4.6 Taste Disorders
Key Features
The sense of taste is mediated by cranial nerves (CNs) VII, IX, and X.
Most complaints of taste dysfunction are in fact olfactory disorders.
Medication effects are the most commonly identifiable cause of taste dysfunction.
Taste or gustation is a proximal chemical sense. Unlike in olfaction (see Chapter 4.5), for taste the primary source of stimulus must be in physical contact with the patient. The qualitative descriptors elicited by stimulation of taste receptors include sweet, sour, salty, bitter, and umami (loanword from Japanese that roughly equates to “savory,” with its own specific receptors stimulated by glutamates).
Anatomy
Epithelial taste receptor cells are located on the anterior and posterior tongue, the soft palate, and in the larynx. Taste receptor cells are arrayed in sensory end organs, the taste buds, and synapse on primary sensory neurons of the facial nerve (CN VII), the glossopharyngeal nerve (CN IX), or the vagus nerve (CN X). Taste innervation is therefore redundant; that is, a lesion of a single cranial nerve would not abolish all taste input. Taste receptor cells in taste buds turn over and are replaced by proliferative basal cells. This indicates that certain clinical conditions that damage or destroy taste receptors may cause only temporary dysfunction since the system has a capacity for repair.