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Neurogenic bladder

MedGen UID:
595
Concept ID:
C0005697
Disease or Syndrome
Synonyms: Bladder Disorder, Neurogenic; Bladder, Neurogenic; Neurogenic Bladder; Neurogenic Bladder Disorder; Neurogenic Bladder Disorders; Neurogenic Dysfunction of the Urinary Bladder; Neurogenic Urinary Bladder; Neurogenic Urinary Bladder Disorder; Neuropathic Bladder; Urinary Bladder Disorder, Neurogenic; Urinary Bladder Neurogenic Dysfunction; Urinary Bladder, Neurogenic
SNOMED CT: Neurogenic bladder (398064005); Neuropathic bladder (398064005); Neurogenic urinary bladder (398064005)
 
HPO: HP:0000011

Definition

A type of bladder dysfunction caused by neurologic damage. Neurogenic bladder can be flaccid or spastic. Common manifestatios of neurogenic bladder are overflow incontinence, frequency, urgency, urge incontinence, and retention. [from HPO]

Conditions with this feature

Oculodentodigital dysplasia
MedGen UID:
167236
Concept ID:
C0812437
Congenital Abnormality
Oculodentodigital dysplasia (ODDD) is characterized by a typical facial appearance and variable involvement of the eyes, dentition, and fingers. Characteristic facial features include a narrow, pinched nose with hypoplastic alae nasi, prominent columella and thin anteverted nares together with a narrow nasal bridge, and prominent epicanthic folds giving the impression of hypertelorism. The teeth are usually small and carious. Typical eye findings include microphthalmia and microcornea. The characteristic digital malformation is complete syndactyly of the fourth and fifth fingers (syndactyly type III) but the third finger may be involved and associated camptodactyly is a common finding (summary by Judisch et al., 1979). Neurologic abnormalities are sometimes associated (Gutmann et al., 1991), and lymphedema has been reported in some patients with ODDD (Brice et al., 2013). See review by De Bock et al. (2013). Genetic Heterogeneity of Oculodentodigital Syndrome An autosomal recessive form of ODDD (257850) is also caused by mutation in the GJA1 gene, but the majority of cases are autosomal dominant.
Currarino triad
MedGen UID:
323460
Concept ID:
C1531773
Disease or Syndrome
The Currarino syndrome is an autosomal dominant form of hereditary sacral dysgenesis that classically consists of the triad of sacral malformation, presacral mass, and anorectal malformations. However, other features include neonatal-onset bowel obstruction, chronic constipation, recurrent perianal sepsis, renal/urinary tract anomalies, female internal genital anomalies, tethered spinal cord, and anterior meningocele. There is marked inter- and intrafamilial variability, and up to 33% of patients are asymptomatic (summary by Wang et al., 2006).
Sacral defect with anterior meningocele
MedGen UID:
325455
Concept ID:
C1838568
Disease or Syndrome
Sacral defect with anterior meningocele (SDAM) is a form of caudal dysgenesis. It is present at birth and becomes symptomatic later in life, usually because of obstructive labor in females, chronic constipation, or meningitis. Inheritance is autosomal dominant (Chatkupt et al., 1994). Welch and Aterman (1984) gave a population frequency of 0.14%. Caudal dysgenesis syndrome and caudal regression syndrome are broad terms that refer to a heterogeneous constellation of congenital caudal anomalies affecting the caudal spine and spinal cord, the hindgut, the urogenital system, and the lower limbs. Approximately 15 to 25% of mothers of children with caudal dysgenesis have insulin-dependent diabetes mellitus (222100) (Lynch et al., 2000). See also Currarino syndrome (176450), a similar disorder caused by mutation in the HLXB9 gene (142994) on chromosome 7q36. Currarino syndrome classically comprises the triad of hemisacrum, anorectal malformation, and presacral mass. However, Currarino syndrome also shows phenotypic variability: Lynch et al. (2000) stated that there is variable expressivity of clinical features and that some patients with Currarino syndrome are asymptomatic. Kochling et al. (2001) found the complete triad of Currarino syndrome in only 8 of 23 patients with mutations in the HLXB9 gene, These reports suggest that some patients previously reported as having forms of sacral agenesis, including SDAM, may have had Currarino syndrome and vice versa. See also spina bifida (182940), which can be seen in some patients with sacral agenesis or caudal regression syndrome and may be etiologically related.
