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MRI appearance of the normal and diseased hypoglossal nerve Poster No.: C-1971 Congress: ECR 2013 Type: Educational Exhibit Authors: I. De Kock , B. Smet , M. Lemmerling ; Ghent/BE, Gent/BE, 1 2 3 1 2 3 Beervelde/BE Keywords: MR, Neuroradiology brain, Head and neck, Structured reporting, Technical aspects, Pathology DOI: 10.1594/ecr2013/C-1971 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. www.myESR.org Page 1 of 17 Learning objectives 1. To present an optimum imaging protocol for hypoglossal nerve imaging. 2. To review the normal course of the hypoglossal nerve using a segmental approach. 3. To present a pictorial overview of pathologic conditions affecting the hypoglossal nerve in each of its four segments. Background The twelfth cranial nerve or hypoglossal nerve is an entire motor nerve, controlling the intrinsic and extrinsic muscles of the tongue, as well as the infrahyoid strap muscles through an anastomosis with the cervical plexus, called the ansa cervicalis. Damage to the hypoglossal nerve produces characteristic clinical and radiological manifestations of which unilateral tongue atrophy is the most common. Dysfunction of the hypoglossal nerve may be a consequence of supranuclear, nuclear or infranuclear disease. The nuclear and infranuclear hypoglossal nerve can be divided into four segments: the medullary, cisternal, skull base and extracranial segments. Because each segment is usually affected by different disorders, localizing a lesion to a particular segment allows the radiologist to narrow the differential diagnosis. ANATOMY: The cortical centre for lingual movement is located within the precentral gyrus, which sends fibers to the hypoglossus nucleus. The paired hypoglossus nuclei are located on the floor of the fourth ventricle, within the medulla oblongata. This is the medullary segment. The fibers course anteriorly, lateral to the medial lemniscus, to exit the medulla in the preolivary sulcus. The rootlets lie posterolateral to the vertebral artery within the premedullary cistern. This is the cisternal segment. Then the rootlets merge to form the hypoglossal nerve within the hypoglossal canal of the occipital bone. This is the skull base segment (Fig. 1). Emerging from the hypoglossal canal, the hypoglossal nerve begins its extracranial course as it enters the nasopharyngeal carotid space. As the nerve passes inferiorly, it comes to lie between the internal jugular vein and the carotid artery, superficial to the vagus nerve (Fig. 2). At the level of the angle of the mandible it then takes an anterior course, lying at the inferior border of the posterior belly of the digastric muscle. After exiting the carotid space the nerve continues anteriorly and inferiorly towards the hyoid bone, crossing the lingual artery to run along the surface of the hyoglossal muscle. This segment of the hypoglossal nerve lies within the sublingual Page 2 of 17 space (Fig. 3). The nerve then continues forward to supply the genioglossus muscle to the tip of the tongue. As already mentioned, the hypoglossal nerve not only supplies motor innervation to the intrinsic and extrinsic muscles of the tongue but also contributes motor innervation to the infrahyoid strap muscles (sternohyoid, sternothyroid and omohyoid muscle) through the ansa cervicalis. The ansa cervicalis is made up of fibers from the first to third cervical nerves (C1-C3) that course through the carotid space together with the hypoglossal nerve (Fig. 4). Images for this section: Page 3 of 17 Fig. 1: On this axial T2WI through the skull base the dots indicate the hypoglossal nuclei. The hypoglossal nerve roots exit the medulla oblongata and pass through the premedullary cistern (arrow heads) toward the hypoglossal canal (asterisk). Page 4 of 17 Page 5 of 17 Fig. 2: On this axial T2WI at the level of the oropharyngeal carotid space the arrows indicate the position of the hypoglossal nerve between the internal jugular vein and the internal carotid artery. Page 6 of 17 Fig. 3: On this axial T2WI at the level of the sublingual space the dots indicate the position of the hypoglossal nerve lateral to the hyoglossus muscle (H). The hypoglossal nerve Page 7 of 17 runs forward into the sublingual space, lying between the paired genioglossus muscles (G) and the mylohyoid muscles (M). Fig. 4: This schematic drawing nicely illustrates the consecutive segments