Should We Trust Perceived Effort for Loading Control and Resistance Exercise Prescription After ACL Reconstruction?

2021 ◽  
pp. 194173812110412
Author(s):  
Daniel Germano Maciel ◽  
Mikhail Santos Cerqueira ◽  
Tim J. Gabbett ◽  
Hassan Mohamed Elsangedy ◽  
Wouber Hérickson de Brito Vieira

Context: The rating of perceived effort (RPE) is a common method used in clinical practice for monitoring, loading control, and resistance training prescription during rehabilitation after rupture and anterior cruciate ligament reconstruction (ACLR). It is suggested that the RPE results from the integration of the afferent feedback and corollary discharge in the motor and somatosensory cortex, and from the activation of brain areas related to emotions, affect, memory, and pain (eg, posterior cingulate cortex, precuneus, and prefrontal cortex). Recent studies have shown that rupture and ACLR induce neural adaptations in the brain commonly associated with the RPE. Therefore, we hypothesize that RPE could be affected because of neural adaptations induced by rupture and ACLR. Study Design: Clinical review. Level of Evidence: Level 5. Results: RPE could be directly altered by changes in the activation of motor cortex, posterior cingulate cortex, and prefrontal cortex. These neural adaptations may be induced by indirect mechanisms, such as the afferent feedback deficit, pain, and fear of movement (kinesiophobia) that patients may feel after rupture and ACLR. Conclusion: Using only RPE for monitoring, loading control, and resistance training prescription in patients who had undergone ACLR could lead to under- or overdosing resistance exercise, and therefore, impair the rehabilitation process. Strength-of-Recommendation Taxonomy: 3C.

2017 ◽  
Author(s):  
Song. Qi ◽  
Demis. Hassabis ◽  
Jiayin Sun ◽  
Fangjian. Guo ◽  
Nathaniel Daw ◽  
...  

Flight initiation distance (FID), the distance at which an organism flees from an approaching threat, is an ecological metric of cost-benefit functions of escape decisions. We adapted the FID paradigm to investigate how fast or slow attacking ‘virtual predators’ constrain escape decisions. We show that rapid escape decisions rely on ‘reactive fear’ circuits in the periaqueductal gray and midcingulate cortex (MCC), while protracted escape decisions, defined by larger buffer zones, were associated with ‘cognitive fear’ circuits which include posterior cingulate cortex, hippocampus and the ventromedial prefrontal cortex, circuits implicated in strategic avoidance and behavioral flexibility. Using a Bayesian Decision Model, we further show that optimization of escape decisions under rapid flight were localized to the MCC, a region involved in adaptive motor control, while the hippocampus is implicated in optimizing decisions that update and control slower escape initiation. These results demonstrate an unexplored link between defensive survival circuits and their role in adaptive escape decisions.SignificanceHumans, like other animals, have evolved a set of circuits whose primary function is survival. In the case of predation, these circuits include ‘reactive fear’ circuits involved in fast and immediate escape decisions and ‘cognitive fear’ circuits that are involved in the conscious feeling of threat as well as slow strategic escape. Using neuroimaging combined with computational modeling, we support this differentiation of fear circuits by showing that fast escape decisions are elicited by the periaqueductal gray and MCC, regions involved in reactive flight. Conversely, slower escape decisions rely on the hippocampus, posterior cingulate cortex and prefrontal cortex, a circuit implicated in behavioral flexibility. These results support the role of the defensive survival circuitry in escape decisions and a separation of fear into reactive and cognitive circuits.


2019 ◽  
Vol 53 (8) ◽  
pp. 794-806 ◽  
Author(s):  
Jooyoung Oh ◽  
Jung Eun Shin ◽  
Kyu Hyun Yang ◽  
Sunghyon Kyeong ◽  
Woo Suk Lee ◽  
...  

Objective: Delirium is an acute brain failure related to uncertain problems in neural connectivity, including aberrant functional interactions between remote cortical regions. This study aimed to elucidate the underlying neural mechanisms of delirium by clarifying the changes in resting-state functional connectivity induced by postoperative delirium using imaging data scanned before and after surgery. Method: Fifty-eight patients with a femoral neck fracture were preoperatively scanned using resting-state functional magnetic resonance imaging. Twenty-five patients developed postoperative delirium, and 14 of those had follow-up scans during delirium. Eighteen patients without delirium completed follow-up scans 5 or 6 days after surgery. We assessed group differences in voxel-based connectivity, in which the seeds were the posterior cingulate cortex, medial prefrontal cortex and 11 subcortical regions. Connections between the subcortical regions were also examined. Results: The results showed four major findings during delirium. Both the posterior cingulate cortex and medial prefrontal cortex were strongly connected to the dorsolateral prefrontal cortex. The posterior cingulate cortex had hyperconnectivity with the inferior parietal lobule, whereas the medial prefrontal cortex had hyperconnectivity with the frontopolar cortex and hypoconnectivity with the superior frontal gyrus. Connectivity of the striatum with the anterior cingulate cortex and insula was increased. Disconnections were found between the lower subcortical regions including the neurotransmitter origins and the striatum/thalamus in the upper level. Conclusions: Our findings suggest that cortical dysfunction during delirium is characterized by a diminution of the anticorrelation between the default mode network and task-positive regions, excessive internal connections in the posterior default mode network and a complex imbalance of internal connectivity in the anterior default mode network. These dysfunctions can be attributed to the loss of reciprocity between the default mode network and central executive network associated with defective function in the salience network, which might be closely linked to aberrant subcortical neurotransmission-related connectivity and striato-cortical connectivity.


NeuroImage ◽  
2016 ◽  
Vol 141 ◽  
pp. 366-377 ◽  
Author(s):  
Katya Krieger-Redwood ◽  
Elizabeth Jefferies ◽  
Theodoros Karapanagiotidis ◽  
Robert Seymour ◽  
Adonany Nunes ◽  
...  

2019 ◽  
Vol 16 (11) ◽  
pp. 1063-1071 ◽  
Author(s):  
Gonzague Foucault ◽  
Guillaume T Duval ◽  
Romain Simon ◽  
Olivier Beauchet ◽  
Mickael Dinomais ◽  
...  

Background: Vitamin D insufficiency is associated with brain changes, and cognitive and mobility declines in older adults. Method: Two hundred and fifteen Caucasian older community-dwellers (mean±SD, 72.1±5.5years; 40% female) received a blood test and brain MRI. The thickness of perigenual anterior cingulate cortex, midcingulate cortex and posterior cingulate cortex was measured using FreeSurfer from T1-weighted MR images. Age, gender, education, BMI, mean arterial pressure, comorbidities, use of vitamin D supplements or anti-vascular drugs, MMSE, GDS, IADL, serum calcium and vitamin B9 concentrations, creatinine clearance were used as covariables. Results: Participants with vitamin D insufficiency (n=80) had thinner total cingulate thickness than the others (24.6±1.9mm versus 25.3±1.4mm, P=0.001); a significant difference found for all 3 regions. Vitamin D insufficiency was cross-sectionally associated with a decreased total cingulate thickness (β=- 0.49, P=0.028). Serum 25OHD concentration correlated positively with the thickness of perigenual anterior (P=0.011), midcingulate (P=0.013) and posterior cingulate cortex (P=0.021). Conclusion: Vitamin D insufficiency was associated with thinner cingulate cortex in the studied sample of older adults. These findings provide insight into the pathophysiology of cognitive and mobility declines in older adults with vitamin D insufficiency.


Sign in / Sign up

Export Citation Format

Share Document