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Brief and mild alcohol intake can increase serum creatine phosphokinase.

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spinal fluid showed 11 lymphocytes and positive treponema assay in a dilution of 5,120. Treatment with
diazepam did not affect the myoclonus. With carbamazepine, 600 mg a day, however, the myoclonus disappeared and did not recur during the subsequent 11 months
under treatment.
Schenck [ 11 reported 24 examples of palatal myoclonus
in various forms of active neurosyphilis. This is the first
time, to our knowledge, that carbamazepine has been used
successfully in the treatment of palatal myoclonus.
Department of Neurology
National Hospital of Bepptl
Oita, Jupan 874-01
amination was normal. Cerebrospinal fluid examination,
isotope brain scan, and C T scan were normal. The electroencephalogram showed typical abnormalities as previously
described [ 11. Biochemical values were satisfactory for a
patient o n maintenance dialysis. The patient was taking
medication similar to the first patient's.
Both patients were treated with clonazepam; this resulted in only unsustained improvement in their abnormal
movements. Subsequently both patients developed progressive dementia and died. Clonazepam had no detectable
effect on their deterioration.
Renal Unit
Groote Schuur Hospital
Cape Town, 7925, South Africa
Reference
1. Schenck E: Analyse der publizierten Fdle von Hirnnewenmyorhythmie. In Die Hirnnervenmyorhythmie. Berlin, Springer,
1965, pp 32-40
References
1. Chokroverty S, Breutman M, Berger V, et al: Progressive
dialytic encephalopathy. J Neurol Neurosurg Psychiatry 39:
411-419, 1976
2. Trauner DA, Clayman M: Dialysis encephalopathy treated with
clonazepam. Ann Neurol6:555-556, 1979
Clonazepam in
Dialysis E ncephalopathy
M. D. Pascoe, MB, ChB, FCP(SA)
Trauner and Clayman [2] reported treating a patient with
dialysis encephalopathy using clonazepam. Two further
patients treated with this drug are presented here.
A 25-year-old man developed end-stage chronic renal
failure on the basis of chronic glomerulonephritis. Maintenance hemod'ialysis was begun and was continued for five
years. At that time he first noted neurological symptoms,
expressed as twitching of the arms, initially on dialysis and
subsequently persisting after dialysis. Speech difficulty was
also noted.
Examination showed the patient to be usually alert but
occasionally inattentive. The striking features were his
dysarthria and dysphasia and the frequent twitching of all
limbs. The remainder of the neurological examination was
unremarkable.
Special investigations, all normal, included cerebrospinal
fluid with normal pressure, isotope brain scan, and C T scan.
Laboratory values for creatinine, electrolytes, calcium, and
phosphorus were within acceptable limits for a patient o n
maintenance dialysis. The electroencephalogram showed
typical symmetrical synchronous spiking activity [l]. H e
was taking no medication other than vitamin supplements
and aluminum hydroxide gel as a phosphate binder.
A 49-year-old man with chronic renal failure from
chronic glomerulonephritis had been on dialysis for four
years at the time of onset of symptoms. A transplant effort
had ended in rejection and return to dialysis after four
weeks. The presentation was with twitching, initially of the
left forearm and subsequently of both arms and legs, and
very marked decline in mental function.
Physical examination was unremarkable apart from the
twitching, which was of the whole body, a marked decline
in cerebral function, and prominent dysarthria and dysphasia. The remainder of the central nervous system ex-
200
Annals of Neurology
Vol 9
No 2
February 1981
Brief and Mild Alcohol
Intake Can Increase Serum
Creatine Phosphokinase
Daniel S. P. Schubert, MD, PhD,"t Karen Brocco, MD,"
Frank Miller, MD,* and Marian Patterson, PhD"t
Lafair and Myerson [3] reported that serum creatine phosphokinase (CPK) in a group of alcoholic subjects reached a
peak 3 to 5 days after binge drinking stopped and that acute
alcoholism without delirium tremens o r clinical muscle involvement produced an increase in CPK in 75% of their
sample. Other work has indicated that volunteers with relatively heavy alcohol intake develop increases in CPK after
10 days of drinking [ 4 ] . However, former alcoholics who
no longer drink d o not have an elevation in serum CPK [ 3 ] .
CPK levels after brief periods of slight to moderate alcohol
consumption have not been reported in the literature.
Patient volunteers admitted to a psychiatric ward were
asked about alcohol intake during the previous 24 hours as
well as the 24-hour to one-week period prior to admission.
Serum CPK was measured as soon as the person had consented to participate in the study, usually within 1 to 4 days
of admission. Subjects were evaluated by the St. Louis Research Criteria [l] for alcoholism and other psychiatric
syndromes. The time after admission when samples were
drawn for CPK determination did not correlate with CPK
level ( r = 0.04, N S ) .
