AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |
Back to Blog
Cardiac coherence brainn injury8/16/2023 Based on the above findings regarding correlations between TBI severity and increasing autonomic impairment during the acute trauma phase, and on the assumption that CAN dysfunction contributes to cardiovascular autonomic dysregulation in patients with a history of mild TBI, we hypothesize that patients with a history of more severe, i.e., with moderate or severe TBI also have more prominent CAN alteration and consequently retain more prominent cardiovascular autonomic dysregulation than do patients with a history of mild TBI. Some studies also suggest that long-term mortality rates after TBI increase with trauma severity. Similarly, Sykora and co-workers recently reported associations between autonomic cardiovascular dysfunction and increased mortality in patients with acute, severe traumatic brain injury. observed episodes of dysautonomia in 11.8% of patients during the acute phase of severe TBI and found associations between dysautonomia and diffuse axonal injury as well as spasticity at follow-up. showed that mortality of acute brain injury patients is linked with decreased heart rate variability and baroreflex sensitivity. In acute brain injuries, Goldstein and co-workers found evidence for cardiovascular and autonomic uncoupling and a deterioration of heart rate and blood pressure variability with increasing trauma severity. In patients with moderate or severe TBI, autonomic dysfunction, so far, has only been reported during the acute phase after the trauma. These findings support the assumption that minor central autonomic network (CAN) dysfunction accounts for the subclinical cardiovascular dysregulation seen in patients even years after mild TBI. Similarly, we found a compromised ability to activate cardiovagal outflow upon eyeball pressure stimulation, which slows heart rate independently from the baroreflex arc. In patients with no clinically overt autonomic dysfunction but with a history of mild TBI, we found a decrease in the overall cardiovascular modulation at rest with a shift towards more sympathetic than parasympathetic activity and a decrease in baroreflex-mediated sympathetic and parasympathetic responses to orthostatic challenge. Particularly, the cause of increased long-term mortality rates is unknown but has been considered to be associated with subtle impairment of the central network assuring autonomic regulation. Patients with a history of mild traumatic brain injury (TBI) frequently have long-lasting post-traumatic complications including neurological, neuro-psychological, and social sequelae, and even an increased risk of unexplained long-term mortality. More than 6 months after TBI, there is autonomic dysfunction at rest and upon standing which is more pronounced after moderate–severe than mild TBI and in part correlates with initial trauma severity. GCS scores correlated positively with LFnu-RRI powers, LF/HF-RRI ratios, and inversely with HFnu-RRI powers, at standing position. Upon standing, only post-mild-TBI patients and controls increased LF-BPsys powers and BPsys and decreased HF-RRI powers. LFnu-RRI powers were higher and HFnu-RRI powers were lower in post-mild-TBI patients than controls. Supine BPsys and LFnu-RRI powers were higher while HFnu-RRI powers were lower in post-moderate–severe-TBI patients than post-mild-TBI patients and controls. We correlated autonomic parameters with initial Glasgow Coma Scale (GCS) scores (Spearman test significance: p < 0.05). We determined mainly sympathetic low (LF) and parasympathetic high (HF) frequency powers of RRI fluctuations, sympathetically mediated LF-BPsys powers, LF/HF-RRI ratios, normalized (nu) LF-RRI and HF-RRI powers, and compared data between groups, at rest and upon standing (ANOVA with post hoc testing). In 20 post-mild-TBI patients (6–78 months after TBI), age-matched 20 post-moderate–severe-TBI patients (6–94 months after TBI) and 20 controls, we monitored respiration, RR intervals (RRI) and systolic blood pressure (BPsys) at supine rest and upon standing. This study was performed to evaluate differences in autonomic modulation at rest and upon standing between patients with a history of mild TBI (post-mild-TBI patients), moderate or severe TBI (post-moderate–severe-TBI patients), and healthy controls. Central autonomic dysfunction might depend on initial trauma severity. After traumatic brain injury (TBI), central autonomic dysfunction might contribute to long-term increased mortality rates.
0 Comments
Read More
Leave a Reply. |