Cubital tunnel syndrome is the second most common compressive neuropathy of the upper limb after carpal tunnel syndrome and results from entrapment of the ulnar nerve around the elbow. High-resolution ultrasound has become a central diagnostic modality because of its excellent spatial resolution, capacity for dynamic assessment, and broad availability in clinical practice. This review offers an integrated and updated overview of the ultrasonographic evaluation of the ulnar nerve in cubital tunnel syndrome, detailing relevant anatomy, characteristic normal and pathological appearances, and key considerations in postoperative follow-up. The ulnar nerve may be compressed at several anatomical sites, including the arcade of Struthers, the retrocondylar groove, Osborne’s ligament within the cubital tunnel, and the aponeurosis between the two heads of the flexor carpi ulnaris. Typical sonographic abnormalities include focal or segmental nerve enlargement, disruption or loss of the normal fascicular architecture, and changes in echogenicity. Dynamic maneuvers during ultrasound examination can further identify nerve subluxation, dislocation, or snapping over the medial epicondyle, all of which may contribute to clinical symptoms. Postoperative ultrasound evaluation is increasingly important for detecting complications or persistent compression following in-situ decompression, medial epicondylectomy, or anterior transposition. A standardized and reproducible ultrasound protocol is therefore essential for accurate diagnosis, appropriate management, and follow-up. Radiologists play a pivotal role in this multidisciplinary approach by providing detailed imaging assessments that guide surgical decision-making and help optimize patient outcomes.
AIM:Pelvic exenterations are complex operations associated with significant morbidity and resource implications. Resection is undertaken with curative intent, and achieving clear margins is paramount to successful oncological outcomes. Comprehensive pathological reporting is essential, yet there are no internationally agreed guidelines describing an optimal approach. METHODS:This article presents a standardised approach to the pathological dissection and reporting of pelvic exenteration specimens, endorsed by the UK Pelvic Exenteration Network (UKPEN). This includes all relevant steps of the clinical pathway, from acknowledging the importance of pathology involvement in pre-operative radiological planning to post-operative correlation meetings. Key recommendations are exemplified with illustrative examples. CONCLUSION:Standardisation of pelvic exenteration pathology will contribute to optimal patient care, enhance multidisciplinary learning and service development, provide quality assurance and auditable standards and facilitate national and international research.
Forensic facial reconstruction is the reproduction of a deceased person’s antemortem face, most commonly achieved using population-based data of facial soft tissue thickness. Facial soft tissue thickness (FSTT) data have been documented for many populations. However, there are no published data for Nigerian female adults. This study measured the facial soft tissue thickness of 32 subjects based on computed tomography scans. Measurements were taken from 50 facial soft tissue thickness points, including 12 mid-sagittal and 19 bilateral (right and left) points, across a diverse age range of 18 to 95 years. The Nigerian female adult consistently shows marginal increase in soft tissue thickness on the left side of the face when compared with the right, with the greatest relative difference at the zygomatic arch and mid-lateral orbit. When compared with the published data of populations in South Africa, Turkey, Korea, and Belgium, there were similarities at the midline but appreciable differences at the lip and chin regions. The right side of the face of the Nigerian female adults was also compared with other populations; the differences at the lateral side of the face were greater than the midline differences. These differences reflects the greater thickness of bilateral soft tissue. This study demonstrates that although the data between different populations are similar, there are still measurable differences at several points. This new dataset will be most applicable for forensic facial reconstruction in Nigerian female adults.
Blinatumomab is increasingly incorporated into frontline therapy for B-cell acute lymphoblastic leukaemia (B-ALL), yet risk stratification remains based on chemotherapy-era factors that may not apply in the immunotherapy setting. We analysed a national cohort to define determinants of relapse following frontline blinatumomab. Children and young people (1-24 years) in the UK and Ireland diagnosed with B-ALL between 2018 and 2025 who were chemotherapy-intolerant or resistant received blinatumomab in place of selected components of the frontline chemotherapy backbone. Outcomes were analysed according to conventional prognostic variables, genetic features, and response to blinatumomab. Among 225 patients, 195 received chemotherapy following blinatumomab (Blin-CT) and 30 underwent first-remission HSCT. In the Blin-CT cohort, traditional risk factors, including age, white cell count, high-risk genetics, and pre-blinatumomab end-of-induction measurable residual disease (MRD) did not predict relapse. On univariable analysis, relapse risk was increased with detectable MRD after blinatumomab cycle 1 (C1-END; hazard ratio HZR 6.61, p<0.001), IKZF1plus (HZR 3.64, p=0.04), JAK-STAT abnormalities (HR 3.56, p=0.05), and DUX4 rearrangements (HZR 4.24, p=0.03). In multivariable modelling, C1-END MRD and IKZF1plus remained independently associated with relapse, whereas DUX4-rearranged cases were strongly associated with persistent MRD at C1-END. An integrated model incorporating C1-END MRD, IKZF1plus, and DUX4-r defined a high-risk subgroup (33%) with an 18% 2-year relapse rate versus 0% in remaining patients (bootstrapped HZR 12.82, p=0.001, C-index=0.81). Relapse following frontline blinatumomab is determined by early treatment response and genetic subtype rather than conventional chemotherapy-derived risk factors. These findings support immunotherapy-specific risk stratification to guide treatment intensity.