of the course of the hypoglossal nerve (medullary, cisternal, skull base, carotid space, sublingual space). The anastomosis via the ansa cervicalis is also shown. Page 8 of 17 Imaging findings OR Procedure details MRI is the imaging modality of choice for the study of a patient with hypoglossal nerve palsy. It supplies superior soft-tissue contrast and allows direct visualization of the different segments of the nerve. Multiple sequences are available to study the nerve and each has specific advantages according to the segments being studied. For the intra-axial segment or above (nuclear or supra-nuclear lesions) a brain protocol is used with fast spin-echo (FSE) T2WI of the brain and T1WI of the skull base. After intravenous injection of gadolinium T1WI are repeated. High resolution T1W images preand post-contrast with fat suppression allow further anatomical characterization of the remaining segments. The use of contrast is especially useful in infectious/inflammatory pathology where abnormal enhancement of the nerve may be the only presentation of the disease. The hypoglossal nerve should be routinely studied in the axial and coronal plane. Sometimes the sagittal plane may be useful, e.g. for distal lesions involving the floor of the mouth or the tongue base. The imaging approach of a patient with hypoglossal nerve palsy consists of analyzing the different anatomical segments of the nerve and recognizing the most common differential diagnosis in each. The most common diseases affecting each segment are discussed below and are listed in table 1. Unilateral atrophy of the tongue musculature is the most important radiologic feature of hypoglossal nerve palsy. Imaging changes in the tongue after damage to the hypoglossal nerve vary according to the time gone by between the initial nerve lesion and the imaging examination. MRI is the most useful imaging modality to characterize these various muscle changes. In the subacute phase of denervation, the tongue is hyperintense on T2WI and hypointense on T1WI, mainly due to edema. Enhancement of the denervated part can be seen after intravenous gadolinium administration. In the chronic phase, as fatty infiltration progresses, the tongue volume on the affected side will decrease. On MRI the affected tongue will have high signal on both T1WI and T2WI. Once tongue atrophy is identified at imaging, systemic evaluation of the hypoglossal nerve should be performed. MEDULLARY SEGMENT: Page 9 of 17 Pathology of this segment of the nerve is frequently associated with damage to other nuclei, resulting in a complex lower cranial neuropathy. Disease that involves both hypoglossal nerve nuclei leads to bulbar palsy with complete paralysis of the tongue. The most common pathology in this region is infarction, due to ischemia or hemorrhage. Neoplasms are also among the most common causes and may be primary or secondary. Most frequent are metastases followed by gliomas. Metastases have a variety of imaging appearances but should always be thought of. Gliomas are heterogeneous lesions with high signal intensity on T2WI, causing expansion of the brainstem (Fig. 5). Other less common pathologic processes of inflammatory, infectious or demyelinating nature may also occur, such as multiple sclerosis, amyotrophic lateral sclerosis or poliomyelitis. CISTERNAL SEGMENT: As described in the anatomical layout of the hypoglossal nerve, there is a close relationship between the nerve and the vertebral artery. Thus, vertebrobasilar pathology or anatomic variants may cause compression of the rootlets resulting in paralysis. Other pathologic entities in this region include skull base bony pathology such as clival tumors, meningioma, osteomyelitis or pathology involving the odontoid such as rheumatoid arthritis, trauma or Chiari malformation (Fig. 6). Basal meningitis or subarachnoidal hemorrhage with exsudation and organization can also compromise the nerve. Primary tumors of the hypoglossal nerve, although uncommon, may also affect the cisternal portion of the nerve. SKULL BASE SEGMENT: Tumors, both benign and malignant, and trauma may damage the hypoglossal nerve along its course through the skull base. Tumors of the skull base may affect the hypoglossal canal by expansion or destruction. The most common malignant tumors are metastasis from breast, lung and prostate cancer and direct extension of nasopharyngeal carcinoma through the skull base. Benign