NOTES A N D LETTERS Choline Chloride in Alzheimer Disease Leon J. Thal, MD,” Wilma Rosen, PhD,” Nansie S. Sharpless, P h D , t and Howard Crystal, MD” During the past several years, numerous investigators have claimed that choline improves or fails to improve cognitive defects in Alzheimer disease. Many of the reported studies were open, nonblind trials 12, 51. Some investigators reported subjective improvement 131. Most reports have appeared in the medical o r psychiatric literature 11-51 rather than in primary neurology journals available to most clinical neurologists. We therefore wish to report on the treatment of seven carefully chosen, mildly to moderately demented patients with Alzheimer disease. Each patient received either placebo or choline chloride (50, 100, o r 200 mg/kg/day in four divided doses). Each patient was evaluated eight times during the study at the end of two-week intervals, including a baseline pretest, three placebo sessions, three drug sessions, and a posttest session. Psychometric testing included: verbal learning on a contingent learning task; recall after organization; immediate and delayed recall o n the Wechsler Memory Scale; constructional ability; verbal fluency from a category naming task; and category recognition and motor performance on the Purdue Pegboard. Despite more than doubling of the baseline plasma choline level with the 100 and 200 mg/kg doses, no subject at any dose level showed overall improvement greater than would be expected by chance. Contrary to the many claims in the literature suggesting amelioration of symptoms in Alzheimer disease, this carefully performed study failed to demonstrate objective improvement. Subjectively, three patients stated that they “felt better” during the study, but none believed that their memory was improved in day-to-day living. Five of the subjects developed a mildly “fishy” odor and one had mild diarrhea at the highest choline dose. By using three different dosages in each patient, we minimized the possibility of missing an effective dose. Higher doses would not be tolerated by most patients. We conclude that despite the known cholinergic deficiency in Alzheimer disease, administration of choline chloride is not effective in improving cognitive deficits. Departments of *‘Neuro/oRya n d tPsycbiatry Albert Einstein College of Medicine 1300 Morris Park Ave Bronx, N Y 10461 References 1. Boyd WD, Graham-White J, Blackwood G , Glen I, McQueen J: Clinical effects of choline in Alzheimer senile dementia. Lancet 2:711, 1977 2. Etienne P, Gauthier S, Johnson G, Collier B, Mendes T, Dastoor D, Cole M, Muller HF: Clinical effects of choline in Alzheimer’s disease. Lancet 1:508, 1978 3. Fovall P, Dysken W, Lazarus LW, Davis JM, Kahn RL, Jope R, Finkel S, Rattan P: Choline bitartrate treatment of Alz- 580 heimer-type dementia. Commun Psychopharmacol 4: 14 1145, 1980 4. Renvoize EB, Jerram T: Choline in Alzheimer’s disease. N Engl J Med 301:330, 1979 5. Signoret JL, Whiteley A, Lhermitte F: Influence of choline on amnesia in e x l y Alzheimer’s disease. Lancet 2:537, 1978 Spinal Seizures Following Intravenous Contrast in a Patient with a Cord AVM George R. Uhl, MD, PhD,” Carlos R. Martinez, MD,t and Benjamin R. Brooks, MD“ Grand mal, focal motor, and psychomotor seizures infrequently complicate intravenous injection of iodinated radiographic contrast materials [3-51. We report the occurrence of stimulus-sensitive spinal seizures following intravenous administration of meglumine iothalamate (Conray) to a patient subsequently proven to have an arteriovenous malformation of the spinal cord. A 40-year-old policeman was evaluated for progressive lower extremity weakness, hypesthesia, and dysesthesias with more recent decrease in bowel and bladder control. O n examination he had diminished tone, strength, sensation, and reflexes in his lower extremities. Broad-based and circumducting gait, bilateral foot drop, hypoactive to absent ankle and patellar reflexes, mild hypesthesia below the twelfth thoracic dermatome bilaterally, and dense hypesthesia below the knees were noted. A 300 ml intravenous infusion of 30% meglumine iothalamate (Conray 30) was performed during the course of a C T scan. Near the end of the infusion, the patient developed extensor spasms of the trunk and extremities that were abrupt in onset and one to two seconds in duration. Vigorous tonic extension of both legs was followed by several symmetrical clonic jerks. There was less vigorous extension of the arms. No abnormal facial movements, eye deviation, incontinence, tongue biting, o r alteration in consciousness was seen. The spasms were stimulus sensitive; movements of the CT scanner table repeatedly triggered the response. The episodes ceased one hour after the contrast infusion. There were no lasting additional neurological deficits. Subsequent iophendylate (Pantopaque) myelography revealed tortuous filling defects along the dorsal surface of the thoracic cord consistent with an arteriovenous malformation extending from the second through tenth thoracic nerve roots, which was later removed surgically. Two features of the observed seizures parallel reported characteristics of other complications of contrast media. First, the stimulus sensitivity has also been noted in seizures evoked during selective intraarterial administration of contrast agents for human diagnostic spinal angiography o r for experimental studies in dogs [ l , 21. Second, the apparent relation to an underlying structural lesion is also frequently noted for the grand mal, focal motor, and psychomotor seizure that occasionally complicate intravenous contrast administration for C T scans [3-51.