Neuromuscular dysfunction of the bladder and urethra

Neuromuscular

Dysfunction

of the Bladder and Urethra

By Gerald W. Friedland and lnder Perkash

A

T LEAST 25 million people in the United States suffer from neuromuscular dysfunction of the bladder and urethra. Since the bladder and urethra are also the targets for many drugs and neuromuscular disorders associated with common diseases, the consequences are even greater than this enormous number of victims would indicate. A hypotonic areflexic bladder occurs in 50% of diabetics over age 50. Since many of them can void only when upright, problems arise if they become bedridden. Patients with benign prostatic hyperplasia may also have a hyperreflexic bladder from cerebrovascular disease. As the population in the western world and particularly in the U.S. ages, more and more patients will enter nursing homes, 50% because of urinary incontinence. Thus, the cost of neuromuscular dysfunction of the bladder and urethra is enormous, not only in terms of direct medical care, but also in lost productivity. During the past decade, dramatic improvement has occurred in our understanding and treatment of neuromuscular dysfunction of the bladder and urethra. This has taken place because of recent research into the pathophysiology of the bladder, information that is now well-documented, and every practicing physician should realize is no longer highly specialized. NEUROANATOMY AND NEUROPHARMACOLOGY

The muscles that are active in voiding and that maintain continence are the detrusor muscle of the fundus of the bladder, the bladder neck muscles, the urethral smooth muscle, the periurethral striated sphincter, and the striated pelvic muscles (Fig. I).’ The detrusor has three intermingled layers, but as it converges on the internal urethral orifice its muscle fibers become organized into three separate layers. The most caudal fibers of the middle circular layer are the most prominent and form the true bladder neck. The bladder neck is complete anteriorly; posteriorly, it fuses with the trigone to form a flat area at the bladder base, the baseplate.’ The whole of the female urethra and the male posterior urethra closely resemble each other. A great deal of smooth muscle extends from the Seminars in Roentgmology,

Vol. XVIII, No. 4 (October).

1983

bladder into the proximal urethra, ending at an indistensible collagenous area that lies transverse to the urethral lumen, the intermuscular incisura, which in men lies opposite the middle of the verumontanum. The periurethral striated sphincter extends from the urogenital diaphragm upward to the intermuscular incisura.’ When the detrusor contracts during voiding, it changes the baseplate to a funnel shape, called the trigonal canal. Several constrictions are visible during voiding: (1) at the bladder neck, (2) at the intermuscular incisura, and (3) at the urogenital diaphragm (Fig. 1). The bladder and posterior urethra are supplied by the parasympathetic nerves, the sympathetic nerves, and the pudendal nerve (Fig. 2). The periurethral striated sphincter and urogenital diaphragm are supplied by all of these nerves (Fig. 3), which is why there is normally perfect synergy between the bladder and the urethra during voiding.2,3 The periurethral striated sphincter relaxes, the bladder neck relaxes, and the detrusor contracts, so voiding occurs through a completely open urethra. Prostaglandins may play an important role in coordinating voiding.” All these peripheral nerves are controlled by the bladder center located in the pons and by complex pathways within the nervous system, with positive and negative feedback loops originating in the cerebral cortex.’ Initiation and termination of voiding are thus under voluntary control. TYPES OF NEUROMUSCULAR

DISORDERS

Patients may have a contractile bladder (Table I) or a noncontractile bladder (Table 2 and From the Department of Radiology and the Spinal Cord Injury Cenier. Palo Alto Veterans Administration Medical Center, Palo Alto, CA. Gerald W. Friedland: Professor of Radiology, Stanford Universit.y Medical School; Siaff Radiologist. Palo Alto Veterans Administration Medical Center. lnder Perkash: The Paralyzed Veterans of America Professor of’ Spinal Cord Injury, Stanford University Medical School and Palo Alto Veterans Administration Medical Center. Address reprint requests to Gerald W. Friedland. M.D., Radiology #I 14. D-219, Palo Alto Veterans Administration Medical Center. 3801 Miranda, Palo Alto, CA 94304. 0 I983 by Grune & Stratton, Inc. 0037-/98X/83/1804-0005 $02.00/O 2%

256

FRIEDLAND

FILLINGPHASE ILateralView] DETRUSOR

AND PERKASH

VOIOING [LateralView]

_ e

BLADDER NECK k SMOOTH MUSCLE

TRIGONAL CANAL

BLADDER NECK ’ VERUMONTAN

INTERMUSCULAR

INCISURA STRIATED SPHINCTER

Fig. 1.

