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Hepatic cirrhosis and intracranial hemorrhage Significance of the association in 53 pathological cases.

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phenytoin for many years and may never develop a clinical
correlate of their radiological abnormality.
Rush-Presbyterian -St. Luke’s Medical Center
Chicago, IL 60612
Rde rences
McLain LW Jr, Martin JT, Allen JH: Cerebellar degeneration
due to chronic phenytoin therapy. Ann Neurol7:18-23, 1980
Salcman M, Defendini R, Correll J, Gilman G: Neuropathological changes in cerebellar biopsies of epileptic patients. Ann Neurol 3:lO-19, 1978
Victor M, Adams RD, Mancall E L A restricted form of cerebellar cortical degeneration occurring in alcoholic patients.
Arch Neurol 1:579-688, 1959
agreement with reports of a beneficial effect of bromocriptine in detrusor dysfunction and favors observations made
in later studies [ l , 4,51. This patient probably developed
ongoing detrusor instability with long-term bromocriptine
therapy. If a patient taking bromocriptine develops incontinence of urine, it may be worthwhile stopping the drug
before embarking on an elaborate work-up.
Experimental Therapeutics Branch
National Institute of Neurological
azd Communicative Disorders and Stroke
National Institutes of Health
Bethesda, M D 20205
References
r r r .
Incontinence ot u rine
with Long-Term
Bromocriptine Therapy
Govindan Gopinathan, MD, FRCP(C),
and Donald B. Calne, DM, FRCP
We report a patient with Parkinson disease who developed
incontinence of urine during long-term bromocriptine
therapy. The patient was a 47-year-old man who had had
Parkinson disease since 197 1 and was taking six tablets of
Sinemet-25/250 daily. Bromocriptine was started in December, 1976, and the dosage had remained at 50 mg daily
since then. He had not undergone any surgical procedures
on the genitourinary tract. Six months before this writing
the patient developed constant dribbling of urine. He experienced several on-off swings daily and also had episodes
of confusion and hallucinations. The incontinence was
present throughout the day, even when he was lucid and
ambulatory.
He was admitted for evaluation of his incontinence on
September 9, 1979. Physical examination revealed nothing
other than features of parkinsonism. The prostate was not
enlarged. Urinalysis was normal and cultures were negative. Plain roentgenograms of the kidney, ureter, and bladder and an intravenous pyelogram were normal. Spine
roentgenograms did not reveal any abnormalities. Cerebrospinal fluid was normal. Because of severe dyskinesias and
frequent on-off phenomena, bromocriptine was stopped on
the fifth hospital day. Within 24 hours the incontinence
started to improve, and it disappeared in three more days.
The patient was discharged from the hospital and has been
seen in follow-up twice. The incontinence has not recurred
since withdrawal of bromocriptine.
The pathophysiology of this patient’s incontinence is uncertain. Incontinence of urine with long-term bromocriptine therapy has not been reported in the series reviewed
[2, 3, 6, 71. The fact that it disappeared promptly on discontinuation of bromocriptine suggests that the drug was
the causative factor. Our observation in this case is in dis-
204 Annals of Neurology Vol 8 N o 2 August 1980
1. Abrams PH, Dunn M: A double blind trial of bromocriptine in
the treatment of bladder instability. Br J Urol5 124-27, 1979
2. Calne DB, Williams AC, Neophyrides A: Long term treatment
of parkinsonism with bromocriptine. Lancet 1:735-737, 1978
3. Fahn S, Cole LJ, Snider SR: Role of bromocriptine in the
treatment of parkinsonism. Neurology 29: 1077-1083, 1979
4. Farrar DJ, Osborne JC: Use of bromocriptine in the treatment
of unstable bladder. Br J Urol 48235-238, 1976
5. Farrar DJ, Pryor JS: Effects of bromocriptine in patients with
benign prostatic hypertrophy. Br J Urol 48:73-75, 1976
6. Lieberman AN, Kupersmith M, Gopinathan G, et al: Bromocriptine in Parkinson disease: further studies. Neurology
29:363-369, 1979
7. Parkes D: Drug therapy-bromocriptine. N Engl J Med
301:873-878, 1979
Hepatic Cirrhosis
and Intracranial
Hemorrhage : Significance
of the Association
in 53 Pathological Cases
GPrard Boudouresques,* MD, Jean-Jacques Hauw, MD,
Vincent Meininger, MD, Raymond Escourolle, MD,
Bernard Pertuiset, MD, AndrC Buge, MD,
Francois Lhermitte, MD, and Paul Castaigne, MD
In a recent survey of 43 1 neuropathological observations of
intracranial hemorrhage with pathological examination of
the liver collected from 1962 to 1977 at the Laboratoire de
Neuropathologie Charles Foix [l], we found 53 (12%)
examples of hepatic cirrhosis (Table). Forty-four cases were
associated with intracerebral hemorrhage. This high incidence of intracerebral hemorrhage in hepatic cirrhosis was
surprising, as it has not previously been reported in the
literature [2-41. To check the significance of these data, we
compared the 44 cases of intracerebral hemorrhage with a
control group of 100 sex- and age-matched cases from the
same laboratory collected during the same period and
Distribution of 53 Cases of Hepatic Cirrhosis According to Type of Hemorrhage
HeDatic Cirrhosis Associated with:
+
Type of
Hemorrhage
Intracerebral
(44/282 cases)
Subarachnoid
(5/ 115 cases)
Subdural
(4/34 cases)
+
ATH
ATH
Anticoagulant
Therapy
Vascular
Malformation
ATH
Arterial
Aneurysm
Trauma
ATH
Trauma +
Anticoagulant
Therapy
13
26
5
0
0
0
0
0
0
0
3
2
0
0
1
0
0
0
0
2
1
Isolated
Hepatic
Cirrhosis
+
ATH = arterial hypertension.
