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Clonazepam in dialysis encephalopathy.

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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
1. Schenck E: Analyse der publizierten Fdle von Hirnnewenmyorhythmie. In Die Hirnnervenmyorhythmie. Berlin, Springer,
1965, pp 32-40
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
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-
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
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encephalopathy, dialysis, clonazepam
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