ABSTRACT Background Acute invasive fungal rhinosinusitis (AIFRS) represents a diagnostic emergency where imaging findings often precede clinical deterioration. While paranasal sinus opacification is commonly encountered in radiology practice, the distinction between benign inflammatory disease and angioinvasive fungal infection carries profound therapeutic implications. This case illustrates the importance of recognizing subtle radiologic red flags that transform “incidental sinusitis” into a life‐threatening diagnosis. Case Presentation A 47‐year‐old male with poorly controlled type II diabetes mellitus (HgbA1c of 9.8%) presented to the radiology department with a 15‐day history of headache, vomiting, and giddiness. Contrast‐enhanced MRI revealed a large extra‐axial lesion centered in the anterior cranial fossa measuring 5.1 × 4.5 × 5.1 cm 3 , characterized by T2W hypointensity, diffusion restriction, and heterogeneous enhancement. Imaging demonstrated multi‐compartmental bony erosion involving the cribriform plate, sphenoid sinus roof, bilateral ethmoidal air cells, and medial orbital walls, with intracranial extension into the bilateral basifrontal lobes causing mass effect and early subfalcine herniation. Orbital involvement with optic nerve encasement was also demonstrated. Histopathology confirmed invasive aspergillosis with characteristic septate, acute‐angle branching hyphae and infarct necrosis. The patient got a multidisciplinary management involving trans‐nasal clearance and bi‐frontal craniotomy, followed by liposomal amphotericin B therapy. Conclusion This case highlights that sinusitis on imaging must never be dismissed as incidental in immunocompromised patients. The radiologist serves as the front‐line diagnostician, where recognition of bone erosion, T2 hypointensity, diffusion restriction, and extra‐sinus extension mandates immediate clinical correlation and surgical consultation.
ABSTRACT Background Vertebral Artery Compression Syndrome (VAMCS) is a rare but increasingly recognized vascular compression disorder of the medulla oblongata, most commonly presenting with paroxysmal symptoms such as hemi‐facial spasm, vertigo, or dysphagia. Longstanding, fixed hemiplegia is an atypical presentation that poses a significant diagnostic challenge. Case Presentation We report a case of a 29‐year‐old male with a longstanding history of left hemiplegia, initially presumed to be of cerebral origin. Non‐contrasted brain and spine MRI was performed. The spine MRI was essentially normal, showing only a loss of cervical lordosis. However, dedicated brain MRI with vascular assessment revealed a dilated and tortuous left vertebral artery compressing the left part of the distal medulla that ascended and looped medially, crossing the midline to compress and flatten the right part of the rostral medulla oblongata, approximately 1.5 cm cranial to the foramen magnum. Discussion This case highlights a crucial radiological tenet: a normal spine MRI does not exclude an intracranial vascular cause for myelopathy‐like symptoms. The distal medulla houses the decussation of the cortico‐spinal tracts. Chronic, fixed compression above this level can mimic a cervical myelopathy or a brainstem infarct, leading to a longstanding contralateral hemiparesis. Conclusion VAMCS should be considered in the differential diagnosis of young patients with unexplained, longstanding hemiplegia, especially when conventional spine imaging and cerebral imaging is unremarkable. Radiologists must actively evaluate the vertebrobasilar system and its relationship to the medulla in such cases, as the finding directly impacts clinical management and surgical planning.
ABSTRACT Ocular ultrasound (OUS) has become an essential diagnostic modality, enabling noninvasive imaging of intraocular and orbital structures. OUS is particularly valuable in emergency medicine, ophthalmology, and critical care, facilitating rapid diagnosis of acute vision loss and other systemic diseases. This review covers the ultrasound technique, detailed ocular anatomy, pathologies with ultrasound findings, clinical applications, limitations, and future perspectives. Emphasis is placed on both common and rare ocular conditions to offer a comprehensive guide for health care providers, especially in the emergency and critical care setting.
