Nutritional and metabolic disorders in multiple system atrophy and their management

Abstract

The causes of nutritional disorders in neurological diseases include dysphagia, cognitive dysfunction, and an increase in the energy requirement. Body weight, reflecting nutritional status, controlled by brain–mediated organ interactions. Leptin suppresses appetite and increases energy expenditure through the sympathetic nervous system from the hypothalamus. Ghrelin secreted by stomach shows appetite stimulation and energy storage effects through the hypothalamus.

In multiple system atrophy (MSA), patients needing tube feeding or tracheostomy showed a remarkable BMI decline, yet in the advanced stable stage with gastrostomy and tracheostomy, BMI increased despite low–calorie intake. We found that this advanced stage showed subcutaneous fat accumulation and increased leptin levels correlated to the autonomic symptom onset duration. It suggested that fat accumulation occurred due to leptin resistance caused by autonomic nervous system disorders. Sato et al. noted low albumin levels despite maintained body weight in the advanced MSA, indicating malnutrition.

In amyotrophic lateral sclerosis (ALS), weight loss is a poor prognostic factor, and high–calorie nutritional therapy may improve prognosis. We have shown that low ghrelin levels in male ALS patients are a poor prognostic factor, which may also be the case in MSA. Metabolic regulation via ghrelin suggests the potential for improving prognosis of some neurological diseases. We also found that serum albumin, BMI reduction rate, and prognostic nutritional index (PNI) are prognosis factors in the early stage of MSA to have diagnosis.

Appropriate nutritional intervention may improve the prognosis and quality of life in neurological diseases, underscoring the need for more evidence in MSA.