tumors include peripheral nerve sheath tumors (such as schwannoma), glomus tumors, and meningiomas (Fig. 7). Primary bony tumors such as giant cell tumors or osteogenic sarcomas may also involve the hypoglossal canal. Infection of the skull base (pseudomonas infection, tuberculous osteomyelitis) is even much rarer, but should also be included in the differential diagnosis, especially in the diabetic or immunocompromised patient. EXTRACRANIAL SEGMENT: • Carotid space segment: Page 10 of 17 In the carotid space the hypoglossal nerve lies in close contact with the internal carotid artery and internal jugular vein. As a result, ectasia and aneurysm of the carotid artery, as well as arterial dissection and jugular thrombosis can compress the nerve and lead to palsy (Fig. 8). However, the most common cause of hypoglossal nerve palsy in the carotid space are malignant tumors, both primary and secondary pathologies, including squamous cell carcinoma, lymphoma, salivary gland tumors and metastatic disease. Benign tumors such as paragangliomas and lipomas should also be in the differential diagnosis. Iatrogenic lesions (endarterectomy, vascular punction) or trauma (stab, gunshot wounds or infection spreading from other neck spaces) may also cause dysfunction of the twelfth cranial nerve. • Sublingual segment: The most common cause of dysfunction in this segment is nerve damage due to squamous cell carcinoma of the base or lateral regions of the tongue (Fig. 9). Odontogenic lesions such as abscesses or iatrogenic damage after tooth extraction are other causes to be considered. Images for this section: Table 1: Segmental differential diagnosis of hypoglossal palsy. Page 11 of 17 Fig. 5: These consecutive T2WI and postgadolinium T1WI in a 40-year-old female glioma patient with impaired sensibility and motor dysfunction of the left half of the tongue shows a T2 hyperintense mass in the left half of the pons and in the left hemicerebellum extending into the medulla oblongata. Heterogeneous enhancement is noted after gadolinium injection. Page 12 of 17 Fig. 6: Three consecutive T1WI are shown in a 52 year-old male with right sided hypoglossal nerve paralysis and rectal cancer in the previous history. A hypointense lytic metastasis is shown in a right paraclival location, extending to the hypoglossal canal on the right side (thick arrows) and to the foramen magnum (thin arrows). Page 13 of 17 Page 14 of 17 Fig. 7: Three consecutive T2WI and T1WI are shown (before and after intravenous injection of gadolinium) in a 49-year-old male with left sided atrophy of the tongue. A dumbbell-shaped mass is seen (arrows) in the left hypoglossal canal, extending into the cistern anterior to the medulla oblongata. The mass is hyperintense on T2WI, hypointense on T1WI, and enhances heterogeneously after intravenous injection of gadolinium: schwannoma. Fig. 8: On these T1WI in a 37-year-old female with sudden left sided partial Horner's syndrome a semilunate T1 hyperintensity is seen (arrows) in the wall of the internal carotid artery on the left side, indicative of dissection of the artery. Page 15 of 17 Fig. 9: T1WI in a 62-year-old male with left sided paralysis of the tongue and dysphagia show a hypointense squamous cell carcinoma posterolaterally in the left half of the tongue (thick arrows), with beginning extension to the left sublingual space. On the fat-suppressed T1WI after intravenous injection of gadolinium moderate enhancement is noted (thick arrows), and it is obvious that the genioglossus muscle is spared (thin arrows). Page 16 of 17 Conclusion • • MRI is the preferred imaging technique to visualize the hypoglossal nerve. For the radiologist approaching a patient with hypoglossal nerve damage, a segmental anatomical approach and knowledge of the most common pathologic conditions occurring in each segment will narrow the differential diagnosis. References 1. 2. 3. 4. Alves P. Imaging the hypoglossal nerve. Eur J Radiol 2010;74:368-77. Thompson EO, Smoker WRK. Hypoglossal nerve palsy: a segmental approach. Radiographics 1994;14:939-58. Loh C, Maya MM, Go JL. Cranial nerve XII: The hypoglossal nerve. Semin. Ultrasound CT MR 2002;23(3):256-65. Lemmerling M, Crevits L, Defreyne L, Achten E, Kunnen M. Traumatic dissection of the internal carotid artery as an unusual cause of hypoglossal nerve dysfunction. Clin Neurol Neurosurg. 1996;98(1):52-4. Personal Information Page 17 of 17