Lower urinary tract dysfunction is a common sequel of neurological disease resulting in symptoms that significantly impacts quality of life. The site of the neurological lesion and its nature influence the pattern of dysfunction. The risk for developing upper urinary tract damage and renal failure is considerably lower in patients with slowly progressive nontraumatic neurological disorders, compared with those with spinal cord injury or spina bifida. This acknowledged difference in morbidity is considered when developing appropriate management algorithms. The preliminary evaluation consists of history taking, and a bladder diary and may be supplemented by tests such as uroflowmetry, post-void residual measurement, renal ultrasound, (video-)urodynamics, neurophysiology, and urethrocystoscopy, depending on the clinical indications. Incomplete bladder emptying is most often managed by intermittent catheterization, and storage dysfunction is managed by antimuscarinic medications. Intra-detrusor injections of onabotulinumtoxinA have revolutionized the management of neurogenic detrusor overactivity. Neuromodulation offers promise for managing both storage and voiding dysfunction. In select patients, reconstructive urological surgery may become necessary. An individualized, patient-tailored approach is required for the management of lower urinary tract dysfunction in this special population.

Neurogenic Bladder: Epidemiology, Diagnosis, and Management.

The lower urinary tract (LUT) in health is regulated by coordinated multi-level neurological inputs which require an intact central and peripheral nervous system. Lower urinary tract dysfunction is, therefore, a common sequelae of neurological disease and the patterns of bladder storage and voiding dysfunction depend upon the level of neurological lesion. Evaluation includes history taking, bladder diary, urological examination when relevant, ultrasonography and urodynamic testing when indicated. Antimuscarinic agents are the first line treatment for patients with storage dysfunction. Alternative treatments include intradetrusor injection of onabotulinumtoxinA, which has been shown to be of benefit in patients with neurogenic detrusor overactivity (NDO), and neuromodulation. Intermittent catheterization remains the option of choice in patients with significant voiding dysfunction resulting in high post-void residual volumes.

/pdf/neurogenic-lower-urinary-tract-dysfunction-evaluation-and-2t00z73x4u.pdf

Neurogenic lower urinary tract dysfunction: evaluation and management

Background

Nocturia is one of the commonest nonmotor symptoms in Parkinson's disease (PD) and has a significant impact on quality of life both for patients and their carers. There exists a relation between nocturia and poor sleep quality, falls, and institutionalization. Nocturia may manifest as a result of reduced functional bladder capacity or nocturnal polyuria; however, most often the cause is multifactorial. Disorders of circadian rhythm regulation are known to occur with sleep disturbances in PD may also contribute to nocturia.



Methods and Results

In this review, an overview of the assessment and management of nocturia in patients with PD is presented. History taking, medication review, and a bladder diary form the cornerstone of the evaluation. Urinalysis, ultrasonography, and urodynamic studies help to assess the cause for lower urinary tract symptoms and exclude concomitant pathologies, such as bladder outlet obstruction. Antimuscarinic medications are the first-line treatment for the overactive bladder; however, caution is needed when using these medications in individuals predisposed to cognitive impairment. Desmopressin is effective for managing nocturnal polyuria.



Conclusions

An individualized approach is recommended to optimize the management of nocturia in PD.

https://movementdisorders.onlinelibrary.wiley.com/doi/pdf/10.1002/mdc3.12374

Nocturia in Parkinson's Disease: Why Does It Occur and How to Manage?

Urogenital dysfunction is commonly reported in Parkinson’s disease (PD), and history taking and a bladder diary form the cornerstone of evaluation. The assessment of lower urinary tract (LUT) symptoms include urinalysis, ultrasonography, and urodynamic studies and help to evaluate concomitant urological pathologies such as benign prostate enlargement. Antimuscarinic medications are the first line treatment for overactive bladder (OAB) symptoms and solifenacin has been specifically studied in PD. Antimuscarininc drugs may exacerbate PD-related constipation and xerostomia, and caution is advised when using these medications in individuals where cognitive impairment is suspected. Desmopressin is effective for the management of nocturnal polyuria which has been reported to be common in PD. Intradetrusor injections of botulinum toxin have been shown to be effective for detrusor overactivity, however, are associated with the risk of urinary retention. Neuromodulation is a promising, minimally invasive treatment for PD-related OAB symptoms. Erectile dysfunction is commonly reported and first line treatments include phosphodiesterase-5 inhibitors. A patient-tailored approach is required for the optimal management of urogenital dysfunction in PD.

