Review Article

Functional Brain Plasticity Associated with ACL Injury: A Scoping Review of Current Evidence

Table 2

Summary of included EEG and fMRI studies (effect size is presented for between or within-group comparisons).

StudyLevel of evidenceGroup (, sex, mean age)Type of surgery; time from injury/surgeryEquipment, outcomesTaskResultsEffect size, Cohen’s

Baumeister et al. [47]Case-control, 3bACLR (, 7M, 2F, )
Healthy (, 7M, 2F, )
All hamstrings; months from surgeryEEG, power spectral analysisKnee extension force reproduction (50% of MVIC)Significantly higher frontal theta power in ACLRACLR vs. healthy, -1.33

Ochi et al. [45]Case-control, 3bACLD (, 2M, 24F, )
ACLR (, 21M, 21F, )
Normal ACL (, 7M, 12F, )
All hamstrings; >13 months after surgery in 38 ACLR participantsEEG—SEP of the ACLDirect mechanical stimulation of the ACL during arthroscopy (under general anaesthesia)Mechanically reproduced SEPs were observed in 58% of ACLD, 86% of ACLR, and 100% of healthy ACL
No differences in SEP mean voltage between the ACLD (1.3 μV), ACLR (1.27 μV), and normal ACL (1.42 μV)
ACLD vs. ACLR,
ACLD vs. healthy,
ACLR vs. healthy, d = 0.30

Ochi et al. [46]Case-control, 3bACLD (, 16M, 16F, )
ACLR (, 13M, 10F, )
Normal ACL (, 9M, 5F, )
Hamstring graft in 22 patients and 1 allogeneic fascia lata graft; >18 months after surgeryEEG—SEP of the ACLElectrical stimulation of the ACL during arthroscopy (under general anaesthesia)Reproducible SEPs in 47% of ACLD, 96% of ACLR, and 100% of healthy ACL
The mean SEP voltage of the ACLD (0.74 μV) was significantly lower () than the healthy group. No differences between ACLD and ACLR
ACLD vs. ACLR,
ACLD vs. healthy,
ACLR vs. healthy,

Miao et al. [56]Case-control, 3bACLD (, all males, )
Healthy (, all males, )
months since injuryEEG, power spectral analysisEEG was recording during the following:
(1) Walking (20 m at a natural speed)
(2) Jogging (20m)
(3) Landing task (25 cm height)
The ACLD group showed a significant increase in band power of all frequencies, during all tasksACLD vs. healthy
Walking, -4.07
Jogging, -3.76
Landing, -4.46

Valeriani et al. [42]Case-control, 3bACLD (, no information on sex of patients, )
Healthy (, 9M, 11F, )
Between 12 and 96 months after injuryEEG—SEP of the common peroneal nerve and posterior tibial nervePatients relaxed in supineSeven subjects from the ACLD group showed SEP abnormalities (loss of P27) after common peroneal nerve stimulationUnable to determine

Valeriana et al. [43].Case-series, 4ACLR (, sex and age unknown)All patellar tendon; time from surgery/injury unknownEEG—SEP of the common peroneal nervePatients relaxed in supineAbsence of cortical P27 response in the injured limb before, and after, ACL reconstruction surgeryUnable to determine

Baumeister et al. [29]Case-control, 3bACLR (, 7M, 3F, )
Healthy (, 9M, 3F, )
All hamstrings; months from surgeryEEG, power spectral analysisReproduce a given knee angle of 40°Significantly higher theta and alpha 2 power in ACLRUnable to determine

Courtney et al. [34]Case-control, 3b17 ACLD patients (7M, 10F), divided in the following: noncopers (, ), adapters (, ), and copers (, )Overall after injury: noncopers: 90 months, adapters: 59 months, and copers: 69 monthsEEG—SEP of the common peroneal nervePatients relaxed in supineThe adapter group showed normal SEPs, 75% of noncopers had normal SEPs, and all copers had altered SEPsUnable to determine

Courtney et al. [57]Case-control, 3b15 ACLD patients (5M, 10F, ), divided in the following: noncopers (), adapters (), and copers ()Overall mean = 67 months after injury: noncopers: 85 months, adapters: 63 months, and copers: 69 monthsEEG—SEP of the common peroneal nervePatients relaxed in supineThe adapter group showed normal SEPs, 75% of noncopers had normal SEPs, and all copers had altered SEPsUnable to determine

Lavender et al. [41]Case-control, 3b11 patients: 4 with intact ACL, 6 with complete rupture, and 1 with partial rupture. No information on sex and age28 months (-96) after injuryEEG—SEP of the ACLElectrical stimulation of the ACL during arthroscopyAll intact ACLs (and the partially ruptured) showed reproducible SEPs; ruptured ACL did not show reproducible SEPsUnable to determine

Kapreli et al. [23]Case-control, 3bACLD (, all male, )
Healthy (, all male, )
months after injuryfMRICycles of 45° knee extension/flexion (1.2 Hz), during 25 s, positioned in supine inside the scannerACLD showed less activation of thalamus, PP, PM, cerebellum, iSM1, cSM1, BG GPe, and CMA and showed higher activation of pre-SMA, SIIp, and pITGUnable to determine

Grooms et al. 2017 [49]Case-control, 3bACLR (, 7M, 8F, )
Healthy (, 7M, 8F, )
13 hamstrings and 2 patellar tendons; months after surgeryfMRI s cycles of 45° knee extension/flexion (1.2 Hz), positioned in supine inside the MRI scannerACLR showed less activation of iMC and cerebellum and showed higher activation of cMC, lingual gyrus, and iSII for the following: , , , lingual , and

ACLR = anterior cruciate ligament reconstruction; ACLD = anterior cruciate ligament deficiency; BG GPe = basal ganglia-external globus pallidus; CMA = cingulated motor area; cMC = contralateral motor cortex; cSM1 = contralateral primary sensorimotor area; EEG = electroencephalography; ES = effect size; F = females; fMRI = functional magnetic resonance imaging; iMC = ipsilateral motor cortex; iSM1 = ipsilateral primary sensorimotor area; iSII = ipsilateral secondary somatosensory area; M = males; pITG = posterior inferior temporal gyrus; PM = premotor cortex; PP = postparietal cortex; pre-SMA = presupplementary motor area; SII = secondary somatosensory area; SEPs = somatosensory-evoked potentials; SIIp = posterior secondary somatosensory area.