or to abnormal responses of receptor to the transmitter. The predominance of one or other form of receptor may determine the clinical state of the myasthenic patient and his response to anticholinesterase medication.
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PMID:Characteristics and mechanism of neuromuscular block in myasthenia gravis. 18 86

In rat skeletal muscle, trimetazidine (TMZ) caused a transmission defect without directly blocking binding of acetylcholine--ionophore impairment. In vivo, TMZ produced low-amplitude and cumulative depression of successive muscle responses, and immediate posttetanic exhaustion. These features differed from the effects of alpha-bungarotoxin (alpha-BuTx) or immunization with acetylcholine receptor (experimental autoimmune myasthenia gravis [EAMG]). In vitro, TMZ-induced block was similar to both alpha-BuTx-induced block and EAMG in many respects, but there were differences in endplate potentials evoked during and after rapid repetitive activations. These differences suggest that antibodies to the acetylcholine receptor do not affect the ionophore.
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PMID:Neuromuscular defect after suppression of ion conductance. 22 54

Clinical investigations of infants hospitalized with botulism demonstrate a remarkable uniformity of complaints and physical findings. Constipation precedes a course of progressive weakness and cranial nerve dysfunction. Examination reveals hypotonia, hyporeflexia, and a variable pattern of involvement of the motor cranial nerves. Initial laboratory investigations should include electrodiagnostic tests, because findings of an incremental response to rapid, repetitive nerve stimulation and of brief, small-amplitude motor units on electromyography are virtually pathognomonic of botulism in the infant. Differential diagnosis includes disorders that may produce generalized depression of the central nervous system, such as septicemia, meningitis, metabolic disturbances, and intoxications. Specific involvement of the neuromuscular system includes acute polyneuropathies, diseases of the anterior horn cell, congenital myopathies or muscular dystrophy, and neonatal myasthenia gravis. Recent studies have expanded the clinical spectrum of infant botulism to include some cases of sudden infant death syndrome and otherwise nonspecific constipation.
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PMID:Differential diagnosis of infant botulism. 23 67

Physiologic studies were carried out in six patients with botulism. Abnormalities were those of a defect of acetylcholine release. Although the most consistent findings were small, evoked muscle action potentials (MAP) and posttetanic facilitation similar to the Eaton-Lambert syndrome, there were differences. In botulism as opposed to the Eaton-Lambert syndrome, the following were true: (1) posttetanic facilitation of the amplitude of the evoked MAP was considerably less and did not approach the normal value when the block was severe; (2) posttetanic facilitation persisted at least several minutes during the postactivation cycle; (3) posttetanic depression did not occur; (4) significant tetanic facilitation of the amplitude of the MAP occurred in less than half the patients and, even then, did not approach normal (on the other hand, a decremental response, as in myasthenia gravis, is not seen); and (5) no decremental response of the MAP occurred during slow rates (two per second) of nerve stimulation. Evidence of transient physiologic denervation occurred as in experimental animals affected by botulinum toxin. All physiologic abnormalities revert to normal in association with clinical recovery.
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PMID:Pathophysiologic aspects of human botulism. 125 59

Analyses of serum immunoglobulin (Ig) levels were performed in patients with myasthenia gravis, polymyositis and dermatomyositis, and in normal subjects. The mean IgG levels were elevated in the disease groups and there was minimal depression of serum IgM levels in nonthymectomized myasthenic patients. There was no consistent pattern with regard to selective immunoglobulin class abnormalities, effect of thymectomy in serial studies, and no evidence of gross humoral immunological deficiency as manifested by consistent depression of serum IgA, IgG, or IgM in the disease groups.
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PMID:Serum immunogloblin levels in myasthenia gravis, polymyositis, and dermatomyositis. 125 9

Retrospectively 20% of more than 200 patients with myasthenia gravis reported being initially diagnosed as having a psychiatric disorder. Younger women are significantly most at risk of a psychiatric misdiagnosis whereas men are more often subject to somatic misdiagnoses. The sample's mean duration of the disease was 10 years. Nevertheless misdiagnoses still coincide with higher depression scores. Depression is also related to the dosage of anticholinesteratic medication as well as to the self-reported muscular weakness. Personality assessment through an inventory reveals only slight emotional instabilities and no illness specific profiles.
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PMID:[Myasthenia gravis in the frontier of psychiatric diagnosis]. 143 10

