ANALYSIS OF VOIDING DISORDERS IN PATIENTS

WITH CEREBROVASCULAR ACCIDENTS

Z . KHAN, M .D.P STARER, M .D .W C . YANG, M .D .A. BHOLA, M .D .

From the Department of Urology, Beth Israel Medical Center,New York, New York

TRACT-Urodynamic evaluation was undertaken in 33 patients (15 males and 18 females, ages"'48-90 years) with voiding problems following cerebrovascular accidents . In the majority ofatients (26) cystometry revealed involuntary contractions of the bladder. The critical volume

iiYtioluntary bladder contractions was approximately 200 mL . The majority of patients withal ,cortex and/or internal capsule lesions had uninhibited relaxation of the sphincter during

;1untary bladder contractions, while all of the patients with lesions only in the basal ganglia orlafnus had normal sphincter function . The remaining 7 patients had poor bladder contractions .relation of bladder dysfunction with the area of brain injury was not conclusive, but was sug-tiroe of directions to be taken in future research .

prevalence of stroke in persons over sixty-years of age is about 60 in every 1,000 ; inons over seventy-five years the prevalence isX1,000 persons .' Bladder dysfunction mayt,?following a cerebrovascular accidentA) : 2 Detrusor hyperreflexia occurring fol-iig a CVA has been explained by the loss ofMary control of the reflex arc between theaer and the sacral spinal cord . 3 However,ary retention also occurs in patients whoesuffered from a CVA . In a study by Borrie1 ;i4 22 poststroke patients with urinary in-fluence underwent cystometric studies . Thei9rity of the patients had detrusor hyper-

however 2 patients were reported as?g'in urinary retention .here have been few studies to delineate arologic lesion by correlating computerizedography (CT) scans of the brain with uro-afnic findings. In a previous report by Khan1 .5 of 20 CVA patients, involuntary bladderttactions were documented in 19 patients .e patient had a stable bladder. Abnormali-

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MARCH 1990 , VOLUME XXXV, NUMBER 3

ties of bladder function were seen in patientswith lesions of the frontal area of the brain,while dysfunction of both the bladder and theexternal sphincter were observed in patientswith lesions of the frontoparietal cerebral areaor lesions in the basal ganglia .

In an effort to understand the correlation ofneurologic lesion with bladder dysfunction, wepresent a follow-up report of urodynamic eval-uations and CT scan localization of brain dam-age in patients with urinary symptoms after acerebrovascular accident .

Material and Methods

Thirty-three patients with urinary dysfunc-tion and a previous history of a cerebrovascularaccident underwent urodynamic studies . Acerebrovascular accident was defined as therapid onset of a neurologic deficit, secondary toa vascular lesion, which persisted for longerthan forty-eight hours. There were 15 malesand 18 females, with an age range of forty-eight

26.5

URODYNAMICS

TABLE 1 . Cystometric evaluation of patientsfollowing cerebrovascular accident

Slop loo nmH20

100

200 m1

100

200m1

FIGURE 1 . Diagrammatic representation of uro-dynamic studies . (A) Involuntary bladder contrac-tion (hyperreflexia) : reduced threshold-200 mL ca-pacity; loss of voluntary external sphinctercontraction. (B) Voluntary external sphincter con-traction .

to ninety years and a mean age of seventy-twoyears . Patients underwent urodynamic studiesduring a time period ranging from less than onemonth to twenty-eight years after the cere-brovascular accident . However, only 2 patientswere studied more than one year after the CVA(1 patient at 2 years, the other at 28 years) . Themajority of the patients (28) were studiedwithin three months of the CVA .

Urodynamic evaluation was performed witha DISA four-channel recording unit and 14AI1electromyography (EMG) equipment . Gas cys-tometry (12-F catheter, filling rate = 100 cc!min) was performed simultaneously with nee-dle electromyography of the external analsphincter. To elicit involuntary bladder contrac-

tions, subjects underwent testing in an upposition and with coughing . Detrusor hreflexia was defined as involuntary contraeof the bladder occurring spontaneously orprovocation . Detrusor underactivity wfined as bladder contractions with a pres,less than 60 cm of water with the Madderto a volume of 500 mL . A patient with a nosphincter was able voluntarily to contra'`sphincter during an involuntary detrusor .traction, while a patient with uninhibitlaxation of the sphincter could not contrsphincter during an involuntary detrusortraction .

