Facial sensory loss may occur in the setting of lesions involving the trigeminothalamic pathways, corona radiata or internal capsule white matter projections from the VPM nucleus of the thalamus to primary sensory cortex, or within sensory cortex itself. Specific pathological processes affecting these pathways include ischemia, hemorrhage, neoplasm, and demyelinating diseases. All result in contralateral hemifacial and hemibody numbness. In seizures, facial tingling often occurs in association with hand numbness and suggests a lesion in the postcentral gyrus. In the cheiro-oral syndrome, ipsilateral numbness in the hand and at the corner of the mouth reflects an insult, typically vascular, at adjoining portions of the ventroposterolateral and VPM nuclei of the thalamus where the anatomical distributions of these regions are directly adjacent to one another. In contrast, a persistent deep, aching, poorly localized facial pain has been reported in patients with thalamic lesions including tumors, infarctions, and multiple sclerosis affecting the VPM nucleus. Often this syndrome is associated with small vessel infarctions of the thalamogeniculate artery.y The syndrome begins with transient facial hemisensory loss but then evolves into painful facial dysesthesias. Migraine headache may be misdiagnosed as trigeminal neuralgia, especially if pain is unilateral, although the duration of most headaches makes this distinction straightforward.
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