• Home
• Instructions
• Introduction
• Lab 1
• Lab 2
• Lab 3
• Lab 4
• Lab 5
• Lab 6
• Lab 7
• Lab 8
• Lab 9
• Lab 10
• Lab 11
• Contact Us

Lab 9 (ƒ 10) - Cranial Nerve Nuclei and Brain Stem Circulation

Ambiguus Nucleus in CN IX, X, and XI

The axons of the nucleus ambiguus innervate the muscles of the palate, larynx and pharynx via three cranial nerves:

• The axons of the most rostral portion of the nucleus ambiguus contribute fibers to the glossopharyngeal (IX) nerve.
• The axons of the mid-portion of the nucleus ambiguus join the vagus (X) nerve.
• Axons from the caudal pole of the nucleus ambiguus emerge from the lateral surface of the medulla caudal to the lowest filaments of the vagus nerve to join the accessory (XI) nerve. These cranial accessory fibers later join the vagus nerve and innervate the intrinsic muscles of the larynx.

Unilateral damage to the lower motor (nucleus ambiguus) neurons produces an ipsilateral paralysis of the palate, pharynx and larynx. Speech disorders, hoarseness, dyspnea (shortness of breath) and dysphagia (difficulty in swallowing) occur. Bilateral lesions may result in death due to the complete paralysis of the larynx (i.e., inability to abduct the vocal cords during inspiration).

The nucleus ambiguus receives short connecting fibers from the neighboring cranial sensory nuclei, i.e., the spinal trigeminal nucleus and nucleus solitarius. These fibers complete reflex arcs controlling swallowing, coughing, vomiting and control laryngeal motor output.

The cortical input to the nucleus ambiguus is bilateral and indirect. Unilateral damage of the corticobulbar tract produces mild forms of weakness. Bilateral lesions produce a weakness or absence of the ability to speak, swallow and breathe.