Repetitive use injuries are commonly seen by musculoskeletal providers, usually in the form of tendinopathies. However, focal peripheral nerve entrapment can mimic or coexist with tendon pathology, particularly when weakness, sensory symptoms, or imaging findings are subtle or nonspecific. This review provides a practical, symptom-first framework to help clinicians distinguish tendon-dominant, nerve-dominant, and mixed presentations in clinical practice. Five clinically relevant tendon-nerve mimic pairs are emphasized: (1) rotator cuff tendinopathy versus suprascapular neuropathy; (2) lateral epicondylitis versus radial tunnel syndrome; (3) iliotibial band syndrome versus common peroneal neuropathy; and (4) peroneal tendinopathy versus superficial or deep peroneal nerve entrapment; (5) plantar fasciitis versus tarsal tunnel syndrome or Baxter nerve entrapment. Across these conditions, diagnosis is most strongly informed by symptom pattern, pain distribution, and focal neurologic deficits, with imaging and adjunctive testing used selectively when they are likely to clarify the diagnosis or change management. Therefore, a symptom-first approach may reduce diagnostic anchoring, improve recognition of atypical or refractory presentations, and support more targeted rehabilitation strategies.

External snapping hip affects approximately 5% to 10% of the population. Surgical intervention, typically via endoscopic or open iliotibial band release, is generally reserved for recalcitrant cases. This article describes a step-by-step guide to the endoscopic treatment of persistent external snapping hip. The technique may be performed in isolation to address external snapping hip or in conjunction with procedures for intra-articular pathology, such as femoroacetabular impingement and labral tears. It involves releasing the iliotibial band and the gluteus maximus tendon at its femoral attachment, with the goal of minimizing recurrence and achieving sustained pain relief.

Background: Plantar pressure analysis provides insight into load distribution at the foot-pedal interface during cycling; however, its modulation by pedaling power, cadence, and overuse injury status remains poorly understood by professional cyclists. It is unclear whether common overuse injuries, such as Achilles tendinopathy, patellofemoral pathology, and iliotibial band syndrome, are associated with distinct plantar loading patterns. This study aimed to characterize plantar pressure distribution in elite cyclists and determine how power, cadence, and injury status influence this pattern. Methods: Professional cyclists completed a single integrated protocol using a high-resolution in-shoe pressure system. Plantar forces were recorded across nine anatomical regions and grouped into the transverse and longitudinal segments of the foot. Three phases were included: absolute power manipulation (100 and 200 W), cadence manipulation (80 and 100 rpm) at fixed power, and an ecological combined protocol using relative power (1.5 and 3 W·kg-1) with individualized cadence. The cyclists used their habitual bike setups. Participants were classified into the non-pathological (NP), AT, PFP, or ITBS groups. Mixed repeated-measures ANOVAs were used to analyze the effects of power, cadence, zone, foot, and injury status. Results: The plantar pressure distribution was consistently dominated by the medial forefoot. Increasing the absolute power from 100 to 200 W increased the maximal plantar pressures by 84.74% (p < 0.001), whereas increasing the cadence from 80 to 100 rpm at a fixed power increased the pressures by 15.90% (p = 0.003). Under individualized conditions, increasing relative power from 1.5 to 3 W·kg-1 increased pressures by 39.59% (p < 0.001), whereas cadence had no global main effect but significantly altered the regional pressure distribution (p < 0.001). Injury groups showed pathology-specific deviations, including higher overall pressures and asymmetry in Achilles tendinopathy, bilateral asymmetry in patellofemoral pathology, and asymmetric loading patterns in iliotibial band syndrome. Conclusions: Power is the main determinant of plantar pressure, and cadence modulates load distribution. Overuse injuries induce pathology-specific pressure patterns, supporting plantar pressure analysis for injury prevention and performance optimization in athletes.

A 59-year-old woman runner was referred for left knee pain, with suspicion of stress fracture of the lateral femoral condyle. 99m Tc-HDP bone scintigraphy using a new 3D-ring CZT system (StarGuide) was performed. Blood pool SPECT/CT revealed hyperemia between the iliotibial band and the lateral femoral condyle of the left knee, suggestive of iliotibial band syndrome (ITBS), while late-phase SPECT/CT did not demonstrate any abnormality in the left knee. The patient underwent an MRI, which confirmed ITBS. Our case emphasizes the potential of blood pool SPECT/CT using a new 3D-ring CZT system to identify relevant extraosseous conditions such as ITBS.

Background: The plantaris muscle (PM) shows substantial variability in its proximal belly attachments. Although often deemed vestigial, specific variants may narrow or reshape the popliteal corridor and contribute to vascular (popliteal artery entrapment syndromes, PAES) and neural conflict (TN, CPN, sural nerves). Despite abundant anatomical descriptions of the plantaris, its contribution to neurovascular compression has not been organised into a classification-linked, imaging-integrated framework. Objective: To synthesise adult and foetal anatomical data with clinical-radiological evidence into a classification-linked framework that stratifies vascular and neural compression risk by proximal PM variants, and to propose an integrated risk matrix and variant-directed diagnostic/operative pathway. Methods: Narrative, classification-centred review centred on the Olewnik schema (Types I-VI) and multi-headed/accessory variants. We mapped variant geometry to (1) physiological compromise on provoked Doppler US and (2) anatomical correlates on MRI/MR angiography (MRA) (axial "band sign"), deriving graded risk for vascular and neural axes and an integrated, action-oriented grade per limb. Results: Baseline risk is low for canonical/compact footprints (Type I-IA, Type V), moderate for capsular-junction patterns (Types II/III), and potentially higher-risk for lateral linkage (Type IV; iliotibial band (ITB)/Kaplan fibres continuity) and multi-headed configurations (duplication, bifurcation, ≥3-4 heads; accessory proximal slips). The integrated matrix upgrades risk for a clear band sign, reproducible compromise on provoked Doppler US, or multi-headed/Type IV anatomy and downgrades when rigorous provocation is negative and muscle volume is small. We provide a variant-indexed imaging checklist, common pitfalls (e.g., Type IV misread as ITB thickening; multi-headed variants misread as cyst/tumour), and operative checkpoints to target capsular clefts, lateral bands, tunnels, and accessory slips. Conclusions: A classification-linked, imaging-integrated approach clarifies which proximal PM variants are plausibly associated with neurovascular entrapment (based on case-level evidence) and aligns work-up with targeted decompression and may improve diagnostic precision and inform surgical planning. Clinical relevance: The framework operationalises variant naming in reports, standardises dynamic provocation and axial mapping, and prioritises variants considered higher risk (Type IV; multi-headed) for early multidisciplinary review. Given that most clinical signals derive from case reports/series (Level IV), these recommendations are inferential and should be applied with clinical judgement.