From the Institute of Anatomy, School of Medicine, University of Belgrade, Belgrade, Serbia (Dr. Marinković); Department of Experimental Pathology and Cytology, Institute for Medical Research, University of Belgrade, Belgrade, Serbia (Drs. Todorović, Budeč, Drndarević, and Pešić); Neurosurgical Service, Showa-Inan General Hospital, Komagane City, Japan (Dr. Gibo); Department of Neurosurgery, University of Belgrade, Belgrade, Serbia (Dr. Joković); Department of Histology, School of Medicine, University of Belgrade, Belgrade, Serbia (Dr. Ćetković).
The Trigeminal Vasculature Pathology in Patients With Neuralgia
Version of Record online: 9 OCT 2007
Headache: The Journal of Head and Face Pain
Volume 47, Issue 9, pages 1334–1339, October 2007
How to Cite
Marinković, S., Todorović, V., Gibo, H., Budeč, M., Drndarević, N., Pešić, D., Joković, M. and Ćetković, M. (2007), The Trigeminal Vasculature Pathology in Patients With Neuralgia. Headache: The Journal of Head and Face Pain, 47: 1334–1339. doi: 10.1111/j.1526-4610.2007.00933.x
Conflict of Interest: None
- Issue online: 9 OCT 2007
- Version of Record online: 9 OCT 2007
- Accepted for publication May 4, 2007.
- endothelial cell;
- smooth muscle cell;
- basement membrane;
- trigeminal neuralgia;
Objective.—To examine the possible pathological changes of the trigeminal vasculature in patients with neuralgia.
Background.—Such a study has never been performed before. The alterations of the trigeminal vessels could have important pathophysiological implications in the trigeminal neuralgia pathogenesis.
Methods.—The biopsy specimens for the electronmicroscopic (EM) and immunohistochemical examination were taken during a partial rhizotomy in 6 patients with trigeminal neuralgia and in 2 persons with trigeminal neuropathy. In addition, the 32 normal trigeminal nerves were used as the control specimens.
Results.—The vascular pathological alterations were noticed in 3 out of 6 neuralgia patients. The EM study revealed signs of apoptosis or degeneration, respectively, of some endothelial and smooth muscle cells in the wall of the trigeminal arterioles. The immune reactions against CD31, CD34, and α-smooth muscle actin in these cells were weaker than in the control specimens, but stronger against factor VIII. In addition, the arteriolar basement membranes, which were thickened, showed an intense laminin, fibronectin, and collagen IV immunoreactivity. Similarly, some endothelial cells and pericytes of the intratrigeminal capillaries also showed signs of apoptosis or degeneration, respectively. Their basement membrane was very thick and showed an intense immune reaction against laminin, fibronectin, and collagen IV.
Conclusion.—The observed pathological changes of the trigeminal vasculature could be the primary factor, while demyelination of the trigeminal nerve fibers could be the secondary process in some patients with neuralgia.