By L. Barnes
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Extra info for Surgical Pathology of the Head and Neck [Vol 2]
Sample text
7%) developed a traumatic neuroma after treatment for recurrent pleomorphic adenoma (15). Rare cases of pharyngeal traumatic neuromas are associated with hoarseness, dysphagia, choking spells, intermittent aphonia, and cough (9). The common symptoms of facial traumatic neuromas include facial weakness, hearing loss, tinnitus, and vertigo or dizziness (14). C. Macroscopy Traumatic neuromas are circumscribed, gray-white, firm bulbous nodules without a true capsule. The nodules arise either at the proximal stump of a severed nerve or along the course of an injured nerve.
Pathogenesis NEs develop as a result of ectopic protrusion of CNS tissue through a defect in the cranium (52,53). Theories of formation of NE include arrested closure of bone of the frontal floor and early outgrowth of neural tube preventing closure of cranial coverings (54). The transsphenoidal type may occur as part of the median facial cleft syndrome, which includes median craniofacial dysraphism (55). Not uncommon, NEs may be associated with neurofibromatosis (NF). Patients with orbitotemporal NF often have partial or complete absence of the greater wing of the sphenoid, resulting in a defect in the posterolateral wall of the orbit (36,56).
The neuroglial tissue is often tranversed by interlacing bands of vascularized fibroconnective tissue that merge with the collagen of the mucosal lamina propria or dermis (2,3,12–25). The relative amounts of glial and fibrous tissue vary (Fig. 5). Recurrent NG or lesions presenting in children older than 18 months tend to contain a considerable amount of fibrosis and may be misdiagnosed as a fibrotic nasal polyp or fibroma (3). Neurons are Figure 4 Higher magnification shows an intact nasal mucosa and a neuroglial component with occasional neurons without fibrosis or inflammatory cells (H&E, 200Â).