Schematic

UROGENITAL

illustration

DIAPHRAGM

of the muscles

of the bladder

and urethra

in the male. (After

Hutch.‘)

PARASYMPATHETIC [Cholinergic] NERVE SUPPLY INTRAMURAL

SACRAL SPINAL CORD

NERVE ENDINGS PRODUCE ACETYLCHOLINE WHICH CONTRACTSDETRUSOR DURING VOIDING

ANTERIOR GRAY COLUMNS S2-4

A SYMPATHETIC NERVESUPPLY PUOENOAL NERVE MAIN NERVk SUPPLY TO PERIURETHRAL STRIATED SPHINCTER AND UROGENITAL DIAPHRAGM

Fig. 2. Peripheral Pudendal nerve. (After

nerve supply Perkash.‘)

to the bladder

and urethra.

(A) Parasympathetic

nerves.

(8) Sympathetic

nerves.

(Cl

NEUROMUSCULAR

257

DYSFUNCTION

SACRUM

0

111 (YADRENERGIC

Fig. 3. distribution a-adrenergic

Schematic illustration of the relative of cholinergic, @-adrenergic, and receptors. (Adapted from Perkash.3)

Fig. 4). Depending on the severity and level of the lesion, they may also have detrusor-sphincter dyssynergia (Fig. 5),6 detrusor-bladder neck dyssynergia (Fig. 6),’ or detrusor hyperreflexia (Table 1). Patients with the central cord syndrome usually have a temporary disturbance of bladder function (Fig. 7).

nisms for which are described in Table 3.’ Such patients present clinically with sweating, headache, hypertension, and bradycardia; patients over age 50 may develop cerebral hemorrhage. Any patient who may have autonomic dysreflexia should always receive an tu-adrenergic blocker before a voiding cystourethrogram is performed.

Autonomic Dysrejexia Patients with detrusor-bladder neck and detrusor-sphincter dyssynergia (tetraplegic patients and paraplegic patients with lesions above TS) manifest autonomic dysreflexia, mechaTable

1. Contractile Dysfuncuon

Type Uninhibited

Incontinent

Bladder Common

be-

Suprapontine

cause

voiding

Cerebral

reflex

triggered

before

bladder

Early

multiple

scle-

Disorders

Figure 8 lists the drugs that contract the detrusor, bladder neck, or urethra through their effects on the peripheral autonomic nervous system; Fig. 9 lists the drugs that relax these same areas through similar mechanisms. We wish to emphasize that many hospitalized patients receive many different drugs, eg, to induce sleep, to alleviate pain, or to relieve anxiety. If such drugs are given to patients with

rosis voluntary

voiding Reflex

athero-

sclerosis

full Also

Causes

Drug-Induced

Voiding cord

via spinal reflex

No voluntary

Neoplasm

of brain

Pernicious

anemia

Subpontine Cord

con-

trol

Table 2. Common Causes of Poorly Contractile (Hyporeflexic) or Noncontractile (Areflexic) Bladder -.---Lower

injury

Neoplasm Extradural Disc

Neuron

Degenerative

equlna

Herniated

abscess

Acute

lesion ar-

Sensory

and

Motor

disc transverse

Extensive

collapse

Lesion: lesions

Guillain-Barr6

thritis Vertebral

Motor Cauda

myelitts syndrome

rectal

carcinoma

Abdominoperineal

resectton

Perivesical

(pelwc

surgery

or Injury1

Intact

(Motor

Nerves

fibrosis

Syringomyelia Motor

Suprapontine Extensive

brain

brain

neoplasm Advanced

multiple

contracts

involuntarily (volume 100

ml)

under

Cord

InfarctIon

OverdistensIon Sensory

sclerosis Bladder

or herniated

to Bladder)

disc

lesion

Diabetes

Cervical

cord

lesion

Tabes

Irritated

reflex

(by Infection

bladder or

(Antenor

Cord

Syndrome)

Areflexia

loss

Suprapontine

catheter)

