1,720,976 research outputs found
[Surgical treatment of blepharoptosis in patients with mitochondrial myopathies. Apropos of 4 cases]
No full textThe authors briefly describe the commonest forms of mitochondrial myopathies particularly those associated with disorders of ocular motility. They report their series of four patients suffering from ptosis of the eyelid caused by mitochondrial myopathies. The ptosis was corrected surgically in all cases by means of Müller's muscle adaptation technique. The authors discuss their results and the indication for this technique
[Surgical treatment of blepharoptosis in patients with mitochondrial myopathies. Apropos of 4 cases].
No full textThe authors briefly describe the commonest forms of mitochondrial myopathies particularly those associated with disorders of ocular motility. They report their series of four patients suffering from ptosis of the eyelid caused by mitochondrial myopathies. The ptosis was corrected surgically in all cases by means of Müller's muscle adaptation technique. The authors discuss their results and the indication for this technique
Adverse interaction between acetazolamide and anticholinesterase drugs at the normal and myasthenic neuromuscolar junction level
No full textMyocardial damage due to hypokalaemia and hypophosphataemia.
No full textA case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed
- …
