- •Preface and Acknowledgments
- •Contents
- •Contributors
- •1: Embryology for Urologists
- •Introduction
- •Renal Development
- •Pronephros
- •Mesonephros
- •Metanephros
- •Development of the Collecting System
- •Critical Steps in Further Development
- •Anomalies of the Kidney
- •Renal Agenesis
- •Renal Aplasia
- •Renal Hypoplasia
- •Renal Ectopia
- •Renal Fusion
- •Ureteral Development
- •Anomalies of Origin
- •Anomalies of Number
- •Incomplete Ureteral Duplication
- •Complete Ureteral Duplication
- •Ureteral Ectopia
- •Embryology of Ectopia
- •Clinical Correlation
- •Location of Ectopic Ureteral Orifices – Male (in Descending Order According to Incidence)
- •Symptoms
- •Ureteroceles
- •Congenital Ureteral Obstruction
- •Pipestem Ureter
- •Megaureter-Megacystis Syndrome
- •Prune Belly Syndrome
- •Vascular Ureteral Obstructions
- •Division of the Urogenital Sinus
- •Bladder Development
- •Urachal Anomalies
- •Cloacal Duct Anomalies
- •Other Bladder Anomalies
- •Bladder Diverticula
- •Bladder Extrophy
- •Gonadal Development
- •Testicular Differentiation
- •Ovarian Differentiation
- •Gonadal Anomalies
- •Genital Duct System
- •Disorders of Testicular Function
- •Female Ductal Development
- •Prostatic Urethral Valves
- •Gonadal Duct Anomalies
- •External Genital Development
- •Male External Genital Development
- •Female External Genital Development
- •Anomalies of the External Genitalia
- •References
- •2: Gross and Laparoscopic Anatomy of the Upper Urinary Tract and Retroperitoneum
- •Overview
- •The Kidneys
- •The Renal Vasculature
- •The Renal Collecting System
- •The Ureters
- •Retroperitoneal Lymphatics
- •Retroperitoneal Nerves
- •The Adrenal Glands
- •References
- •3: Gross and Laparoscopic Anatomy of the Lower Urinary Tract and Pelvis
- •Introduction
- •Female Pelvis
- •Male Pelvis
- •Pelvic Floor
- •Urinary Bladder
- •Urethra
- •Male Urethra
- •Female Urethra
- •Sphincter Mechanisms
- •The Bladder Neck Component
- •The Urethral Wall Component
- •The External Urethral Sphincter
- •Summary
- •References
- •4: Anatomy of the Male Reproductive System
- •Testis and Scrotum
- •Spermatogenesis
- •Hormonal Regulation of Spermatogenesis
- •Genetic Regulation of Spermatogenesis
- •Epididymis and Ductus Deferens
- •Accessory Sex Glands
- •Prostate
- •Seminal Vesicles
- •Bulbourethral Glands
- •Penis
- •Erection and Ejaculation
- •References
- •5: Imaging of the Upper Tracts
- •Anatomy of the Upper Tracts and Introduction to Imaging Modalities
- •Introduction
- •Renal Upper Tract Basic Anatomy
- •Modalities Used for Imaging the Upper Tracts
- •Ultrasound
- •Radiation Issues
- •Contrast Issues
- •Renal and Upper Tract Tumors
- •Benign Renal Tumors
- •Transitional Cell Carcinoma
- •Renal Mass Biopsy
- •Renal Stone Disease
- •Ultrasound
- •Plain Radiographs and IVU
- •Renal Cystic Disease
- •Benign Renal Cysts
- •Hereditary Renal Cystic Disease
- •Complex Renal Cysts
- •Renal Trauma
- •References
- •Introduction
- •Pathophysiology
- •Susceptibility and Resistance
- •Epidemiological Breakpoints
- •Clinical Breakpoints
- •Pharmacodynamic Parameters
- •Pharmacokinetic Parameters
- •Fosfomycin
- •Nitrofurantoin
- •Pivmecillinam
- •b-Lactam-Antibiotics
- •Penicillins
- •Cephalosporins
- •Carbapenems
- •Aminoglycosides
- •Fluoroquinolones
- •Trimethoprim, Cotrimoxazole
- •Glycopeptides
- •Linezolid
- •Conclusion
- •References
- •7: An Overview of Renal Physiology
- •Introduction
- •Body Fluid Compartments
- •Regulation of Potassium Balance
- •Regulation of Acid–Base Balance
- •Diuretics
- •Suggested Reading