Sensory

neoplasm,

Poliomyellt6

jury Extensive

Hyperreflexic

Paralysis, Injury,

in-

mellitus

Alcoholic

neuropathy

Untreated

chrontc

SIO”

overdistension

from

upper

motor --__

le-

258

FRIEDLAND

AND

PERKASH

VOIOSBY CRiDEOR VALSALVAMANEUVER

S2-4

IC FLOOR ALLOWS

PRESSURE AND FLOW INSUFFICIENT TO DISTEND MEMBRANOUS URETHA

borderline abnormal bladder function, or to elderly patients, or to those with dementia, the mental state of the patient may be so affected that voiding becomes impossible. These drugs may also affect the bladder directly.

Spinal Cord Injury;

The Elderly Incontinent

Spinal cord injury patients and the elderly incontinent are two groups of patients who do not always receive sufficient attention.’ There are between 500,000 and 1.5 million survivors of

\

Fig. 4. Schematic illustration lower motor neuron lesion.

of

spinal cord injury in the U.S., and 20,000 new cases per yr.” Of these, 66% are age 30 or younger. The peak incidence occurs at age 19; almost all such patients are males, usually injured in automobile or diving accidents.” The prognosis for such patients was once bad, but they can now lead virtually normal lives and can even father children. The elderly incontinent are likewise a major growing problem. Table 4 lists the common causes of incontinence in the elderly.‘* Chronic psychogenic polydypsia is a frequently overSITEOFLESION KEY

q

POSSIBLESITESOF LESION-ANYWHERE BETWEENPONSAND CONUS

NEUROMUSCULAR DYSFUNCTION

(Oetrurar - SphinctwDysryntrgia)

IO1OTHER FINOINIiS (1) ELEVATED BLADDER HVPERTROPHIEO

?

/

&I3

WIDE BLAODER

(4) PROMINENT VERUMONTANUM REFLUX OF URINE

Fig. 5. Schematic sphincter dyssynergia.

illustration

of

detruaor-

F

CONUS

REFLUX OF URINE INTO PROSTATIC DUCTS (occasionally)

NEUROMUSCULAR

DYSFUNCTION

259

KEY

. ,

a

;'%$L;SITES

-

CORDABOVETS CONUS(Sympathetic) NervesUnopposed)

EFFECT OFu ADRENEAGIC BLOCKERS IPhetiolrmine or Phenoxybenzrminel

NEUROMUSCULAR GYSFUNCTION [Oelrusor-Wadder Neck Oyssynergial

bT5

111 WHENDETRUSOR CONTRACTS

ELEVATED BLADDER PRESSURE

Fig. 6. Schematic of detrusor-bladder synergia.

'?I BLADDERNECK RILAXES

illustration neck dys-

8 NO VOIDING ORONLY DRIBBLES

looked cause of incontinence in the elderly and in psychiatric patients.13 DANGERS OF CATHETERIZATION

Many medical centers currently treat patients with neuromuscular disorders of the bladder and urethra with intermittent catheterization. Although this is important for the acute stage and is safer than prolonged use of an indwelling catheter, it does give rise to many complications.‘4-‘7 A EARLY

EDEMAAND HEMORRHAGE

,3 VOIDS

recent study suggests that as many as 56,000 people die in the U.S. each year as a result of catheterization,‘x which is why we have come to regard it as an invasive procedure. We are now able to render patients suffering from detrusor-sphincter dyssynergia catheterfree by performing transurethral sphincterotomy through the periurethral striated sphincter and bladder neck.6.‘7 Although some patients with detrusor-bladder neck dyssynergia respond to oral phenoxybenzamine (an a-adrenergic blocker),19 most require a new kind of sphincterotomy devised by one of us (I.P.), in which the bladder neck is incised so deeply that it blocks the n-adrenergic response almost completely.’ Thus, we can now successfully manage two of the most Table 3. Autonomic

BLADDERFIBERS INITIALLYINVOLVEDBLADDERDYSFUNCTION.

1.

Detrusor-bladder relax

2.

LATER

Dysreflexia: neck

when

Bladder

detrusor

neck

Sequence

dyssynergia

(bladder

of Events neck

fails

to

contracts1

forced

open

against

fibers

overstimulated

resistance

during

void-

w

EDEMAANDHEMORRHAGE SUBSIDE

3.

cr-Adrenergic

4.

