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HYPOGLOSSAL NUCLEUS (C.N. XII)

This nucleus lies just off the midline beneath the floor of the fourth ventricle. Axons from cells within the hypoglossal nucleus course ventrally to exit the medulla between the pyramid and the inferior olive. The hypoglossal nerve then passes through the hypoglossal foramen to emerge from the base of the skull. Each nerve innervates the ipsilateral intrinsic and extrinsic muscles of the tongue (you referred to this nerve as somatomotor in Gross Anatomy and learned that the palatoglossus is innervated by C.N X; this is tooo detailed for neuro!). These muscles are arranged as paired groups, fused at the midline and oriented in multiple planes that allow the extremely varied and complex movement capabilities of the tongue in speaking, chewing, swallowing, and buccal cleaning processes.


Following a lesion of the hypoglossal nucleus or nerve, there is ATROPHY of the muscles of the IPSILATERAL one-half of the tongue. This is a lower motor neuron lesion (the damaged neuron or axon directly innervates skeletal muscle). Upon closer examination, FASCICULATIONS (tiny, spontaneous contractions) can be seen. Both fasciculations and atrophy result from the loss of the normal innervation of the muscle by the lower motor neurons in the hypoglossal nucleus. Upon protrusion, the tongue will deviate TOWARD the side of the lesion (i.e., same side). This is due to the unopposed action of the genioglossus muscle on the normally innervated side of the tongue (the genioglossus pulls the tongue forward). Remember, the genioglossus arises laterally in the tongue and inserts on the midline of the mandible.



You have already heard of corticospinal axons. By their name, they arise from cortical neurons and end in the spinal cord. Another important group of axons that arise from cortical neurons do not reach the spinal cord. Instead, they end in motor nuclei of cranial nerves. These axons are called CORTICOBULBAR (“bulb” is a term that some neuroanatomists use when referring to the medulla because of its appearance as a bulb-like expansion of the spinal cord).



The corticobulbar input to the hypoglossal nucleus arises from motor cortex (you can voluntarily move your tongue) and is predominantly CROSSED. Thus, a lesion in motor cortex will result in deviation of the tongue toward the opposite side or CONTRALATERAL to the lesion. In contrast to the atrophy and fasciculations seen in lesions of the hypoglossal nucleus and nerve (lower motor neuron), NO such signs are present after lesions of the corticobulbar tract (remember, the neurons in the hypoglossal nucleus are still alive). A lesion of the corticobulbar input to the hypoglossal nucleus is called a supranuclear lesion (i.e., above or rostral to the hypoglossal nucleus). In a lesion of the motor cortex there is also involvement of corticospinal fibers. For example, a lesion in the LEFT motor cortex (which involves both corticospinal and corticobulbar axons) would result in a RIGHT hemiplegia and deviation of the tongue to the RIGHT. There would NOT be any atrophy.

Weakness of the tongue manifests itself as a slurring of speech. The patient’s tongue feels “thick” and lingual sounds are slurred. This is called dysarthria (dys-articulation) and is more apparent in hypoglossal nerve lesions but can occur following supranuclear lesions.





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