The trigeminal system contains both sensory and motor components and thus subserves and controls ipsilateral facial sensation and masticatory movements. The trigeminal sensory and motor nuclei extend in the brain stem from the pons to the upper cervical spinal cord. Pain, thermal, tactile, and kinesthetic sensory stimuli are received from the facial skin, oropharynx, nasal mucous membranes, sinuses, teeth, palate, dura, and masticatory muscles themselves. Motor fibers extend to the muscles of mastication as well as the tensor tympani and tensor veli palatini. Clinically, trigeminal dysfunction commonly is manifested as sensory changes such as paresthesias, dysesthesias, or anesthesia; paroxysmal or chronic pain; or difficulty chewing and swallowing. Traumatic, vascular, infectious, inflammatory, neoplastic, and demyelinating disorders can affect the trigeminal nerve at multiple points along the anatomical pathway from cortex, through the brain stem and trigeminal sensory ganglion, and out into peripheral trigeminal branches.
The first adequate clinical description of trigeminal neuralgia was made by Fothergill in 1773. Thereafter, Charles Bell (1829) demonstrated that the trigeminal nerve subserved sensation to the face. The trigeminal ganglion was excised in the late 19th century by Rose (1890), and the celebrated surgeon Horsley first sectioned the fifth cranial nerve through an intradural middle fossa approach in 1891. Early 20th century studies focused primarily on physiology, and more modern research has integrated neurochemistry, neuropharmacology, and microsurgical interventions in the treatment of trigeminal lesions.
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