Impaired sense of smell or taste can raise a person’s risk of developing Parkinson’s disease 2.5 times, a study suggests.
The study, “Incidence of Parkinson’s disease in a large patient cohort with idiopathic smell and taste loss,” was published in the Journal of Neurology.
Currently, Parkinson’s disease is diagnosed mainly on the assessment of patients’ motor symptoms and their severity. However, evaluation scales can be subjective and might fail to detect small changes.
Non-motor symptoms have gained increased attention because of their potential to anticipate Parkinson’s-related motor manifestations. Approximately 90% of Parkinson’s patients have altered smell sensitivity during the disease’s initial and moderate stages, thought to be partly because of brain connectivity changes.
To explore the incidence and diagnostic potential of smell and taste disorders in Parkinson’s disease, researchers reviewed the clinical records of 474 people who had been diagnosed with smell and taste loss of unknown cause.
Patients diagnosed and followed over a period of 15 years at the Smell and Taste Clinic in Dresden, Germany, were interviewed by phone using a standardized questionnaire to record their condition and clinical history.
At the time of the first assessment at the clinic, patients had already experienced reduced or lost odor and taste sensitivity for a mean period of 4.6 years. Onset of olfactory (smell) disturbances was in general noticed at a mean age of 57.9 years; gustatory (taste) disorders, 59.3 years.
Of the 474 participants, 14.3% had a normal sense of smell, 40.5% had reduced, and 45.1% had complete loss of smell. Regarding taste, 90.1% of the participants had normal sensation, 9.5% had reduced, and 0.4% had complete loss of taste.
Collectively, 242 people were diagnosed with a qualitative olfactory or gustatory disorder, of whom 21.1% had parosmia (distortions of the sense of smell), 32.9% had phantosmia (olfactory hallucinations), and 7.6% had parageusia (distortions of the sense of taste).
Participants’ clinical reports revealed that 45 (9.5%) had developed Parkinson’s disease after the initial idiopathic smell and/or taste loss diagnosis.
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Six of the Parkinson’s patients had combined olfactory and gustatory disorders at the time of diagnosis, whereas 38 had pure olfactory disorders and one patient had a pure gustatory disorder.
The frequency of taste disorders was similar between those with and without Parkinson’s. In contrast, Parkinson’s patients had a higher prevalence of initial complete loss of smell compared to those without the disease.
The team did not find a significant association between taste or smell loss and the development of the disease. Still, patients who developed Parkinson’s reported a decrease in olfactory and gustatory function more frequently than non-Parkinson’s patients.
Researchers found that “patients with a decrease in olfactory or gustatory function developed Parkinson’s with a significantly higher rate compared to patients with a stable smell or taste function.” Overall, impaired smell or taste sense increased the risk of developing Parkinson’s disease 2.47 times.
“Risk stratification might be considerably improved by correct diagnostic allocation of smell and taste loss, the use of both olfactory and gustatory testing, and subsequent long-term monitoring of these functions,” researchers said.