- •8: Ureteral Physiology and Pharmacology
- •Ureteral Anatomy
- •Modulation of Peristalsis
- •Ureteral Pharmacology
- •Conclusion
- •References
- •Introduction
- •Afferent Signaling Pathways
- •Efferent Signaling
- •Parasympathetic Nerves
- •Sympathetic Nerves
- •Vesico-Spinal-Vesical Micturition Reflex
- •Peripheral Targets
- •Afferent Signaling Mechanisms
- •Urothelium
- •Myocytes
- •Cholinergic Receptors
- •Muscarinic Receptors
- •Nicotinic Receptors
- •Adrenergic Receptors (ARs)
- •a-Adrenoceptors
- •b-Adrenoceptors
- •Transient Receptor Potential (TRP) Receptors
- •Phosphodiesterases (PDEs)
- •CNS Targets
- •Opioid Receptors
- •Serotonin (5-HT) Mechanisms
- •g-Amino Butyric Acid (GABA) Mechanisms
- •Gabapentin
- •Neurokinin and Neurokinin Receptors
- •Summary
- •References
- •10: Pharmacology of Sexual Function
- •Introduction
- •Sexual Desire/Arousal
- •Endocrinology
- •Steroids in the Male
- •Steroids in the Female
- •Neurohormones
- •Neurotransmitters
- •Dopamine
- •Serotonin
- •Pharmacological Strategies
- •CNS Drugs
- •Enzyme-inducing Antiepileptic Drugs
- •Erectile Function
- •Ejaculatory Function
- •Premature Ejaculation
- •Abnormal Ejaculation
- •Conclusions
- •References
- •Epidemiology
- •Calcium-Based Urolithiasis
- •Uric Acid Urolithiasis
- •Infectious Urolithiasis
- •Cystine-Based Urolithiasis
- •Aims
- •Who Deserves Metabolic Evaluation?
- •Metabolic Workup for Stone Producers
- •Medical History and Physical Examination
- •Stone Analysis
- •Serum Chemistry
- •Urine Evaluation
- •Urine Cultures
- •Urinalysis
- •Twenty-Four Hour Urine Collections
- •Radiologic Imaging
- •Medical Management
- •Conservative Management
- •Increased Fluid Intake
- •Citrus Juices
- •Dietary Restrictions
- •Restricted Oxalate Diet
- •Conservative Measures
- •Selective Medical Therapy
- •Absorptive Hypercalciuria
- •Thiazide
- •Orthophosphate
- •Renal Hypercalciuria
- •Primary Hyperparathyroidism
- •Hyperuricosuric Calcium Oxalate Nephrolithiasis
- •Enteric Hyperoxaluria
- •Hypocitraturic Calcium Oxalate Nephrolithiasis
- •Distal Renal Tubular Acidosis
- •Chronic Diarrheal States
- •Thiazide-Induced Hypocitraturia
- •Idiopathic Hypocitraturic Calcium Oxalate Nephrolithiasis
- •Hypomagnesiuric Calcium Nephrolithiasis
- •Gouty Diathesis
- •Cystinuria
- •Infection Lithiasis
- •Summary
- •References
- •12: Molecular Biology for Urologists
- •Introduction
- •Inherited Changes in Cancer Cells
- •VEGR and Cell Signaling
- •Targeting mTOR
- •Conclusion
- •References
- •13: Chemotherapeutic Agents for Urologic Oncology
- •Introduction
- •Bladder Cancer
- •Muscle Invasive Bladder Cancer
- •Metastatic Bladder Cancer
- •Conclusion
- •Prostate Cancer
- •Other Chemotherapeutic Drugs or Combinations for Treating HRPC
- •Conclusion
- •Renal Cell Carcinoma
- •Chemotherapy
- •Immunotherapy
- •Angiogenesis Inhibitor Drugs
- •Conclusion
- •Testicular Cancer
- •Stage I Seminoma
- •Stage I non-seminomatous Germ Cell Tumours (NSGCT)
- •Metastatic Germ Cell Tumours
- •Low-Volume Metastatic Disease (Stage II A/B)
- •Advanced Metastatic Disease
- •Salvage Chemotherapy for Relapsed or Refractory Disease
- •Conclusion
- •Penile Cancer
- •Side Effects of Chemotherapy
- •Conclusion
- •References
- •14: Tumor and Transplant Immunology
- •Antibodies
- •Cytotoxic and T-helper Cells
- •Immunosuppression
- •Induction Therapy
- •Maintenance Therapy
- •Rejection
- •Posttransplant Lymphoproliferative Disease
- •Summary
- •References
- •15: Pathophysiology of Renal Obstruction
- •Causes of Renal Obstruction
- •Effects on Prenatal Development