ABSTRACT Background Artificial intelligence (AI) applied to neuroimaging has expanded in Alzheimer's disease (AD) research, yet recent model types, data sources, and clinical aims remain heterogeneous. This scoping review maps AI‐based neuroimaging studies in AD by clinical task, data modality, study tag (specific vs multimodal), and data collection design. Methods We compiled recent AD studies in which AI models were applied to neuroimaging data from adult participants. We extracted neuroimaging modality, AI approach, clinical purpose, high‐level classification (diagnosis/detection, prognosis/outcome prediction, subtype discovery, biomarker prediction, image enhancement, workflow integration), study tag (Specific vs Multimodal), and data collection design (Retrospective vs Prospective). We focused on studies using MRI, PET, or combinations with clinical, cognitive, genetic, or plasma biomarkers. Results Most studies were retrospective and used structural T1‐weighted MRI. “Specific” studies applied deep learning models to MRI for multi‐class diagnosis and staging, distinguishing cognitively normal individuals, mild cognitive impairment (MCI) subtypes, and AD. PET‐based models were used for diagnosis and biomarker‐related tasks, including prediction of metabolic or tau changes and classification of amyloid or tau positivity. “Multimodal” studies integrated imaging with clinical or biomarker data and were prominent in prognostic and biomarker‐focused applications. Several studies targeted subtype discovery using generative or normative modeling, while explainability and workflow‐oriented tools were less common. Discussion AI‐based neuroimaging in AD is dominated by retrospective MRI‐ and PET‐driven deep learning models focused on diagnosis and prognostication. Multimodal approaches are increasing, but real‐world implementation studies remain limited. This scoping review provides a map of current AI–neuroimaging applications to inform future development.
ABSTRACT Introduction The diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) in patients with diabetic sensorimotor polyneuropathy (DSP) is challenging when both diseases coexist, as patients with DSP may have demyelinating features in nerve conduction studies (NCS). We aimed to investigate the value of nerve ultrasound (US) to differentiate patients with DSP, CIDP and DSP+CIDP. Methods We prospectively included adult patients diagnosed with CIDP, DSP or DSP+CIDP based on clinical assessments and NCS, who had US of the median, ulnar, fibular and tibial nerves. Patients with DSP, who presented with unexpected progression in a pattern consistent with CIDP and supportive changes in magnetic resonance imaging (MRI) or cerebrospinal fluid (CSF) analysis, were diagnosed with DSP+CIDP. Results Of 57 patients (20 DSP, 20 CIDP and 17 DSP+CIDP), 3 had Type1 diabetes mellitus (DM) and 34 Type2 DM. There were no differences in age, sex and neuropathy duration between the groups (p = 0.42, 0.72 and 0.87 respectively). Patients with CIDP or DSP+CIDP had larger cross‐sectional areas (CSA) in three sites: left median at mid‐arm (p = 0.001), right ulnar (p = 0.002) and left ulnar (p = 0.009) nerves at mid‐arm. There were no differences in the median CSA at the wrists (p = 0.62), or ulnar CSA at the grooves (p = 0.84). Discussion Nerve US may be helpful to differentiate patients with CIDP or CIDP+DSP from those with DSP only. Proximal upper limb nerve segments show enlarged areas in CIDP or CIDP+DSP patients.