The brain damage was assessed inddently by one of us (WCY) with a G .E . 80scanner. The CT scan reports and urod)findings were reviewed retrospectively.

Results

Cystometric studies revealed detrusorreflexia in 26 patients and poor bladdertractions (average = 30 cm H 2O) in 7 pa(Table I) . In the patients with detruscflreflexia, a strong (90 cm H 2O) invoh'bladder contraction was produced at areduced threshold (average bladder capa200 mL) . The patients with detrusor instwere studied during a time period ranginless than one month following the ('twenty-eight years after the event (av819 months) . Except for 2 patients, all pwith detrusor hyperreflexia were studiedone year after the stroke . Although podder contractions were documented in 1as late as eight months after the CVAmaining 6 patients with poor bladder c4 .tions were all studied within two , monthsstroke. One of these patients was studied(one and two months after the CVA'showed partial recovery of bladder funetl

Of the 7 patients with poor bladderstions, CT scan revealed combined lesions :frontal lobe and the basal ganglia in 3 pa

(ipsilateral lesions in 1 patient, contralatsions in 1 patient, and both contra- andTeral lesions in 1 patient) (Fig . 2. Table,,patient had a left parietal infarct and 1"`

had a left frontoparietal infarct . i t wastient with the left frontoparietal infarshowed partial recovery of bladder flwhen restudied two months after the CV .remaining 2 patients with poor bladd?Ptractions had a right thalamic hemgt(Figs . 3, 4) and a normal CT scan, rape

UROLOGY . MARCH 1990 1 VO : .GL1E XXx N

CT ScanLocalization

Cystometric StudyDetrusor

Detrusorof Brain Lesion No. Hyperreflexia Underactivity

Cerebral cortex 13 11 2Internal capsule 1 1 0Basal ganglia 3 3 0Thalamus 3 2 1Combined cerebral

cortex/internalcapsule 2 2 0

Combined cerebralcortex/basalganglia 7 3

Combined thalamus/internal capsule 1 1 0

Normal CT scan 3 2 1To'rALs 33 26 7

ns 2 . CT scan reveals presence of left frontal3'i;and right basal ganglion infarct-poor bladderljtraction and coordinated external sphincter.

TABLE It . Localization of brain lesions.1n patients with poor bladder contractions

following cerebrovascular accident

1JFlle 26 patients with detrusor hyperreflexia,vmajority (11) had lesions in the cerebral cor-«'''alone (frontal lobe, 2; temporal lobe, 1 ;(r%ptoparietal, 2 ; temporal-occipital, 1 ; pa-etotemporal, 1 ; multiple areas, 4) (Table I) .M r patients with detrusor hyperreflexia had

lyernent of the internal capsule (2 of theseclients also had lesions in the cerebral cortex, 1~d'- a'thalamic lesion) . Two patients with le-

1 .qs onlin the thalamus had detrusor hyper-'Seven patients with detrusor byper-hadeXia had involvement of the basal ganglia .

cases the basal ganglia alone were in-`'tl'ed, while in 4 cases there were also lesions

the : cerebral cortex (frontoparietal, 2 ; tem-''omparietal, 1 ; multiple areas, 1) . In these 4

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MARCH 1990 ! VOLUME XXXV, NUMBER 3

FIGURE 3 . CT scan reveals presence of right tha-lamic hemorrhage in patient with poorly contract-ing bladder and nonrelaxing external sphincter .

100cmH2O

100

200 ml

FIGURE 4 . Diagrammatic representation of patientwith right thalamic infarct (Fig . 3), in urinary re-tention due to poor bladder contraction and nonre-laxing external sphincter

cases with combined basal ganglia-cortical le-sions, a significant residual urine volume wasnot demonstrated . In the 3 cases in which thebasal ganglia alone were involved, the residualurine ranged from 10 mL-300 mL .

