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The article by Heckmann et al1 regarding the neurological aspects of taste disorders deserves merit for the description of a generally neglected field of neurology. Although the introduction, ancillary examinations, and classification of gustatory dysfunction are concise, the description and classification of clinical disorders require some comments.
The authors point out that a fifth type of taste, namely umami (taste of glutamate), has been added. An affinity of certain receptors for fat is also widely discussed. Concerning the methods of investigation, descriptions of several peripheral examinations of the facial nerve as well as methods of detecting function of the lingual nerve are omitted,2 which can be of practical importance for assessment of the most peripheral area of taste perception. Concerning the ancillary examinations, another central point is that functional magnetic resonance imaging enables the direct detection of gustatory perception and will become an important tool in the future evaluation of taste and olfaction.3
Practically all patients with anosmia also have a diminished perception of taste, and the two are often confused in clinical settings. From a neuro-oncologic standpoint, smell and taste disturbances are usually noted in patients who have undergone cranial (local or whole) radiation and cause a lot of discomfort for these people. Olfactory disorders may be caused by several medications or general disease.
We disagree with the description of peripheral neurological causes; the lingual nerve, which carries the taste fibers from the anterior two thirds of the hemitongue, should have been mentioned. The causes of mandibular nerve lesions are most often iatrogenic, including local anesthetic procedures or tooth extractions,4 but may also be caused by trauma as fractures of the mandibula. Bilateral involvement has been described in a patient with Guillain-Barré syndrome.5
To continue with the trigeminal nerve, 2 circumstances have to be considered: the ganglionopathy of the gasserian ganglion in connective tissue disease and sensory neuronopathies6as well as the observation that neurosurgical treatment of the gasserian ganglion may cause a taste disorder.7 This has led to the speculation that some taste fibers travel with trigeminal fibers.
Although it makes sense that a disturbance of taste might occur in the facial nerve (Bell palsy), it would have been helpful if the authors had pointed out that not all peripheral facial nerve palsies results in a disturbed gustatory sense and that this peculiar feature allows precise localization within the temporal bone. The quoted article by Roob et al8 does not mention this point. The literature suggests that between 30% and 50% of cases of Bell palsy are associated with a disturbance of taste. Another interesting observation is the phenomenon of ephaptic transmission in ageusia, which at the time of improvement may cause a metallic taste in the tongue.9
Finally rare entities such as "neuritis due to neuroborreliosis"1(p669) and herpes zoster may cause facial nerve paralysis. The frequency and relevance to gustatory disorders are unclear. Lesions of the cerebellopontine angle may cause disorders of taste, but what kind of lesions are meant by the submandibular region? The same applies to dissection of cervical arteries; would this apply only to the carotid arteries?
The paragraph on central neurological causes also merits comment. Although the authors point out that taste and smell cannot be precisely discriminated, this combination has to be considered in degenerative disorders such as Alzheimer disease, variant Creutzfeldt-Jakob disease,10 Huntington disease, Korsakoff syndrome, and Parkinson disease. The anatomically based classification into brainstem, thalamic, and cortical taste disorders is theoretical and lacks practical clinical examples. It remains unclear to what extent hemihypogeusia is observed in brainstem and cortical disorders.
From the standpoint of dealing with geriatric patients, disorders of taste are frequent and cause practical problems for this population. Although these disorders are not life threatening, they are unpleasant and occur in great quantity.
Regarding therapy, it seems courageous to suggest zinc gluconate according to preliminary data on the basis of a small series. Although this possibility is mentioned in a textbook of internal medicine,11 this treatment lacks evidence and cannot be recommended.
These points need to be taken into consideration in clinical practice. Additional differential diagnostic tables, as in the study by Sanchez-Juan and Combarros,12 would make this article more useful for the reader.
Grisold W, Nussgruber V. Comments on Neurological Aspects of Taste Disorders. Arch Neurol. 2004;61(2):297–298. doi:10.1001/archneur.61.2.297
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