Parkinson’s disease and nocturnal polyuria

Sakakibara R1, Shimizu A2, Takahashi O2, Sekido N3, Ogata T1, Sawai S1, Uchiyama T4, Yamamoto T5, Yamanishi T6, Shibata C6

Research Type

Clinical

Abstract Category

Neurourology

Abstract 247
Nocturia
Scientific Podium Short Oral Session 17
Friday 9th September 2022
10:42 - 10:50
Hall G1
Neuropathies: Central Nocturia Voiding Diary Overactive Bladder
1. Neurology, Sakura Medical Center, Toho University, 2. Clinical Physiology Unit, Sakura Medical Center, Toho University, 3. Urology, Ohashi Medical Center, Toho University, 4. Neurology, International University of Health and Welfare, Narita, 5. Neurology, Chiba Prefectural University of Health Sciences, 6. Continence Center, Dokkyo Medical College
Online
Presenter
Links

Abstract

Hypothesis / aims of study
The question of whether Parkinson’s disease (PD) patients have nocturnal polyuria (NP) has not yet been fully answered. 
Objective is to determine whether NP was present in PD patients and if so, what its relevant factors were.
Study design, materials and methods
This was a retrospective analysis. We had 36 consecutive referred PD patients: age, 71.5 years (range, 54-83 years); 24 men, 12 women; mean disease duration, 2.5 years (1.0-4.5 years); Hoehn and Yahr motor scale, 3.0 (2.0-3.5); all ambulatory; all on treatment. All PD patients completed a lower urinary tract symptom (LUTS questionnaire) and a bladder diary, and underwent urodynamics testing.
Results
NP was identified in 56% of patients. NP was more common in patients with nocturia (p<0.05), and in patients with urodynamic detrusor overactivity (p<0.01). There was no relation between NP and gender, age, PD medications, blood pressure, or comorbid diabetes.
Interpretation of results
There may be two PD-related mechanisms in NP. First, hypothalamic arginine vasopressin (AVP) neurons (originating in the suprachiasmatic nucleus [SCN] and the paraventricular nucleus [PVN], which project fibers to the posterior pituitary gland, relevant to circadian rhythm generation, nausea, analgesia, antidiuresis [reabsorption of salt and water in the kidneys], etc.) are affected in PD, leading to either the syndrome of inappropriate antidiuretic hormone secretion (SIADH, clinically manifested as hyponatremia in rare cases) or the loss of nocturnal surge/increase of AVP (loss of NAVP, clinically manifested as NP).15 Similar conditions have been documented in multiple system atrophy that also affects hypothalamic AVP neurons. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model dogs, NP and loss of NAVP were reported, and the administration of levodopa resumed NP and loss of NAVP. In another study, DAergic stimulation increased plasma AVP. Therefore, DA neurons are thought to facilitate NAVP. In the present study, NP was found to have a close relation with detrusor overactivity. Detrusor overactivity in PD is most probably a reflection of lesion in the nigrostriatal DA pathways. Considering the results of the present study, we postulate that in PD, loss of DA neurons leads to both NP (hypothalamic circuit) and detrusor overactivity (nigrostriatal circuit). However, it is important to note that loss of NAVP is not noted solely in brain diseases but also in general NP, at least in some cases. The second mechanism is orthostatic hypotension, although this relationship was not obvious in the present study. PD affects extra-brain periarterial noradrenergic (NAergic) fibers (innervating alpha1B receptors), producing orthostatic hypotension. In this condition, the glomerular filtration rate (GFR) depends on posture (on standing: diurnal peripheral fluid shift, edema and decreased GFR [immobility is also a factor]; on lying: nocturnal rostral fluid shift, increased GFR and NP). Other etiologies relevant to orthostatic hypotension, such as cervical spinal cord injury 22 and diabetic neuropathy, also cause NP.
Concluding message
A total of 56% of PD patients had NP, which had a close relation with detrusor overactivity (p<0.01). These findings suggest that in PD, the loss of dopaminergic neurons leads to NP (hypothalamic circuit) and detrusor overactivity (nigrostriatal circuit).
Figure 1 Figure 1. Relationship between nocturnal polyuria and other factors in Parkinson’s disease (PD).
References
  1. Sakakibara R, Panicker J, Finazzi-Agro E, Iacovelli V, Bruschini H; Parkinson’s Disease Subcomittee, The Neurourology Promotion Committee in The International Continence Society. A guideline for the management of bladder dysfunction in Parkinson’s disease and other gait disorders. Neurourol Urodyn. 2016; 35: 551-563.
  2. Romain J, Torny F, Dumas JP, Gamé X, Descazeaud A. Is nocturnal polyuria more frequent among patients with Parkinson’s disease? Prog Urol. 2015; 25: 312-317.
  3. Smith M, Seth J, Batla A, Hofereiter J, Bhatia KP, Panicker JN. Nocturia in patients with Parkinson’s disease. Mov Disord Clin Pract. 2015; 3: 168-172.
Disclosures
Funding None Clinical Trial No Subjects Human Ethics Committee Ethics committee in Sakura Medical Center, Toho University Helsinki Yes Informed Consent Yes
Citation

Continence 2S2 (2022) 100336
DOI: 10.1016/j.cont.2022.100336

20/11/2024 14:03:26