Facial Myocloni and Stroke as Late Sequelae of Metrizamide Myelography

An 85-year old man with negative stroke risk factors was admitted to the neurological department because of sudden onset vertigo, dysarthria, and left-sided hemiparesis. His history was remarkable for recurrent lumbalgias in his seventies, successfully relieved with analgesics, and jerks of the left eyelids since 2 years previously. Metrizamide myelography in 1980 was normal. Initially, the jerks lasted for up to half an hour and recurred up to four times a day, decreased in frequency or disappeared occasionally for several weeks later on, and recurred two to three times per week during the last months before admission. Because he was hardly disturbed by his symptoms and not affected by any other illness, he had not been seen by a doctor since 1980. Neurological examination showed partial disorientation, dysarthria, moderate left-sided hemiparesis sparing the upper facial muscles, left-sided facial hypesthesia, and recurring myocloni of the left orbicularis oculi muscle, lasting for a few minutes. Blood pressure and ECG were normal. The initial cerebral CT showed moderate leukoaraiosis, diffuse cerebral atrophy, and multiple disseminated hyperdense circular formations intraventricularly and in the subarachnoidal space, including the sulci, with right hemispheric accentuation. These findings were interpreted as remaining droplets of metrizamide, used in the aforementioned myelography. A second CT of the head, 4 days later, additionally showed right basal ganglia infarction. Ultrasonography of the extracranial and intracranial arteries and transthoracic echocardiography were normal. Repeated EEGs disclosed bitemporal slowing without increased cerebral excitability. Under adequate therapy, stroke symptoms continuously improved, but the myocloni remained unaffected until discharge.

The residual droplets of metrizamide were assumed to be responsible for the patient's symptoms because 1) previous reports imply that metrizamide is not completely benign and can result in persistent neurological dysfunction,³ 2) metrizamide penetrates into the brain and spinal cord with a possibly toxic effect to the neurons and vessels,⁵ and 3) no other risk factors or abnormalities were found that could have been responsible for the myocloni and stroke. The patient had no history of hypertension, hypotension, hyperlipidemia, anemia, exsiccosis, or nicotine or other drug abuse. On ultrasonography there was no indication for extracranial or intracranial atherosclerosis. The transthoracic echocardiography was not indicative of thrombi, endocarditis, or open foramen ovale. Thus, a chronic toxic effect of metrizamide was speculated to have caused the myocloni and the stroke. The same agent's causing myocloni and stroke might be due to a toxic effect not only on the neurons but also on the cerebral vessels. The reason why the myocloni and stroke occurred not until 15 and 17 years, respectively, after the application of metrizamide remains speculative, but possibly additional pathogenetic factors were necessary for metrizamide to become symptomatic.

This case demonstrates that intracranial metrizamide residue may cause facial myocloni and stroke, even years after application of the contrast medium.