Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with sick sinus syndrome (SSS) presented with episodic lightheadedness and weakness. The electrocardiographic features were marked supraventricular bradyarrhythmias and paroxysmal atrial flutter. The symptoms lasted for four years and disappeared with the onset of stable atrial flutter which has persisted for the past seven years. Over the 11-year period of observation, there has been progressive involvement of the His-Purkinje system manifested by the development of left anterior fascicular block, right bundle-branch block, and prolongation of the HV conduction time. The patient has refused pacemaker implantation. In the absence of angina and in the presence of a normal heart size, the etiology of his SSS is postulated to be idiopathic fibrosis of his conduction system.
Pacing Clin Electrophysiol 1978 Oct
PMID:Symptomatic improvement in a patient with sick sinus syndrome after the onset of stable atrial flutter. 9 40

Twenty patients were treated for acute acromioclavicular separation using a Dacron vascular prosthesis and followed for an average period of 13.1 months. None demonstrated loss of motion, or muscle weakness. All resumed their prior level of athletic activity. Satisfactory results were obtained in 18 patients. Residual deformity was the primary reason for an unsatisfactory rating. Recurrence of deformity can be minimized by technical skill and perfection of the surgical reduction.
Clin Orthop Relat Res
PMID:Repair of acromioclavicular separation using a dacron prosthesis graft. 14 91

A 56-year-old woman with symptoms of weakness, visual blurring, and sweating underwent diagnostic studies to evaluate the etiology of her hypoglycemia. Fasting hypoglycemia was never documented; in diagnostic studies performed during her two hospitalizations and several outpatient glucose tolerance tests, the lowest fasting plasma glucose recorded was 56 mg/dl. The patient displayed exaggerated plasma insulin responses following oral glucose (peak response: 447 muU/ml at 30 min) and following 1 gm of iv tolbutamide (peak response: 719 muU/ml at 5 min) with symptomatic profound hypoglyceria during both tests. Basal per cent proinsulin was elevated at 49% (normal range 5-22%). Throughout a 72 h fast, values for plasma glucose, insulin, and glucose/insulin ratios were all within the normal range. During the infusion of exogenous insulin (0.1 U/kg for 60 min) serum C-peptide reactivity suppressed to less than 1.3 ng/ml when the plasma glucose fell below 40 mg/dl representing normal suppression. At surgery, a pancreatic beta cell adenoma was found and removed. This patient represents the uncommon circumstances in which stimulation tests with tolbutamide and glucose were more helpful in establishing a preoperative diagnosis than were the suppression tests.
J Clin Endocrinol Metab 1976 Dec
PMID:Nonautonomous function of a pancreatic insulinoma. 18 13

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
J Lab Clin Med 1978 Oct
PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

The myopathy associated with vitamin D deficiency has not been well characterized, and it is not known if weakness is a result of a specific effect of vitamin D deficiency on skeletal muscle. Chicks were raised from hatching on a vitamin D-deficient diet, and by 3 wk of age were hypocalcemic and appeared weak. Tension generated by triceps surae during repetitive stimulation of posterior tibial nerve was significantly less than that developed by chicks given vitamin D(3) supplements (309 g tension/g wet weight of triceps surae, SD 60, for vitamin D-deficient chicks; 470, SD 77, for vitamin D(3)-treated chicks, P < 0.01). Histochemical and electron microscopic examination of skeletal muscles of these chicks showed no abnormalities, and there were no electrophysiologic evidences of motor nerve or neuromuscular junction dysfunction. The concentration of ATP in skeletal muscle of the vitamin D-deficient chicks (5.75 mumol/g wet weight, SD 0.17) was not significantly different from that in vitamin D-treated chicks (5.60, SD 0.50). There was no correlation between strength and serum calcium, serum inorganic phosphate, or skeletal muscle inorganic phosphate. Relaxation of tension after tetanic stimulation was slowed in the vitamin D-deficient chicks (20.6 ms, SD 1.7, vs. 15.4, SD 1.3, in vitamin D-treated chicks and 15.3, SD 1.0, in normal control chicks), and in vitro (45)Ca(++) transport by sarcoplasmic reticulum from the vitamin D-deficient chicks was reduced. Calcium content of mitochondria prepared from leg muscles of vitamin D-deficient chicks (24 nmol/mg mitochondrial protein, SD 6) was considerably lower than that of mitochondria from normal control chicks (45, SD 8) or from chicks treated with vitamin D for 2 wk or more (66-100, depending upon level and duration of therapy). Treatment of the vitamin D-deficient chicks from hatching with sufficient dietary calcium to produce hypercalcemia did not significantly raise skeletal muscle mitochondrial calcium content (31 nmol/mg mitochondrial protein, SD 7) and did not prevent weakness. These studies demonstrate objective weakness as a result of myopathy in vitamin D-deficient chicks, and provide evidence that vitamin D deficiency has effects on skeletal muscle calcium metabolism not secondary to altered plasma concentrations of calcium and phosphate.
J Clin Invest 1979 Nov
PMID:Skeletal muscle calcium metabolism and contractile force in vitamin D-deficient chicks. 22 25