Adult polyglucosan body disease
MedGen UID:
342338
Concept ID:
C1849722
Disease or Syndrome
Most individuals with classic GBE1 adult polyglucosan body disease (GBE1-APBD) present after age 40 years with unexplained progressive neurogenic bladder, gait difficulties (i.e., spasticity and weakness) from mixed upper and lower motor neuron involvement, sensory loss predominantly in the distal lower extremities, autonomic dysfunction (associated with orthostatic hypotension and constipation), and mild cognitive difficulties (often executive dysfunction). Some affected individuals without classic GBE1-APBD have atypical phenotypes including Alzheimer disease-like dementia and axonal neuropathy, stroke-like episodes, and diaphragmatic failure; others may have a history of infantile liver disease.
Lateral meningocele syndrome
MedGen UID:
342070
Concept ID:
C1851710
Disease or Syndrome
NOTCH3-related lateral meningocele syndrome (LMS) is characterized by multiple lateral spinal meningoceles (protrusions of the arachnoid and dura through spinal foramina), distinctive facial features, joint hyperextensibility, hypotonia, and skeletal, cardiac, and urogenital anomalies. Neurologic sequelæ of the meningoceles depend on size and location and can include neurogenic bladder, paresthesia, back pain, and/or paraparesis. Other neurologic findings can include Chiari I malformation, syringomyelia, and rarely, hydrocephalus. Additional findings of LMS include developmental delay, mixed or conductive hearing loss, and cleft palate. Skeletal abnormalities may include scoliosis, vertebral fusion, scalloping of vertebrae, and wormian bones. Infants may demonstrate feeding difficulties with poor weight gain.
Wolfram syndrome 2
MedGen UID:
347604
Concept ID:
C1858028
Disease or Syndrome
Wolfram syndrome-2 (WFS2) is an autosomal recessive neurodegenerative disorder characterized by diabetes mellitus, high frequency sensorineural hearing loss, optic atrophy or neuropathy, and defective platelet aggregation resulting in peptic ulcer bleeding (summary by Mozzillo et al., 2014). For a discussion of genetic heterogeneity of Wolfram syndrome, see WFS1 (222300).
Spastic ataxia 3
MedGen UID:
370715
Concept ID:
C1969645
Disease or Syndrome
A rare genetic autosomal recessive spastic ataxia disease with characteristics of cerebellar ataxia, spasticity, cerebellar (and in some cases cerebral) atrophy, dystonia and leucoencephalopathy. Caused by homozygous or compound heterozygous complex genomic rearrangements involving the MARS2 gene on chromosome 2q33.
COG7 congenital disorder of glycosylation
MedGen UID:
419311
Concept ID:
C2931010
Disease or Syndrome
CDG IIe is caused by a mutation that impairs the integrity of the conserved oligomeric Golgi (COG) complex and alters Golgi trafficking, resulting in the disruption of multiple glycosylation pathways. For a general discussion of CDGs, see CDG1A (212065).
COG5-congenital disorder of glycosylation
MedGen UID:
462226
Concept ID:
C3150876
Disease or Syndrome
COG5-congenital disorder of glycosylation (COG5-CDG, formerly known as congenital disorder of glycosylation type IIi) is an inherited condition that causes neurological problems and other abnormalities. The pattern and severity of this disorder's signs and symptoms vary among affected individuals.\n\nIndividuals with COG5-CDG typically develop signs and symptoms of the condition during infancy. These individuals often have weak muscle tone (hypotonia) and delayed development. Other neurological features include moderate to severe intellectual disability, poor coordination, and difficulty walking. Some affected individuals never learn to speak. Other features of COG5-CDG include short stature, an unusually small head size (microcephaly), and distinctive facial features, which can include ears that are set low and rotated backward, a short neck with a low hairline in the back, and a prominent nose. Less commonly, affected individuals can have hearing loss caused by changes in the inner ear (sensorineural hearing loss), vision impairment, damage to the nerves that control bladder function (a condition called neurogenic bladder), liver disease, and joint deformities (contractures).
