1	IMAGING CHANGES SECONDARY TO CRANIAL NERVE DYSFUNCTION N Chaudhary, S Fareedi, E Woo, SEJ Connor Department of Neuroradiology, King’s College Hospital, London.
2	Contents Abstract Introduction General concepts in muscle denervation of head and neck Trigeminal (V) nerve dysfunction imaging features Abducent (VI) nerve dysfunction imaging features Facial (VII) nerve dysfunction imaging features Vagus (X) nerve dysfunction imaging features Spinal Accessory (XI) nerve dysfunction imaging features Hypoglossal (XII) nerve dysfunction imaging features. References
3	ABSTRACT The effects of motor cranial nerve dysfunction on the CT and MRI appearances of head and neck muscles are reviewed. Patterns of denervation changes are described and illustrated for V, VII, X, XI and XII cranial nerves. Recognition of the range of imaging manifestations, including the temporal changes in muscular appearances and associated muscular grafting or compensatory hypertrophy is emphasises. It will prompt the radiologist to search for underlying cranial nerve pathology which may be clinically occult. The relevant cranial nerve motor division anatomy will be described to enable a focussed search for such a structural abnormality.
4	INTRODUCTION Lower motor cranial nerve denervation results in an alteration of morphology, either due to reduced bulk of muscle or due to the loss of tone and position. Occasionally, the radiological changes in deep inaccessible muscle groups are clinically occult. By recognising the patterns of muscular involvement, and understanding the relevant motor cranial nerve anatomy, the radiological search and scan volume may be focused appropriately. The imaging appearances of muscular denervation secondary to V, VII, X, XI and XII motor cranial nerve dysfunction will form the basis of this review. Appearances which may be misconstrued as local pathology will be emphasised.
5	Muscular denervation in the head and neck: General concepts and temporal changes
6	Trigeminal (V) nerve motor supply and anatomy
7	Trigeminal (V) nerve dysfunction: Pattern of nerve damage and likely Causes
8	Trigeminal (V) nerve Dysfunction: Pseudolesions Subacute phase – inflammatory, neoplastic and traumatic aetiology Chronic phase – disuse, congenital facial asymmetry, connective tissue disorder and posttraumatic reflex sympathetic dystrophy.
9	Imaging changes due to subacute trigeminal (V) nerve dysfunction
10	Imaging Changes in Chronic proximal Trigeminal (V) nerve dysfunction
11	Imaging changes in Chronic distal trigeminal (V) nerve dysfunction
12	Imaging changes due to chronic Abducent (VI) nerve dysfunction
13	Facial (VII) nerve: Anatomy and motor supply
14	Facial (VII) nerve dysfunction: Likely causes and Pseudolesions Lesions - The likely causes of denervation changes in the facial muscles have only been described in the context of facial nerve dysfunction due to malignant infiltration of the parotid and following skull base surgery. Whilst viral infection and trauma (typically related to temporal bone fracture or parotid surgery) are the most common pathologies to affect the facial nerve, the effects are transient. Pseudolesions - It is unlikely that imaging changes in these small muscles will mimic pathology however regional and free muscle flap transfers used for the treatment of chronic facial nerve paralysis may simulate a mass lesion within the facial soft tissues.
15	Imaging changes due to chronic Facial (VII) nerve dysfunction.
16	Vagus (X) nerve Anatomy and Motor supply
17	Vagus (X) nerve dysfunction: Distribution and Pathology
18	Vagus (X) nerve denervation: Psedolesions The alteration in morphology of the hemilarynx should not be misinterpreted as tomour infiltration. A fixed immobile cord due to mechanical interference from tumour infiltration of the thyroarytenoid muscle will often result in soft tissue within the paralaryngeal fat. A paramedian vocal cord may also result from arytenoid cartilage dislocation (typically secondary to traumatic intubation), and inflammatory pathology of the cricoarytenoid joint. However in the setting of dislocation, the arytenoid cartilage would be situated anterior to the cricoid margin. Pharyngeal wall atrophy and MRI signal alteration should not be misconstrued as contralateral wall thickening due to inflammation or neoplasm.
19	Imaging changes due to subacute proximal Vagus (X) nerve dysfunction
20	Imaging changes due to distal Vagus (idiopathic recurrent laryngeal) nerve (X) dysfunction
21	Spinal Accessory (XI) nerve: Anatomy and motor supply The spinal accessory nerve arises from the spinal accessory nucleus in the anterolateral grey matter of the upper cervical cord. The nerve then ascends through the foramen magnum and exits the skull base through the jugular foramen. Within the jugular foramen, it exchanges fibres with the cranial part of the accessory nerve (bulbar motor supply). The spinal accessory nerve initially lies adjacent to the internal jugular vein and descends obliquely across the posterior triangle. It innervates the sternoocleidomastoid muscle and together with the upper cervical nerves, it supplies the trapezius muscle.
22	Spinal Accessory (XI) nerve dysfunction: Pathology and Pseudolesions Lesions - The radiological findings of denervation are only described in the later stages. If the denervation results from a classical radical neck dissection then the internal jugular vein and sternocleidomastoid muscle will also have been resected. An underlying lesion is usually secondary to neck dissection with surgical sacrifice or tumour infiltration in the presence of gross metastatic nodal disease of the posterior triangle, high jugulodigastric region or skull base. Pseudolesions - The asymmetry produced by muscle atrophy may be misconstrued as an enlarged “normal” trapezius or sternocleidomastoid muscle. Alternatively, the compensatory enlargement of the levator scapulae muscle may present as an inflammatory or neoplastic pseudolesion, both clinically and radiologically.
23	Imaging changes due to Spinal Accessory (XI) nerve dysfunction
24	Hypoglossal (XII) nerve: Anatomy and motor supply The hypoglossal nerve is almost completely formed by somatic motor fibres. The nerve rootlets from the medulla traverse the premedullary cistern and unite after passing through the hypoglossal canal in the occipital bone. It then passes into the carotid space between the internal carotid artery and internal jugular vein and loops inferiorly to the level of the hyoid bone. It then travels upward to the sublingual space where it supplies the intrinsic and extrinsic muscles of the tongue (genioglossus, styloglossus, and hyoglossus). Additional branches to the strap muscles, omohyoid muscle (arising in the mid neck) and geniohyoid muscle (within the sublingual space) are principally derived from a supply to the hypoglossal nerve from the first and second cervical nerves.
25	Hypoglossal (XII) nerve dysfunction: Distribution and Imaging changes The muscles affected by hypoglossal nerve denervation include the extrinsic and intrinsic muscles of tongue. However, if the nerve is damaged in the mid neck then there is additional denervation of the strap muscles and geniohyoid. The altered appearances of the hemitongue should prompt imaging of the nerve from the medulla to the sublingual space and from the posterior fossa to the hyoid bone.
26	Hypoglossal (XII) nerve: Pathology and Pseudolesions The lesions causing denervation are - skull base tumours (meningioma, nasopharyngeal tumour extension, metastasis, sarcoma, chordoma, glomus tumour), hypoglossal nerve schwannoma, surgery, radiotherapy, metastatic nodal disease in the carotid sheath and upper aerodigestive tract or salivary carcinoma.
27	Imaging changes due to chronic Hypoglossal (XII) nerve dysfunction
28	References:
29	References: