Introduction. Osteolytic skull lesions pose significant surgical challenges because of their destructive nature and potential involvement of adjacent soft tissues. Complete resection of the affected bone is essential to reduce the risk of recurrence and ensure cranial stability; however this frequently results in large defects that require precise and immediate reconstruction. Advances in three-dimensional printing have enabled patientspecific surgical planning and the creation of customized tools and implants, thereby improving surgical accuracy, operative efficiency, and cosmetic outcomes. Case Report. We present a case of a patient with an osteolytic skull lesion treated using a customized three-dimensional-printed bone resection guide and a polylactic acid mold for intraoperative polymethyl methacrylate cranioplasty. Preoperative computed tomography and magnetic resonance imaging data were used to generate a virtual three-dimensional model, allowing accurate definition of resection margins and precise implant design. This approach enabled controlled lesion excision and immediate reconstruction using a well-fitting polymethyl methacrylate implant. Postoperative imaging confirmed complete lesion resection and optimal implant positioning, with excellent cosmetic and functional outcomes observed at one-year follow-up. Discussion. The integration of three-dimensional printing into cranial reconstructive surgery enhances surgical precision, reduces operative time, and offers a cost-effective method for individualized reconstruction. This case highlights the practical applicability of three-dimensional-printed surgical guides and molds in managing complex osteolytic skull lesions. Conclusion. The use of three-dimensional-printed resection guides combined with intraoperative polymethyl methacrylate molding enables accurate bone resection and immediate cranial reconstruction, achieving high precision, reproducibility, and favorable clinical outcomes.

To externally validate the 3-point Simplified Motor Score (SMS) against the 15-point Glasgow Coma Scale (GCS) for predicting outcomes after traumatic brain injury (TBI). Retrospective cohort of consecutive adult patients with TBI evaluated at the Department of Neurosurgery, University Clinical Centre of Vojvodina, Serbia, in 2017. Discrimination for in-hospital mortality, emergency intubation, and non-home discharge was assessed using the area under the receiver operating characteristics (ROC) curve (AUC), with pairwise comparisons by the DeLong test. Agreement was quantified by Cohen's κ. Of 823 patients, with a median age of 58 years, 66.1% were male, 7.7% died, 9.7% required emergency intubation, and 16.5% had non-home discharge. The AUCs for GCS and SMS were 0.882 versus 0.837 for mortality; 0.967 versus 0.927 for intubation; and 0.835 versus 0.762 for non-home discharge respectively. The AUC differences between GCS and SMS ranged from 0.040 to 0.072. Agreement between SMS ≤ 1 and GCS ≤ 13 was high (κ = 0.84). The GCS was more accurate in patients aged ≥ 65 years. The SMS preserved most of the discriminative ability of the full GCS for acute outcomes but underperformed for disposition outcomes and in older patients. The SMS is best used as a rapid bedside complement to the GCS.

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder primarily known for progressive kidney cysts, and it is the most common hereditary syndrome linked to intracranial aneurysms (IAs). Approximately 5–20% of ADPKD patients have IAs (versus ~3% in the general population). Key risk factors for IAs in ADPKD include a family history of aneurysmal subarachnoid hemorrhage (SAH), early-onset or poorly controlled hypertension, and possibly more severe kidney disease (e.g., large total kidney volume and reduced kidney function). The PKD1 and PKD2 mutations in ADPKD lead to polycystin-1/-2 dysfunction in vascular cells, causing intrinsic vessel wall weakness. This weakness—compounded by chronic hemodynamic stress and inflammation—predisposes ADPKD patients to aneurysm formation. Clinically, most aneurysms in ADPKD are small (<7 mm), asymptomatic, and located in the anterior cerebral circulation. Their growth and rupture risk appears similar to aneurysms in non-ADPKD patients; however, ruptures in ADPKD occur at younger ages, underscoring the need for vigilant management. This narrative review provides a nephrology-oriented overview of intracranial aneurysms in ADPKD, including pathophysiology, epidemiology, and clinical management. Key Messages: -ADPKD carries a higher prevalence of intracranial aneurysms (≈5–20%) than the general population (≈3%). Key risk factors include a family history of aneurysm/SAH, early or poorly controlled hypertension, and possibly advanced renal disease. -Guidelines support targeted rather than universal screening, mainly in patients with family history or prior SAH. -Non-contrast MRA is the preferred modality, usually initiated around age 30 in at-risk individuals. -Most aneurysms are small and asymptomatic; small lesions are monitored with BP control and imaging, while larger or high-risk aneurysms are treated prophylactically. -Broader screening remains debated. Future genetic insights may improve risk stratification, but current practice requires balancing rupture prevention against over screening.