- •Prenatal Hydronephrosis
- •Spectrum of Renal Abnormalities
- •Renal Functional Changes
- •Renal Growth/Counterbalance
- •Vascular Changes
- •Inflammatory Mediators
- •Glomerular Development Changes
- •Mechanical Stretch of Renal Tubules
- •Unilateral Versus Bilateral
- •Limitations of Animal Models
- •Future Research
- •Issues in Patient Management
- •Diagnostic Imaging
- •Ultrasound
- •Intravenous Urography
- •Antegrade Urography and the Whitaker Test
- •Nuclear Renography
- •Computed Tomography
- •Magnetic Resonance Urography
- •Hypertension
- •Postobstructive Diuresis
- •References
- •Introduction
- •The Normal Lower Urinary Tract
- •Anatomy
- •Storage Function
- •Voiding Function
- •Neural Control
- •Symptoms
- •Flow Rate and Post-void Residual
- •Voiding Cystometry
- •Male
- •Female
- •Neurourology
- •Conclusions
- •References
- •17: Urologic Endocrinology
- •The Testis
- •Normal Androgen Metabolism
- •Epidemiological Aspects
- •Prostate
- •Brain
- •Muscle Mass and Adipose Tissue
- •Bones
- •Ematopoiesis
- •Metabolism
- •Cardiovascular System
- •Clinical Assessment
- •Biochemical Assessment
- •Treatment Modalities
- •Oral Preparations
- •Parenteral Preparations
- •Transdermal Preparations
- •Side Effects and Treatment Monitoring
- •Body Composition
- •Cognitive Decline
- •Bone Metabolism
- •The Kidneys
- •Endocrine Functions of the Kidney
- •Erythropoietin
- •Calcitriol
- •Renin
- •Paraneoplastic Syndromes
- •Hypercalcemia
- •Hypertension
- •Polycythemia
- •Other Endocrine Abnormalities
- •References
- •General Physiology
- •Prostate Innervation
- •Summary
- •References
- •Wound Healing
- •Inflammation
- •Proliferation
- •Remodeling
- •Principles of Plastic Surgery
- •Tissue Characteristics
- •Grafts
- •Flap
- •References
- •Lower Urinary Tract Symptoms
- •Storage Phase
- •Voiding Phase
- •Return to Storage Phase
- •Urodynamic Parameters
- •Urodynamic Techniques
- •Volume Voided Charts
- •Pad Testing
- •Typical Test Schedule
- •Uroflowmetry
- •Post Voiding Residual
- •Further Diagnostic Evaluation of Patients
- •Cystometry with or Without Video
- •Cystometry
- •Videocystometrography (Cystometry + Cystourethrography)
- •Cystometric Findings
- •Comment:
- •Measurements During the Storage Phase:
- •Measurements During the Voiding Phase:
- •Abnormal Function
- •Disorders of Sensation
- •Causes of Hypersensitive Bladder Sensation
- •Causes of Hyposensitive Bladder Sensation
- •Disorders of Detrusor Motor Function
- •Bladder Outflow Tract Dysfunction
- •Detrusor–Urethral Dyssynergia
- •Detrusor–Bladder Neck Dyssynergia
- •Detrusor–Sphincter Dyssynergia
- •Complex Urodynamic Investigation
- •Urethral Pressure Measurement
- •Technique
- •Neurophysiological Evaluation
- •Conclusion
- •References
- •Endoscopy
- •Cystourethroscopy
- •Ureteroscopy and Ureteropyeloscopy
- •Nephroscopy
- •Virtual Reality Simulators
- •Lasers
- •Clinical Application of Lasers
- •Condylomata Acuminata
- •Urolithiasis
- •Benign Prostatic Hyperplasia
- •Ureteral and Urethral Strictures
- •Conclusion
- •References
- •Introduction
- •The Prostatitis Syndromes
- •The Scope of the Problem
- •Category III CP/CPPS
- •The Goal of Treatment
- •Conservative Management
- •Drug Therapy
- •Antibiotics
- •Anti-inflammatories
- •Alpha blockers
- •Hormone Therapies
- •Phytotherapies
- •Analgesics, muscle relaxants and neuromodulators
- •Surgery
- •A Practical Management Plan
- •References
- •Orchitis
- •Definition and Etiology
- •Clinical Signs and Symptoms
- •Diagnostic Evaluation
- •Treatment of Infectious Orchitis
- •Epididymitis
