Orbital fractures represent a common and complex challenge in maxillofacial surgery, with functional and aesthetic sequelae. Advances in computer-aided design and manufacturing, virtual planning, and three-dimensional printing have enabledpatient-specific implants (PSIs). Polyetheretherketone (PEEK), a bioinert polymer with properties similar to cortical bone, has emerged as a suitable material for orbital reconstruction. Surgical navigation has also been advocated to enhance accuracy in challenging regions. This retrospective service evaluation analysed ten patients with unilateral orbital fractures reconstructed using customised PEEK PSIs, placed either with navigation (n = 5) or freehand (n = 5). Orbital volumes were measured preoperatively, after virtual planning, and postoperatively; implant positioning was assessed by translational and rotational deviations; and clinical outcomes were evaluated using standardised ophthalmic and maxillofacial criteria. Fractured orbits were larger than contralateral orbits preoperatively, with postoperative volumes close to those of the intact side in both groups. Planned-treated volume discrepancies were small (navigation median 1.50 cm3, IQR 0.30-1.60; freehand 0.20 cm3, IQR 0.20-0.50; median difference 1.00 cm3, 95% CI -0.30 to 1.60; p = 0.151). Translational deviations remained below 2 mm, while rotational discrepancies were greater without navigation, though not statistically significant. Clinical success was achieved in six of the nine evaluable patients, with persistent diplopia in three cases attributed to traumatic muscle injury rather than implant malposition. PEEK PSIs provided a reliable orbital reconstruction, accurate volume restoration, and favourable clinical outcomes. Customised PEEK PSIs were typically designed and manufactured within 4 weeks after clinical assessment and imaging, consistent with a delayed reconstruction pathway in complex cases. Navigation may enhance intraoperative confidence and refine rotational control; however, no statistically demonstrable advantage over freehand placement was shown in this small exploratory cohort, in which satisfactory outcomes were achieved with both approaches, consistent with the inherent 'one-fit' characteristic of PSI.

Adenoid cystic carcinoma (ACC) with intracranial metastasis and sixth cranial nerve (CN VI) palsy, spinal metastases, and malignant spinal cord compression is an uncommon clinical entity. We present a case of a patient exhibiting this constellation of findings secondary to the parotid ACC. A 55-year-old man with no identifiable risk factors for ACC presented with a 10-year history of a left parotid tumor. He underwent two surgical resections and received one cycle of chemotherapy. Subsequently, his disease progressed locoregionally and systemically. He developed diplopia due to left sixth cranial nerve palsy caused by an intracranial metastatic lesion, together with complete spinal cord syndrome secondary to thoracic spinal metastases with malignant spinal cord compression. The patient was treated with whole-brain radiotherapy for intracranial metastasis and palliative spinal radiotherapy for spinal cord compression, achieving neurological stabilization without further deterioration. Systemic therapy with a tyrosine kinase inhibitor was subsequently initiated (lenvatinib 24 mg QD). The lungs are the most common site of distant metastasis in ACC, followed by bone and liver involvement. However, intracranial dissemination may occur rarely and should be considered in the clinical evaluation of these patients.

We report a case of a 20-year-old male who presented with a two-month history of progressively worsening binocular diplopia, dizziness, chest tightness, and significant weight gain. A comprehensive evaluation, including serial imaging, biopsy, and cerebrospinal fluid analysis, ultimately led to the diagnosis of an extragonadal seminoma with simultaneous involvement of the anterior mediastinum and the brain. Notably, the patient had a longstanding history of nonspecific testicular microlithiasis. The patient exhibited a favorable clinical and radiological response to treatment with whole-brain radiation combined with BEP (cisplatin, etoposide, bleomycin) chemotherapy. This rare presentation, together with the positive therapeutic outcome, provides meaningful insights into the existing literature on extragonadal germ cell tumors, particularly regarding atypical metastatic patterns, diagnostic challenges, therapeutic considerations, and prognosis in complex clinical scenarios.

Guillain-Barré syndrome (GBS) is an immune-mediated disorder of the peripheral nervous system characterized by progressive weakness and often triggered by infections. GBS has an estimated mortality rate of approximately 5%, with a worldwide incidence of 0.81-1.91 cases per 1,00,000 person-years. This case reported a 23-year-old man presented with progressive weakness in all four extremities. An initial neurological examination revealed bilateral total ophthalmoplegia, ptosis on both eyes, bilateral facial palsy lower motor neuron (LMN) type, dysarthria, dysphagia, flaccid tetra-paresis, gloves, and stocking paresthesia. Lumbar puncture showed cytoalbumin dissociation. Nerve conduction studies showed a demyelinating sensorimotor polyradiculoneuropathy lesion. The patient received intravenous immunoglobulin (IVIG) treatment 0.4 g/kg/day for 5 days, physical rehabilitation therapy, nutritional support, multidisciplinary care involving anesthesiology and intensive care teams, and other symptomatic treatments. At five-month follow-up, the patient demonstrated complete recovery. GBS typically presents as an acute ascending sensorimotor neuropathy; however, atypical presentations may occur. Extensive cranial nerve involvement-including complete ophthalmoplegia, bilateral facial palsy, and bulbar dysfunction-in AIDP is uncommon and may mimic other GBS spectrum disorders. Early recognition, prompt immunotherapy, and careful electrophysiological evaluation are essential for optimizing patient outcomes. Because electrodiagnostic classification of GBS may evolve over time, serial nerve conduction studies should be considered whenever feasible to improve subtype classification and diagnostic confidence.