Excessive

noradrenalin

5.

Peripheral

vasoconstriction

6.

In lesions

below

does

rise

7.

BLADDERFIBERS RECOVER-BLADDER REGAINSNORMAL FUNCTION. Schematic

illustration

of the central

In lesions splanchnic

8.

above

T5 (above

veins

Baroreceptors

and

splanchnic

do not

in carotid

sweating veins

greater

reflexly

dilate:

splanchnic

dilate;

BP rises

sinus

stimulated.

BP

nerve), causing

brady-

cardia 9.

Fig. 7. drome.

not

T5.

secretion

cord

syn-

Decreased rises

cardiac

considerably

output

insuffuent

to lower

BP, which -

-.-__

260

FRIEDLAND

AND PERKASH

Cholinergic drugs: delrusor contracts. Acetylcholine, Bethanecol. Methacholine. Nicotme

Drugs which increase bladder neck and urethral pressure: u Adrenergic Phenylephrine, Ephedrine, lmipramine Fig. 8. Drugs that contract the detrusor, the bladder neck, or the urethra through their effects on the peripheral autonomic nervous system. (After Perkash.‘)

Drugs whi& increase urethral pressure: p Blockers - Propanalol

serious conditions in patients with neuromuscular dysfunction of the bladder and urethra, catheter complications and elevated blood pressure. URODYNAMIC

STUDIES

We perform urodynamic studies simultaneously with either a radiographic or a sonographic voiding cystourethrogram. These include the following tests performed simultaneously: (1) measurement of bladder pressure during filling and during voiding; (2) measurement of urine flow rate during voiding; (3) measurement of urethral pressure when the patient is and is not voiding; (4) electromyography of the periurethral striated sphincter. Screening Tests. In patients in whom a neuromuscular dysfunction of bladder and urethra is suspected, and in elderly patients with urinary incontinence, the following tests and procedures are available.

(1) Observation of voiding. This simple recourse helps to determine the flow rate. Most people can empty the bladder in about 15-20 set; if it requires more than 30 set, a problem exists. (2) Determination of residual urine. Catheterization is no longer necessary for this purpose; transabdominal ultrasound can perform the same task. (3) Uroflowmeter and chart recorder studies, if available, The urine flow rate can be monitored directly, which is better than visual observation. The patient should be well hydrated beforehand because the results are difficult to interpret if the volume of urine voided is less than 150 ml. The normal maximum flow rates are as follows: For men under 40 yr, over 22 ml/set; 40-60 yr, over 18 ml/set; past 60 yr, over 13 ml/set. For women under 50 yr, over 25 ml/set; beyond 50 yr, over 18 ml/sec.20~2’ (4) A new method pioneered in our institution

Orupswhich roduco bladdercontr~ctlllly and raayloadto urlntrv ratsllllon: Anticholinergics - Propantheline. 6 - Tubocurarine, Aeserpine. Guanethedine, Phenothiazine. Antihistaminics.

-

Drugsrhlch lowor bladdernook and urathral prarruraa: n Blockers - Phentolamine. Phenoxybenzamine. Prazocin HCL Fig. 9. Drugs that relax the detrusor, the bladder neck, or the urethra through their effects on the peripheral autonomic nervous system. IAfter Perkash.‘)

Orup: which lower urethral prossure: 0-Stimulants Isoproterenol. Progesterone

NEUROMUSCULAR

Table 4. Common

A. Neurogenic

261

DYSFUNCTION

Causes of Urinary in the Elderly

Incontinence

(see Tables 1 and 2)