- •Definition and Etiology
- •Clinical Signs and Symptoms
- •Diagnostic Evaluation of Epididymitis
- •Treatment of Acute Epididymitis
- •Treatment of Chronic Epididymitis
- •Treatment of Spermatic Cord Torsion
- •Fournier’s Gangrene
- •Definition and Etiology
- •Risk Factors
- •Clinical Signs and Symptoms
- •Diagnostic Evaluation
- •Treatment
- •References
- •Fungal Infections
- •Candidiasis
- •Aspergillosis
- •Cryptococcosis
- •Blastomycosis
- •Coccidioidomycosis
- •Histoplasmosis
- •Radiographic Findings
- •Treatment
- •Tuberculosis
- •Clinical Manifestations
- •Diagnosis
- •Treatment
- •Schistosomiasis
- •Clinical Manifestations
- •Diagnosis
- •Treatment
- •Filariasis
- •Clinical Manifestations
- •Diagnosis
- •Treatment
- •Onchocerciasis
- •References
- •25: Sexually Transmitted Infections
- •Introduction
- •STIs Associated with Genital Ulcers
- •Herpes Simplex Virus
- •Diagnosis
- •Treatment
- •Chancroid
- •Diagnosis
- •Treatment
- •Syphilis
- •Diagnosis
- •Treatment
- •Lymphogranuloma Venereum
- •Diagnosis
- •Treatment
- •Chlamydia
- •Diagnosis
- •Treatment
- •Gonorrhea
- •Diagnosis
- •Treatment
- •Trichomoniasis
- •Diagnosis
- •Treatment
- •Human Papilloma Virus
- •Diagnosis
- •Treatment
- •Scabies
- •Diagnosis
- •Treatment
- •References
- •26: Hematuria: Evaluation and Management
- •Introduction
- •Classification of Hematuria
- •Macroscopic Hematuria
- •Microscopic Hematuria
- •Dipstick Hematuria
- •Pseudohematuria
- •Factitious Hematuria
- •Menstruation
- •Aetiology
- •Malignancy
- •Urinary Calculi
- •Infection and Inflammation
- •Benign Prostatic Hyperplasia
- •Trauma
- •Drugs
- •Nephrological Causes
- •Assessment
- •History
- •Examination
- •Investigations
- •Dipstick Urinalysis
- •Cytology
- •Molecular Tests
- •Blood Tests
- •Flexible Cystoscopy
- •Upper Urinary Tract Evaluation
- •Renal USS
- •KUB Abdominal X-Ray
- •Intravenous Urography (IVU)
- •Computed Tomography (CT)
- •Retrograde Urogram Studies
- •Magnetic Resonance Imaging (MRI)
- •Additional Tests and Renal Biopsy
- •Intractable Hematuria
- •Loin Pain Hematuria Syndrome
- •References
- •27: Benign Prostatic Hyperplasia (BPH)
- •Historical Background
- •Pathophysiology
- •Patient Assessment
- •Treatment of BPH
- •Watchful Waiting
- •Drug Therapy
- •Interventional Therapies
- •Conclusions
- •References
- •28: Practical Guidelines for the Treatment of Erectile Dysfunction and Peyronie´s Disease
- •Erectile Dysfunction
- •Introduction
- •Diagnosis
- •Basic Evaluation
- •Cardiovascular System and Sexual Activity
- •Optional Tests
- •Treatment
- •Medical Treatment
- •Oral Agents
- •Phosphodiesterase Type 5 (PDE 5) Inhibitors
- •Nonresponders to PDE5 Inhibitors
- •Apomorphine SL
- •Yohimbine
- •Intracavernosal and Intraurethral Therapy
- •Intracavernosal Injection (ICI) Therapy
- •Intraurethral Therapy
- •Vacuum Constriction Devices
- •Surgical Therapy
- •Conclusion
- •Peyronie´s Disease (PD)
- •Introduction
- •Oral Drug Therapy
- •Intralesional Drug Therapy
- •Iontophoresis
- •Radiation Therapy
- •Surgical Therapy
- •References
- •29: Premature Ejaculation
- •Introduction
- •Epidemiology
- •Defining Premature Ejaculation
- •Voluntary Control
- •Sexual Satisfaction
- •Distress
- •Psychosexual Counseling
- •Pharmacological Treatment
- •On-Demand Treatment with Tramadol
- •Topical Anesthetics
- •Phosphodiesterase Inhibitors
- •Surgery
- •Conclusion
- •References
- •30: The Role of Interventional Management for Urinary Tract Calculi
- •Contraindications to ESWL
- •Complications of ESWL
- •PCNL Access
- •Instrumentation for PCNL