The population resident in the skilled nursing home of a Veterans Administration Hospital on the 27th of June 1988 was screened for the presence of depression. Only 74% of the patients (59 of 80) were able to complete most of the screening battery: the Folstein Mini-Mental State Examination, the 15-item Geriatric Depression Scale, and the Hamilton Depression Scale. Thirty-four percent of the sample (20 of 59) met the criteria for a DSM-III-R psychiatric diagnosis; 22% (13 patients) had a major depressive disorder, and 12% (seven patients) had an adjustment disorder with depressed mood. The 15-item version of the Geriatric Depression Scale was more effective than the Hamilton Depression Scale as a screening instrument in this population of frail elderly veterans who had multiple and severe medical problems (end-stage cardiac disease, progressive myasthenia gravis, terminal pulmonary disease, and multiple cerebrovascular accidents) that limited verbal and nonverbal communication, as well as physical endurance.
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PMID:Screening a skilled nursing home population for depression. 178 10

A cumulative dose followed by an infusion was used to determine the dose response to suxamethonium in a patient with diagnosed myasthenia gravis who was in true remission (asymptomatic while receiving no therapy). The ED50 and ED90 values for suxamethonium were 0.08 mg/kg and 0.20 mg/kg, and an infusion rate of 3.2 mg/kg/hour was required to maintain a 90-95% depression of the single twitch response as monitored by integrated electromyography. These values are within the range for normal patients, and we conclude that myasthenic patients during a true remission may not demonstrate resistance to suxamethonium.
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PMID:Response to suxamethonium in a myasthenic patient during remission. 199 50

Pyridostigmine bromide (Pyr), the current drug of choice in the management of myasthenia gravis, has been suggested for use in Alzheimer's dementia, and as a prophylactic treatment for intoxication with organophosphate cholinesterase inhibitors. The present study was undertaken to evaluate the dose-response and time-course effects of acute oral administration of Pyr over a broad dose range (3-40 mg/kg) on the lever pressing of rats maintained under a multiple fixed-ratio (FR-20) time-out schedule of reinforcement for water reward. The drug produced a dose-dependent biphasic response depression in the overall rate of FR responding. Low doses of Pyr (less than or equal to 12 mg/kg) that caused no gross signs of toxicity only moderately decreased rates of responding, primarily due to a decrease in response rates. Whereas high doses of Pyr (greater than 24 mg/kg) which produced overt signs of peripheral cholinergic intoxication markedly suppressed overall responding, primarily due to cessation of responding. The lowest effective dose of performance disruption was 6 mg/kg, and the ED50 was calculated as 23.3 (17.9-28.7) mg/kg. The time-course data of performance disruption showed that low doses of Pyr (less than or equal to 12 mg/kg) had an onset latency within 40-80 min and a duration of 20-80 min, whereas high doses (greater than or equal to 24 mg/kg) had an onset latency of 20-40 min and a duration greater than 80 min. These results suggest the recommended human therapeutic or prophylactic regimen of 30-120.mg Pyr, orally taken each 8 hours, might adversely affect behavioral performance.
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PMID:Acute effects of oral pyridostigmine bromide on conditioned operant performance in rats. 206 91

Myasthenia gravis is an autoimmune disease involving the acetylcholine receptors at neuromuscular junctions. Perioperative management of patients with myasthenia gravis is complicated by their enhanced sensitivity to nondepolarizing neuromuscular blocking agents and their resistance to depolarizing drugs (1). Prolonged respiratory depression commonly occurs when these agents are used. Atracurium dibesilate is one of a new series of nondepolarizing agents and is promising by virtue of its rapid degradation by 'Hoffmann elimination', leaving products with little or no muscle blocking activity. After encouraging results were obtained with atracurium (2-6), we investigated the neuromuscular blocking effect of different doses of the drug (0.2 mg/kg, 0.5 mg/kg) in sixteen myasthenic patients undergoing thymectomy, with continuous monitoring of neuromuscular function.
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PMID:Evaluation of atracurium in myasthenic patients undergoing thymectomy. 224 32


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