B. Nonneurogenic Chronic psychogenic polydypsia Drugs: phenothlazines, diazepam, chlorodiazepoxide. furosemlde, lithium salts, phenytoln sodium, reserp~ne Medical diseases: renal insufficiency, diabetes mellItUS Obstruction (false incontinence, overflow): benign prostatIc hyperplasia, prostatic carcinoma, urethral stricture, impacted stool pressing on urethra Irritation of bladder: neoplasm, stone, chronic interstitial cystitis, radiation cystitis Stress inconunence, or urethral diverticulum I” women Postoperative: prostatectomy (damaged periurethral striated sphincter)

involves the use of transrectal real time gray scale ultrasonography with a linear array transducer.” This examination can determine whether prostate or seminal vesicle disease is present, the state of the bladder neck and urethra, and completeness of bladder emptying. (5) A complete history, physical examination, urinalysis, routine blood chemistry studies, and neurologic examination should never be omitted. A neuro-urologic examination should also be obtained; it includes testing anal tone, anal reflexes, voluntary control of the anal sphincter, and the bulbocavernosus reflex. If the screening tests show dysfunction or if the patient is tetraplegic or paraplegic, the next step is the use of invasive tests to define exactly what the problem is. These tests should be used only under these circumstances. They involve urodynamic studies performed simultanesouly with either a radiographic or a sonographic voiding cystourethrogram. Drug Studies. During the combined urodynamic-ultrasonographic study, drug studies are performed on selected patients. Those with uninhibited contractions or a hyperreflexic bladder receive an anticholinergic drug such as propantheline or oxybutynin; if the contractions decrease or disappear, the patient is then treated with that drug. If none of the tests reveal whether the patient has a denervated bladder, bethanecol is administered.12 Phentolamine is given intravenously to patients with detrusor-bladder neck

Fig. 10. Voiding cystourethrogram. ron lesion (compare with Fig. 4).

Lower

motor

neu-

dyssynergia, and to patients with benign prostatic hyperplasia; in the latter, voiding improves in about 20%. If phentolamine is effective, the patient is subsequently treated with oral phenoxybenzamine.” If there is suspicion that a drug is causing neuromuscular dysfunction of the bladder or urethra, the above studies are performed with and without the suspected drugs, so that the offending pharmaceutical is discovered by process of elimination.

Fig. 11. Voiding cystourethrogram. sphincter dyssynergia (compare with Fig. 5).

Detrusor-

262

FRIEDLAND

AND PERKASH

Fig. 12. Voiding cystourethrogram. sor-bladder neck and detrusor-sphincter synergia (compare with Fig. 6).

Interpretation

of Urodynamic Studies

Perkash” pioneered the Electromyography. procedure in which the needle is inserted in the periurethral striated sphincter rather than the perianal sphincter, as had previously been done. This enabled him to detect 20% more cases of neuromuscular dysfunction of the bladder and urethra than previously. A normal person at rest and not voiding will have moderate electrical activity in the periurethral striated sphincter. On bearing down, the periurethral striated sphincter is tightened, and electrical activity is increased. This indicates that all the pathways from the frontal lobes to the periurethral striated sphincter must be intact. If there is no increase in electrical activity, neuromuscular dysfunction exists. The patient is then asked to void. In the normal case, all the electrical activity will cease, as the sphincter is completely relaxed. If electrical activity does not stop, or if it increases during the voiding attempt, then the patient has detrusor-sphincter dyssynergia. If the patient has a narrowing in the posterior urethra on the voiding cystourethrogram but the electrical activity ceases when voiding occurs, then the narrowing is due to a stricture or, in older patients, to benign prostatic hyperplasia. A patient with a lower motor neuron lesion will have no electrical activity at any time. Cystometrogram. During normal voiding, the bladder pressure will not usually exceed 60 cm water. However, with bladder outlet obstruction due either to dyssynergia, an enlarged prostate, or stricture, bladder pressure will be higher. Our data suggest that if sustained bladder pressure greater than 70 cm water is present, the patient may develop vesicoureteral reflux.

Detrudys-

Urethral pressure. The main functional reasons for high urethral pressures are detrusorbladder neck dyssynergia or detrusor-sphincter dyssynergia. Electromyography will show whether detrusor-sphincter dyssynergia is present. If the urethral pressure falls dramatically with intravenous phentolamine, the patient has detrusor-bladder neck dyssynergia. Our studies

Detrusor-sphincter dyssynergia, treated elseFig. 13. where by intermittent catheterization. Bilateral vesicoureteral reflux with intrarenal reflux on left, which could lead to chronic reflux nephropathy.=