ABSTRACT Background and Purpose Over the past decades, whole‐body PET‐CT scanning has undergone considerable innovation, with a considerable increase in clinical indications becoming a key diagnostic imaging method. Subsequently PET is contributing to the growth in imaging incidentaloma rates, including those of the brain, a critical functional tissue. Investigation of etiologies and prevalence of PET incidentalomas, notably of brain, is crucial in order to enhance their recognition and managing by concerned physicians. Thus, for educational purposes, we have chosen to collect and analyze cases of cerebral PET incidentalomas that are published in relevant international literature. Methods Following PRISMA checklist guidelines, a systematic review and a meta‐analysis were executed. Literature was searched through several engines including PubMed and Cochrane Library. Data extracted from selected studies were qualitatively and quantitatively analyzed. Results Among a total of 2211 studies collected, only 18 retrospective observational studies, using different kind of radiotracers, were eligible. Descriptive analysis revealed that the most frequent brain PET incidentalomas were meningiomas (30%), metastatic tumors (23.1%), and pituitary adenomas (9.2%). The meta‐analyses concluded a pooled prevalence rate of 1.2% (95% CI: 0.7%–2%; p‐value < 0.0001) and 3.5% (95% CI: 1.6%–7.5%; p‐value < 0.0001) of incidentalomas as disclosed by 18F‐FDG and 68Ga‐DOTA‐peptides respectively. Conclusions This review is the first to have summarized findings available in the literature on the identification of brain incidentalomas using PET‐CT techniques with different kinds of radiotracers. It fulfilled its main objective by presenting the compiled findings and deducing a pooled prevalence rate along with a description of their etiologies. Results undeniably solicit more research for better management of these entities whose etiologies are quite diverse.
ABSTRACT Pediatric neurosonology is an important component of non‐invasive brain monitoring. The combination of transcranial and ocular ultrasound enables real‐time assessment of cerebral blood flow velocities, autoregulation, and intracranial dynamics across different clinical settings. This narrative review synthesizes the main themes presented at the Pediatric Neurosonology Symposium, held in August 2025 to celebrate 50 Years of Ultrasound Education at Wake Forest University, reflecting the expanding clinical use of ultrasound in the pediatric brain. The review integrates anatomical and physiological foundations of pediatric neurosonology with bedside applications across acute, perioperative, and intensive care medicine. Structured into key thematic domains—B‐mode for rapid assessment of skull fractures and intracranial pathology and ocular ultrasound, transcranial Doppler use in hemodynamic assessment, critical illness and extracorporeal life support, and real‐time cerebral autoregulation— the review presents practical insights in this emerging field. Topics include point of care evaluation in head trauma in the emergency department, optic nerve sheath diameter for intracranial pressure assessment, pediatric stroke monitoring, cerebral autoregulation, transcranial Doppler thresholds for vasospasm and perfusion failure, and cerebral circulatory arrest. Real‐world examples illustrate how ultrasound can transform cerebral physiology into actionable, bedside decision‐making, potentially complementing other neuromonitoring modalities. Broader clinical integration of pediatric neurosonology will require standardized training, multicenter validation studies, and reduced variability in implementation across institutions. With scientific and clinical collaboration, pediatric neurosonology may bridge gaps in understanding of anatomy, physiology, and individualized care, offering a dynamic and repeatable window into the pediatric brain during illness.
ABSTRACT Background and Purpose Whether neuromuscular ultrasound (NMUS) can help differentiate between different types of immune‐mediated neuropathy remains unclear. This study aims to investigate the sonographic features of Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) and other immune‐mediated neuropathies. Methods This exploratory study was performed in our center between August 2022 and June 2025. Thirty‐one patients were enrolled after providing written consent. Twelve patients met the criteria for CIDP, and 19 were diagnosed with immune‐mediated demyelinating neuropathy, which is not CIDP; 12 multifocal motor neuropathy (MMN), 4 anti‐MAG (DADS) neuropathy, and others. CIDP diagnosis was established according to the EAN/PNS 2021 guidelines. Results CIDP group had higher cross‐sectional area (CSA) values, compared to the non‐CIDP immune neuropathy group. This was demonstrated in two nerve segments reaching statistical significance (median nerve in the forearm and ulnar nerve in the groove, p< 0.05) and in the overall average of the value ‘measured CSA divided by expected normal CSA’; 131% versus 102%, p = 0.004. Similar results were found between CIDP versus MMN (with no other non‐CIDP disorders). Honeycomb architecture was more distorted in the non‐CIDP immune neuropathy group, whereas echogenicity was similar. Conclusions We provided a sonographic characterization for CIDP and non‐CIDP cases, highlighting neuroimaging parameters that differentiate between the two groups, such as CSA. This study enriches the existing information about the utility of NMUS and improves our ability to differentiate between CIDP and other immune‐mediated neuropathies.
