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Archive for August 2009OLFACTORY DYSFUNCTION —AN EARLY DIAGNOSTIC FOR PARKINSON’S DISEASEAugust 8, 2009 by mike.
SAN DIEGO—A simple smell test may soon be used to aid the diagnosis of Parkinson’s disease and to identify relatives and others at risk for the disease. Research on the use of smell tests in Parkinson’s disease was presented at the 58th Annual Meeting of the American Academy of Neurology. Since at least 1955, hyposmia has been known to occur in patients with Parkinson’s disease, according to Nicolaas Bohnen, MD, Associate Professor of Radiology and Neurology at the University of Michigan in Ann Arbor. But interest in the phenomenon has grown markedly in the past few years, driven by the hope of developing neuroprotective treatment for patients in the early stage of the disorder. “The idea is to have biomarkers for early diagnosis,” said Dr. Bohnen, “and this interest is related to neuroprotective treatment.” While no definitive neuroprotective treatment has emerged, recent studies of coenzyme Q10 and rasagiline have hinted that such a therapy might be possible. PASSING THE SMELL TEST Dr. Bohnen’s team sought to determine whether a selective pattern of smell deficit might exist in patients with Parkinson’s disease. They used the University of Pennsylvania Smell Identification Test (UPSIT), a self-administered battery of 40 scratch-and-sniff odors ranging from turpentine to roses to pizza. The researchers compared smell ability in 26 Parkinson’s disease patients and 26 controls matched for age, sex, and smoking history. The existence of a selective deficit corroborates well with findings from a similar study in the United Kingdom, although there were some differences. In particular, British patients especially had trouble identifying wintergreen, while the American patients in Dr. Bohnen’s study had fewer difficulties in identifying this odor. “The cultural affinity for specific smells may differ between groups, as people are more exposed in daily life to specific smells,” he said. Difficulty recognizing banana was common to both groups. “I’m unaware of any good explanation for why there is this specific deficit in Parkinson’s disease,” said Dr. Bohnen. While the disease is characterized by well-described pathology in the olfactory nucleus, “smell recognition is also a cognitive function. It’s relatively complex.” CAFFEINE AND HYPOSMIA Hyposmia in first-degree relatives of Parkinson’s disease patients also correlates with low caffeine intake, according to a third study. High caffeine consumption previously has been shown to be associated with a lower risk of Parkinson’s disease. In this study of 159 relatives of patients with Parkinson’s disease, Matthew Stern, MD, and colleagues from Pennsylvania Hospital in Philadelphia found that lifetime caffeine intake was negatively correlated with UPSIT score. Twenty-five percent of those consuming one cup or less per day of a caffeinated beverage over their lifetime were at or below the 10th percentile in UPSIT performance, compared with only 8% of those consuming more than one cup per day. “The effect may be the result of poor olfactory performance in individuals who will go on to develop Parkinson’s disease,” the researchers concluded, although they noted an alternative explanation is that hyposmia is “an intermediate phenotype” for the disease, due to the sharing of epidemiologic associations and risk factors with those for clinical Parkinson’s disease. —Richard Robinson Posted in Research, Parkinson's Disease Categories | Print | No Comments »
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