NEUROMUSCULAR

263

DYSFUNCTION

show that with detrusor-sphincter dyssnergia, the urethral pressure falls to some degree but not dramatically, because the periurethral striated sphincter has some a-adrenergic receptors. Radiologic voiding cystourethrogram. To make sense of the voiding cystourethrogram, the radiologist must have urodynamic data available, and be able to understand their significance. The findings on the voiding cystourethrogram are predictably the result of the changes in anatomy and function wrought on the urinary tract by neuromuscular dysfunction of the bladder and urethra (Figs. 4 to 6 and 10 to 12). The examination can also show the presence of bladder trabeculation and vesicoureteral reflux,24 although neither is common now. Both are related to voiding against an obstruction (Fig. 13). The data from our urodynamic studies suggest that vesicoureteral reflux occurs when there is sustained bladder pressure greater than 70 cm water. Vesicoureteral reflux and bladder trabeculation can be prevented by appropriate medical or surgical treatment early in the course of the disease. Even a “pine tree” or “Christmas tree” bladder deformity will disappear with appropriate treatment (Fig. 14). Following successful medical or surgical therapy, a narrowed bladder neck or posterior urethra may regain normal caliber or may even become dilated. Transrectal sonographic voiding cystoureRecently, a linear array transducer throgram. that can be inserted into the rectum has become available, enabling the bladder and urethra to be visualized at rest and during voiding (Fig. 15). We monitor patients with this transducer continuously throughout urodynamic studies, and have in every case obtained just as good an image of the urethra as that available from the radiologic voiding cystourethrogram.2’ The sonographic voiding cystourethrogram has many other advantages. The surrounding soft tissue can be visualized, enabling us to detect benign prostatic hyperplasia, carcinoma, or prostatic calculi that are invisible radiologically. These may be responsible for recurrent Proteus urinary infections. We can also see the seminal vesicles and, to our surprise, have found that patients receiving phenoxybenzamine have very large seminal vesicles (Fig. 16). The seminal vesicles contract because their muscles have

a-adrenergic receptors. When these are blocked by phenoxybenzamine, the vesicles become large, a discovery that might not have been made without transrectal sonography. This explains why phenoxybenzamine may render young men sterile.25 Transrectal sonography has also revealed that as the bladder is being emptied, the holes of the catheter may become stuck in the mucosa, thus preventing the bladder from completely emptying. By moving the catheter tip under sono-

(A) Pine tree Fig. 14. resident’s aide-memoire) sphincterotomy.

or Christmas tree bladder which disappeared (6)

(with after

264

graphic control, we have been able to obtain a more accurate residual volume. Furthermore, catheters may irritate reflex bladders, causing them to become hyperreflexic. Patients receiving intermittent catheterization may have a small

FRIEDLAND

AND PERKASH

residual volume, but when the catheterization is stopped they may develop retention, as the bladder is no longer being irritated by the catheter. Transrectal sonography has also permitted an accurate measurement of the length of the male

265

NEUROMUSCULARDYSFUNCTION

Fig. 16. Transrectal gray scale ultrasonogram showing seminal phenoxybenzamine. (6) Large seminal vesicles in patient receiving cm. Both sonograms were taken at the same mag&ication.

urethra. We found it to be much shorter than commonly believed, which explains why the catheter is sometimes pushed too deep into the bladder. For all these reasons we have found transrectal real time gray scale sonography to be an ideal screening tool for detecting neuromuscular dysfunction of the bladder and urethra, and for determining the reasons for incontinence in elderly men. We routinely use it for these purposes. Transrectal sonography involves no radiation, which has long been a concern when performing radiologic voiding cystourethrograms on young men. We have also been able to reduce radiation by cutting back the frequency of intravenous urogram in patients with neuromuscular dysfunction of the bladder and urethra from once yearly (recommended nationally) to once every 3-5 yr, because fewer problems now arise in the upper urinary tract than formerly. The advent of all these new techniques and treatments has meant a marked improvement in the prognosis of these patients. We can now keep

vesicles (arrowheads). (A) Normal in patient not receiving phenoxybenzamine. Markers on right hand edge indicate

