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Neurogenic bladder in neurolepticmalignant syndrome
NEUROGENIC BLADDER IN NEUROLEPTIC MALIGNANT SYNDROME ZAFAR KHAN, M.D. R. RAJARATNAM, M.D. VINOD K. SINGH, M.D. From the Department of Surgery, Division of Urology, Beth Israel Medical Center, New York, New York
~STRA CT--Urinary retention or incontinence is not an inyrequent clinical finding in patients th neuroleptic malignant syndrome. We studied the pathophysiology o] this voiding disorder by ~dynamic testing. It revealed involuntary bladder contraction and rigidity of external sphincter rskinesia). These findings are analogous to those in Parkinson disease patients and support the ~amine deficiency theory as the cause o] neuroleptic malignant syndrome.
lis report presents a study of neurogenic bladr in a patient with neuroleptic malignant synome.
Case Report A sixty-six-year-old white woman, a known ise of chronic paranoid schizophrenia, was adiffed with complaints of paranoia and anxty, vague body pain, and disorientation of e and place of one-week duration. On exination, her pupils were dilated with minii~ reaction to light, and she had cog wheel i~dity of upper limbs. ~Prior to this admission, she had been taking loperidol (Haldol) and benztropine (Cogen0. During hospitalization, benztropine was scontinued and haloperidol was replaced ith perphenazine (Trilafon). Neurologist suprted the diagnosis of organic brain syndrome eondary to antieholinergie etiology. During the first week of hospitalization, the ltient became diaphoretic; taehyeardia develIped and she refused to eat. Increase in her ri~ t y was noticed. On the thirteenth day, she ~iecamefebrile (101.4 °F) and alternating symp~ s of urinary incontinence and retention deeloped. Creatinine phosphokinase (CPK) was [crated (532 U/L), and she had increased ihite blood cell count (13.8). On the basis of !ese findings, a diagnosis of neuroleptic malig-
~
~OLOGY / JUNE 1991 / VOLUME XXXVII, NUMBER 6
nant syndrome was made. Perphenazine was discontinued and she was managed with hydration (I/V fluids). Because of her inability to empty the bladder, indwelling catheter was maintained. Her general condition gradually improved over a period of four days but urinary retention continued. Urodynamic test revealed the following. Bladder capacity was 1,200 cc. Although she experienced lower abdominal discomfort, she failed to interpret it as a desire to void. Involuntary bladder contraction of 72 cm of water occurred; but external sphincter remained rigidly contracted, and she failed to relax it even after repeated commands to void (Fig. 1). She denied any urge to void. She attempted to void by abdominal straining during which the periodic relaxation of the external sphincter was seen and urine was voided in spurts. At the end of voiding she had residual urine of 500 cc. Management consisted of continued indwelling catheter. The indwelling catheter was removed when the generalized rigidity improved and the patient passed the trial of voiding. Comment Neuroleptic malignant syndrome is a rare disorder. It is a serious and potentially lethal adverse reaction to antipsyehotie medication. It occurs after therapeutic doses of neuroleptie 543
S cmH20 Pressure C02 C02CYSTOMETRY
III!NI
250[-
200~-
~, ~
I00~0
y '
,-,T.. '"L~F'.
....
..
•
~
20#V EMG M'~
vJ¢
A i
#!i . . . . . . .
