This composite diagnostic image displays radiological findings from six patients with trigeminal neuralgia, primarily using axial Magnetic Resonance Imaging (MRI) and Computed Tomography (CT) focusing on the posterior fossa and cerebellopontine angle (CPA). Panels A, B, and E demonstrate neurovascular compression (NVC) of the trigeminal nerve (yellow arrowheads). Specifically, panels A and E show compression by the petrosal vein (blue arrowheads), while panel B shows compression by the superior cerebellar artery (red arrowhead). Panel C illustrates a left trigeminal nerve without apparent vascular contact. Panel D provides a non-contrast CT view of the left cerebellopontine cistern (pink arrowheads) in a patient where MRI was contraindicated. Panel F displays a T1-weighted gadolinium-enhanced MRI showing a pathological mass/tumor (green arrowhead) within the left cerebellopontine cistern, representing secondary trigeminal neuralgia. The collection serves as an educational comparison between idiopathic, neurovascular, and secondary causes of trigeminal nerve dysfunction, highlighting the anatomical relationship between the nerve root entry zone and adjacent vascular or neoplastic structures.

This composite medical image presents a comparison between pre-operative axial MRI scans (a, c, e) and corresponding intra-operative clinical photographs (b, d, f) illustrating neurovascular conflict (NVC) in cases of trigeminal neuralgia. The MRI images demonstrate the spatial relationship between the trigeminal nerve (TGN, blue arrows) and adjacent vascular structures, primarily the superior cerebellar artery (SCA, red arrows) and other vessels (yellow arrows) in the cerebellopontine angle. The intra-operative views provide direct visualization of these structures during microvascular decompression (MVD) surgery. The series highlights clinical discrepancies where routine MRI might suggest arterial compression that is later identified intra-operatively as non-contacting (white arrow gap in b), compression by venous structures (white arrow in d), or arterial compression that was subtle on imaging (white arrow in f). This comparison serves as an educational tool for neurosurgical planning, emphasizing the importance of identifying the Root Entry Zone (REZ) and distinguishing between arterial and venous compression in the management of trigeminal nerve syndromes.

This composite image illustrates the clinical progression and surgical treatment of trigeminal neuralgia using microvascular decompression (MVD). Panel A is a preoperative axial MRI scan of the brain, with a red circle highlighting neurovascular compression at the root entry zone of the right trigeminal nerve in the cerebellopontine angle. Panels B through F provide a sequence of intraoperative endoscopic photographs showing the surgical workflow. Key anatomical structures identified include the trigeminal nerve (blue arrow), brainstem (purple arrow), petrosal vein (orange arrow), and facial nerve (green arrow). The sequence demonstrates the exploration and dissection of arachnoid adhesions (Panels B-D), identifying a petrosal vein branch (red arrow) as the offending vessel compressing the nerve (Panel E). The final panel (F) depicts the therapeutic intervention, where a Teflon pad (yellow arrow) is surgically interposed between the trigeminal nerve and the offending vessel to achieve mechanical decompression. This sequence serves as an educational tool for neurosurgical training, demonstrating the suboccipital retrosigmoid approach and the efficacy of endoscopic visualization in identifying subtle vascular compression.

Histology image obtained from a temporal artery biopsy, prepared with Hematoxylin and Eosin stain and viewed under light microscopy at low magnification. The specimen demonstrates classic giant cell arteritis with transmural, granulomatous inflammation encompassing the full thickness of the arterial wall (intima, media, and adventitia) in a segmental distribution. Multinucleated giant cells are interspersed with a dense lymphohistiocytic infiltrate, and fragmentation or disruption of the internal elastic lamina is evident. The inflammatory process extends to the vasa vasorum and small venules within the adventitia, indicating widespread perivascular involvement. Accompanying features include marked intimal hyperplasia producing marked luminal narrowing and, in this field of view, near-occlusive lumen occlusion. The arterial media may show loss of elastic fibers and necrosis is not conspicuous here. These findings are diagnostic of GCA and help differentiate from other large-vessel vasculitides and nonspecific atherosclerotic changes. Clinically, such histology supports a diagnosis of temporal arteritis in patients with new headaches, visual symptoms, jaw claudication, and elevated inflammatory markers, guiding urgent corticosteroid therapy to prevent ischemic complications. This image exemplifies the radiologic-pathologic correlation typical of vasculitic arteritis. The slide highlights diagnostic relevance, research utility, and educational value for trainees and clinicians in practice. For medical education and research.

This histology image captures a cross-sectional temporal artery biopsy illustrating the hallmarks of giant cell arteritis. Prepared as a paraffin-embedded tissue section and stained with Hematoxylin and Eosin, the slide reveals a transmural inflammatory infiltrate that traverses all arterial wall layers. At the center, a narrowed lumen is surrounded by concentric intimal hyperplasia with marked medial disruption. Multinucleated giant cells and mononuclear macrophage clusters are present within the media, accompanied by lymphocytic infiltrate along the vessel wall. The elastic lamina appears disrupted, and fragmentation of the media is evident, consistent with robust granulomatous vasculitis. These features produce near-occlusive narrowing of the artery, explaining the ischemic risk associated with temporal arteritis. Clinically, such histopathology confirms a diagnosis of GCA and helps differentiate from atherosclerotic disease, infectious vasculitis, or other large-vessel vasculitides. The image underscores the systemic nature of the disease, as inflammation can extend from cranial vessels to the aorta. The diagnostic significance lies in correlating histology with patient presentation, including age-related cranial symptoms and risk of vision loss; timely immunosuppressive therapy can prevent irreversible ischemic complications. This specimen exemplifies classic angiitis with granulomatous inflammation and intimal hyperplasia driving luminal compromise.

Imaging modality and technique: Brightfield light microscopy of a temporal artery biopsy stained with Hematoxylin and Eosin (H&E). Specimen: arterial wall from the temporal region; cross-sectional vascular biopsy showing inflammatory arteritis. Key features include granulomatous inflammatory infiltrate surrounding the media and adjacent to the internal elastic lamina, composed of lymphocytes, plasma cells, epithelioid histiocytes, and multinucleated giant cells. Giant cells are often present but may be absent; their presence supports diagnosis but is not required. The inflammatory infiltrate disrupts the media and may extend into the adventitia; fragmentation and phagocytosis of the internal elastic lamina are characteristic. Medial necrosis is minimal to absent; there is usually no well-formed granuloma or extensive necrosis. Neointimal hyperplasia and luminal narrowing can be observed as secondary consequences of chronic vasculitis. The image demonstrates a granulomatous arteritis pattern typical of giant cell arteritis. Diagnostic significance: classic histopathology includes granulomatous inflammation of medium-sized arteries with IEL fragmentation; biopsy positivity confirms temporal arteritis; however, skip lesions can yield false negatives; clinical correlation with headache, scalp tenderness, jaw claudication, visual symptoms and elevated inflammatory markers (CRP/ESR) is essential. Differential considerations include Takayasu arteritis, atherosclerosis, infectious vasculitis, and other granulomatous vasculitides. This slide is used in educational settings to illustrate GCA pathology and IEL involvement.