ABSTRACT Background and Purpose Type 2 diabetes (T2D) is a major metabolic risk factor for Alzheimer's disease dementia (ADD), yet it remains unclear whether cognitive decline in T2D follows a distinct cerebral metabolic trajectory. We investigated whether [18F]FDG‐PET hypometabolism differs between T2D patients with mild cognitive impairment (MCI) versus ADD, and whether peripheral metabolomic profiles mirror AD‐sensitive brain vulnerability. Methods Nineteen patients with T2D (11 MCI, 8 ADD) underwent [18F]FDG‐PET and plasma metabolomics. Cerebral glucose metabolism was assessed voxel‐wise and region‐wise using global‐mean normalization, with group comparisons adjusted for age, sex, HbA1c, and systolic blood pressure. Metabolite group differences and ROI–metabolite associations were evaluated using multiple‐comparison–corrected statistical models. Results ROI analyses showed lower global‐mean–normalized FDG uptake in T2D + ADD versus T2D + MCI, with the right hippocampus and right parahippocampal gyrus (PHG) remaining significant after BH–FDR correction. Voxel‐wise analysis identified one FWE‐corrected cluster of relative hypometabolism in T2D + ADD centered in the left inferior temporal gyrus. Several metabolites differed between groups at the uncorrected level, but none remained significant after BH–FDR correction. ROI–metabolite coupling patterns were stage dependent: in T2D + MCI, right parahippocampal uptake was negatively correlated with glutamine and amino acids and positively correlated with lipoproteins (BH–FDR significant), whereas in T2D + ADD the same ROI showed positive correlations with dimethylglycine (DMG), dimethylamine (DMA), albumin‐lysyl, and 2‐oxoglutarate, and the left inferior temporal gyrus correlated negatively with amino acids. Conclusions In T2D, ADD is characterized by medial temporal and lateral temporal–parietal hypometabolism accompanied by stage‐specific peripheral metabolite coupling, supporting a progression‐sensitive neuro‐metabolic vulnerability signature.
ABSTRACT Background Freezing of gait (FoG) is a debilitating motor feature that affects individuals with Parkinson's disease (PD). The mechanism underlying FoG is not entirely understood, which poses a challenge in finding effective treatment. The goal of this study is to advance the understanding of FoG pathophysiology. This study aims to assess the differences in structural connectivity (SC) and functional connectivity (FC) patterns among PD patients with freezing of gait (FoG+), gait disturbances other than freezing (FoG−), and no gait disturbances (NGD). Methods Diffusion‐weighted MRI (dwMRI) and resting‐state functional MRI (rs‐fMRI) were obtained from 9 FoG+, 13 FoG−, and 10 NGD patients. The FC data was processed by a region of interest (ROI)‐to‐ROI analysis using the default preprocessing pipeline from the MATLAB‐based CONN toolbox. SC analysis was performed via diffusion‐based tractography and subsequent connectome reconstructions in MRtrix3. Results Compared to the FoG− and NGD groups, the FoG+ group showed substantial involvement, in both SC and FC, of the limbic system, putamen, parietal lobes, and cerebellum. Furthermore, our results reveal FC alteration between the cerebellum and the median raphe nuclei, which is part of the pontomedullary reticular formation. Conclusions Our results confirmed previous research regarding the alterations in multiple brain areas in those with FoG, particularly the limbic system, putamen, parietal lobe, and cerebellum. We further establish unique FC between the cerebellum and the median raphe nucleus in those with FoG. This finding highlights the role of the cerebellum in regulating posture, gait, and locomotive signals, potentially through serotonergic projections.
