Gastrointestinal (GI) involvement in the pathogenesis of Parkinson’s Disease (PD) has been widely recognized and supported in recent literature. Prospective and retrospective studies found non-motor symptoms within the GI, specifically constipation, precede cardinal signs and cognitive decline by almost 20 years. In 2002, Braak et al. were the first to propose that PD is a six-stage propagating neuropathological process originating from the GI tract (GIT). Aggregated α-synuclein (α-syn) protein from the GIT is pathognomonic for the development of PD. This article reviews the current literature from the past 10 years as well as original research found in PubMed on the combined effects of enteric glial cells and lectins on the development of Parkinson’s Disease. Studies have found that these aggregated and phosphorylated proteins gain access to the brain via retrograde transport through fast and slow fibers of intestinal neurons. Plant lectins, commonly found within plant-based diets, have been found to induce Leaky Gut Syndrome and can activate enteric glial cells, causing the release of pro-inflammatory cytokines. Oxidative stress on the enteric neurons, caused by a chronic neuro-inflammatory state, can cause a-syn aggregation and lead to Lewy Body formation, a hallmark finding in PD. Although the current literature provides a connection between the consumption of plant lectins and the pathophysiology of PD, further research is required to evaluate confounding variables such as food antigen mimicry and other harmful substances found in our diets.

Crouzon syndrome (CS) is a rare autosomal dominant disorder that requires care from a multidisciplinary team and early surgical management to minimize complications. Despite the shared similarities across craniosynostoses, CS can be differentiated by the presence of normal bone development of the hands and feet and hypertelorism (large distance between the eyes). Other common features include midface hypoplasia, shallow orbits, ocular proptosis, and dental abnormalities including possible bifid uvula or Vshaped maxillary arch. In this report, we present a case of prolonged foot pain in a four-year and twomonth-old boy with CS; we also engage in a brief review of the literature. The patient's physical exam and laboratory work were unremarkable on the initial presentation. Radiographic films showed signs of potential demineralization of bone tissue. He was prescribed calcium and vitamin D supplementation with complete resolution of his symptoms at the three-month follow-up visit.