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Disturbances of Smell and Taste
Disorders of smell and taste can jeopardize human safety and produce loss of appetite, unintended weight loss, malnutrition, occupational disability, and reduced quality of life. In a study of 750 patients with chemosensory disturbances, 68% reported altered quality of life, 46% changes in appetite or body weight, and 56% adverse influences on daily living or psychological well-being ( ). In another study of 445 such patients, at least one hazardous event, such as food poisoning or failure to detect fire or leaking natural gas, was reported by 45.2% of those with anosmia, as compared with 19.0% of those with normal function ( ). Importantly, older persons with smell loss are three times more likely to die over the course of 4 or 5 years ( ). Of particular relevance to the neurologist is the fact that smell dysfunction is among the earliest “preclinical” or “presymptomatic” signs of neurodegenerative diseases such as Alzheimer disease (AD) and Parkinson disease (PD) ( ). Indeed, olfactory tests are as effective in detecting PD as single-photon emission computed tomography (SPECT) imaging of the dopamine transporter ( ).
Both smell and taste disorders have been documented in a wide range of diseases, although meaningful smell disturbances are much more common than taste disorders. The vast majority of patients complaining of “taste” disturbances actually have decreased smell, not taste, function ( ). Flavor sensations such as cola, coffee, chocolate, strawberry, pizza, licorice, steak sauce, and vanilla depend upon stimulation of the olfactory receptors by molecules that enter the nasal pharynx during deglutition ( ). Such “taste” sensations disappear when the olfactory epithelium is severely damaged, leaving intact only tactile and the taste bud–mediated sensations of sweet, sour, salty, bitter, and savory.
In this chapter, olfactory and gustatory system anatomy and physiology are reviewed, with an emphasis on pathophysiology. Chemosensory disturbances in diseases commonly encountered by the neurologist are described, along with means for patient assessment and symptom management.
Anatomy and Physiology
Olfaction
The approximately 6 million olfactory receptor cells are located within a pseudostratified columnar neuroepithelium lining the cribriform plate and sectors of the superior septum, the middle turbinate, and the superior turbinate. This epithelium also contains sustentacular, microvillar, and basal cells (the precursors of other cell types within the epithelium) and is supported by a highly vascularized lamina propria containing Bowman glands, the major source of the olfactory mucus. The bipolar receptor cells, which project 3–30 receptor-bearing cilia into the mucus, serve as both a receptor cell and a first-order neuron and can regenerate, to some degree, from basal cells after being damaged. Such cells exhibit the most diverse molecular phenotype of any neuron, expressing a wide range of receptor protein types and cell surface antigens. A photomicrograph of the surface of the olfactory epithelium is shown in Fig. 19.1 .
Each olfactory receptor cell expresses only 1 of nearly 400 functional types of receptor proteins. Odor receptor genes are found in approximately 100 locations on all chromosomes except 20 and Y. Remarkably, the olfactory subgenome spans 1%–2% of the total genomic DNA. Most single-chemical odorants stimulate more than one type of receptor and overlap typically exists among the sets of receptors stimulated by various chemicals, implying complex across-fiber sensory coding.
After coalescing into bundles (fila) within the lamina propria, the olfactory receptor axons traverse the foramina of the cribriform plate and enter sphere-like glomeruli located within an outer layer of the olfactory bulb, an ovid structure composed of afferent and efferent nerve fibers, multiple interneurons, microglia, astrocytes, and blood vessels ( Fig. 19.2 ). Those receptor cells expressing the same odorant protein converge onto the same glomerulus. The bulb’s primary output neurons—the mitral and tufted cells—are modulated by input from olfactory receptor cells and local interneurons, including the γ-aminobutyric acid (GABA) ergic granule cells, the most numerous cells of the bulb. Granule cells receive numerous inputs from central brain regions and, unlike nearly all other central nervous system (CNS) neurons, undergo periodic replacement from neuroblasts that migrate from the anterior subventricular zone of the brain. Some of these differentiating neuroblasts further migrate within the bulb to repopulate periglomerular cells ( ).
The axons of the mitral and tufted cells project centrally, via the lateral olfactory tract, to the anterior olfactory nucleus, the piriform cortex, the anterior cortical nucleus of the amygdala, the periamygdaloid complex, and the rostral entorhinal cortex. Pyramidal cells from the anterior olfactory nucleus project to numerous ipsilateral and contralateral brain structures, the latter via the anterior commissure. Although most bulbar output neurons project ipsilaterally to cortical structures without synapsing in the thalamus, connections via the thalamus do exist between primary (e.g., entorhinal) cortex and secondary (i.e., orbitofrontal) olfactory cortices.
The relative roles of central brain structures in odor perception are poorly understood. The piriform cortex encodes higher-order representations of odor quality, identity, and familiarity, and is involved in odor learning and memory ( ). The entorhinal cortex preprocesses information entering the hippocampus, whereas the amygdala seems to respond to the intensity of emotionally significant odors. The orbitofrontal cortex combines input from taste, texture, and smell and plays a vital role in flavor perception and hedonics ( ).
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