Table 2.
Study | Level of evidence | Group (n, sex, mean age) | Type of surgery; time from injury/surgery | Equipment, outcomes | Task | Results | Effect size, Cohen's d |
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Baumeister et al. [47] | Case-control, 3b | ACLR (n = 9, 7M, 2F, age = 25 ± 5) Healthy (n = 9, 7M, 2F, age = 24 ± 3) |
All hamstrings; 12.0 ± 4.7 months from surgery | EEG, power spectral analysis | Knee extension force reproduction (50% of MVIC) | Significantly higher frontal theta power in ACLR | ACLR vs. healthy, d = 0.91-1.33 |
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Ochi et al. [45] | Case-control, 3b | ACLD (n = 45, 2M, 24F, age = 29.8) ACLR (n = 42, 21M, 21F, age = 32.9) Normal ACL (n = 19, 7M, 12F, age = 28.4) |
All hamstrings; >13 months after surgery in 38 ACLR participants | EEG—SEP of the ACL | Direct 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, d = 0.06 ACLD vs. healthy, d = 0.21 ACLR vs. healthy, d = 0.30 |
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Ochi et al. [46] | Case-control, 3b | ACLD (n = 32, 16M, 16F, age = 25.5 ± 9.3) ACLR (n = 23, 13M, 10F, age = 27.8 ± 10.0) Normal ACL (n = 14, 9M, 5F, age = 22.9 ± 12.3) |
Hamstring graft in 22 patients and 1 allogeneic fascia lata graft; >18 months after surgery | EEG—SEP of the ACL | Electrical 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 (P = 0.001) than the healthy group. No differences between ACLD and ACLR |
ACLD vs. ACLR, d = 0.98 ACLD vs. healthy, d = 1.37 ACLR vs. healthy, d = 0.65 |
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Miao et al. [56] | Case-control, 3b | ACLD (n = 16, all males, age = 26.4 ± 6.3) Healthy (n = 15, all males, age = 26.2 ± 3.8) |
9 ± 7 months since injury | EEG, power spectral analysis | EEG 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 tasks | ACLD vs. healthy Walking, d = 2.07-4.07 Jogging, d = 3.58-3.76 Landing, d = 2.43-4.46 |
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Valeriani et al. [42] | Case-control, 3b | ACLD (n = 19, no information on sex of patients, age = 28.0 ± 4.1) Healthy (n = 20, 9M, 11F, age = 23.9 ± 5.2) |
Between 12 and 96 months after injury | EEG—SEP of the common peroneal nerve and posterior tibial nerve | Patients relaxed in supine | Seven subjects from the ACLD group showed SEP abnormalities (loss of P27) after common peroneal nerve stimulation | Unable to determine |
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Valeriana et al. [43]. | Case-series, 4 | ACLR (n = 7, sex and age unknown) | All patellar tendon; time from surgery/injury unknown | EEG—SEP of the common peroneal nerve | Patients relaxed in supine | Absence of cortical P27 response in the injured limb before, and after, ACL reconstruction surgery | Unable to determine |
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Baumeister et al. [29] | Case-control, 3b | ACLR (n = 10, 7M, 3F, age = 27 ± 5) Healthy (n = 12, 9M, 3F, age = 25 ± 3) |
All hamstrings; 12.5 ± 4.6 months from surgery | EEG, power spectral analysis | Reproduce a given knee angle of 40° | Significantly higher theta and alpha 2 power in ACLR | Unable to determine |
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Courtney et al. [34] | Case-control, 3b | 17 ACLD patients (7M, 10F), divided in the following: noncopers (n = 4, age = 32), adapters (n = 10, age = 36), and copers (n = 3, age = 37) | Overall mean = 68 months after injury: noncopers: 90 months, adapters: 59 months, and copers: 69 months | EEG—SEP of the common peroneal nerve | Patients relaxed in supine | The adapter group showed normal SEPs, 75% of noncopers had normal SEPs, and all copers had altered SEPs | Unable to determine |
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Courtney et al. [57] | Case-control, 3b | 15 ACLD patients (5M, 10F, age = 34), divided in the following: noncopers (n = 4), adapters (n = 8), and copers (n = 3) | Overall mean = 67 months after injury: noncopers: 85 months, adapters: 63 months, and copers: 69 months | EEG—SEP of the common peroneal nerve | Patients relaxed in supine | The adapter group showed normal SEPs, 75% of noncopers had normal SEPs, and all copers had altered SEPs | Unable to determine |
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Lavender et al. [41] | Case-control, 3b | 11 patients: 4 with intact ACL, 6 with complete rupture, and 1 with partial rupture. No information on sex and age | 28 months (range = 1-96) after injury | EEG—SEP of the ACL | Electrical stimulation of the ACL during arthroscopy | All intact ACLs (and the partially ruptured) showed reproducible SEPs; ruptured ACL did not show reproducible SEPs | Unable to determine |
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Kapreli et al. [23] | Case-control, 3b | ACLD (n = 17, all male, age = 25.5 ± 5.0) Healthy (n = 18, all male, age = 27.0 ± 5.0) |
26.2 ± 23.0 months after injury | fMRI | Cycles of 45° knee extension/flexion (1.2 Hz), during 25 s, positioned in supine inside the scanner | ACLD showed less activation of thalamus, PP, PM, cerebellum, iSM1, cSM1, BG GPe, and CMA and showed higher activation of pre-SMA, SIIp, and pITG | Unable to determine |
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Grooms et al. 2017 [49] | Case-control, 3b | ACLR (n = 15, 7M, 8F, age = 21.7 ± 2.7) Healthy (n = 15, 7M, 8F, age = 23.2 ± 3.5) |
13 hamstrings and 2 patellar tendons; 38.1 ± 27.2 months after surgery | fMRI | 4 × 30 s cycles of 45° knee extension/flexion (1.2 Hz), positioned in supine inside the MRI scanner | ACLR showed less activation of iMC and cerebellum and showed higher activation of cMC, lingual gyrus, and iSII | d for the following: iMC = 0.78, cerebellum = 3.05, iSM = 2.01, lingual gyrus = 1.14, and cMC = 0.94 |
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.