- •Nephrostomy Drains Post PCNL
- •Contraindications to PCNL
- •Complications of PCNL
- •Semirigid Ureteroscopy
- •Flexible Ureteroscopy
- •Electrohydraulic Lithotripsy (EHL)
- •Ultrasound
- •Ballistic Lithotripsy
- •Laser Lithotripsy
- •Ureteric Stents
- •Staghorn Calculi
- •Lower Pole Stones
- •Horseshoe Kidneys and Stones
- •Calyceal Diverticula Stones
- •Stones and PUJ Obstruction
- •Treatment of Ureteric Colic
- •Medical Expulsive Therapy (MET)
- •Intervention for Ureteric Stones
- •Stones in Pregnancy
- •Morbid Obesity
- •References
- •Anatomy and Function
- •Pathophysiology
- •Management
- •Optical Urethrotomy/Dilatation
- •Urethral Stents
- •Preoperative Assessment
- •Urethroplasty
- •Anastomotic Urethroplasty
- •Substitution Urethroplasty
- •Grafts Versus Flaps
- •Oral Mucosal Grafts
- •Tissue Engineering
- •Graft Position
- •Conclusion
- •References
- •32: Urinary Incontinence
- •Epidemiology and Risk Factors
- •Pathophysiology
- •Urge Incontinence
- •Conservative Treatments
- •Pharmacotherapy
- •Invasive/ Surgical Therapies
- •Stress Urinary Incontinence
- •Male SUI Therapies
- •Female SUI Therapies
- •Mixed Urinary Incontinence
- •Conclusions
- •References
- •33: Neurogenic Bladder
- •Introduction
- •Examination and Diagnostic Tests
- •History and Physical Examination
- •Imaging
- •Urodynamics (UDS)
- •Evoked Potentials
- •Classifications
- •Somatic Pathways
- •Brain Lesions
- •Cerebrovascular Accident (CVA)
- •Parkinson’s Disease (PD)
- •Multiple Sclerosis
- •Huntington’s Disease
- •Dementias
- •Normal Pressure Hydrocephalus (NPH)
- •Tumors
- •Psychiatric Disorders
- •Spinal Lesions and Pathology
- •Intervertebral Disk Prolapse
- •Spinal Cord Injury (SCI)
- •Transverse Myelitis
- •Peripheral Neuropathies
- •Metabolic Neuropathies
- •Pelvic Surgery
- •Treatment
- •Summary
- •References
- •34: Pelvic Prolapse
- •Introduction
- •Epidemiology
- •Anatomy and Pathophysiology
- •Evaluation and Diagnosis
- •Outcome Measures
- •Imaging
- •Urodynamics
- •Indications for Management
- •Biosynthetics
- •Surgical Management
- •Anterior Compartment Repair
- •Uterine/Apical Prolapse
- •Enterocele Repair
- •Conclusion
- •References
- •35: Urinary Tract Fistula
- •Introduction
- •Urogynecologic Fistula
- •Vesicovaginal Fistula
- •Etiology and Risk Factors
- •Clinical Factors
- •Evaluation and Diagnosis
- •Pelvic Examination
- •Cystoscopy
- •Imaging
- •Treatment
- •Conservative Management
- •Surgical Management
- •Urethrovaginal Fistula
- •Etiology and Presentation
- •Diagnosis and Management
- •Ureterovaginal Fistula
- •Etiology and Presentation
- •Diagnosis and Management
- •Vesicouterine Fistula
- •Etiology and Presentation
- •Diagnosis and Management
- •Uro-Enteric Fistula
- •Vesicoenteric Fistula
- •Pyeloenteric Fistula
- •Urethrorectal Fistula
- •References
- •36: Urologic Trauma
- •Introduction
- •Kidney
- •Expectant Management
- •Endovascular Therapy
- •Operative Intervention
- •Operative Management: Follow-up
- •Reno-Vascular Injuries
- •Pediatric Renal Injuries
- •Adrenal
- •Ureter
- •Diagnosis
- •Treatment
- •Delayed Diagnosis
- •Bladder and Posterior Urethra
- •Bladder Injuries: Initial Management
- •Bladder Injuries: Formal Repair
- •Anterior Urethral Trauma
- •Fractured Penis
- •Penile Amputation
- •Scrotal and Testicular Trauma
- •Imaging
- •CT-IVP (CT with Delayed Images)
- •Technique
- •Cystogram
- •Technique
- •Retrograde Urethrogram (RUG)
- •Technique
- •Retrograde Pyelogram (RPG)
- •Technique
- •One-Shot IVP
- •Technique
- •References
- •37: Bladder Cancer
- •Who Should Be Investigated?
