Cerebral Palsy (CP) is a limiting deficiency, characterized by a permanent neuromotor disorder which affects movements, resulting in non-progressive lesions of the immature brain during the neuro psychomotor stages. Epidemiological studies of premature births correlated with the presence of high levels of inflammation in the umbilical cord, amniotic fluid, and fetal blood, being that one of the most relevant underlying physiopathological mechanisms includes inflammation and intra-amniotic infection, with inflammatory response and damage to the developing brain. Recently attributed to the excessive production of cytokines, CP inflammation is mostly modulated through diet restriction, intestinal dysfunction, and drug intake. The high prevalence of convulsive crises in individuals with CP (77%) on its own does not bring about post inflammatory and post convulsive cytokine synthesis, treated with antiepileptic medication. In these individuals, there is high incidence of intestinal constipation (47%), besides oral dysbiosis, gingival bleeding and even greater increase in chronic inflammation. The dysbiosis causes an increase in mucous permeability (leaky-gut) of the gut-brain axis, and increase in seric endotoxin, demonstrating a persistent inflammatory state, and supporting the emergence of new side effects, which can become the object of future research.

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