Spondylocostal dysostosis 4, autosomal recessive
MedGen UID:
462292
Concept ID:
C3150942
Disease or Syndrome
Spondylocostal dysostosis (SCDO), defined radiographically as multiple segmentation defects of the vertebrae (M-SDV) in combination with abnormalities of the ribs, is characterized clinically by: a short trunk in proportion to height; short neck; non-progressive mild scoliosis in most affected individuals, and occasionally, more significant scoliosis. Respiratory function in neonates may be compromised by reduced size of the thorax. By age two years lung growth may improve sufficiently to support relatively normal growth and development; however, even then life-threatening complications can occur, especially pulmonary hypertension in children with severely restricted lung capacity from birth. Males with SCDO appear to be at increased risk for inguinal hernia.
Hermansky-Pudlak syndrome 6
MedGen UID:
854714
Concept ID:
C3888007
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. Ocular findings include reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in variable bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.
Frontotemporal dementia and/or amyotrophic lateral sclerosis 2
MedGen UID:
863085
Concept ID:
C4014648
Disease or Syndrome
CHCHD10-related disorders are characterized by a spectrum of adult-onset neurologic phenotypes that can include: Mitochondrial myopathy (may also be early onset): weakness, amyotrophy, exercise intolerance. Amyotrophic lateral sclerosis (ALS): progressive degeneration of upper motor neurons and lower motor neurons. Frontotemporal dementia (FTD): slowly progressive behavioral changes, language disturbances, cognitive decline, extrapyramidal signs. Late-onset spinal motor neuronopathy (SMA, Jokela type): weakness, cramps, and/or fasciculations; areflexia. Axonal Charcot-Marie-Tooth neuropathy: slowly progressive lower-leg muscle weakness and atrophy, small hand muscle weakness, loss of tendon reflexes, sensory abnormalities. Cerebellar ataxia: gait ataxia, kinetic ataxia (progressive loss of coordination of lower- and upper-limb movements), dysarthria/dysphagia, nystagmus, cerebellar oculomotor disorder. Because of the recent discovery of CHCHD10-related disorders and the limited number of affected individuals reported to date, the natural history of these disorders (except for SMAJ caused by the p.Gly66Val pathogenic variant) is largely unknown.
Webb-Dattani syndrome
MedGen UID:
863145
Concept ID:
C4014708
Disease or Syndrome
Webb-Dattani syndrome is an autosomal recessive disorder characterized by frontotemporal hypoplasia, globally delayed development, and pituitary and hypothalamic insufficiency due to hypoplastic development of these brain regions. Patients present soon after birth with multiple pituitary hormonal deficiencies and subsequently develop microcephaly, seizures, and spasticity. Other features include postretinal blindness and renal abnormalities (summary by Webb et al., 2013).
Hypomyelinating leukodystrophy 12
MedGen UID:
905068
Concept ID:
C4225247
Disease or Syndrome
Hypomyelinating leukodystrophy-12 (HLD12) is an autosomal recessive neurologic disorder characterized by severely delayed or even lack of psychomotor development that becomes apparent in the first months of life. Patients are markedly disabled, with acquired microcephaly, lack of speech, and often lack of spontaneous movement due to hypotonia and spasticity. Brain imaging shows delayed myelination (summary by Edvardson et al., 2015). For a general phenotypic description and a discussion of genetic heterogeneity of HLD, see 312080. In a review of the pathogenesis of disorders with prominent dystonia or opisthotonic posturing as a feature, Monfrini et al. (2021) classified HLD12 as belonging to a group of neurologic disorders termed 'HOPS-associated neurologic disorders (HOPSANDs), which are caused by mutations in genes encoding various components of the autophagic/endolysosomal system, including VPS11.
Frontometaphyseal dysplasia 2
MedGen UID:
934664
Concept ID:
C4310697
Disease or Syndrome