screened for hepatic cirrhosis. A significantly higher percentage of hepatic cirrhosis was found in the cases of intracerebral hemorrhage compared with the controls (15.6%
versus 7%; xz = 596, df = 1,p < 0.00005).
It appears that hepatic cirrhosis can be considered a risk
factor for intracerebral hemorrhage. An independent comparison by two-way contingency tables showed no difference (p < 0.5) in the incidence of arterial hypertension and
anticoagulant therapy between cirrhotic and noncirrhotic
patients having intracerebral hemorrhage. The incidence of
hepatic cirrhosis in our study is higher than that found by
McCormick and Schochet [ 3 ] : 3 cases of hepatic disease
among 12 1 cases exhibiting our criteria for intracerebral
hemorrhage (4%).Among our cases, the topographical localization and number of hemorrhages were not statistically
different from those of the noncirrhotic population by a
similar statistical test (p < 0.5).
No significant correlation between hepatic cirrhosis and
subarachnoid or subdural hemorrhage could be demonstrated, perhaps because of the small number of cases in the
latter groups.
Hzpital de la Salp^etrdwe
47 Blud de I'Hzpital
75651 Paris Gedex 13, France
"HGpitalde la Timone
Blud Jean Moulin
F13385 Marseille Cedex 4, France
References
Boudouresques G , Hauw JJ, Meininger V, et al: Etude
neuropathologique des hbmorragies intracraniennes de
I'adulte. I. DonnGes g6nerales ipropos de 500 observations.
Rev Neurol (Paris) 135:197-210, 1979
Fisher CM: The pathology and pathogenesis of intracerebral
hemorrhage. In Fields WS (ed):Pathogenesis and Treatment of
Cerebrovascular Disease. Springfield, IL, Thomas, 1961, pp
295-3 17
McCormick WF, Schochet SS: Atlas of Cerebrovascular Disease. Philadelphia, Saunders, 1976, pp 251-264
Stehbens WE: Pathology of the Cerebral Blood Vessels. St.
Louis, Mosby, 1972, pp 284-350
Plasma Exchange
in Polyradiculoneuropathy
Klaus V. Toyka, MD, Regine Augspach, MD,
Walter Paulus, MD, Bernd Grabensee, MD,
and Ditmar Hein, M D
The report by Drs Server et al[3] on plasma exchange (PE)
in relapsing polyradiculoneuropathy states that despite
marked improvement in muscle strength after the treatment, nerve conduction velocities were unchanged. We
have recently treated a 17-year-old, wheelchair-bound girl
who has the severe chronic type of Guillain-Bark syndrome with two series of three PE treatments using a new
hollow-fiber filter [ 2 ] (Asahi Medical) connected to a
computer-aided dialysis pump (Fresenius). The patient had
not shown any benefit from six months' treatment with steroids and azathioprine. After PE a dramatic increase in
strength was seen, following a similar time course as in the
Hopkins case. In contrast to that case, however, nerve conduction velocities, distal latencies, and, most strikingly,
amplitudes of the compound muscle action potentials reverted toward normal values concomitantly with clinical
improvement. Five weeks after the first PE series the patient relapsed while on azathioprine, but another course of
PE reproduced the clinical and electrophysiological improvement seen before. The findings in this patient suggest
that the putative serum factor somehow relates to the impaired nerve conduction.
After we had initiated PE in this patient, another short
communication appeared reporting the successful use of
PE in chronic progressive polyneuropathy [ 11. Therefore, a
larger controlled trial of PE, as suggested by Drs Server et
al, is warranted. The rarity of the severe chronic type of
Guillain-Bark syndrome may pose difficulties if such a
study is conducted by a single center.
Departments of Neurology and Medicine
Uniwersity of Dusseldorf
Dusseldorf; West Germany
Notes and Letters
205
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associations, pathologic, hemorrhagic, hepatica, case, cirrhosis, intracranial, significance
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