- •Epidemiology
- •Risk Factors
- •Role of Screening
- •Signs and Symptoms
- •Imaging
- •Cystoscopy
- •Urine Tests
- •PDD-Assisted TUR
- •Pathology
- •NMIBC and Risk Groups
- •Intravesical Chemotherapy
- •Intravesical Immunotherapy
- •Immediate Cystectomy and CIS
- •Radical Cystectomy with Pelvic Lymph Node Dissection
- •sexual function-preserving techniques
- •Bladder-Preservation Treatments
- •Neoadjuvant Chemotherapy
- •Adjuvant Chemotherapy
- •Preoperative Radiotherapy
- •Follow-up After TUR in NMIBC
- •References
- •38: Prostate Cancer
- •Introduction
- •Epidemiology
- •Race
- •Geographic Variation
- •Risk Factors and Prevention
- •Family History
- •Diet and Lifestyle
- •Prevention
- •Screening and Diagnosis
- •Current Screening Recommendations
- •Biopsy
- •Pathology
- •Prognosis
- •Treatment of Prostate Cancer
- •Treatment for Localized Prostate Cancer (T1, T2)
- •Radical Prostatectomy
- •EBRT
- •IMRT
- •Brachytherapy
- •Treatment for Locally Advanced Prostate Cancer (T3, T4)
- •EBRT with ADT
- •Radical Prostatectomy
- •Androgen-Deprivation Therapy
- •Summary
- •References
- •39: The Management of Testis Cancer
- •Presentation and Diagnosis
- •Serum Tumor Markers
- •Primary Surgery
- •Testis Preserving Surgery
- •Risk Stratification
- •Surveillance Versus Primary RPLND
- •Primary RPLND
- •Adjuvant Treatment for High Risk
- •Clinical Stage 1 Seminoma
- •Risk-Stratified Adjuvant Treatment
- •Adjuvant Radiotherapy
- •Adjuvant Low Dose Chemotherapy
- •Primary Combination Chemotherapy
- •Late Toxicity
- •Salvage Strategies
- •Conclusion
- •References
- •Index
457
nEUrogEnic BladdEr
from the Onuf’s nucleus. Acetylcholine acts on |
initiates low-level afferent activity in the pelvic |
|
nicotinic receptors located at the motor end |
nerve. Afferent firing originating from the ure- |
|
plate and causes muscle contraction. Botulinum |
thra stimulates sympathetic efferent outflow to |
|
toxin and its various serotypes prevent acetyl- |
the bladder base and urethra as well as somatic |
|
choline-containing vesicles from fusing to the |
outflow to the EUS. The storage reflexes are |
|
prejunctional terminal membrane interfering |
organized at spinal level, whereas the spinal |
|
with the release process. Botulinum toxin A |
reflex pathways are under influence by a lateral |
|
(BoTNA) injections into the EUS have been used |
pontine area designated the urine storage |
|
for treating DSD.10 Intravesical BoTNA injec- |
center. |
|
tions have been useful to treat urinary inconti- |
During bladder filling, the intravesical pres- |
|
nence due to neurogenic DO.11 |
sure remains low and constant (5–10 cm H O) |
|
|
2 |
|
|
until the threshold for inducing voiding is |
|
|
reached. Once this threshold is achieved, the |
|
Central Control of Urine Storage |
central and peripheral parasympathetic efferent |
|
pathways are activated, whereas sympathetic |
||
and Release and the Pontine |
and somatic pathways are inhibited. SCI, MS, |
|
cervical disk disease, tumors, or inflammatory |
||
Micturition Center (PMC) |
||
processes that interrupt these pathways are |
||
|
associated with loss of coordination between |
|
The central regulation of the micturition reflex |
the bladder and its outlet and DSD. |
|
involves the cerebral cortex, diencephalon, and |
In predicting the impact of neurological con- |
|
pons. The command and control center for the |
ditions on urinary control, it is helpful to envi- |
|
bladder is the pons. Stimulation of the dorsome- |
sion a hierarchical scheme divided into brain, |
|
dial pontine center causes urinary bladder con- |
spine, and periphery, and consider whether |
|
traction and simultaneous EUS inhibition.12 |
pathology exists rostral or caudal to the SPN. |
|
Stimulation of the dorsolateral pons increases |
However, urodynamic findings and clinical |
|
activity of EUS while inhibiting the bladder. |
expression of disease do not always clearly fit |
|
Neurons in the dorsomedial pons send axons to |
into known pathophysiological mechanisms. |
|
the sacral spinal. Onuf’s nucleus also receives |
For example, although only lesions between the |
|
projections from the dorsolateral pons and the |
pons and sacral cord should lead to DSD, some- |
|
medial hypothalamus as well as axons from a |
times DSD is seen in other conditions either |
|
lateral region of the PMC. Other brain regions |
because of multiple levels of pathology or |
|
implicated in bladder control include the central |
because of erroneous interpretations of UDS. |
|
