AimsBladder dysfunction is frequent during the course of multiple
sclerosis (MS), observed in up to 75% of patients. Urinary
symptomatology can be a feature of the first episode of MS in a minority
of cases, and most often shows characteristics of an overactive bladder
(OAB), with voiding symptoms seen less frequently, often in combination
with OAB. The neural control of micturition is complex, involving
systems located in the brain, spinal cord, and periphery, and
implicating central noradrenergic, serotonergic, and dopaminergic
activities. Urinary disorders are also linked to anxiety and depression,
conditions connected to hypothalamus-pituitary-adrenal axis activity. In
this study we aimed to investigate neurochemical and neuroendocrine
correlates of bladder dysfunction in early MS.
MethodsWe included 101 patients at first demyelinating episode
suggestive of MS that were drug-free at assessment. We evaluated the
presence of urinary symptomatology and estimated CSF levels of the main
metabolites of noradrenaline, serotonin, and dopamine, as well CSF-ACTH
and serum cortisol.
ResultsIn total, 15 patients (15%) reported urinary dysfunction
suggestive of OAB. Four of these had coexistent voiding symptomatology.
The serotonin metabolite 5-HIAA was significantly reduced (P=0.017) in
patients with OAB syndrome, while there were no differences in the
metabolites of noradrenaline (MHPG) and of dopamine (HVA). Additionally,
significantly lower serum cortisol (P=0.009) and borderline lower
CSF-ACTH (P=0.08) were found in patients with OAB.
ConclusionsMS patients with OAB syndrome at the first demyelinating
episode show reductions in central serotonergic activity and stress
hormones. Whether the same changes persist at later disease stages
remains to be investigated. Neurourol. Urodynam. 35:955-958, 2016. (c)
2015 Wiley Periodicals, Inc