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Choline chloride in Alzheimer disease.

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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.
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