Neuroscience Quiz: Facial and Glossopharyngeal Nerves

The facial nerve (CN VII) is a mixed nerve responsible for facial expression, taste sensation from the anterior two-thirds of the tongue, and innervating salivary glands. It also carries sensory information from the external ear.

The facial nerve has several branches, with the chorda tympani carrying taste fibers to the anterior two-thirds of the tongue and parasympathetic fibers to the submandibular and sublingual glands. The greater petrosal nerve carries parasympathetic fibers to the lacrimal gland and nasal mucosa.

The facial nerve's main motor nucleus controls facial muscles for expressions. The superior salivatory nucleus controls parasympathetic innervation to salivary glands. The nucleus of the solitary tract receives taste information.

The facial nerve exits the skull through the stylomastoid foramen, branching within the parotid gland.

The facial nerve travels through the internal acoustic meatus, facial canal, and makes a bend at the geniculate ganglion before exiting the stylomastoid foramen.

The geniculate ganglion houses cell bodies of sensory fibers responsible for taste from the front of the tongue.

The pterygopalatine ganglion lies in the pterygopalatine fossa and receives parasympathetic input from the greater petrosal nerve, relaying it to the lacrimal gland, nasal mucosa, and other glands.

The submandibular ganglion lies near the submandibular gland and receives parasympathetic input from the chorda tympani nerve, innervating the submandibular and sublingual glands.

A mixed nerve with sensory, motor, and parasympathetic functions. It controls swallowing, phonation, and taste from the posterior pharynx and epiglottis.

The main motor nucleus of the vagus nerve, controlling muscles involved in swallowing and speech.

The parasympathetic nucleus of the vagus nerve, influencing the heart, lungs, and digestive tract.

The sensory nucleus for the vagus nerve, receiving taste and general sensation from the pharynx, larynx, and organs.

The vagus nerve's general sensory fibers receive sensory information from the pharynx, larynx, thorax, and abdomen. These fibers are also involved in regulating nausea, oxygen intake, and lung inflation.

The vagus nerve's general visceral efferent fibers innervate glands, cardiac muscles, trachea, bronchi, esophagus, stomach, and intestines. This allows the vagus to control important functions like digestion and heart rate.

The vagus nerve's special sensory fibers carry taste signals from the posterior pharynx and epiglottis, contributing to our sense of flavor.

The vagus nerve's special visceral efferent fibers control the muscles of the larynx, pharynx, and soft palate. These muscle movements are essential for phonation, swallowing, and resonance.

The vagus nerve exits the skull from the jugular foramen and descends down the neck. It then divides into right and left branches that travel through the thorax and abdomen.

The vagus nerve splits into right and left branches as it descends through the thorax, each with unique paths and innervations. The right vagus travels near the trachea and superior vena cava, while the left vagus crosses the aortic arch.

The facial nerve (VII) controls facial expressions, taste in anterior 2/3 of the tongue, and lacrimal gland secretions. Damage to the upper motor neuron (UMN) can result in a unilateral paresis of the lower facial muscles, but the muscles above the eyebrow are spared. This is because the upper facial muscles have bilateral innervations from the motor cortex.

Damage to the lower motor neuron (LMN) of the facial nerve results in a unilateral paralysis of all facial muscles on the same side of the face, as well as the stapedius muscle and taste in the anterior 2/3 of the tongue. This complete paralysis is caused by the interruption of the entire motor pathway to those muscles.

A sudden onset of paralysis of the facial muscles on one side of the face. It is caused by inflammation, infection, or degeneration of the facial nerve, often affecting the LMN. The affected side of the face may droop, and the person may have difficulty closing their eye, smiling, or making other facial expressions on that side.

A nerve that plays a vital role in both hearing and maintaining balance. It has two branches: the cochlear nerve, which is responsible for hearing, and the vestibular nerve, which is responsible for maintaining balance and registering head position in space.

The glossopharyngeal nerve (IX) has a mix of functions, including taste in the posterior third of the tongue, touch sensation of the soft palate and tongue, salivary gland secretion, and motor control for swallowing. It involves several nuclei in the brainstem.

Glossopharyngeal nerve (IX) damage can result in various issues like swallowing difficulty (dysphagia), loss of taste in the posterior tongue, dry mouth, and loss of the gag reflex. Bilateral damage is usually required for stronger clinical signs.

Sensory signals from the carotid body and carotid sinus travel through the carotid nerve, inferior glossopharyngeal ganglion, and nucleus of the solitary tract before reaching the reticular formation and hypothalamus. This pathway is crucial for regulating blood pressure and breathing.

Taste information from the posterior third of the tongue travels via the inferior glossopharyngeal ganglion to the tractus solitarius, then to the nucleus of the solitary tract, and finally to the thalamus and sensory cortex for processing. This pathway allows us to experience and recognize flavors.

Motor commands originating from the motor cortex travel through the corticobulbar tracts and activate the nucleus ambiguus. This activates the stylopharyngeus muscle, which is involved in swallowing, via branches of the glossopharyngeal (IX) and vagus (X) nerves.

The external acoustic meatus, external surface of the tympanic membrane, pharynx, and larynx are all innervated by the vagus nerve (CN X) for sensory functions. This pathway involves the superior vagal ganglia, spinal trigeminal tract, medial lemniscus, and the contralateral ventral posterior medial (VPM) nucleus of the thalamus, ultimately reaching the sensory cortex. Some fibers also project to the contralateral dorsomedial nucleus (DM) and the cingulate gyrus.

The vagus nerve (CN X) also carries sensory information from the pharynx, larynx, trachea, esophagus, thoracic, and abdominal viscera. This signal travels through the inferior vagal ganglion, nucleus tractus solitarius, and then bilaterally to the reticular formation and the hypothalamus.

The motor cortex sends signals to the nucleus ambiguus via bilateral corticobulbar fibers. From there, motor commands are sent to the vagus nerve, controlling the muscles of the pharynx, larynx, and soft palate.

The dorsal motor nucleus of the vagus nerve sends parasympathetic signals to the heart and other organs. These signals travel through the vagal nerve to the cardiac ganglia and cardiac plexus, regulating heart rate and digestion.

Damage to both sides of the brainstem involving the vagus nerve can cause respiratory failure, leading to death. Single-sided lesions can result in weakness or paralysis of the soft palate, pharynx, and larynx on the affected side.

A unilateral lesion of the vagus nerve can lead to weakness or paralysis on one side of the soft palate, pharynx, and larynx. This can cause the uvula to deviate to the unaffected side, and both sides of the soft palate to droop.

A one-sided lesion of the vagus nerve can cause vocal cord paralysis. Damage to both vocal cords can lead to stridor (noisy breathing) and loss of voice (aphonia) due to the inability to produce sound.

Damage to the vagus nerve can also affect autonomic reflexes, like the gag reflex, and cause numbness in the pharynx and larynx. Additionally, taste sensation can be lost. Lesions on the superior laryngeal branch can impair the ability to change the pitch of the voice.

The spinal accessory nerve (CN XI) has a motor function, controlling the movement of the trapezius and sternocleidomastoid muscles. These muscles are essential for head movement and positioning.

Damage to the spinal accessory nerve (CN XI) can affect the ability to control head movement. When testing, ask the patient to rotate and tilt their head to assess the strength of these muscles.