I
I
340 40 60 80 00 '280 300 360 :380 400 20 FIGURE 1. This combined CMG and EMG study reveals presence of involuntary bladder con but no simultaneous relaxation o] sphincter is seen. During straining (S) partial relaxation of sphiz
drugs and is unrelated to the duration of therapy. This syndrome is one end of the range of well-recognized extrapyramidal side effects of neuroleptic drugs that occurs in up to 15 percent of patients treated with these drugs. ] The incidence of neuroleptic malignant syndrome has been reported to vary from 0.2 percent in one study 2 to 0.5-1,0 percent in another? The clinical signs consist of fever, altered consciousness, rigidity, and autonomic dysfunction. 4 Urinary ineontinenee was reported to be present in 21 percent of cases. ~ Urinary retention has also been reported. 6 The exact pathophysiology of this syndrome is not clear, but it is considered to be a depletion of d o p a m i n e within the central nervous system, affecting both the basal ganglia and the hypothalamus, v The other school of thought believes it to be a direct toxic (hypermetabolic) effect on skeletal muscle. This syndrome has been noted in patients with Parkinson disease when dopamine agonists, levodopa/earbidopa and amantadine were withdrawn. 7,~ Urinary incontinence due to detrusor hyperreflexia is a common finding in patients 'with Parkinson disease. 9 Disturbance of striate muscle component of external sphincter is also well known. Poor relaxation of external sphincter (dyskinesia) can cause poor urinary flow, high residual urine, and urinary retention in a male patient. In neuroleptie ma-
544
lignant syndrome the urodynamic f: similar to that of Parkinson disease. it lends support to the theory of dop~ ciency as the cause of neuroleptic syndrome. 130 East New York, New i~?/i
References 1. Marsden CD, and Jenner P: The pathophysioh pyramidal side-effects of neuroleptie drugs, Psychol (1980). 2. Singh G: The malignant neuroleptie syndrorr with a report of three eases), Indian J Psychiatry 22~ 3. Delay J, Pichot P, and Lemperiere T: L'em] tyrophenones en syehiatrie. Etudes statisqe et psye Sumpos Internazionale Sull L'Haloperidol et Triperi, 1963, p 305. 4. Caroff SN: The neuroleptie malignant syndr Psychiatry 41:79 (1980). 5. Levenson JL: Neuroleptie malignant syndrom~ chiatry 142:1137 (1985). 6. Janieak PG, Bresnahan DB, and Comaty JE: T tie malignant syndrome: a clinical update, Psychiat (1987). 7. Henderson VW, and Wooten GF: Neurolepti syndrome: a pathogenetic role for dopamine receptq Neurology 31:132 (1981). 8. Burke RE, et ah Neuroleptic malignant syndror dopamine-depleting drugs in a patient with Huntinl Neurology 31:1022 (1981). 9. Bradley WE: Neurologic disorders affecting bladder, in Krane RJ, and 8iroky MD (Ed): Clinical ogy, Boston, Little, Brown, 1979, p 245.
UROLOGY / JUNE1991
/ VOLUME XXX V I I ' N U ' ' ~ I ~
~STRA CT--Urinary retention or incontinence is not an inyrequent clinical finding in patients th neuroleptic malignant syndrome. We studied the pathophysiology o] this voiding disorder by ~dynamic testing. It revealed involuntary bladder contraction and rigidity of external sphincter rskinesia). These findings are analogous to those in Parkinson disease patients and support the ~amine deficiency theory as the cause o] neuroleptic malignant syndrome.
lis report presents a study of neurogenic bladr in a patient with neuroleptic malignant synome.
Case Report A sixty-six-year-old white woman, a known ise of chronic paranoid schizophrenia, was adiffed with complaints of paranoia and anxty, vague body pain, and disorientation of e and place of one-week duration. On exination, her pupils were dilated with minii~ reaction to light, and she had cog wheel i~dity of upper limbs. ~Prior to this admission, she had been taking loperidol (Haldol) and benztropine (Cogen0. During hospitalization, benztropine was scontinued and haloperidol was replaced ith perphenazine (Trilafon). Neurologist suprted the diagnosis of organic brain syndrome eondary to antieholinergie etiology. During the first week of hospitalization, the ltient became diaphoretic; taehyeardia develIped and she refused to eat. Increase in her ri~ t y was noticed. On the thirteenth day, she ~iecamefebrile (101.4 °F) and alternating symp~ s of urinary incontinence and retention deeloped. Creatinine phosphokinase (CPK) was [crated (532 U/L), and she had increased ihite blood cell count (13.8). On the basis of !ese findings, a diagnosis of neuroleptic malig-
~
~OLOGY / JUNE 1991 / VOLUME XXXVII, NUMBER 6
nant syndrome was made. Perphenazine was discontinued and she was managed with hydration (I/V fluids). Because of her inability to empty the bladder, indwelling catheter was maintained. Her general condition gradually improved over a period of four days but urinary retention continued. Urodynamic test revealed the following. Bladder capacity was 1,200 cc. Although she experienced lower abdominal discomfort, she failed to interpret it as a desire to void. Involuntary bladder contraction of 72 cm of water occurred; but external sphincter remained rigidly contracted, and she failed to relax it even after repeated commands to void (Fig. 1). She denied any urge to void. She attempted to void by abdominal straining during which the periodic relaxation of the external sphincter was seen and urine was voided in spurts. At the end of voiding she had residual urine of 500 cc. Management consisted of continued indwelling catheter. The indwelling catheter was removed when the generalized rigidity improved and the patient passed the trial of voiding. Comment Neuroleptic malignant syndrome is a rare disorder. It is a serious and potentially lethal adverse reaction to antipsyehotie medication. It occurs after therapeutic doses of neuroleptie 543
S cmH20 Pressure C02 C02CYSTOMETRY
III!NI
250[-
200~-
~, ~
I00~0
y '
,-,T.. '"L~F'.
