The John Hunter Hospital and John Hunter Children's Hospital (sometimes known as the JHH and JHCH respectively, or more colloquially The John Hunter) is the principal referral centre and a tertiary hospital for Newcastle, and northern New South Wales, Australia. The 796 bed hospital is the main teaching hospital of the University of Newcastle. The hospital contains the only trauma centre in New South Wales outside the Sydney Metropolitan Area, and has the busiest emergency department in the state. John Hunter is the busiest trauma hospital in the state, and the second-busiest in the country behind The Alfred Hospital in Victoria[citation needed].
The use of standardised structured radiology reports improves the consistency, reproducibility and overall quality of radiological reporting while enhancing communication with referring physicians and ultimately contributing to improved patient care. To develop a standardised structured report template for foetal and neonatal postmortem magnetic resonance imaging through expert consensus. A Delphi survey was conducted between September and December 2025 among members of the ESPR Postmortem Task Force and other recommended international PM imaging experts. The surveyed items were derived from clinically used MRI reporting templates across the expert group. Consensus was defined using a ≥75
BACKGROUND:The left atrial posterior wall (LAPW) is often targeted in atrial fibrillation (AF) ablation due to its shared properties with pulmonary veins. However, substrate-guided approaches using structural markers have shown inconsistent results. We investigated posterior wall conduction time (PWCT) as a novel and functional marker of LAPW remodeling in AF patients. METHODS:In our pilot study, 40 patients undergoing first-time AF ablation (20 paroxysmal, 20 persistent AF) were included. AF cycle length (AF CL), PW linear conduction, PW conduction area (PWCA) and PWCT were evaluated on electroanatomical mapping at different pacing CLs. Major decremental PWCT was defined as PWCT increase ≥ 17% at 400 ms compared to 600 ms. RESULTS:Persistent AF patients had a larger posterior wall area (PWA; 20.4 ± 5.2 vs. 16.8 ± 4.9 cm², p = 0.033), greater low voltage area (LVA; 16.5 ± 25.8% vs. 6.1 ± 19.8%, p = 0.044) and shorter left atrial appendage AF CLs (shortest AF CL 146.2 ± 36.3 vs. 179.1 ± 37.1 ms, p = 0.012) than paroxysmal AF patients. PWCT was numerically longer in persistent AF, with major ΔPWCT observed exclusively in 6 persistent AF patients. In this subgroup, PWCA was reduced at each 10 ms increment during 400 ms pacing, a finding not observed in non-major ΔPWCT subgroup. Major ΔPWCT did not correlate with PWA size, LVA, or AF CL. CONCLUSION:PWCT may represent a novel functional biomarker of LAPW remodeling, independent of structural changes, potentially identifying patients who may benefit from targeted LAPW ablation. Further studies are needed to validate PWCT as a guide for personalized AF ablation.
BACKGROUND:Contrast induced encephalopathy (CIE) is an increasingly recognized but uncommon complication of endovascular procedures. Despite increased reports, there is limited evidence to guide clinical management. We sought to identify commonly used treatments for CIE and propose management strategies to aid clinical decision making. METHODS:A retrospective multicenter study was conducted across 10 neurovascular centers in Australia. Cases were included based on previously proposed diagnostic criteria for CIE. Clinical features, treatments, and outcomes were extracted and analyzed. Descriptive statistics were used to characterize management strategies, and associations with clinical outcomes were assessed using Fisher's exact and χ2 tests. RESULTS:56 patients were identified (median age 65 years; 80.4% women). Common interventions included corticosteroids (66.1%), intravenous fluids (66.1%), and antiseizure medications (prophylactic 51.8% and therapeutic 12.5%). Half required intensive care admission for neurological monitoring. Complete recovery was achieved in 87.5% of cases. Corticosteroid administration was significantly associated with symptom resolution within 72 hours (OR 4.51, 95% CI 1.19 to 17.85, P=0.022), while intravenous fluids showed a non-significant trend toward shorter symptom duration (OR 2.25, 95% CI 0.64 to 8.15, P=0.170). CONCLUSIONS:CIE generally carries a favorable prognosis. Corticosteroids appeared to shorten symptom duration and may be considered in management. Based on our findings and the existing literature, we propose a treatment algorithm to guide clinicians. Prospective validation is warranted.
BACKGROUND:Contrast-induced encephalopathy (CIE) is an increasingly observed complication following neurointervention, but remains poorly defined with limited evidence for clinical decision-making. We sought to characterize the stereotypical clinical features of CIE in a nationwide, multicenter cohort. METHODS:A multicenter cohort study was conducted between 10 neurovascular sites across Australia. Patients were screened according to the previously proposed Australian diagnostic criteria. Descriptive analysis was conducted to characterize the clinical course and outcomes of CIE, and associations between clinical and radiological variables on patient outcomes were analyzed using Fisher's exact and χ2 tests. RESULTS:A total of 56 patients (median age 65 years) were included. The median contrast volume was 170 mL (IQR 140-229). Median time to symptom onset was 6 hours (IQR 1-12), with frequent symptoms including motor deficit (55.4%), dysphasia (39.3%), and confusion (35.7%). Common radiological findings included sulcal effacement (45.5%) and subarachnoid contrast staining (30.9%) on CT. Hemianopia (p=0.001) and cortical blindness (p=0.018) were associated with posterior circulation interventions, while motor deficit was correlated with anterior circulation interventions (p=0.001). At discharge, 87.5% of patients achieved complete resolution of symptoms, of which 69.4% achieved complete recovery within 72 hours. CONCLUSION:CIE is a recognized complication of neurointervention. Symptoms occur within hours of contrast administration and correlate with the territory of contrast administration. Most patients achieve complete symptom resolution. Ongoing investigation is required to further define CIE as a clinical entity.
The aetiology of childhood motor speech disorders of dysarthria and apraxia has been poorly understood. Recent evidence suggests a moderate genetic contribution for these rare and severe speech disorders. To date, however, no studies have examined genetic diagnostic yield for childhood apraxia of speech (CAS) and dysarthria in a clinical setting. Here, we used a clinically accredited genomics pipeline to investigate genetic diagnostic yield and variables predictive of a genetic diagnosis in a tertiary hospital speech clinic. A cohort of 153 children (range 2;7-16;5 years, 42 female) ascertained for motor speech disorder were assessed by a clinical geneticist and speech pathologist and underwent chromosomal microarray, Fragile X and exome sequencing. Odds ratios identified predictors of genetic diagnosis. 44/153 (29%, 15 female) had pathogenic variants (30 de novo), encompassing monogenic conditions (n = 35) and copy number variants (n = 9) across 38 distinct disorders. Delayed walking, fine and gross motor disorder, receptive language impairment and/or cognitive impairment, and dysmorphism were associated with a genetic diagnosis. The presence of CAS and dysarthria was more commonly associated with a genetic diagnosis than CAS alone. Autism spectrum disorder was less commonly associated with a genetic diagnosis. No child had a Fragile X diagnosis. The clinical genetic diagnostic yield for motor speech disorders is comparable to epilepsy and cerebral palsy, conditions where genetic testing is routine in most centres, unlike for motor speech disorders. Children with motor speech disorder with co-occurring motor, language and/or learning deficits, should be prioritised for genomic testing.
