The non-motor manifestations of Parkinson’s disease have been known since the description of the disease by James Parkinson in 1817. In his ‘Essay of the Shaking Palsy’, he clearly stated ‘sleep becomes much disturbed … .the bowels, which had been all along torpid, in most cases demand stimulating medicines of very considerable power … .sometimes the expulsion of feces requiring mechanical aid’ [1]. However, for years the emphasis has been on the motor features which define the disease, largely by the availability of dopaminergic and other agents which alleviate the bradykinesia and rigidity, and partly also the tremor. In fact, these drugs added new non-motor manifestations.

Parkinson’s disease (PD) in pregnancy is a rare occurrence. PD presents before the age of 40 in only 5% of cases and less than 400 women less than 50 years of age are diagnosed with PD each year in the United States [1]. However, as the average maternal age is increasing, it may become more common. Incidence of pregnancy in PD is unknown and knowledge is limited to case reports.

Animal models suggest estrogen has a neuroprotective effect on dopaminergic neurons by influencing anti-oxidative, anti-inflammatory, and anti-apoptotic pathways with studies showing cell death can be significantly decreased by administration of estrogen [2]. Other animal studies showed estrogen has dopaminergic effect by inhibiting catechol-O-methyltransferase (COMT) and striatal dopamine transporter activity as well as enhancing tyrosine hydroxylase [3, 4]. Incidence of PD is less in women, yet after menopause risk of PD increases [5]. Women tend to have less severe disease but more dyskinesia [6, 7].