ABSTRACT Background and Purpose Arterial spin labeling (ASL)‐MRI measures cerebral blood flow (CBF) by magnetically labeling red blood cells (RBC). ASL‐MRI shows reduced CBF in diseases including Alzheimer's Disease (AD). ASL‐measured CBF is affected by hematocrit, the proportion of blood volume composed of RBC. Hematocrit affects the ASL signal by affecting the T1 relaxation time of blood, and also physiologically, via rheological effects and autoregulation. This may confound comparisons between groups with differing hematocrit levels, such as men and women. We evaluated the influence of hematocrit on sex differences in ASL‐MRI‐measured CBF using two independent datasets. Methods 403 participants (252 women) from a local dataset and 119 participants (67 women) from ADNI underwent ASL‐MRI to measure cortical CBF and blood sampling for hematocrit. Using multiple regression, we assessed sex differences in CBF with and without accounting for hematocrit. Results Hematocrit was strongly and inversely correlated with CBF calculated using two different ASL‐MRI methods. Without adjusting for hematocrit, women appeared to have higher CBF than men, but this difference was no longer statistically significant when hematocrit was included in the model. Conclusions Hematocrit significantly affects ASL‐MRI‐measured CBF and must be considered when comparing groups with differing hematocrit. We demonstrate this for sex differences, and discuss its relevance to menopause, which is associated with increased hematocrit due to cessation of menstruation. Since female sex and post‐menopause are important AD risk factors, accounting for hematocrit is essential when using ASL‐MRI to investigate how sex and menopause influence brain perfusion, function, and vulnerability to AD.
ABSTRACT Background and Purpose The optic nerve sheath diameter (ONSD) measured by sonography is a well‐known noninvasive technique for estimation of intracranial pressure (ICP). Still, test‐retest reliability and the minimal detectable change (MDC) for ONSD sonography remains unexplored in the setting of acute brain injury (ABI), which this study aimed to evaluate. Methods This was a post‐hoc study based on data extracted from two previous studies of ONSD measured with a 10 MHz linear probe in ABI patients with invasive ICP monitoring. We included repeated measurements of ONSD in short time intervals with invasively measured ICP fluctuating ≤2 mmHg between observations. Intraclass correlation coefficient (ICC) with absolute agreement, standard error of measurement (SEM), MDC and limits of agreement (LOA) were calculated for right, left and mean ONSD. Results 31 patients were included. Test–retest reliability was considered good to excellent, with intraclass correlation coefficients values ranging from 0.80 (95%CI:0.63–0.90) to 0.91 (95%CI:0.82–0.95). Measurement errors were small, with SEM values ranging from 0.31 mm to 0.17 mm and MDC values ranging from 0.87 mm to 0.47 mm. The best SEM and MDC were achieved using a bilateral mean of ONSD measured internal of the dura mater (ONSDint). Conclusions According to our results, a bilateral mean ONSDint is recommended for noninvasive estimation of ICP in an ABI population. Using this technique, a change ≥0.5 mm may be safely assumed to represent underlying physiological or anatomical changes, most likely changes in the ICP.
ABSTRACT Sudden sensorineural hearing loss (SSNHL) is most often idiopathic or related to benign conditions such as Meniere's disease. However, SSNHL caused by vertebrobasilar ischemia is rare and may precede life‐threatening neurological deficits. We present the case of a 67‐year‐old male with hypertension and hyperlipidemia who developed acute vertigo, left‐sided hearing loss, dysarthria, right facial droop, and right‐sided weakness. Initial non‐contrast CT was unremarkable, but computed tomography angiography (CTA) revealed a near‐occlusive thrombus in the mid‐basilar artery. MRI showed an acute infarct in the left cerebellum within the anterior inferior cerebellar artery (AICA) distribution, which supplies the internal auditory artery. Subsequent audiometry confirmed bilateral SSNHL, more severe on the left. The patient was outside the thrombolysis window but underwent cerebral angiography, which confirmed chronic left vertebral occlusion and high‐grade basilar stenosis. He was started on dual antiplatelet therapy and high dose statin therapy and discharged to rehabilitation with residual vertigo and hearing loss. This case emphasizes that SSNHL and vertigo can be early signs of posterior circulation stroke. High‐grade basilar stenosis affecting AICA flow may compromise perfusion to the auditory and vestibular systems. Clinicians should maintain a high index of suspicion for vertebrobasilar ischemia in patients presenting with audiovestibular symptoms, even in the absence of classic stroke findings. Early imaging with MRI and CTA is critical for diagnosis. Recognizing these atypical presentations enables timely management and may reduce long‐term neurologic impairment.