most elderly patients continent and catheterfree, and in younger patients we can eliminate catheters, reduce blood pressure problems, and control upper urinary tract complications (hydronephrosis, chronic reflux pyelonephritis, infection stones, and renal failure). For these reasons, every radiologist and urologist should strive to make these new advances available to as many patients as possible. REFERENCES I. Hutch JA: Anatomy and Physiology of the Trigone, Bladder and Urethra. New York: Appleton-Century-Crofts, 1972. pp. 1066122 2. El-Badawi A, Schenk EA: A new theory of the tnnervation of bladder musculature. Part 4. Innervation of the vesicourethral junction and external urethral sphincter. J Ural 1974:l I1:613-615 3. Perkash I: Management of neurogenic dysfunction of the bladder and bowel. In: Kottke FJ, Stillwell CK, Lehman JF (eds): Krusen’s Handbook of Physical Medicine and Rehabilitation (ed 3). Philadelphia: Saunders. 1982;724745 4. Ghoneim MA, Fretin influence of vesical distension

JA, Ganon DJ, et al: The on the urethral resistance to

FRIEDLAND

266

flow:

A

possible

role

for

prostaglandins?

J Ural

1976; 116:739-743

5. Bradley WE, Rockwold CL, Timm GW, et al: Neurology of micturition. J Ural 1976;115:48 I-486 6. Perkash 1: Detrusor-sphincter dyssynergia and dyssynergic responses: Recognition and rationale for early modified transurethral sphincterotomy in complete spinal cord injury lesions. / Ural 1978;120:469~74 I. Perkash I: Pressure response during cystomanometry in spinal injury patients complicated with detrusor-sphincter dyssynergia. JUrol 1979; 12 1:778-782 8. Naftchi NE, Denemy M, Lowman EW, et al: Hypertensive crises in quadraplegic patients: Changes in cardiac output, blood volume, serum dopamine hydroxylase activity, and arterial prostaglandin PGE,. Circulation 1978;57:336341

9. Perkash I: Hearing Before the Subcommittee on Hospitals and Health Care of the Committee on Veterans’ Affairs, US House of Representatives, 97th Cong, 2d sess. Washington DC: US Government Printing Office, 1982; Serial 9772:27-28

10. McKnew L: ibid, p 27 11. Schuman SH, Pelz DC, Erhlich NJ, et al: Young male drivers. Impulse expression, accidents and violation. JAMA 1967;200:1026-1030

12. Keegan CT, McNichols DW: The evaluation and treatment of urinary incontinence in the elderly. Surg Clin North Am 1982;62:261-274 13. Blum A, Friedland GW: Urinary tract abnormalities due to chronic psychogenic polydipsia. Am J Psychiatry 1983;140:915-916

14. Perkash I: Detrusor-sphincter

dyssnergia and detru-

AND

PERKASH

sor hyperreflexia leading to hydronephrosis during intermittent catheterization. J Ural 1978;120:640-642 15. Perkash I: Intermittent catheterization failure and an approach to bladder rehabilitation in spinal cord injury patients. Arch Phys Med Rehabil 1978;59:9-19 16. Rhame F, Perkash I: Urinary tract infections occurring in recently injured spinal cord injury patients on intermittent catheterization. J Ural 1979;122:669-673 17. Perkash I: Urodynamic findings, procedure and results for decatheterization of long-term indwelling drainage in 50 spinal injury patients. J Ural 1980;124:249-253 18. Platt R, Polk F, Murdock B, et al: Mortality associated with nosocomial urinary tract infections. N Engl J Med 1982;307:637-642 19. McGuire EJ, Wagner FM, Weiss RM: Treatment of autonomic dysreflexia with phenoxybenzamine. J Ural 1976;l I5:53-55 20. Drach GW, Ignatoff J, Langton T: Peak urinary flowrate. Observations in female subjects and comparison to male subjects. J Urol 1979;122:215-219 21. Siroky MB, Oleson CA, Krane RJ: The flowrate nomogram. I. Development. J Ural 1979; I22:665-668 22. Shapeero LG, Friedland GW, Perkash I: Transrectal sonographic voiding cystourethrography: Studies in neuromuscular dysfunction. AJR 1983;141:83-90 23. Perkash I: Urodynamic evaluation: Periurethral striated EMG versus perianal striated EMG. Paraplegia 1980;18:275-280 24. Hodson CJ, Cotran RS: Reflux nephropathy. Hosp Pratt 1982;26:133-156 25. Kedia KR, Persky L: Effect of phenoxybenzamine (Dibenzyline) on sexual function in man. Urology 1981;18:620-622