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  4. Pathophysiology of Neurogenic Obesity After Spinal Cord Injury

Pathophysiology of Neurogenic Obesity After Spinal Cord Injury

Top Spinal Cord Inj Rehabil, 2021 · DOI: 10.46292/sci20-00067 · Published: January 1, 2021

Spinal Cord InjuryEndocrinology

Simple Explanation

Spinal cord injury (SCI) leads to a unique physiology characterized by muscle loss, bone density reduction, anabolic hormone deficiency, sympathetic nervous system dysfunction and altered satiety, impacting energy balance and body composition. Neurogenic obesity in SCI patients increases the risk of metabolic dysfunction, including inflammation, high blood sugar, abnormal lipid levels and high blood pressure. This article highlights the relationship between neurogenic obesity and metabolic syndrome in SCI, explaining mechanisms related to adipose tissue pathology and comorbidities.

Study Duration
Not specified
Participants
Representative studies of persons with SCI
Evidence Level
Not specified

Key Findings

  • 1
    Individuals with SCI have altered energy balance due to sarcopenia, neurogenic osteoporosis, neurogenic anabolic deficiency, sympathetic dysfunction, and blunted satiety.
  • 2
    Neurogenic obesity is associated with metabolic syndrome, increasing the risk of systemic inflammation, hyperglycemia, dyslipidemia, and hypertension.
  • 3
    Adipose tissue in SCI patients produces proinflammatory adipokines, which mediate dyslipidemia, insulin resistance, and hypertension.

Research Summary

Physiological changes in adipose tissue following SCI should be characterized as neurogenic obesity due to an obligatory sarcopenia, neurogenic osteoporosis, neurogenic anabolic deficiency, sympathetic dysfunction, and blunted satiety associated with SCI, all of which alter energy balance and subsequently body composition. Because of these findings, recent guidelines recommend characterizing obesity in SCI as BMI ≥22 kg/m2 or as %BF >22% for men and >35% for women. The epidemic of neurogenic obesity associated with SCI puts individuals at high risk for the metabolic syndrome, due to AT-related systemic inflammation, hyperglycemia, dyslipidemia, and HTN.

Practical Implications

Clinical Vigilance

Greater vigilance among SCI specialists and primary care providers is needed to manage the epidemic of neurogenic obesity and metabolic syndrome from a public health perspective.

Optimized Screening

Clinicians should optimize their screening practices and management strategies for comorbidities associated with neurogenic obesity in SCI patients.

Targeted Interventions

Future research should focus on prevention and management of neurogenic obesity through exercise and nutrition.

Study Limitations

  • 1
    Space and reference restrictions may have limited the identification, review, or inclusion of all pertinent and seminal studies.
  • 2
    Lack of consensus for an SCI-screening tool to accurately classify obesity in this special population
  • 3
    The need for a transparent and unbiased review using systematic evidence synthesis methodology to fully describe the pathophysiology, prevalence, and incidence of neurogenic obesity in persons with SCI.

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