Lacunar strokes are small subcortical infarcts that result from the occlusion of small perforating arteries, and they comprise about 25% of all strokes. Unlike other types of infarcts, lacunar strokes are primarily due to cerebral small vessel disease. Detection of acute lacunar infarcts may be challenging due to their small size, but it can be improved with clinical-radiologic correlation. Numerous mimics should also be kept in mind in the differential diagnosis. While lacunar infarcts are more often asymptomatic, they may manifest with distinct clinical syndromes. Five classic lacunar syndromes are commonly recognized: pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, and dysarthria-clumsy hand syndrome. Beyond these, numerous atypical lacunar syndromes such as internuclear ophthalmoplegia, isolated dysarthria, hemichorea and hemiballismus, and paramedian thalamic syndrome have been described. Each of these has a unique clinical manifestation linked to lesions in specific neuroanatomic pathways. The authors provide a comprehensive overview of lacunar strokes, emphasizing their diverse clinical manifestations and the crucial role of imaging in diagnosis of these infarcts. ©RSNA, 2026 Supplemental material is available for this article.

Lymphocytic hypophysitis (LYH), attributed to autoimmune mechanisms, typically causes multiple anterior pituitary hormone deficiencies, with corticotroph dysfunction occurring earliest; predominant thyrotroph dysfunction is uncommon. A 65-year-old woman presented with headache, fever, and diplopia. Laboratory tests revealed marked systemic inflammation and cerebrospinal fluid (CSF) pleocytosis. Pituitary magnetic resonance imaging (MRI) demonstrated diffuse enlargement and homogeneous contrast enhancement of the pituitary gland and stalk. Endocrinological evaluation showed paradoxically decreased thyroid-stimulating hormone (TSH) despite low thyroid hormone levels, contrasting with elevated adrenocorticotropic hormone (ACTH) levels. Endocrinological stimulation tests revealed a markedly blunted TSH response, with preserved gonadotropin and growth hormone responses, indicating predominant thyrotroph dysfunction despite preserved corticotroph function. Glucocorticoid therapy resulted in prompt improvement of clinical, laboratory, and MRI findings, with complete recovery of anterior pituitary functions. A presumptive diagnosis of LYH with reversible predominant thyrotroph dysfunction and meningitis secondary to direct extension of pituitary inflammation was established. This case demonstrates that LYH can present with atypical anterior pituitary hormone dysfunction, may be complicated by aseptic meningitis, and requires prompt glucocorticoid therapy for favorable outcomes.

A 48-year-old man was diagnosed with IgG4-related disease (IgG4-RD) during an evaluation for exophthalmos and unexplained pain on the left side of his face. The diagnosis was made by ruling out all other possible conditions and was based on histopathological findings. After initiating immunosuppressive therapy with corticosteroids (GC), most of the symptoms resolved. As the GC-dose was gradually reduced, a relapse occurred, leading to two courses of Rituximab. Reflecting the success of the therapy, long-term follow-up revealed a marked radiological reduction in the retrobulbar mass and a significant clinical improvement in pain.

SLC25A4, solute carrier family 25 member 4, gene is a member of the mitochondrial carrier subfamily within the solute carrier protein family. Pathogenic variants in SLC25A4 are associated with a spectrum of mitochondrial disorders that exhibit variable inheritance patterns and clinical manifestations. Specifically, dominantly inherited variants are typically associated with progressive external ophthalmoplegia with mitochondrial DNA deletions, recessively inherited variants are linked to myopathy and cardiomyopathy, and de novo variants can result in early-onset fatal disease presentations. In this study, we aimed to identify and characterize the disease-causing mutation(s) in a nine-year-old female patient from a consanguineous Saudi family. The patient was asymptomatic until the age of 3 years, when she presented with cardiomyopathy and myopathy. Comprehensive genetic analysis inclusive of whole exome sequencing and segregation analysis using Sanger sequencing identified an SLC25A4 variant (NM_001151.4: exon 2: c.112-1G>C) as the most likely cause of the disease. To assess transcript-level effects, we performed RT-PCR on RNA extracted from the patient's cultured lymphoblast cell lines (LCLs) and fibroblast cell lines (FCLs). RT-PCR analysis demonstrated that the variant causes aberrant splicing, resulting in a 6 bp in-frame deletion (p.Gln37_Val38del) in the ANT1 protein. Quantitative RT-PCR demonstrated reduced SLC25A4 transcript levels in both FCLs and LCLs. Quantitative PCR analysis of mitochondrial DNA demonstrated a trend toward increased mtDNA copy number in patient-derived FCLs compared with controls, suggesting a possible compensatory response to mitochondrial dysfunction. Furthermore, Seahorse assays revealed marked reductions in both oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) in patient-derived FCLs compared with controls. These findings expand the molecular and functional spectrum of SLC25A4-associated disease and may inform clinical practice, including genetic interventions such as preimplantation genetic diagnosis, premarital genetic screening, targeted genetic counseling, and cascade testing of at-risk family members.