metrizamide and Stuttering

Aphasia following metrizamide myelography has been reported infrequently. During a seven-month period, we examined two patients who developed Broca's aphasia, apraxia of speech, oral-buccal-facial apraxia and neurogenic stuttering after intrathecal metrizamide administration. In each case, focal neurologic deficits were accompanied by clinical, electroencephalographic and radiologic signs of generalized neurologic disease. Serial speech and language evaluations initially revealed severe deficits that were largely resolved by the third day post-myelography. Out-patient follow-up examinations demonstrated persistence of mild speech and language abnormalities in each case. Our findings suggest that metrizamide may cause longlasting neurologic dysfunction.

Topics: Aphasia; Aphasia, Broca; Apraxias; Humans; Male; Metrizamide; Middle Aged; Myelography; Stuttering

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.

Topics: Animals; Brain Diseases, Metabolic; Confusion; Hexokinase; Humans; Male; Metrizamide; Middle Aged; Myelography; Neuromuscular Diseases; Rats; Stuttering