Neuroanatomy, Nucleus Gustatory

Structure and Function

The nucleus gustatory is a paired structure found in the nucleus of the solitary tract located on both sides of the posterolateral portion of the medulla oblongata. The nucleus of the solitary tract or nucleus solitarius runs longitudinally and divides into 2 parts: a caudal and a rostral. The caudal portion primarily regulates the function of the cardiopulmonary center of the brainstem as well as regulating functions of the gastrointestinal system. The rostral portion is what is known as the gustatory nucleus. It receives inputs from chemoreceptors on the tongue and epiglottis via afferent cranial nerve fibers from VII, IX, and X. One notable difference in the 2 portions of the nucleus solitarius is the afferent inputs. In the rostral portion of the nucleus solitarius, the nucleus gustatory receives inputs from cranial nerves VII, IX, and X. In contrast, the nucleus solitarius's caudal portion lacks cranial nerve VII input.[3]

The function of the gustatory nucleus is to relay information regarding gustation from taste buds to the gustatory cortex. This process depends on the convergence of visceral afferent taste fibers from the cranial nerves and an intact pathway to the thalamus. Taste from the anterior two-thirds of the tongue travels along the chorda tympani, a branch of cranial nerve VII. It then moves toward the geniculate ganglion, which houses the cell bodies of the first-order neurons in this pathway. The bipolar neuron in this ganglion synapses in the medulla at the nucleus gustatory. Taste from the posterior one-third of the tongue travels along the lingual branch of cranial nerve IX to the petrosal ganglion. The bipolar neuron found here also serves as the first-order neuron in the taste pathway and synapses in the nucleus gustatory. Finally, taste from the pharynx, specifically the epiglottis, travels along the vagus nerve to the nodose ganglion. This ganglion also houses a bipolar neuron, and it is the last location for the cell body of a first-order neuron in the taste pathway. The vagus nerve continues until it synapses in the nucleus, gustatory in the medulla. After receiving these inputs, second-order neurons in the nucleus gustatory project to the thalamus's ventral posterior medial (VPM) nucleus. The third-order neurons found in the thalamus project to the gustatory cortex after synapsing in the thalamus with neurons from the gustatory nucleus.[4][1]

Embryology

Cranial nerves VII, IX, and X carry functional modalities that are gustatory and non-gustatory. This duality in function results from a subsequent duality in embryonic origin. The non-gustatory functions of these nerves are derived from the cranial neural crest. In contrast, the gustatory function is exclusively derived from epibranchial placodes and projects centrally to the nucleus gustatory.[5]

Blood Supply and Lymphatics

The blood vessels in the brainstem are closely associated with the structures they supply. The blood supply in the medulla can be divided into 2 categories: the rostral medullary blood supply and the caudal medullary blood supply. The rostral medullary blood supply comprises the vertebral artery, basilar artery, and posterior inferior cerebellar artery (PICA). The caudal medullary blood supply consists of the anterior and posterior spinal arteries (PSA). The arteries of the medulla supply the nucleus of the solitary tract; therefore, the nucleus gustatory is the PICA rostrally and the PSA caudally.[6]

Surgical Considerations

Surgery in the medulla poses significant risks due to the proximity of several structures vital for survival. With such a small margin of error, surgical interventions should only occur when necessary, as even millimeters of invasion into normal, healthy tissue can cause devastating effects on the body.

Clinical Significance

Although the brainstem location where the nucleus gustatory resides is arguably the most critical for unconscious human functioning, it has limited clinical significance. Several terms are used to characterize pathologies in taste perception. As mentioned above in conjunction with the COVID-19 pandemic, olfaction is strongly linked to gustation, and dysfunction of the olfactory mechanism is the primary failure in taste (gustatory) disturbances.

• Ageusia – the absence of taste
• Hypogeusia – diminished taste
• Hypergeusia – enhanced perception of taste
• Dysgeusia or parageusia – the unpleasant perception of taste

The perception of taste can be localized into 2 functional components: the peripheral and central arms. The peripheral arm is most commonly the culprit in taste-related disorders. Abnormal saliva production, damage to taste buds, or damage to any of the branches of the cranial nerves supplying these taste buds can cause a decrease or absence in the perception of taste in the peripheral arm. One example is the damage to the Chorda Tympani, a possible complication of surgery in the middle ear. This finding is, however, infrequent as studies have documented the chorda tympani’s significant neuroplasticity, allowing for the maintenance of taste in the presence of a damaged nerve.[7][8][9]

Many taste disorders are reversible and associated with various drugs, including antibiotics, anticonvulsants, and antidepressants. Regarding peripheral lesions of the cranial nerves VII, IX, and X, the facial nerve VII (chorda tympani) is affected most frequently. In idiopathic CN VII palsy (Bell palsy), taste dysfunction usually, hypogeusia can be the presenting complaint. Other considerations include Lyme disease (neuroborreliosis), herpes zoster, or a space-occupying lesion in the cerebellopontine angle, such as a meningioma or neurinoma. Rare causes of peripheral gustatory dysfunction include polyneuropathies such as porphyria, connective tissue diseases, amyloidosis, diphtheria, and posttraumatic iatrogenic neuropathy following intubation or other laryngoscopic manipulations.

An isolated taste disorder is rarely the presenting symptom of a brainstem, thalamic, or cortical lesion. Hemiageusia or hemi-hypogeusia at the level of the nucleus of the solitary tract presents with demyelinating diseases such as multiple sclerosis, ischemia, hemorrhage, or cavernous angiomas. A taste disturbance is usually associated with other neurologic symptoms, including hemiparesis, hemi-hypoesthesia, or ocular motor disturbance. Beyond losing taste perception, bilateral thalamic lesions may result in a psychological indifference to the pleasure in food intake (hedonic loss), resulting in considerable weight loss. Disturbances of taste can understandably go unrecognized in the face of major neurologic deficits due to ischemic stroke, intraparenchymal hemorrhage, neoplasm, and infections involving the insular cortex and frontal operculum.[10][11][12]