Frontometaphyseal dysplasia (FMD) is a progressive sclerosing skeletal dysplasia characterized by supraorbital hyperostosis, undermodeling of the small bones, and small and large joint contractures, as well as extraskeletal developmental abnormalities, primarily of the cardiorespiratory system and genitourinary tract. Patients with FMD2 appear to have a propensity for keloid formation (summary by Wade et al., 2016). For a discussion of genetic heterogeneity of frontometaphyseal dysplasia, see FMD1 (305620).
Intellectual disability, autosomal dominant 42
MedGen UID:
934741
Concept ID:
C4310774
Mental or Behavioral Dysfunction
GNB1 encephalopathy (GNB1-E) is characterized by moderate-to-severe developmental delay / intellectual disability, structural brain abnormalities, and often infantile hypotonia and seizures. Other less common findings include dystonia, reduced vision, behavior issues, growth delay, gastrointestinal (GI) problems, genitourinary (GU) abnormalities in males, and cutaneous mastocytosis.
Peroxisome biogenesis disorder 10B
MedGen UID:
1379481
Concept ID:
C4479254
Disease or Syndrome
Alkaline ceramidase 3 deficiency
MedGen UID:
1622324
Concept ID:
C4540358
Disease or Syndrome
A rare genetic disorder with characteristics of infantile onset of stagnation and regression of motor and language development resulting in complete lack of communication and purposeful movement. Further neurological manifestations include truncal hypotonia, appendicular spasticity, dystonia, optic disc pallor, peripheral neuropathy and neurogenic bladder. Patients also present multiple contractures, late-onset relative macrocephaly, short stature and facial dysmorphism (including coarse facial features, sloping forehead, thick eyebrows, low-set ears, prominent nose, flat philtrum, and prominent lower lip). Brain imaging at advanced stages shows diffuse abnormal white matter signal and severe atrophy. Sural nerve biopsy reveals decreased myelination.
Wolfram syndrome 1
MedGen UID:
1641635
Concept ID:
C4551693
Disease or Syndrome
WFS1 Wolfram syndrome spectrum disorder (WFS1-WSSD) is a progressive neurodegenerative disorder characterized by onset of diabetes mellitus (DM) and optic atrophy (OA) before age 16 years, and typically associated with other endocrine abnormalities, sensorineural hearing loss, and progressive neurologic abnormalities (cerebellar ataxia, peripheral neuropathy, dementia, psychiatric illness, and urinary tract atony). Although DM is mostly insulin-dependent, overall the course is milder (with lower prevalence of microvascular disease) than that seen in isolated DM. OA typically results in significantly reduced visual acuity in the first decade. Sensorineural hearing impairment ranges from congenital deafness to milder, sometimes progressive, hearing impairment.
Mitochondrial complex 1 deficiency, nuclear type 27
MedGen UID:
1648481
Concept ID:
C4748826
Disease or Syndrome
Ichthyotic keratoderma, spasticity, hypomyelination, and dysmorphic facial features
MedGen UID:
1682428
Concept ID:
C5193147
Disease or Syndrome
Ichthyotic keratoderma, spasticity, hypomyelination, and dysmorphic features (IKSHD) is characterized by epidermal hyperproliferation and increased keratinization, resulting in ichthyosis; hypomyelination of central white matter, causing spastic paraplegia and central nystagmus; and optic atrophy, resulting in reduction of peripheral vision and visual acuity (Mueller et al., 2019). In addition, patients exhibit mild facial dysmorphism (Kutkowska-Kazmierczak et al., 2018).
Urinary bladder, atony of
MedGen UID:
1684829
Concept ID:
C5231389
Disease or Syndrome
Autonomic bladder dysfunction with impaired pupillary reflex and secondary CAKUT (congenital anomalies of the kidney and urinary tract) is an autosomal recessive neurogenic disorder with onset in utero or early childhood. Affected individuals have impaired neuronal bladder and ureteral innervation causing coordination defects that result in secondary structural defects of the renal system, including hydronephrosis, vesicoureteral reflux (VUR), and small kidneys, that may result in chronic kidney disease as well as recurrent urinary tract infections (UTIs). Surgical treatment of VUR is not effective. Most individuals also have additional autonomic features, most commonly impaired pupillary reflex and sometimes orthostatic hypotension (summary by Mann et al., 2019).