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.
Electroencephalogr Clin Neurophysiol Suppl 1978
PMID:Reciprocal Ia inhibition in spastic paralysis in man. 28 52

Fifty-five patients with mild to moderately severe essential hypertension were treated with guanabenz (2, 6-dichlorobenzylidene aminoguanidine acetate) in doses from 4 to 16 mg twice daily in a randomized, placebo-controlled study. The patients treated with placebo in the initial phase of the study were subsequently treated with guanabenz. The mean arterial pressure in the guanabenz group decreased from 130.6 to 107.6; that in the placebo group decreased from 129.6 to 126.6 standing and from 126.6 tp 109.9 and 128.8 to 120.5, respectively, supine. The principle adverse effects included sedation, dry mouth, weakness, and tiredness. Of the guanabenz-treated patients 84% had sustained decrease in supine diastolic blood pressure of 10 mm Hg or more, whereas in the placebo-treated patients only 32% had such a response. There was no significant orthostatic hypotension. Guanabenz thus appears to be an effective antihypertensive drug in patients with mild to moderately severe hypertension.
Clin Pharmacol Ther 1977 Mar
PMID:Guanabenz in essential hypertension. 31 38

Congenital pseudarthrosis of the clavicle, as observed in a review of the literature, is a rare condition of uncertain etiology which usually presents on the right side. Four of 10 cases were treated by surgical repair of the pseudarthrosis with excision of the non-union and internal fixation with a Steinmann pin and cancellous bone graft. A major postoperative complication in one case consisted of an acute massive neuropraxia of the brachial plexus (recognized 6 hours postoperatively), and was successfully treated by immediate removal of the internal fixation. Ten months postoperatively, the patient was experiencing only minimal weakness of the right opponens muscle. Roentgenograms at this time showed that the pseudarthrosis had healed but with angulation of the clavicle.
Clin Orthop Relat Res
PMID:Severe complication of surgical treatment of congenital pseudarthrosis of the clavicle. 45 52

A case of muscle weakness with hypertension is presented. The patient had symptoms of depression. Diagnosis of hyperaldosteronism was suspected because of a low serum potassium and confirmed by discovery of an adrenal adenoma. The role of hypokalemia in mental disturbances is reviewed. Emphasis is placed on possible metabolic etiologies when mood changes, muscle paresis and hypertension coexist.
J Clin Psychiatry 1979 Aug
PMID:Hyperaldosteronism (Conn's disease) presenting as depression. 46 62

Postoperative physiatric treatment is an integral part of the replacement of hips, knees, ankles, shoulders, elbows, wrists, and digital joints. Neuromuscular substitution patterns and incoordination usually prevail after joint replacement because of the usual long-term expectation and experience of pain, limitation of motion, fatigue, weakness, and the unavoidable operative trauma. The goals of postoperative physiatric treatment, in line with those of joint replacement surgery, are relief of pain and reestablishment of comfortable, normal neuromuscular functions and their reasonable, safe application in appropriate activities of daily living and of locomotion. By close collaboration between the Department of Orthopedic Surgery and that of Physical Medicine and Rehabilitation, certain principles and detailed protocols of postoperative management have been developed over the last 10 years. These are described in some detail for each of the joint replacements. Optimal results can be achieved only through meticulous attention to physical and psychosocial details, with close cooperation and communication among the involved services and persons.
Mayo Clin Proc 1979 Sep
PMID:Total joint arthroplasty: principles and guidelines for postoperative physiatric management. 47 Apr 59


1 2 3 4 5 6 7 8 9 10 Next >>