Initial imaging. The hypoglossal nerve (CN XII) nucleus arises in the dorsal medulla. The hypoglossal rootlets traverse the premedullary cistern dorsal to the vertebral artery and then form the nerve, which enters the hypoglossal canal where it is surrounded by a venous plexus. The extracranial hypoglossal nerve travels caudally within the carotid space after which it courses anteriorly inferior to the hyoid where it distributes terminal branches providing somatic motor innervation to the intrinsic and extrinsic muscles of the tongue (except the palatoglossus muscle) and the infrahyoid strap muscles via the ansa cervicalis [2,13,181]. Hypoglossal nerve palsy typically presents clinically when a nuclear or infranuclear lesion is present and is characterized by dysarthria and deviation of the tongue to the side of the lesion upon tongue protrusion. Hypoglossal nerve palsy can occur because of injury of the nerve at any point along its course. There are a multitude of causes for hypoglossal nerve palsy including brainstem infarct, demyelinating disease, tumors, vascular lesions, trauma, inflammatory, and infectious processes. Nuclear lesions are usually accompanied by additional neurologic deficits indicative of brainstem involvement. Most hypoglossal nerve palsies are due to neoplasm involving the hypoglossal canal [2,182,183]. Within the extracranial segment, the most common causes of isolated hypoglossal nerve palsy are malignant tumors both along the course of CN XII Cranial Neuropathy in the carotid space and in the sublingual space [184]. Dissection of the internal carotid artery can result in isolated acute CN XII palsy or multiple variable patterns of CN palsies including involvement of CN IX through CN XII [185-187]. Associate denervation signal alterations can be seen on MRI that vary with the duration of the palsy [2,186-188].
Cranial Neuropathy. Initial imaging. The hypoglossal nerve (CN XII) nucleus arises in the dorsal medulla. The hypoglossal rootlets traverse the premedullary cistern dorsal to the vertebral artery and then form the nerve, which enters the hypoglossal canal where it is surrounded by a venous plexus. The extracranial hypoglossal nerve travels caudally within the carotid space after which it courses anteriorly inferior to the hyoid where it distributes terminal branches providing somatic motor innervation to the intrinsic and extrinsic muscles of the tongue (except the palatoglossus muscle) and the infrahyoid strap muscles via the ansa cervicalis [2,13,181]. Hypoglossal nerve palsy typically presents clinically when a nuclear or infranuclear lesion is present and is characterized by dysarthria and deviation of the tongue to the side of the lesion upon tongue protrusion. Hypoglossal nerve palsy can occur because of injury of the nerve at any point along its course. There are a multitude of causes for hypoglossal nerve palsy including brainstem infarct, demyelinating disease, tumors, vascular lesions, trauma, inflammatory, and infectious processes. Nuclear lesions are usually accompanied by additional neurologic deficits indicative of brainstem involvement. Most hypoglossal nerve palsies are due to neoplasm involving the hypoglossal canal [2,182,183]. Within the extracranial segment, the most common causes of isolated hypoglossal nerve palsy are malignant tumors both along the course of CN XII Cranial Neuropathy in the carotid space and in the sublingual space [184]. Dissection of the internal carotid artery can result in isolated acute CN XII palsy or multiple variable patterns of CN palsies including involvement of CN IX through CN XII [185-187]. Associate denervation signal alterations can be seen on MRI that vary with the duration of the palsy [2,186-188].