Electromyographic studies of the externalsphincter were conducted in 19 of the patientswith detrusor hyperreflexia (Table III) . The re-maining 7 patients did not tolerate EMG stud-ies . Ten of the patients were unable voluntarilyto contract the sphincter during involuntarybladder contraction (Fig . 1), while 9 patientshad normal sphincters . All of the patients withlesions only in the basal ganglia or thalamushad normal sphincters, while the majority ofpatients with involvement of the cerebral cortexand/or internal capsule had uninhibited relax-ation of the sphincter.

267

Age(Years) Sex CT Scan Findings

77 F Left frontal lobe, rightbasal ganglia

65 F Right frontal lobe,bilateral basal ganglia

2 50 F Left frontal lobe, leftbasal ganglia

64 F Right thalamic hemorrhage88 F Left parietal lobe69 F Left frontoparictal lobe78 F Normal CT scan

2 f35

*EMG studies not performed in 7 patients .

Comment

Detrusor hyperreflexia was the most com-mon cystometric finding in the patients westudied who had urinary complaints after acerebrovascular accident. The majority of thepatients were studied within three months ofthe CVA. This result is not unexpected since de-trusor hyperreflexia occurs when there is dis-ruption of the voluntary control by the cerebralcortex of the brain stem and the sacral spinalreflex arc (S2-S4) . 3 During the bladder's fillingphase, a reflex contraction was provoked at acritical volume of approximately 200 mL . Theresult was a functional reduction in bladder ca-pacity. This finding was observed byLangworthy' in animal experiments . When CTscans of the brain were reviewed, it was foundthat the majority of patients with a cerebral le-sion or an internal capsule lesion had detrusorhyperreflexia . This is similar to the findings ofTsuchida et al .' who concluded that damage tothe frontal lobe or internal capsule results in de-trusor hyperreflexia . Of the 26 patients with de-trusor hyperreflexia, 2 patients had normal CTscans. One of these subjects was found to havebladder outflow obstruction, while the otherhad incomplete relaxation of the externalsphincter during bladder contraction, suggest-ing other causes of involuntary bladder contrac-tion ."

It is more difficult to explain the finding ofpoor bladder contractions in a minority (7 of 33

patients) of our cases. All of these patientsstudied within eight months of the CVA . If .true that the detrusor underactivity seersthese patients will eventually be followeddetrusor h, perreflexia, 2 then it is unclear'some patients persist longer in the underaestate than others . Although the possible eatitions of detrusor underactivity may includedetected spinal cord problems or anotherulated neurologic or urologic abnormality,interest that all 3 patients with involvedreboth the basal ganglia and the frontal lobes})poor bladder contractions .

In addition, of the 7 patients with intary bladder contractions and involvemtithe basal ganglia, 3 patients (2 females, 1had residual urine of 100 mL, due to poor Bder contractions . These 3 patients had ininvolving the basal ganglia alone . By detering the effect of this area of the brain on 'b

der function, we may be able to predict voii

problems following a CVA .The concept of a "cortical inhibitory

acting on a sacral reflex arc" may be ansimplification,' Tang,' in his work with'described "micturition facilitatory and infitort' areas at different levels of the neuralwhich influence the sacral micturitiori rDiencephalic and brain stem areas contrethe micturition reflex include a cerebral intory region, a hypothalamic facilitatory,the mammillary region of the posterior Lz

thalamus, a midbrain inhibitory area locbilaterally in the tegmentum lateral to thetral gray matter at the caudal superior . cofar level, and a pontine facilitatory araized bilaterally in the dorsal tegmentum"isthmus level immediately ventral to the 1angles of the periventricular gray matter,

The basal ganglia are subcortical nUmasses which include the caudate nucleu,putamen, the globus pallidus, and the arm,loid nuclear complex . The corpus strictcomprised of the caudate nucleus, putsand glohus pallidus . In studies of the cat, ;

trical stimulation of the globus pallidus in"inhibition of spontaneous urinary bladder ;

tractions ." In other animal studies„'itfound that stimulation of the amygda'aduced micturition.72 14 The finding of b4hibitory and facilitatory influences by the'on the sacral micturition reflex arc suggescomplexity involved in predicting bladder'function which may occur in the settingstructive or irritative neurologic lesions

UROLOGY r MARCH 1900 1 VOLUME XXXV NC

TABLE III . EMG studies of external sphincter inpatients with detrusor hyperreflexia*

NormalCT Scan

Localization ofBrain Tissue No .

