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February 2004

Comments on Neurological Aspects of Taste Disorders—Reply

Arch Neurol. 2004;61(2):298. doi:10.1001/archneur.61.2.298

In reply

We thank Grisold and Nussgruber for their comments on our review of neurological aspects of taste disorders. A neurological review is limited to 3000 words and a maximum of 50 references. For this reason, not all available information could be thoroughly debated.

It is correct that "fat receptors" have been discussed,1 but so far they have limited clinical relevance. A detailed investigation of the olfactory system is necessary to complete the diagnostic procedures in patients with complaints of taste dysfunction.2 The additional information on taste disorder due to radiation and to lesions of the lingual, trigeminal, and facial nerves is also of interest. The dissection of cervical arteries in association with cranial nerve palsy mostly affects the carotid artery, although the vertebral artery can be affected too.

We feel that the classification of central taste disorder into brainstem, thalamic, and cortical taste disorders is expedient in clinical practice, easy to memorize, and follows the traditional—and still applied—neurological question "Where is the lesion?" For instance, hemihypogeusia can occur with an ipsilateral brainstem lesion.3

We agree with the authors that gustatory dysfunction with aging is frequent, although it is relatively mild compared with age-related olfactory loss. Currently, the diagnosis of age-related gustatory dysfunction is possible only through exclusion. The present knowledge on extent, severity, and course of taste disorders in dementia and related diseases is sparse.4

Finally, we would like to thank Grisold and Nussgruber for the opportunity to provide more details on our study indicating the usefulness of zinc gluconate in gustatory dysfunction.5 This randomized, double-blind, placebo-controlled clinical trial was recently performed with 50 patients (43 women, 7 men; mean ± SD age, 61.1 ± 7.4 years) who had idiopathic dysgeusia. Twenty subjects received placebo, and 26 subjects received zinc gluconate (140 mg/d). Gustatory function was quantitatively assessed, the Beck Depression Inventory score was determined, and a mood scale score was obtained before and after 3 months of therapy. When compared with placebo, therapy with zinc improved gustatory function (P<.001). Following therapy, patients in the zinc group were less depressed than those in the placebo group, as indicated by changes in the Beck Depression Inventory (P= .01) and mood scale scores (P= .04). Patients who received zinc also found suprathreshold tastants to be less unpleasant than patients in the placebo group (P= .05). No significant group differences were seen for other parameters investigated, including blood and saliva chemistry. These findings lead us to conclude that zinc is useful in the treatment of dysgeusia in terms of (1) improvement in general gustatory function, (2) improvement of dysgeusic sensations, and consequently (3) improvement in general mood scores.

To conclude, we see the comments made by Grisold and Nussgruber as a useful addendum to our review and welcome any discussion on taste dysfunction in the field of neurology.

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