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Objectives: MR neurography has the ability to detect and depict peripheral nerve injuries. This study evaluated the potential of MR neurography in the diagnosis of post-traumatic trigeminal neuropathy.
Methods: Forty-one participants prospectively underwent MR neurography of the lingual and inferior alveolar nerves using a 3D TSE STIR black-blood sequence. Two blinded and independent observers recorded the following information for each nerve of interest: presence of injury, nerve thickness, nerve signal intensity, MR neurography Sunderland class, and signal gap. Afterwards, the apparent nerve-muscle contrast-to-noise ratio and apparent signal-to-noise ratio were calculated. Clinical data (neurosensory testing score and clinical Sunderland class) was extracted retrospectively from the medical records of patients diagnosed with post-traumatic trigeminal neuropathy.
Results: Compared to neurosensory testing, MR neurography had a sensitivity of 38.2% and specificity of 93.5% detecting nerve injuries. When differentiated according to clinical Sunderland class, sensitivity was 19.1% in the presence of a low class injury (I to III) and improved to 83.3% in the presence of a high class (IV to V). Specificity remained unchanged. The area under the curve using the apparent nerve-muscle contrast-to-noise ratio, apparent signal-to-noise ratio, and nerve thickness to predict the presence of an injury was 0.78 (p < .05). Signal intensities and nerve diameter increased in injured nerves (p < .05). Clinical and MR neurography Sunderland scores positively correlated (correlation coefficient = 0.53; p = .005).
Conclusions: This study shows that MR neurography can accurately differentiate between injured and healthy nerves, especially in the presence of a more severe nerve injury.
Clinical Relevance Statement: MR neurography is not only able to detect trigeminal nerve injuries, but it can also provide information about the anatomical specifications of the injury, which is not possible with clinical neurosensory testing. This makes MR neurography an added value in the management of post-traumatic trigeminal neuropathy.
Key Points: • The current diagnosis of post-traumatic trigeminal neuropathy is mainly based on clinical examination. • MR neurography is able to visualize and stratify peripheral trigeminal nerve injuries. • MR neurography contributes to the diagnostic process as well as to further decision-making.
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http://dx.doi.org/10.1007/s00330-023-10363-2 | DOI Listing |
Spec Care Dentist
September 2025
Department of Pediatric Dentistry, Faculty of Dentistry of Ribeirao Preto, University of São Paulo, Ribeirão Preto, Brazil.
Neuropathic pain and its high impact on patient's quality of life, must be thoroughly assessed to be adequately managed. Unfortunately, there remains a lack of evidence for different treatment options that could improve the quality of life of those patients. Beyond first-choice therapies, complementary integrative therapies can emerge as a highly valuable option for controlling chronic pain.
View Article and Find Full Text PDFToxins (Basel)
August 2025
Department of Oral Medicine, Sedation and Imaging, Hadassah Medical Center, Faculty of Dental Medicine, Hebrew University of Jerusalem, Jerusalem 91120, Israel.
Orofacial pain encompasses a spectrum of disorders ranging from musculoskeletal disorders, such as myofascial pain, and temporomandibular disorders to neuropathic situations, such as trigeminal neuralgia and painful post-traumatic trigeminal neuropathy, and neurovascular pain such as orofacial migraine and cluster orofacial pain. Each require tailored prophylactic pharmacotherapy, such as carbamazepine, gabapentin, pregabalin, amitriptyline, metoprolol, and topiramate. Yet a substantial subset of patients remains refractory.
View Article and Find Full Text PDFBiochem Pharmacol
August 2025
Department of Pharmacology, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. Electronic address:
Post-traumatic trigeminal neuropathy (PTTN) is a debilitating sensory disorder resulting from trigeminal nerve damage for which effective therapies are lacking.Pretreatment with neutralizing antibodies against high mobility group box-1 (HMGB1), a damage-associated molecular pattern (DAMP), has shown promise in preventing PTTN development; however, the specific receptor mediating HMGB1-driven neuropathic pain in this context remains undefined. This study investigates the role of the receptor for advanced glycation end-products (RAGE), a key HMGB1 receptor, in PTTN pathogenesis using a distal infraorbital nerve chronic constriction injury (dIoN-CCI) model in both male and female mice.
View Article and Find Full Text PDFJ Headache Pain
August 2025
Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA.
Background: Posttraumatic headache (PTH) is a common and debilitating consequence of traumatic brain injury (TBI), characterized by neuroinflammation and pain hypersensitivity. Current treatments are limited, and novel therapeutics are needed. Indomethacin morpholinamide (IMMA), a substrate-selective cyclooxygenase-2 (COX-2) inhibitor, enhances endocannabinoid signaling without disrupting prostaglandin homeostasis and may offer a mechanistically distinct approach to managing PTH.
View Article and Find Full Text PDFBrain
August 2025
Harvard Medical School, Boston, MA 02115, USA.
Emerging evidence implicates pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) in migraine and other headache disorders. Systemic infusion of PACAP-38 induces migraine headache in people with migraine and mild headache in healthy adults. However, the precise mechanism and site of action remain poorly characterized.
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