....
..
•
~
20#V EMG M'~
vJ¢
A i
#!i . . . . . . .
I
I
340 40 60 80 00 '280 300 360 :380 400 20 FIGURE 1. This combined CMG and EMG study reveals presence of involuntary bladder con but no simultaneous relaxation o] sphincter is seen. During straining (S) partial relaxation of sphiz
drugs and is unrelated to the duration of therapy. This syndrome is one end of the range of well-recognized extrapyramidal side effects of neuroleptic drugs that occurs in up to 15 percent of patients treated with these drugs. ] The incidence of neuroleptic malignant syndrome has been reported to vary from 0.2 percent in one study 2 to 0.5-1,0 percent in another? The clinical signs consist of fever, altered consciousness, rigidity, and autonomic dysfunction. 4 Urinary ineontinenee was reported to be present in 21 percent of cases. ~ Urinary retention has also been reported. 6 The exact pathophysiology of this syndrome is not clear, but it is considered to be a depletion of d o p a m i n e within the central nervous system, affecting both the basal ganglia and the hypothalamus, v The other school of thought believes it to be a direct toxic (hypermetabolic) effect on skeletal muscle. This syndrome has been noted in patients with Parkinson disease when dopamine agonists, levodopa/earbidopa and amantadine were withdrawn. 7,~ Urinary incontinence due to detrusor hyperreflexia is a common finding in patients 'with Parkinson disease. 9 Disturbance of striate muscle component of external sphincter is also well known. Poor relaxation of external sphincter (dyskinesia) can cause poor urinary flow, high residual urine, and urinary retention in a male patient. In neuroleptie ma-
544
lignant syndrome the urodynamic f: similar to that of Parkinson disease. it lends support to the theory of dop~ ciency as the cause of neuroleptic syndrome. 130 East New York, New i~?/i
References 1. Marsden CD, and Jenner P: The pathophysioh pyramidal side-effects of neuroleptie drugs, Psychol (1980). 2. Singh G: The malignant neuroleptie syndrorr with a report of three eases), Indian J Psychiatry 22~ 3. Delay J, Pichot P, and Lemperiere T: L'em] tyrophenones en syehiatrie. Etudes statisqe et psye Sumpos Internazionale Sull L'Haloperidol et Triperi, 1963, p 305. 4. Caroff SN: The neuroleptie malignant syndr Psychiatry 41:79 (1980). 5. Levenson JL: Neuroleptie malignant syndrom~ chiatry 142:1137 (1985). 6. Janieak PG, Bresnahan DB, and Comaty JE: T tie malignant syndrome: a clinical update, Psychiat (1987). 7. Henderson VW, and Wooten GF: Neurolepti syndrome: a pathogenetic role for dopamine receptq Neurology 31:132 (1981). 8. Burke RE, et ah Neuroleptic malignant syndror dopamine-depleting drugs in a patient with Huntinl Neurology 31:1022 (1981). 9. Bradley WE: Neurologic disorders affecting bladder, in Krane RJ, and 8iroky MD (Ed): Clinical ogy, Boston, Little, Brown, 1979, p 245.
UROLOGY / JUNE1991
/ VOLUME XXX V I I ' N U ' ' ~ I ~