ABSTRACT Background and Purpose Chiari II deformation in open neural tube defect (ONTD) includes hindbrain herniation (HBH) and posterior fossa remodeling. While HBH reversal after prenatal ONTD repair is well described, associated changes in cerebellar morphology, torcular position, and bony configuration remain poorly characterized. This study evaluated longitudinal changes in posterior fossa anatomy following fetal ONTD repair and their associations with HBH reversal and evolving ventriculomegaly. Methods We retrospectively reviewed 112 fetuses who underwent prenatal ONTD repair at a single center (2011–2023), each with fetal MRI before surgery (median 22.9 [19.1–25.4] weeks) and 6 weeks after surgery (31.4 [28.6–34.0] weeks). Two independent examiners assessed cerebellar and brainstem position, occipital bone outpouching, clivus concavity, torcular position, and preservation of supratentorial subarachnoid space. HBH reversal was defined as cerebellar ascent above the foramen magnum. Severe ventriculomegaly was defined as a mean atrial width ≥15 mm. Associations were tested using Chi‐square or McNemar tests. Results At referral, 17.9% had severe ventriculomegaly and 79.5% had lesions below L2. After surgery, clivus concavity (97.3% vs 84.1%, p<0.01) and subarachnoid space preservation (82.1% vs 3.6%, p<0.01) increased significantly, while occipital outpouching and low torcular position showed no change. Complete HBH reversal occurred in 62.5%. Subarachnoid space preservation was more frequent with HBH reversal (98% vs 63.3%, p<0.01). Severe ventriculomegaly at postoperative MRI (58.9%) was not associated with posterior fossa abnormalities. Conclusions Prenatal ONTD repair improves HBH and supratentorial CSF space preservation but has limited impact on deeper posterior fossa remodeling, which appears only partially reversible.
ABSTRACT Transcranial color‐coded duplex (TCCD) ultrasound enables rapid bedside assessment of cerebral hemodynamics in pediatric intensive care units (PICUs), yet its use is underreported in resource‐limited settings. We retrospectively reviewed five pediatric cases from a single tertiary PICU in which TCCD was performed as part of neurocritical care, applying standardized protocols and operator training. Median mean flow velocity (MFV) increased from 70 to 98 cm/s post‐intervention, while pulsatility index (PI) decreased from 1.30 to 1.05. The cases demonstrated diagnostic contributions in suspected brain death, cerebral vasospasm, arteriovenous malformation, and raised intracranial pressure. These findings suggest that TCCD is a feasible, noninvasive neuromonitoring tool in pediatric neurocritical care, even in resource‐limited settings, although larger studies are needed to validate its diagnostic accuracy.
ABSTRACT Background Posterior reversible encephalopathy syndrome (PRES) is a well‐described neuro‐clinical syndrome characterized by acute‐onset symptoms, seizures, headache, visual disturbances, encephalopathy, and distinctive neuroimaging findings of vasogenic edema, typically in parieto‐occipital regions. A cardinal feature is the reversibility of both clinical and radiological abnormalities, often within days to weeks of addressing the inciting trigger. Case presentation This report presents a highly atypical case of a 47‐year‐old hypertensive male being managed for abdominal sepsis with a history of recurrent seizures and altered mentation with symptoms persisting more than 4 months after the initial brain magnetic resonance imaging (MRI). The MRI 5 days post symptoms revealed bilateral, symmetrical occipital lobe vasogenic edema consistent with PRES, in the absence of acute infarction, hemorrhage, or vasculopathy. Conclusion This case challenges the conventional temporal boundaries of PRES, demonstrating that the “reversible” component may, in rare instances, extend over several months, thereby expanding the recognized clinico‐radiological spectrum of this syndrome.
