Orbital exenteration is a disfiguring operation involving the removal of the entire contents of the orbit, with or without the eyelids. It is widely felt that such extensive surgery can only be performed under general anesthesia. We report our experience with a patient who underwent orbitalexenteration under trigeminal block with intravenous sedation. A 68-year-old male patient was diagnosed to have orbital cellulitis (mucormycosis), uncontrolled diabetes mellitus, ischemic heart disease, dilated cardiomyopathy with severe left ventricular systolic dysfunction with severe pulmonary artery hypertension, and nephropathy. We decided to avoid general anesthesia for such a high-risk patient with many co-morbid illnesses. We gave trigeminal block using a 22-G spinal needle with local anesthetic solution of bupivacaine 0.5% by classic approach. A standard exenteration was performed and the patient tolerated the procedure well with no complications.
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http://dx.doi.org/10.4103/1658-354X.121051 | DOI Listing |
JA Clin Rep
January 2025
Department of Pain Clinic, NTT Medical Center Tokyo, 5-9-22 Higashi-Gotanda, Shinagawa-Ku, Tokyo, 141-8625, Japan.
Background: Bilateral trigeminal neuralgia secondary to multiple sclerosis is an extremely rare condition. When Gasserian ganglion block is performed, it is necessary to achieve reliable long-term analgesic effects while avoiding treatment-related complications.
Case Presentation: A 49-year-old male with multiple sclerosis exhibited persistent dull pain and paroxysmal electric shock-like pain in his bilateral maxillary molars and mandible.
Br J Pharmacol
January 2025
Center for Clinical Pharmacology, Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri, USA.
Background And Purpose: Pituitary adenylate cyclase activating polypeptide (PACAP) is a human migraine trigger that is being targeted for migraine. The δ-opioid receptor (δ-receptor) is a novel target for the treatment of migraine, but its mechanism remains unclear. The goals of this study were to develop a mouse PACAP-headache model using clinically significant doses of PACAP; determine the effects of δ-receptor activation in this model; and investigate the co-expression of δ-receptors, PACAP and PACAP-PAC1 receptor.
View Article and Find Full Text PDFbioRxiv
December 2024
Center for Pain Therapeutics and Addiction Research, School of Dentistry, University of Texas Health San Antonio, Texas, 78229, USA.
Truncated TrkB (TrkBT1), traditionally considered a dominant-negative regulator of full-length TrkB (TrkBTK+), remains poorly understood in peripheral sensory neurons, particularly nociceptors. Furthermore, sensory neuronal TrkB expression and function has been traditionally associated with non-nociceptive neurons, particularly Aδ low-threshold mechanoreceptors. This study challenges prevailing assumptions by demonstrating that TrkBT1 is the predominant TrkB isoform expressed in sensory neurons and plays a functional role in modulating neuronal activity.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Departamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, Chile.
Cold allodynia is a debilitating symptom of orofacial neuropathic pain resulting from trigeminal nerve damage. The molecular and neural bases of this sensory alteration are still poorly understood. Here, using chronic constriction injury (CCI) of the infraorbital nerve (IoN) (IoN-CCI) in mice, combined with behavioral analysis, Ca imaging and patch-clamp recordings of retrogradely labeled IoN neurons in culture, immunohistochemistry, and adeno-associated viral (AAV) vector-based delivery , we explored the mechanisms underlying the altered orofacial cold sensitivity resulting from axonal damage in this trigeminal branch.
View Article and Find Full Text PDFCells
November 2024
Department of Pharmacology, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Post-traumatic trigeminal neuropathy (PTTN) is a sensory abnormality caused by injury to the trigeminal nerve during orofacial surgery. However, existing analgesics are ineffective against PTTN. Abnormal microglial activation in the caudal part of the spinal trigeminal nucleus caudal part (Sp5C), where the central trigeminal nerve terminals reside, plays an important role in PTTN pathogenesis.
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