Impaired cerebral haemodynamic function associated with chronic traumatic brain injury in professional boxers

Abstract

The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO₂ (cerebrovascular reactivity to changes in CO₂: 5% CO₂ and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitive function (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial blood pressure (finger photoplethysmography), end-tidal CO₂ (capnography) and cortical oxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (P<0.05 compared with controls). Likewise, CVRCO₂ was also reduced resulting in a lower CVRCO₂ range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r=-0.84, P<0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career.

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

“…228,229 In human studies, stimulation-induced increases in blood flow have also been shown to be perturbed after TBI. [232][233][234] Data are also available showing that, in addition to the acute changes in CBF, long-term alterations in rCBF are also observed in experimental and clinical models (Fig. 4).…”

“…4). [233][234][235][236][237][238][239][240][241] Using MRI imaging or other methodologies, evidence for depressed blood flow throughout the injured and contralateral hemisphere have been documented. Moderate reductions in chronic blood flow can augment slow, evolving injury processes or aggravate events that were initiated by the acute insult.…”

Phosphodiesterase‐5 inhibition potentiates cerebrovascular reactivity in chronic traumatic brain injury

“…There are established methods to study CVR non‐invasively in humans including transcranial Doppler (TCD), near infra‐red spectroscopy (NIRS) with hypercapnia,23 and MRI‐Blood Oxygen Level Dependent (MRI‐BOLD) with hypercapnia challenge. In professional boxers, CVR is decreased in the first week after a fight, and correlates with cumulative lifetime concussions 24. A meta‐analysis of CVR after sports concussion concluded that CVR is decreased acutely 25.…”

Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

“…DM has long been considered to be a physiological cause of severe TBI, but abnormalities in cerebrovascular reactivity and cerebral blood flow have also been found in mild TBI, and especially in people who have suffered multiform mild TBIs and who have enduing post-concussive symptoms (18,19) Data from neuroimaging studies (20) using T2*-weighted gradient echo imaging, which is sensitive to DM, found DM in deep white matter in 23 of 98 patients who suffered a TBI.…”