Charcot-Marie-Tooth disease, axonal, mitochondrial form, 1
MedGen UID:
1731194
Concept ID:
C5435765
Disease or Syndrome
Mitochondrial form of axonal Charcot-Marie-Tooth disease-1 (CMTMA1) is inherited only through the maternal line. The disorder is characterized by onset of distal muscle weakness and atrophy mainly affecting the lower limbs and resulting in difficulty walking in the second decade of life, although both earlier and later onset can occur. Upper limb involvement often develops with time, and affected individuals have weakness and atrophy of the intrinsic hand muscles. Other features may include distal sensory impairment, foot deformities, scoliosis, hypo- or hyperreflexia, spastic paraparesis, and neurogenic bladder. Electrophysiologic studies are compatible with an axonal sensorimotor peripheral neuropathy, and muscle and nerve biopsy show evidence of mitochondrial dysfunction with decreased activities of respiratory complexes, mtDNA deletions, and mitochondrial hyperplasia (summary by Fay et al., 2020).
Neurodegeneration, childhood-onset, with hypotonia, respiratory insufficiency, and brain imaging abnormalities
MedGen UID:
1781967
Concept ID:
C5543020
Disease or Syndrome
Neuronal ceroid lipofuscinosis-15 (CLN15) is characterized by severe global developmental delay apparent in infancy or early childhood. Affected individuals have hypotonia with impaired motor development, respiratory insufficiency, and feeding difficulties requiring intervention. Intellectual and speech development is also delayed, and most have visual defects, including cortical visual blindness, nystagmus, and esotropia. The disorder is progressive, as manifest by developmental regression consistent with neurodegeneration. Although overt seizures are not observed, some patients may have episodic hypertonia or apnea, and EEG may show nonspecific abnormalities. Brain imaging shows unique diffusion restriction signal abnormalities affecting the brainstem, cerebellum, and corticospinal tracts. Early death may occur (summary by Polovitskaya et al., 2020).
Endove syndrome, limb-brain type
MedGen UID:
1782954
Concept ID:
C5543142
Disease or Syndrome
Limb-brain ENDOVE syndrome (ENDOVESLB) is characterized by marked mesomelic shortening of the lower limbs due to severe hypoplasia of the tibia and fibula. The talus is absent and foot bones are rudimentary. Hands show short and malformed fingers with a missing digit, and nails are absent on some fingers. In addition, there is cerebellar aplasia with hypoplasia of the brainstem (Allou et al., 2021).
Early-onset progressive encephalopathy-hearing loss-pons hypoplasia-brain atrophy syndrome
MedGen UID:
1798652
Concept ID:
C5567229
Disease or Syndrome
A rare genetic neurological disorder with characteristics of early-onset severe global developmental delay with regression, congenital or acquired microcephaly, hearing loss, truncal hypotonia, appendicular spasticity, and dystonia and/or myoclonus. Additional reported manifestations include seizures, optic atrophy, cortical visual impairment, scoliosis, and dysphagia. Brain imaging shows pontine hypoplasia, partial agenesis of the corpus callosum, and diffuse cerebral atrophy with relative sparing of the cerebellum.
Mitochondrial DNA depletion syndrome 20 (mngie type)
MedGen UID:
1804209
Concept ID:
C5676934
Disease or Syndrome
Mitochondrial DNA depletion syndrome-20 (MTDPS20) is an autosomal recessive multisystem disorder with variable manifestations and severity. Most patients develop symptoms in childhood, although the onset can range from infancy to the teenage years. Prominent features include severe gastrointestinal dysmotility often requiring parenteral nutrition, neurogenic bladder, and muscle weakness and atrophy. Neurologic involvement manifests as headaches, stroke-like episodes, seizures, pyramidal signs, and learning difficulties or cognitive decline. Brain imaging usually shows diffuse leukoencephalopathy and may show cerebellar atrophy. The disorder results from a defect in the maintenance and repair of mitochondrial DNA, resulting in mtDNA depletion and impaired mitochondrial function (summary by Bonora et al., 2021). For a discussion of genetic heterogeneity of mtDNA depletion syndromes, see MTDPS1 (603041).

