patient was given 15 units of regular insulin intravenously while potassium replacement continued, and within 30 minutes he was quadriparetic without antigravity function of any upper or lower extremity muscle group. During this period, the single motor unit amplitude in the left deltoid muscle decreaseil from 750 t o 2 0 p v and the peak-to-peak EMG response fell from 2.8 mv to 2 0 p v . The MNCV remained normal. The patient’s EMG response and strength returned in two hours. Serum potassiuni and glucose levels were monitored every 15 minutes during the insulin challenge. Potassium varied between 2.1 and 2.2 mEq per liter anJ glucose decreased from 280 to 165 mg per deciliter. After four days o f potassium supplementation, the patient’s strength was normal and he no longer became weak after receiving his insulin. A biopsy of the left deltoid muscle revealed vac-uolation of the sarcoplasm in 8% of the fibers by light microscopy. The patient was discharged after ten da\,s, at which time all his laboratory values were essentially normal T h e week after discharge, his EMG before and afrer insulin atlniinistration and muscle biopsy of the right deltoici were normal. H e had no recurrence of p r h e time of his death thirteen months later weakness ~ i to in a motor vehicle accidenr. The most likely cause for this patient’s weakness was fludrocortisone-iii~~uce~i hypokalemia 141. Steroid myopathy is usually associated with mpalgias and generally is not accompanieil by elevated serum levels of muscle enzymes o r clecreaseil s e r u m potassium [ 11. The resolution of weakness with potassium replacement suggests that the weakness was not due t o the patient’s lung tumor [ 2 ] .The vacuolar change is characteristic of hypokalemic myopathy 151. The findings suggest that i n the provocative test for hypokalemic periodic paralysis, insulin may have a direct inhibitory effect o n muscle membrane excitability in a d d t i o n t o lowering serum potassium.

Referewc-ei 1. Askari A, Vignos PJ, hloskowitz RW: Steroid myopathy in connective tissue disease. A m J Med h1:485-492, 1976 2 . Croft PB, Wilkinson M: Carcinomatous neuromyopathy: its incidence in patients with carcinoma of the lung and carcinoma o f the breast. Lancet 1:184--188, 1963 3. Kao I , GorJon AM: Mechanism of insulin-induced paralysis of muscles from potassiuin-~leplete~ rats. Science 188:740-741, 1975 4 . Rivera VIM: lnrcarpretation of serum creatine phosphokinase. J A M A 225:991-~904,1073 5 . Ruheristein AE, W i m a p e l SF: Acute hypokalernic myopathy in alcoholism. Arch Neurol 3 4 : 5 5 3 - 5 5 5 , 1977

More on Epilepsy and Epileptic Drivers William M. Landau. M D In his editorial “The Physician’s Responsibility for Epileptic Drivers” (Ann Neurol 4:485-486, 1978), Dr Masland emphasizes issues and data regarding starutes and practices o n compulsory reporting of epileptic patients who drive. But for the majority of neurologists, who practice in states without such laws, the problem may better be defined as the physician’s responsibility t o the epileptic driver. The fact that the word dwtov means “teacher” is nowhere betrer illustrated than by this responsibility. At the beginning of a discussion with an epileptic patient about driving, the neurologist must explain clearly that both ethics and the law regarding privacy of the doctor-patient relationship require that the physician not be a policeman; responsibili t y lies with the patient. Furthermore, the issue of whether an epilepric patient should not drive is one that must be patiently tackled with empathy and sympathy more than once, for a driving proscription is probably the most onero u s handicap the patient confronts in relation to both occupational and social activities, particularly in the case of the teenager and young adult male. Unfortunately, the neurologist’s motivating argument that the lives of the patient and innocent citizens o n the street are at risk often is not persuasive, nor is the argument that the driver’s license bureau may withdraw a license and prosecute for dishonesty in filling o u t the license application form. The concept of light at the end of the tunnel in the form of freedom from the driving proscription after a year or more of perfect seizure control is a useful selling point that is supported by the licensure law in some states. This may also motivate the patient to understand the importance of compliance with the drug regimen. An argument I have found quite effective, especially with parents, concerns liability insurance coverage: the small print in insurance policies indicates that prevarication about illness in the application, if discovered, can result in retroactive lack of coverage for an accident, even if the accident had no relation at all to a seizure. This logical and realistic threat of uninsured financial catastrophe often provokes more compliance than does consideration of abstract risk to unknown persons. I agree with D r Masland that the physician’s notes should religiously document the transfer to an epileptic patient of information about driving, and further, that a reinforcing formal letter may help persuade the patient that the issue is indeed important. However, I am sure D r Masland would agree that establishing the record for medicolegal purposes is not the end of the road for a noncompliant patient. Each patient visit should be used as an opportunity for reinforcement of the lesson.

From the Department of Neurology and Ncurological Surgery (Neurology), Washington University School of Medicine, 660 S Euclid Ave, St. Louis, MO 631 10.

140 Annals of Ycurology

Vol 6

No 2

August 1979