Smell and taste are the chemical senses — the two systems that detect molecules in the environment and translate them into the conscious experience of flavor, smell, and the visceral responses they produce. They share a peculiar position in clinical neurology: testing of either is often skipped in routine examinations, but specific syndromes turn on them. Anosmia precedes the motor symptoms of Parkinson disease by years. Olfactory hallucinations herald temporal lobe seizures. Loss of taste from a specific tongue region localizes a facial nerve lesion. The chemical senses are small in clinical real estate but worth knowing in detail.

The Olfactory Pathway

Olfaction is the only sensory modality that reaches cortex without a thalamic relay. The pathway:

  1. Olfactory receptor neurons in the olfactory epithelium, in the roof of the nasal cavity. Bipolar neurons with cilia projecting into the mucus.
  2. Central processes pass through the cribriform plate of the ethmoid bone (highly fragile — sheared in head trauma) to the olfactory bulb on the inferior surface of the frontal lobe.
  3. Mitral and tufted cells of the bulb project via the olfactory tract to the primary olfactory cortex (piriform cortex, entorhinal cortex, parts of the amygdala) — all in the medial temporal region.
  4. Secondary projections reach the orbitofrontal cortex (for conscious olfactory perception) and the thalamus (only after primary olfactory cortex relay).

The direct connection to amygdala and entorhinal cortex (without thalamic relay) explains why smells can trigger immediate emotional and memorial responses.

Olfactory Clinical Correlates

  • Anosmia in early Parkinson disease: precedes motor symptoms by years. One of the most reliable prodromal features.
  • Anosmia in head trauma: from shearing of olfactory filaments at the cribriform plate. Often permanent.
  • Anosmia after viral infection: especially COVID-19, but also other URIs. Often improves over weeks to months; sometimes persistent.
  • Olfactory groove meningioma: can grow silently, eventually causing anosmia and frontal lobe symptoms. Foster Kennedy syndrome: ipsilateral anosmia + ipsilateral optic atrophy + contralateral papilledema.
  • Uncinate seizures: temporal lobe seizures originating in the uncus, with olfactory aura (typically unpleasant smells), sometimes with emotional and autonomic features.
  • Anosmia in Alzheimer disease: present in some patients.

Test with mild odorants (coffee, mint, cloves) — never with irritants like ammonia, which stimulate trigeminal nociceptors rather than olfactory receptors.

The Gustatory Pathway

Taste is detected by taste buds on the tongue, palate, and pharynx. The afferent pathway varies by region of the tongue:

  • Anterior two-thirds of the tongue: chorda tympani branch of CN VII.
  • Posterior third of the tongue: CN IX.
  • Epiglottis and adjacent regions: CN X.

The pathway:

  1. Taste afferents → nucleus solitarius in the medulla (rostral portion is the gustatory portion).
  2. Solitary nucleus → ventral posteromedial nucleus (VPM) of thalamus (parvocellular portion).
  3. VPM → primary gustatory cortex in the insular operculum.

Five Basic Taste Modalities

  • Sweet: sugars; detected by G-protein-coupled receptors (T1R2/T1R3).
  • Salty: sodium; detected by epithelial sodium channels.
  • Sour: acids; detected through proton channels.
  • Bitter: toxins; detected by a large family of T2R receptors.
  • Umami: savory (glutamate); detected by T1R1/T1R3 receptors.

Flavor is the integration of taste with smell — “loss of taste” in patients with anosmia is largely loss of flavor (which depends heavily on retronasal smell during eating), with preserved basic taste.

Gustatory Clinical Correlates

  • Loss of taste on anterior tongue with facial nerve palsy at the level above the chorda tympani branch in the mastoid segment.
  • Loss of taste on posterior tongue with CN IX involvement (uncommon as isolated).
  • Burning mouth syndrome: chronic burning sensation, often with altered taste.
  • Cancer chemotherapy: often produces altered taste (dysgeusia).
  • Gustatory sweating (Frey syndrome): after parotid surgery; misdirected regeneration of parasympathetic salivary fibers to sweat glands.

Pitfalls and Pearls

  • Olfaction reaches cortex without thalamic relay. Unique among sensory systems.
  • Anosmia in Parkinson disease precedes motor symptoms by years. Reliable prodromal feature.
  • Test smell with mild odorants, not irritants. Ammonia stimulates trigeminal nociceptors, not olfactory receptors.
  • Olfactory groove meningioma can cause Foster Kennedy syndrome.
  • Uncinate seizures present with unpleasant olfactory hallucinations, often with déjà vu and autonomic features.
  • “Loss of taste” usually means loss of flavor, which depends on intact smell.
  • Anterior two-thirds of tongue taste = CN VII (chorda tympani). Posterior third = CN IX.
  • Primary gustatory cortex is in the insular operculum. Lesions can produce isolated taste abnormalities.

References

  1. Doty RL. Olfactory dysfunction in Parkinson disease. Nat Rev Neurol. 2012;8(6):329-339.
  2. Hawkes CH, Doty RL. The Neurology of Olfaction. Cambridge University Press; 2009.
  3. Bromley SM. Smell and taste disorders: a primary care approach. Am Fam Physician. 2000;61(2):427-436.
  4. Chaudhari N, Roper SD. The cell biology of taste. J Cell Biol. 2010;190(3):285-296.
  5. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Wolters Kluwer; 2017.