Professional guidelines

PubMed

Truzzi JC, de Almeida FG, Sacomani CA, Reis J, Rocha FET
Int Braz J Urol 2022 Mar-Apr;48(2):220-243. doi: 10.1590/S1677-5538.IBJU.2021.0098. PMID: 34156189Free PMC Article
Panicker JN
Semin Neurol 2020 Oct;40(5):569-579. Epub 2020 Oct 16 doi: 10.1055/s-0040-1713876. PMID: 33065745Free PMC Article
Nicolle LE, Gupta K, Bradley SF, Colgan R, DeMuri GP, Drekonja D, Eckert LO, Geerlings SE, Köves B, Hooton TM, Juthani-Mehta M, Knight SL, Saint S, Schaeffer AJ, Trautner B, Wullt B, Siemieniuk R
Clin Infect Dis 2019 May 2;68(10):e83-e110. doi: 10.1093/cid/ciy1121. PMID: 30895288

Recent clinical studies

Therapy

Belko NA, Pohl HG
Urol Clin North Am 2024 Nov;51(4):537-549. Epub 2024 Aug 20 doi: 10.1016/j.ucl.2024.06.004. PMID: 39349021
Bapir R, Bhatti KH, Eliwa A, García-Perdomo HA, Gherabi N, Hennessey D, Magri V, Mourmouris P, Ouattara A, Perletti G, Philipraj J, Stamatiou K, Trinchieri A, Buchholz N
Arch Ital Urol Androl 2022 Dec 28;94(4):492-506. doi: 10.4081/aiua.2022.4.492. PMID: 36576454
Kinnear N, Barnett D, O'Callaghan M, Horsell K, Gani J, Hennessey D
Neurourol Urodyn 2020 Feb;39(2):854-862. Epub 2019 Dec 17 doi: 10.1002/nau.24253. PMID: 31845396
McKibben MJ, Seed P, Ross SS, Borawski KM
Urol Clin North Am 2015 Nov;42(4):527-36. Epub 2015 Jul 7 doi: 10.1016/j.ucl.2015.05.006. PMID: 26475949
Burks FN, Bui DT, Peters KM
Urol Clin North Am 2010 Nov;37(4):559-65. doi: 10.1016/j.ucl.2010.06.007. PMID: 20955907