Patients were excluded whose records or nurses' interviews showed evidence of other factors that might raise
serum CPK, including intramuscular injection, seizure disorder, brain trauma or other brain damage, exercise, restraint, seclusion, and history of muscle disease or heart
damage. Schizophrenia has been found to be associated
with a somewhat elevated CPK [ 5 ] ; therefore, patients who
CPK Levels of Three Patient Groups Differing in Recency of Alcohol Intake
No. of
Patients
Mean
CPK
No. Positive
for Alcoholism
by St. Louis
Research Criteria
Group 1: alcohol in 24 hr PTA but
not between 24 hr and 1 wk PTA
6
85.3
2
Group 2: alcohol in both 24 hr PTA
and between 24 hr and 1 wk PTA
9
83.2
6
Group 3: alcohol not in 24 hr FTA
but in 24 hr to 1 wk FTA
8
44.75
2
Subjects
PTA
=
Patients with
Reported Intake
CPK > 90 ( N = 3): 3 beers, 1 mixed
drink, and 2 glasses wine,
respectively
CPK > 100 (N = 2): 1 beer in 24 hr
P T A - C P K 137; 2 beers in 24 hr
PTA and 30 in 24 hr to 1 wk
PTA-CPK 156
prior to admission
met St. Louis Research Criteria for schizophrenia were excluded from the analysis. In addition, patients were rated
for motor activity in the 24 hours prior to CPK measurement, in most cases by at least two observers, and motor
activity was found to be unrelated to CPK levels.
Six patients reported alcohol intake during the 24 hours
before admission but not during the rest of the week prior
to admission (Group 1, Table). Mean serum CPK for this
group was 85.3. Group 2 comprised 9 patients who reported alcohol intake during both the 24 hours and the
week prior to admission; mean CPK in this group was 83.2.
Group 3 consisted of 8 patients who reported drinking
during the week prior to admission but not within the preceding 24 hours; these patients had a mean serum CPK of
44.75. Examining the individual CPK level shows that for
Group 3, no subject who reported drinking earlier than 24
hours prior to admission had an initial CPK greater than
78. In Groups 1 and 2 , comprising patients who reported
drinking in the 24 hours prior to admission, 4 subjects had
CPK levels between 100 and I56 and 5 had CPKs between
80 and 7 9 .
No significant difference ( t = 0.10, df = 13, NS) in CPK
level separated Groups 1 and 2, so these groups were combined to include 1 5 subjects reporting alcohol intake in the
24 hours before admission. This combined group had a
mean CPK of 84.07, significantly higher than Group 3,
with a mean CPK of 44.75 ( t = 2.59, df = 21,p < 0.02).
The Table shows that the three groups differed in the
proportion of patients who received diagnoses of alcoholism by the St. Louis Research Criteria. Alcoholics
comprised one-third of Group 1 , two-thirds of Group 2 ,
and one-fourth of Group 3. The diagnosis of alcoholism
was found in another study [ 5 ] to be unrelated to CPK
levels in such subjects. Our results suggest that relatively
minor amounts of alcohol consumed over a brief- period
may produce an increase in CPK levels among individuals
who are not necessarily alcoholics. The study is consistent
with prior work in which subjects meeting criteria for alcoholism who denied recent intake were found not to have
elevated CPK [ 3 , 51. It appears that a high amount of dcoho1 intake may be unnecessary to initiate an increase in
CPK, as suggested in prior work.
The explanation for the present findings is speculative.
O n e possibility is a minor alcohol withdrawal syndrome
with heightened sympathetic nervous system activation [ 2 ] .
This would account for the lack of CPK increase immediately after sustained alcohol intake, followed by a gradual
rise over 3 to 5 days [3]. A second explanation is a direct
toxic effect on the muscle membrane or else early muscle
fiber damage. Although alcoholics often distort their histories, we see no reason to suspect that they systematically
did so in order to provide the results in this study.
"Department of Psychiatry
+Department of Psychology
Case Western Reserve University
Cleveland, OH 44 109
Supported in part by NIMH Training Grant 1-TO1-MH14852 and
N I H Internal Medicine Training Grant PE-15 188-01.
The authors would like to thank the 6B nurses for doing the motility ratings and Mr Thomas Grande for assisting with the data
analysis.
References
1. Feighner JP, Robins E, Guze SB, Woodruff RA Jr, Winokur G ,
Munoz R: Diagnostic criteria for use in psychiatric research.
Arch Gen Psychiatry 26:57-63, 1972
2. Ikeda H : Serum creatine phosphokinase activity in newly admitted chronic alcoholics. Folia Psychiatr Neurol Jpn 3 1:9-16,
1977
3. Lafair JS, Myerson RM: Alcoholic myopathy. Arch Intern Med
122:417-42 2, 1968
4. Rubin E, Katz AM, Lieber CS, Stein EP, Puszkin S: Muscle
damage produced by chronic alcohol consumption. Am J
Pathol83:499-516, 1976
5. Schubert DSP, Brocco K, Miller FT,Patterson M: Creatine
phosphokinase in St. Louis Research Criteria schizophrenics.
Am J Psychiatry (in press)
Notes and Letters
201
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