ABSTRACT Background and Purpose Solitary tumefactive demyelinating lesions (TDLs) represent an uncommon but clinically significant manifestation of central nervous system demyelination and pose a major diagnostic challenge due to their radiologic resemblance to high‐grade gliomas, primary central nervous system lymphoma, and other mass‐like lesions. Accurate non‐invasive differentiation is essential to avoid unnecessary biopsy and inappropriate oncologic treatment. This review aims to synthesize the role of advanced MRI techniques in improving diagnostic confidence in TDLs. Methods A narrative review of the literature was performed, focusing on advanced MRI modalities used in the evaluation of TDLs, including proton MR spectroscopy, diffusion tensor imaging, magnetization transfer imaging, and dynamic susceptibility contrast perfusion imaging. Relevant studies were analyzed to identify characteristic imaging patterns and their underlying pathophysiologic correlates. An illustrative case was incorporated to contextualize these findings. Results Advanced MRI techniques demonstrate distinct imaging signatures in TDLs that reflect inflammatory demyelination rather than neoplastic processes. Proton MR spectroscopy typically reveals elevated choline with preserved or relatively less reduced N‐acetylaspartate and the presence of lipid–lactate peaks. Diffusion imaging shows variable restriction corresponding to active inflammatory fronts. Magnetization transfer imaging highlights myelin disruption, often with characteristic peripheral signal changes. Perfusion imaging consistently demonstrates low relative cerebral blood volume, reflecting the absence of neoangiogenesis, in contrast to high‐grade tumors. Integration of these modalities improves diagnostic specificity and reduces reliance on invasive procedures. Conclusions Advanced multimodal MRI provides critical complementary information for differentiating TDLs from neoplastic mimics. A combined imaging approach, supported by pathophysiologic understanding, can enhance diagnostic accuracy and guide appropriate clinical management. Incorporation of illustrative cases further strengthens the practical application of these techniques in routine clinical practice.
ABSTRACT Background and Purpose Glioblastoma (GBM) is a primary CNS neoplasm with a dismal prognosis. Sarcopenia is an indicator of poor overall survival (OS) in a variety of cancers. Temporalis muscle thickness (TMT) and masseter muscle thicknesses (MMT) have been studied as surrogate markers for sarcopenia, while muscle volume has not. Our objective was to determine the utility of temporalis muscle volume (TMV) and masseter muscle volume (MMV) as a prognostic indicator in GBM patients. Methods This retrospective cohort study included adult patients with a primary IDHwt GBM diagnosis between 2008 and 2020, and Karnofsky Performance Scale (KPS) ≥ 60. TMT, MMT, TMV, and MMV were measured on CT Brain closest to date of diagnosis using Varian Eclipse v18.0. Cox proportional hazards regression was used to assess the association of TMT, MMT, TMV, and MMV with OS. Results 99 patients were included. Median age was 61 years, most (71%) were male, and the mean BMI was 28.9 kg/m2. TMT and MMT were moderately correlated with TMV and MMV. None of our muscle indices demonstrated significant association with OS (adjusted p‐value = 0.522 for TMT, 0.066 for TMV, 0.371 for MMT, and 0.597 for MMV). MGMT methylation and extent of resection were associated with significantly improved OS (p < 0.001 for both). Conclusion Neither temporalis nor masseter muscle thickness or volume demonstrated a significant association with OS in patients with GBM. Given the modest sample size and limited statistical power, a prognostic role for these sarcopenia‐related measures cannot be excluded and warrants further investigation.