Prognosis

Werneburg GT, Stoffel JT
Urol Clin North Am 2024 May;51(2):209-220. Epub 2024 Jan 6 doi: 10.1016/j.ucl.2023.12.001. PMID: 38609193
Boussetta A, Jellouli M, Baati R, Gargah T
Tunis Med 2021 Aout;99(8):898-902. PMID: 35261018Free PMC Article
Kinnear N, Barnett D, O'Callaghan M, Horsell K, Gani J, Hennessey D
Neurourol Urodyn 2020 Feb;39(2):854-862. Epub 2019 Dec 17 doi: 10.1002/nau.24253. PMID: 31845396
Stein R, Bogaert G, Dogan HS, Hoen L, Kocvara R, Nijman RJM, Quadackers JSLT, Rawashdeh YF, Silay MS, Tekgul S, Radmayr C
Neurourol Urodyn 2020 Jan;39(1):45-57. Epub 2019 Nov 13 doi: 10.1002/nau.24211. PMID: 31724222
Tseng TY, Stoller ML
Clin Geriatr Med 2009 Aug;25(3):437-43. doi: 10.1016/j.cger.2009.06.003. PMID: 19765491

Clinical prediction guides

Werneburg GT, Stoffel JT
Urol Clin North Am 2024 May;51(2):209-220. Epub 2024 Jan 6 doi: 10.1016/j.ucl.2023.12.001. PMID: 38609193
Bapir R, Bhatti KH, Eliwa A, García-Perdomo HA, Gherabi N, Hennessey D, Magri V, Mourmouris P, Ouattara A, Perletti G, Philipraj J, Stamatiou K, Trinchieri A, Buchholz N
Arch Ital Urol Androl 2022 Dec 28;94(4):492-506. doi: 10.4081/aiua.2022.4.492. PMID: 36576454
Boussetta A, Jellouli M, Baati R, Gargah T
Tunis Med 2021 Aout;99(8):898-902. PMID: 35261018Free PMC Article
Tate DG, Wheeler T, Lane GI, Forchheimer M, Anderson KD, Biering-Sorensen F, Cameron AP, Santacruz BG, Jakeman LB, Kennelly MJ, Kirshblum S, Krassioukov A, Krogh K, Mulcahey MJ, Noonan VK, Rodriguez GM, Spungen AM, Tulsky D, Post MW
J Spinal Cord Med 2020 Mar;43(2):141-164. doi: 10.1080/10790268.2019.1706033. PMID: 32105586Free PMC Article
Kinnear N, Barnett D, O'Callaghan M, Horsell K, Gani J, Hennessey D
Neurourol Urodyn 2020 Feb;39(2):854-862. Epub 2019 Dec 17 doi: 10.1002/nau.24253. PMID: 31845396

Recent systematic reviews

Bapir R, Bhatti KH, Eliwa A, García-Perdomo HA, Gherabi N, Hennessey D, Magri V, Mourmouris P, Ouattara A, Perletti G, Philipraj J, Stamatiou K, Trinchieri A, Buchholz N
Arch Ital Urol Androl 2022 Dec 28;94(4):492-506. doi: 10.4081/aiua.2022.4.492. PMID: 36576454
Salehi-Pourmehr H, Nouri O, Naseri A, Roshangar L, Rahbarghazi R, Sadigh-Eteghad S, Mahmoudi J, Mostafaei H, Roshandel MR, Hoseini L, Abolhasanpour N, Mostafaei A, Hajebrahimi S, Hashim H
Int Urogynecol J 2022 Aug;33(8):2081-2097. Epub 2021 Nov 12 doi: 10.1007/s00192-021-04986-6. PMID: 34767058
Chugh S, Pietropaolo A, Montanari E, Sarica K, Somani BK
Curr Urol Rep 2020 Mar 24;21(4):16. doi: 10.1007/s11934-020-0969-2. PMID: 32211969
Kinnear N, Barnett D, O'Callaghan M, Horsell K, Gani J, Hennessey D
Neurourol Urodyn 2020 Feb;39(2):854-862. Epub 2019 Dec 17 doi: 10.1002/nau.24253. PMID: 31845396
Stein R, Bogaert G, Dogan HS, Hoen L, Kocvara R, Nijman RJM, Quadackers JSLT, Rawashdeh YF, Silay MS, Tekgul S, Radmayr C
Neurourol Urodyn 2020 Jan;39(1):45-57. Epub 2019 Nov 13 doi: 10.1002/nau.24211. PMID: 31724222

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