A double-blind crossover study with imipramine was conducted in 10 patients with absence and myoclonic-astatic seizures who had not responded to conventional medications. Imipramine produced a significant initial decrease in seizure frequency in 5 of the 10 patients, and in 2 patients the beneficial effect was maintained for more than 1 year. An open trial of imipramine in another 16 patients showed an initial reduction in seizure frequency in 10 patients (63 percent), and this decrease persisted for more than 1 year in 4 patients (25 percent). The effect of imipramine on the EEG did not always correlate with the clinical response. Serum content of imipramine in the patients who showed a long-term response was 40 to 120 ng per milliliter, on a total daily dose of 0.7 to 3.5 mg per kilogram. These results suggest that imipramine is a valuable addition to the treatment of seizures.
THE MEASUREMENT of serum en$ zyme activities, particularly those of crea$ tine phosphokinase (CPK), aldolase, and glutamic oxaloacetic transaminase (SGOT), is an important adjunct in the diagnosis of primary muscle disease.1-4 Elevations have been found in patients with muscular dystrophy and polymyositis,5-7 whereas patients with neurogenic atrophy generally have had normal levels.8Altered potassium metabolism has long been associated with muscle dysfunction,9 but only a few references have appeared linking hypokalemia, myopathy, and serum enzyme elevation.10-12 Three patients with hypokalemia and severe muscle weakness were studied; all had marked alterations in their serum enzymes, particularly CPK.
MethodsCreatine phosphokinase determinations were done using the method of Nielsen and Ludvigsen.13 The normal range is 0\g=m\Uto 18\g=m\U per milliliter.Glutamic oxaloacetic transaminase determinations were performed using a modification of the method of Henry and co-workers.14 The normal values are in the range of 10\g=m\Uto 35\g=m\U per milliliter. Aldolase determinations were based on the method of Beisenherz and co-workers15 and the normal values are 3/iU to 8µ per milliliter.Serum potassium values were determined by flame photometry. Normal range is 3.9 to 5.2 mEq/liter ± 0.2 mEq/liter. Muscle strength was evaluated daily by one, and often by two, of the authors. Strength was graded according to the method used by Smith et al16 where 5 is normal and 0 represents no observed activity.
A 22-year-old woman gradually developed depression, dementia, and chorea over an 8-month period. She fulfilled the criteria for the primary antiphospholipid antibody syndrome but not those for systemic lupus erythematosus. Her chorea and neurobehavioral deficits responded favorably to a regimen of prednisone, hydroxychloroquine, and aspirin. This appears to be the first report of a patient with a lupus anticoagulant and reversible dementia. The response to immunosuppressive therapy implies an antibody-mediated condition similar to Sydenham's chorea.
Marked asterixis occurred in two patients following metrizamide myelography. One also suffered generalized seizures and the other had severe stuttering speech for seven days. The spectrum of toxic manifestations of metrizamide is reviewed with emphasis on the unusual lethargy and other depressive effects seen with this relatively safe agent. The hypothesis that metrizamide exerts a ouabain-like effect on the cortical surface was tested. Metrizamide in concentrations as high as 20 mM had no inhibitory effect on rat cerebral K+-para-nitrophenylphosphatase, a partial reaction of (Na+K+)-adenosine triphosphatase. Because metrizamide is a 2-deoxyglucose analogue, a competitive inhibition of hexokinase at the first step in glycolysis was also postulated. Metrizamide was found to competitively inhibit commercial (microbial) hexokinase. The Michaelis constant for glucose rises from 0.13 to 0.25 to 0.33 to 0.91 mM in the presence of 0, 0.4, 1.0, and 2.0 mM metrizamide, respectively. Since the concentration of metrizamide over the cerebral cortex after routine myelography may be approximately 50 mM compared with a glucose concentration of only 3.6 mM (65 mg/dl), it is postulated that impaired brain glucose metabolism may be responsible for some of the toxic effects of metrizamide.
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