/pdf/treatment-options-for-urogenital-dysfunction-in-parkinson-s-459jjys64h.pdf

Treatment Options for Urogenital Dysfunction in Parkinson's Disease.

Progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS; the most common phenotype of corticobasal degeneration) are tauopathies with a relentless course, usually starting in the mid-60s and leading to death after an average of 7 years. There is as yet no specific or disease-modifying treatment. Clinical deficits in PSP are numerous, involve the entire neuraxis, and present as several discrete phenotypes. They center on rigidity, bradykinesia, postural instability, gait freezing, supranuclear ocular motor impairment, dysarthria, dysphagia, incontinence, sleep disorders, frontal cognitive dysfunction, and a variety of behavioral changes. CBS presents with prominent and usually asymmetric dystonia, apraxia, myoclonus, pyramidal signs, and cortical sensory loss. The symptoms and deficits of PSP and CBS are amenable to a variety of treatment strategies but most physicians, including many neurologists, are reluctant to care for patients with these conditions because of unfamiliarity with their multiplicity of interacting symptoms and deficits. CurePSP, the organization devoted to support, research, and education for PSP and CBS, created its CurePSP Centers of Care network in North America in 2017 to improve patient access to clinical expertise and develop collaborations. The directors of the 25 centers have created this consensus document outlining best practices in the management of PSP and CBS. They formed a writing committee for each of 12 sub-topics. A 4-member Steering Committee collated and edited the contributions. The result was returned to the entire cohort of authors for further comments, which were considered for incorporation by the Steering Committee. The authors hope that this publication will serve as a convenient guide for all clinicians caring for patients with PSP and CBS and that it will improve care for patients with these devastating but manageable disorders.

/pdf/best-practices-in-the-clinical-management-of-progressive-4iopm418za.pdf

Best Practices in the Clinical Management of Progressive Supranuclear Palsy and Corticobasal Syndrome: A Consensus Statement of the CurePSP Centers of Care

Background

Waking up from sleep more than once to pass urine, known as nocturia, is an important nonmotor symptom in Parkinson's disease (PD). Very little is known about the cause for nocturia. The aim of this work was to evaluate lower urinary tract (LUT) symptoms in patients with PD reporting nocturia using standardized validated questionnaires and bladder diaries and to assess the impact of nocturia on quality of life and sleep.



Methods

Twenty-three consecutive patients with PD (17 males, 6 females; mean age: 68.5 years; range, 50–85) referred to a specialist uro-neurology clinic reporting nocturia according to the International Continence Society definition were included. Patients measured their daily fluid intake, urinary output per void, and recorded these with the timing of voids on a 3-day bladder diary. Standardized questionnaires were used to assess LUT symptoms (Urinary Symptom Profile, International Prostate Symptom Score, and Qualiveen Short Form) and sleep quality (Parkinson's Disease Sleep Scale).



Results

Mean duration of PD was 10.1 years, and mean severity on H & Y scale was 3.0 (range, 1.0–5.0). Median duration of LUT symptoms was 6.0 years. Mean night-time urinary frequency was 3.5 (range, 1.0–7.3), and mean nocturnal maximum voided volume was 242 mL. Mean Nocturnal Polyuria Index (NPi) was 0.4 (range, 0.13–0.75), and 13 patients (56.5%) had nocturnal polyuria (NPi > 0.33). Patients with nocturnal polyuria reported more-severe LUT symptoms that impacted quality of life and sleep.



Conclusions

In this preliminary study, nocturnal polyuria seems to be common in patients with PD reporting nocturia and appears to affect quality of life and sleep, though this was not statistically significant. The bladder diary is an essential tool in the assessment of nocturia in patients with PD.

https://movementdisorders.onlinelibrary.wiley.com/doi/pdf/10.1002/mdc3.12279

Johann Hofereiter

Papers

Nocturia in Patients With Parkinson's Disease