nucleus of the amygdala, bed nucleus stria ter- |
Neuropathology effects both voiding and stor- |
|
minalis, paraventricular nucleus, and locus |
age reflexes. Changes in neural connections and |
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coeruleus suggesting that stress and alertness |
transmitter following disease or injury, termed |
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could impact on bladder function.13 Many pro- |
neuroplasticity, alter these pathways sometimes |
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jections in these pathways contain corticotropin |
in unpredictable ways. |
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releasing factor (CRF) that when released from |
|
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the hypothalamus causes ACTH release.14 Thus |
Brain Lesions |
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it is not surprising that conditions associated |
||
with severe stress (posttraumatic stress disor- |
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der, abuse) are associated with OAB.15 |
Cerebrovascular Accident (CVA) |
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Ascending pathways from neurons arising in |
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the dorsal horn of the spinal cord are involved in |
LUTS are prevalent in the stroke victim with up |
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transmission of sensory information from the |
to 94% of patients describing at least one uri- |
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lower urinary tract to the dorsolateral pons |
nary symptom with nocturia being the most |
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including the periaqueductal gray. |
common complaint.16 Acute urinary retention is |
|
To promote bladder distension and urethral |
common immediately after a CVA. Bothersome |
|
sphincter contraction during urine storage, the |
urinary incontinence is seen in 25% of patients |
|
micturition reflex is inhibited, whereas sympa- |
at 12 months with a range of UI in the early |
|
thetic and somatic pathways are activated |
period of 57–83%. UI following a CVA is the best |
|
(Fig. 33.2). During storage, bladder distension |
predictor of future disability.17 |
458
Practical Urology: EssEntial PrinciPlEs and PracticE
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Storage reflex |
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Inhibition |
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(Inhibition) |
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Hypogastric nerve |
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SYM |
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Pelvic nerve |
+ M3 |
- b3 |
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(Inhibition) |
No |
+ a1D |
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On Pudendal nerve |
+ N |
+ a1A |
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Figure 33.2. cns control of micturition. lower urinary tract function works as a switch in the pontine micturition center (PMc) from urine storage to voiding. during voiding, as depicted, sacral mechanisms regulating the external urethral sphincter (EUs), onuf’s nucleus (on), and sympathetic centers (syM) are inhibited, whereas preganglionic neurons giving rise to the pelvic nerve are activated. infrapontine but supraspinal neuropa-
Urodynamics studies in stroke patients are variable. In the immediate shock period 21% demonstrate overflow UI secondary to detrusor areflexia (DA). UDS in symptomatic patients revealed 69% had neurogenic DO, 10% hypocontractility, and 22% DSD.18 The latter finding suggests spinal involvement or misinterpretation due to lack of voluntary relaxation.
thology may interfere with this switch and cause detrusor sphincter dyssynergia. acetylcholine released from postganglionic neurons activate M3 receptors expressed by detrusor to contract and no released in urethra relaxes outlet. during storage,postganglionic sympathetic neurons release norepinephrine which activates a1 receptors in bladder neck and urethra and b3 receptors in bladder body to store urine under low pressure.
accurately predict surgical outcomes with only half of patients undergoing a TURP have an excellent result.20 Controversy exists whether men with coexistent PD and obstruction should also undergo surgical intervention. Although such procedures may assist evacuation of the bladder, the risk of UI or persistent storage symptoms is substantial.
