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.
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.