Bariatric Surgery-Associated Myelopathy

Abstract

Bariatric surgery is gaining acceptance as an efficient treatment modality for adults and adolescents with morbid obesity. The early postbariatric period has the potential to induce an immunomodulatory imbalance due to the development or worsening of nutritional deficiencies, changes in hormonal balance (specifically after sleeve gastrectomy), and a shift in the proinflammatory cytokine profile along with a major change in the gut microbiome and permeability. These changes may induce encephalomyelitic T cell activity, change neural barrier permeability, and induce gut dysbioisis, favoring a proinflammatory metabolic profile. Such changes, in genetically prone individuals or those with additional risk factors, may lead to the development of myelopathy, particularly MS. Key Message: Postbariatric myelopathy is rare but should be considered in bariatric patients with relevant complaints in the postoperative period.

Keywords: Bariatric surgery; Myelopathy; Nutritional deficiencies.

Fig. 1

a, c First spinal MRI examination showing longitudinal myelitis with increased T2 signal and slight cord expansion at C6 through vitamin D₁ levels. b, d Following gadolinium injection, there is central, almost complete enhancement, mainly involving the central cord.

Fig. 2

The multiple elements related to bariatric surgery that may be involved in the development of myelopathies. Patients with a specific genetic predisposition who are obese are exposed to additional potential elements related to bariatric procedures that may induce the development of myelopathy and multiple sclerosis.