Parkinson’s Disease (PD)
PD arises from neurodegeneration of dopaminergic neurons in the basal ganglia.An imbalance in activation of excitatory (D2) and inhibitory (D1) dopamine receptors causes LUTs which range from 37% to 71%.19 Storage symptoms of frequency, urgency, nocturia, and urge UI are most common. Voiding symptoms of slow stream, hesitancy, and double voiding are less frequent and can be confused with symptoms due to benign prostatic hyperplasia (BPH). Sixty-seven to ninety-three percent of CMGs show neurogenic DO, 16% reveal hyporeflexia or DA, 7% have pseudodyssynergia, and 11% demonstrate bradykinesia of the EUS.19 Abnormal UDS correlate with disease severity. Although pressure flow studies can be useful to diagnose obstruction due to BPH, they fail to
Multisystem Atrophy (MSA),
Olivopontine Cerebellar Degeneration
(OPCD), ShyDrager
Urinary complaints are nearly universal in patients with MSA. MSA causes striatonigral degeneration in which Parkinsonian symptoms are predominant. OPCD denotes the condition in which cerebellar signs predominate. Shy Drager describes this neurodegenerative disorder when autonomic failure is present. Neurologic and urinary symptoms in PD and MSA may be identical. But as opposed to PD, neuronal degeneration extends beyond the basal ganglia. In Shy Drager autonomic ganglia and Onuf’s nucleus are often involved. In a patient with orthostatic hypotension, UI, retention, and Parkinsonian symptoms, MSA/Shy Drager should be suspected. If physical
459
nEUrogEnic BladdEr
examination reveals lax anal tone or absent |
Dementias |
|
voluntary anal contraction further suspicion of |
|
|
MSA is raised. Nearly a third of MSA patients |
There is wide variation in UI (11–90%) reported |
|
complain of difficulty voiding, 44% have SUI, a |
with dementia. UI is more common with |
|
third note urinary frequency, and a third dem- |
Alzheimer’s than multi-infarct dementia. Incon- |
|
onstrate urge UI.21 |
tinence in patients with dementia is multi-facto- |
|
Video UDS can differentiate MSA from PD. |
rial with social factors; such unwillingness to |
|
While up to a third of PD may show an open |
hold urine after first sensation of fullness, cog- |
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bladder neck, 46–100% of patients with MSA |
nitive inability to get to toilet, physical inability |
|
have this finding.22 UDS show that more than |
to reach a toilet, impact of medications, and |
|
half the patients lack EUS responses to cough or |
access are operative. Underlying these limita- |
|
Valsalva. Sixty-seven percent show DA, a third |
tions are studies demonstrating DO. One study |
|
neurogenic DO, and more than half reduced |
showed that DO was present on CMG in 58% of |
|
compliance.21 Indeed, residual urines greater |
patients with Alzheimer’s disease, 91% with |
|
than 100 cm3 should lead the clinician to suspect |
multi-infarct dementia,and 50% who had both.26 |
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MSA rather than PD. Motor unit responses of |
Half of UI patients had DO, whereas none of the |
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the EUS consistent with denervation include |
continent patients had this urodynamic finding. |
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polyphasic potentials and increased duration of |
Another finding in dementia patients is unin- |
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responses.23 |
hibited sphincter relaxation. Of particular |
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For the urologist, the most important reason |
importance is avoiding the use of nonselective |
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to differentiate MSA from PD is for the manage- |
antimuscarinics to treat UI in these patients |
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ment of a patient in whom bladder outlet |
which may exert adverse effects on cognitive |
|
obstruction is suspected. Since retention and |
function. |
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residuals are common in MSA, these patients |
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more likely to under prostatic surgery to relieve |
Normal Pressure Hydrocephalus (NPH) |
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obstruction. Stress urinary incontinence (SUI) |
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occurs either more commonly or exclusively in |
Dilated cerebral ventricles and normal cerebro- |
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MSA relative to PD.24 |
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spinal fluid pressure, termed NPH, is associated |
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with gait disturbance, memory defects, and UI. |
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Multiple Sclerosis |
Up to 93% of NPH patients have OAB symptoms |
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with 63–100% demonstrating DO.27 Some |
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MS is a demyelinating disorder of axons in the |
patients demonstrate a PVR urine as well poten- |
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brain and spinal cord. Eighty to ninety percent |
tially due to aging-related impaired contractile |
|
of MS patients will develop urologic complaints. |
function. In a substantial proportion of patients |
|
In a systemic review of UDS in MS patients neu- |
shunting improves or eliminates LUTS.28 Care in |
|
rogenic DO was found in 62%, DSD in 25%, and |
the use of antimuscarinics is advised due to |
|
hypocontractility in 20%.25 |
memory defects.29 |
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Although upper tract deterioration is unusual |
|
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in MS, men with lower extremity involvement |
Cerebral Palsy, Cerebellar Ataxia, |
|
may be the one group at greater risk and require |
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close monitoring, if not with UDS, than with fre- |
Epilepsy |
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quent upper tract imaging. |
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DO has been demonstrated in 31–100% of |
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patients with CP.30,31 DSD is uncommon(3–19%). |
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Huntington’s Disease |
UI may be related to underlying bladder dys- |
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function or social limitations imposed by lim- |
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This autosomal dominant neurodegenerative |
ited mobility or cognitive function. |
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disorder causes neuronal loss in the cerebral |
Cerebellar ataxia is usually not associated |
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cortex and caudate nucleus. In the rare studies |
with LUTS unless other neurodegenerative con- |
|
examining urinary complaints, DO was the only |
ditions coexist. When present, UI and urgency |
|
finding. In large surveys, LUTS occurred only in |
are typical symptoms. DO in symptomatic |
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late stages (>10 years) of the disease. |
patients has been described in 25–53%.32,33 One |