Altered levels of α-melanocyte stimulating hormone in cerebrospinal fluid and plasma of patients with traumatic brain injury

Abstract

Traumatic brain injury (TBI) is closely associated with marked inflammation. Although alpha-Melanocyte-Stimulating Hormone (α-MSH) exerts powerful anti-inflammatory effects, changes in endogenous α-MSH levels following TBI remain poorly understood. We investigated the changes of α-MSH levels in the cerebrospinal fluid (CSF) and plasma of post-TBI patients and the association of these changes with the severity of TBI and inflammation. TBI severity was assessed by the GCS coma scale from which, patients were separated into three groups. Clinical data were collected on days 1, 3, 5, and 7 including levels of α-MSH, tumor necrosis factor (TNF-α), and intracranial pressure (ICP). α-MSH levels in CSF steadily increased for one week (peak at day 5) but plasma α-MSH decreased and remained low. These changes were more substantial in the Severe Group of TBI with lower GCS. TNF-α levels were similarly increased in both CSF and plasma (peak at day 3). In the early phase of TBI elevated TNF-α and ICP dominated, and CSF α-MSH displayed a slow and insufficient increase. In later phases of TBI, TNF-α and ICP levels were alleviated concordantly with sustained increases in central α-MSH, wherein an anti-inflammatory environment might predominate. The relationship between plasma α-MSH and TNF-α showed significant negative correlation, and the relationship between CSF α-MSH and TNF-α showed significant positive correlation with a two-day lag. In conclusion, plasma α-MSH levels decreased, but CSF levels increased slowly following TBI. These changes were more substantial in severe patients with a lower GCS. Increases in central α-MSH paralleled alleviation of inflammation.

Keywords: Alpha-melanocyte stimulating hormone (α-MSH); Cerebrospinal fluid (CSF); Intracranial pressure (ICP); Traumatic brain injury (TBI); Tumor necrosis factor-alpha (TNF-α).