The question of whether PD patients have NP has not yet been fully answered.  The aim of this study is to determine whether Parkinson’s disease (PD) causes nocturnal polyuria (NP) and if so, what its relevant factors were.

We retrospectively analyzed 36 consecutive referred PD patients: mean age, 71.5 years, range, 54-83 years; gender, 24 men, 12 women; mean disease duration, 2.5 years, range, 1.0-4.5 years; median Hoehn and Yahr motor scale, 3.0, range, 2.0-3.5; all ambulatory; all on treatment. All PD patients completed 1) a lower urinary tract symptom (LUTS) questionnaire, 2) a bladder diary, and 3) urodynamics testing.

NP was found in 56% of patients. NP was more common in patients with nocturia (p<0.05), and in patients with urodynamic detrusor overactivity (DO) (p<0.01) with statistical significance. In contrast, we found no relation between NP and gender, age, PD medications, blood pressure, or comorbid diabetes.

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 the loss of nocturnal surge/increase of AVP (loss of nocturnal AVP rise, clinically manifested as nocturnal polyuria NP). 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 nocturnal AVP rise were reported, and the administration of levodopa resumed NP and loss of nocturnal AVP rise. In another study, DAergic stimulation increased plasma AVP. Therefore, DA neurons are thought to facilitate nocturnal AVP rise.  
In addition, our study results showed a relation between NP (suggesting hypothalamic DA neuron lesion) and detrusor overactivity (suggesting substantia nigra DA neuron lesion). Therefore, we should care for both DA-depletion-related NP and detrusor overactivity in PD patients.

We found that 56% of PD patients had NP, which had a close relation with DO (p<0.05). These findings indicate that in PD, pathological loss of dopaminergic neurons in the brain leads to NP via the hypothalamic circuit and detrusor overactivity via the nigrostriatal circuit together. Since both NP and DO significantly affect the quality of life, NP should also be checked regularly as a non-motor symptom of PD.

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