UninhibitedRelaxationof Sphincter

VoluntaryContractionof Sphincter

Cerebral cortex 7 4 3Internal capsule 1 1 0Basal ganglia 3 0 3Thalamus 1 0 1Combined cerebral

cortex/internalcapsule 2 1 1

Combined cerebralcortex/basalganglia 4 4 0

Normal CT scan 1 0 1

TOTALS 19 10 9

role of thalamic and hypothalamic nu-

still unclear. One study by Uvnas 10 indi-,hat vesical motility is profoundly af-

d i,y these nuclei . Poor bladder contraction

flexia. with or without changes in ex-sphincter behavior, may well be due to

in these nuclei . The desire to micturate ispt but voluntary vesical contraction is im-

Our data suggest that basal gangliage may play a role in the development ofy retention after a cerebrovascular acci-In the study by Tsuchida et al ., 7 5 pa-were found to have acontractile bladders

s otnetry: 4 had brain atrophy on CT scanhad a lesion in the putamen. Additional

s would be helpful in clarifying this area .irelate neurologic lesions with bladderfiction, a comprehensive assessment of the

us system is essential . Unfortunately, the,,scan is limited in defining areas of the

such as the brain stem . In addition, it

a be important to evaluate for causes of

ai cord nerve root injury, such as protrudeddisk . 1x .18

rusor areflexia has been described duringInitial phase of a cerebrovascular accident,ed by detrusor hyperreflexia . 2 Indeed, 1patients with an underactive bladder

-,strafed evidence of recovery when re-died two months after the stroke . In cases inh underactivity is temporary, the diagnosisbe missed due to delayed referral for uro-mic investigation . In addition, involun-bladder contractions may be present priorerebral trauma . The finding of detrusor hy-flexia in a majority of elderly stroke pa-may reflect the high prevalence of invol-y contractions in elderly patients inal. An elderly patient with involuntaryr contractions may be continent" 11 buta cerebrovascular accident, the combina-of impaired mobility and involuntary con-on may lead to urinary dysfunction . Blad-

ltmction prior to the CVA was not known inu study. In stroke patients, the contribution

pt~t cognitive impairment and immobility toik?'+1 arv incontinence needs to be considered, asrrdl as neurologic injury." Optimally, a pro-

9tive study could be conducted with CT scand urodvnamic studies obtained at set inter-jt aster the onset of the CVA . Where obtain-

4118 autopsy studies would allow more defini-'e:loealization of brain lesions . In our cases,lilies were performed at varying times . In I

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MARCH 1990 ' Vol UMV XXXV, NUMBER 3

case urodynamic studies were performedtwenty-eight years after the CVA .

When EMG studies of the external sphincterwere done in the patients with detrusor hyper-reflexia, it was found that the majority of pa-tients with cerebral cortical lesions or internalcapsule lesions were unable to contract thesphincter during an involuntary contraction .Patients with lesions in the basal ganglia re-tained control of the external sphincter. This issimilar to the findings of Tsuchida et al .' whoconcluded that damage to the frontal lobe orthe internal capsule results in a hyperreflexicbladder with uninhibited relaxation of thesphincter. The majority of their patients withputaminal lesions (7 of 10 patients) had normalsphincter function . A voluntary contraction ofthe external sphincter during filling of the blad-der is an indication of intact corticospinaltracts . The inability to voluntarily contract theexternal sphincter during an involuntary blad-der contraction is an interesting phenomenon .This reflects the powerful inhibitory effect ofinvoluntary bladder contractions on the motoractivity of the external sphincter . Experimentalwork in this area has been conducted by Yama-moto et al .22

Although definitive conclusions cannot bedrawn from a retrospective review of a limitednumber of patients, the data suggest directionswhich may be taken in future research inurinary problems after cerebrovascular acci-dents .

130 East 18th StreetNew York, New York 10003

(DR . KHAN)

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269

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