Manal El Faham

Abstract Background Diffuse axonal injury (DAI) is a severe form of traumatic brain injury associated with high-velocity impact, acceleration–deceleration forces, and rotational trauma. Despite its clinical and forensic importance, DAI frequently eludes detection on gross examination at autopsy, rendering it a “hidden lesion” that necessitates microscopic evaluation and advanced neuroimaging for accurate diagnosis. In forensic practice, DAI plays a pivotal role in determining the mechanism and timing of injury, particularly in fatal trauma and suspected non-accidental head injury. This review aims to synthesize current evidence on the pathophysiology, neuropathological features, diagnostic modalities, and forensic and medicolegal implications of DAI in traumatic brain injury, with particular emphasis on its role in death investigation. Main body The pathophysiology of DAI involves shearing forces that disrupt axons at interfaces of differing brain densities, particularly within the corpus callosum, brainstem, and subcortical white matter. Histopathological findings include axonal swellings and retraction bulbs, with enhanced detection through immunohistochemical markers such as β-amyloid precursor protein (β-APP) and neurofilaments. Radiologically, magnetic resonance imaging (MRI) demonstrates superior sensitivity compared to computed tomography (CT), especially with advanced techniques including susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI). From a forensic perspective, DAI is central to the evaluation of traumatic brain injury, including cases of abusive head trauma (AHT), where it contributes to the assessment of both mechanism and timing of injury. Conclusion Diffuse axonal injury remains a diagnostically challenging yet forensically significant entity in traumatic brain injury. Accurate identification requires a multidisciplinary approach integrating clinical context, advanced neuroimaging, and targeted histopathology. Improved recognition enhances the accuracy and reliability of medicolegal determinations, particularly in complex trauma and suspected abuse, reinforcing its value in forensic practice.

Ménière's disease (MD) is a chronic vestibular disorder characterized by recurrent vertigo, fluctuating sensorineural hearing loss (SNHL), tinnitus, and aural fullness, with an unpredictable course that can significantly impair quality of life. Endolymphatic hydrops (EH) remains the hallmark histopathological finding; however, its underlying pathophysiology is not fully understood and likely reflects a multifactorial process involving immune, viral, allergic, genetic/familial, and vascular mechanisms. Emerging evidence suggests that EH may represent a secondary manifestation rather than the primary driver of symptoms, potentially resulting from endolymphatic sac hyperplasia. Given this complexity, no single unifying mechanism has been confirmed, and etiologic contributors may vary among patients. Presenting a clinical case, therefore, provides valuable insight into this heterogeneity and highlights the need for continued research to clarify the underlying pathology of MD. This report presents a 57-year-old male with recurrent vertigo, progressive moderately severe right-sided SNHL, tinnitus, and severe vitamin D deficiency. Diagnostic pure-tone audiometry, comprehensive vestibular testing, and imaging were performed. Management consisted of lifestyle and dietary modifications, pharmacologic therapy, vestibular rehabilitation, vitamin D supplementation, and hearing aid rehabilitation, resulting in improved vertigo control, balance, and overall quality of life. The discussion integrates current diagnostic criteria, differential considerations, and evidence-based management strategies, emphasizing individualized, patient-centered care and the importance of recognizing emerging modifiable factors such as vitamin D deficiency and potential genetic susceptibility. The central aim of this case report is to enhance medical students' understanding of this multifaceted disorder and to underscore the clinical reasoning skills required for accurate and timely diagnosis.

Background: Vanishing Twin Syndrome (VTS)—the early spontaneous loss of one fetus in a multifetal gestation—occurs in up to 36% of twin pregnancies assisted by reproductive technology and approximately 10–15% of spontaneous twin pregnancies. While historically considered a benign event for the surviving co-twin, emerging evidence indicates that VTS can significantly impair residual placental function and fetal growth trajectories. Case presentation: This report describes a primigravida who presented with early first-trimester ultrasound confirmation of a dichorionic-diamniotic (DCDA) twin pregnancy. Subsequent follow-up imaging demonstrated complete spontaneous reabsorption of one twin sac, indicating VTS. While antenatal monitoring continued as a single gestation, progressive fetal growth restriction (FGR) and altered umbilical artery (UA) Doppler indices were identified in the surviving fetus during the late second and third trimesters. Serial growth tracking and obstetric management resulted in the delivery of a very low birth weight (VLBW) infant at late term without major acute neonatal morbidities. Conclusion: This case highlights that VTS should not be treated as a routine single gestation once twin disappearance is confirmed. Heightened biophysical and Doppler surveillance throughout the second and third trimesters is essential to detect latent FGR and optimize timing of delivery.