The Hypoglossal Nerve (CN XII) is a specialized motor nerve originating in the medulla of the brainstem. Its primary function is controlling movement rather than sensation. Testing CN XII is a standard component of a neurological examination used by clinicians to assess the integrity of the lower brainstem and the pathways that control the tongue.
The Role of the Hypoglossal Nerve
The Hypoglossal Nerve controls nearly all the muscles of the tongue. It provides motor innervation to both the intrinsic muscles, which change the tongue’s shape, and the extrinsic muscles, which change its position (e.g., the genioglossus, hyoglossus, and styloglossus). These actions are fundamental for speech and swallowing.
Proper articulation requires rapid and precise tongue movement, which depends entirely on CN XII signaling. The nerve also facilitates the oral phase of swallowing by manipulating food and forming a cohesive mass, known as a bolus. The genioglossus muscle is specifically responsible for protruding the tongue, a movement focused on during the clinical examination.
Step-by-Step Examination Procedure
The clinical evaluation begins with a visual assessment of the tongue at rest inside the patient’s mouth. The clinician looks for muscular wasting, known as atrophy, which appears as a loss of bulk on one side. They also watch for small, involuntary muscle contractions called fasciculations, which resemble a subtle rippling or twitching beneath the surface.
The patient is then asked to stick their tongue straight out (protrusion), a maneuver driven primarily by the genioglossus muscle. If one side is weak, the tongue will deviate toward the side of the damaged nerve or muscle. This deviation happens because the healthy, unopposed genioglossus muscle on the stronger side pushes the weak side out of the midline.
Finally, the strength of the tongue is tested. The patient is asked to push the tip of the tongue firmly against the inside of their cheek. The clinician applies external resistance with a finger on the outside of the cheek to gauge the muscle’s power. This resistance test confirms unilateral weakness and provides a comparative measure of strength between the left and right sides.
Understanding Abnormal Findings
When the tongue deviates upon protrusion, accompanying signs help localize the site of nerve damage.
Lower Motor Neuron (LMN) Lesions
LMN lesions are characterized by flaccid weakness, often accompanied by visible atrophy and fasciculations. Since the LMN directly connects the brainstem nucleus to the muscle, damage at this level causes the tongue to point toward the side of the lesion and results in associated muscle wasting.
Upper Motor Neuron (UMN) Lesions
A different set of findings suggests an UMN lesion, which occurs in the brain pathways that control the nerve nucleus, such as from a stroke. UMN lesions cause weakness resulting in deviation toward the affected side, but they do not cause the muscle atrophy or fasciculations seen with LMN damage. This is because the connection between the nerve and the muscle remains intact, preventing the rapid denervation and muscle wasting that defines LMN injury. The presence or absence of atrophy and fasciculations is key to distinguishing the location of the neurological issue.
Conditions Leading to Hypoglossal Nerve Damage
Damage to the Hypoglossal Nerve can arise from medical conditions or physical trauma. One common cause is a stroke, particularly one that affects the brainstem or the corticobulbar tracts, which contain the UMN fibers that descend to control CN XII. This type of event results in sudden onset of weakness and deviation.
Neurodegenerative diseases, such as Amyotrophic Lateral Sclerosis (ALS), often involve the lower motor neurons of CN XII, leading to progressive atrophy and persistent fasciculations. Tumors in the head and neck region, including those at the base of the skull, can directly compress or invade the nerve as it exits the skull. Surgical procedures in the neck, such as carotid endarterectomy, also carry a risk of localized injury to the nerve.