Volume 24, Issue 2, Pages 268-273
Published Online: October 29, 2008
Authors: Tomoyuki Miyamoto, MD, PhD,, Masayuki Miyamoto, MD, PhD, Masaoki Iwanami, MD, Keisuke Suzuki, MD, PhD, Yuichi Inoue, MD, PhD, Koichi Hirata, MD, PhD
Read Article | Listen to Podcast Review
Reduction of olfactory function in idiopathic rapid-eye-movement (REM) sleep behavior disorder (iRBD) is of the same magnitude as that found in patients with Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We assessed olfactory function using the Odor Stick Identification Test for Japanese (OSIT-J) in 48 Japanese patients with iRBD, 21 with PD, and 34 with obstructive sleep apnea syndrome (OSAS). Possible score of the OSIT-J ranges from 0 to 12. OSIT-J scores were 4.9 ± 2.8 in patients with iRBD, 4.8 ± 2.8 in patients with PD, and 9.9 ± 1.4 in OSAS patients. An OSIT-J score of 8.5 was associated with a sensitivity of 88.2 and 85.3%, respectively, and specificity of 83.3 and 85.7%, respectively, in differentiating iRBD or PD patients from OSAS patients. Odor identification is impaired in Japanese patients with iRBD and PD. The results suggest that OSIT-J, which is a short and simple nonlexical olfactory identification test, can be useful as a clinical indicator for iRBD with Lewy body formation and is appropriate in the Japanese elderly population.
© 2008 Movement Disorder Society
Podcast review by Dr. Matthew B. Stern, MD
Idiopathic REM Sleep Behavior Disorder (RBD) is increasingly recognized as potential harbinger of neurodegenerative diseases involving synuclein pathology, including Parkinson's disease (PD) and Lewy Body Disease (DLBD). Previous studies have demonstrated a variety of shared risk factors in PD and RBD including hyposmia and subtle motor impairment.
The study by Miyamoto and colleagues extends these observations using an olfactory identification test tailored to the Japanese population. Using the Odor Stick Identification Test for Japanese (OSIT-J), the authors found that smell loss was similar in patients with RBD and PD and distinct from a control group of patients with obstructive sleep apnea. They used a cutoff value of 8.5 (out of 12 items) to yield a sensitivity and specificity in the mid to high 80% range for differentiating RBD and PD from controls.
A fascinating new concept in understanding neurodegeneration in PD and DLBD is the evolution of pathology and the potential to detect features of the disease before neurologic symptoms predominate. Olfactory function has emerged as a key target of early detection. This has been fueled by a number of observations including the presence of significant olfactory dysfunction in early PD independent of disease stage or duration and likely beginning well before the cardinal clinical manifestations. Further, Lewy pathology might first affect lower brainstem structures and the anterior olfactory nucleus, suggesting that smell loss be explored as part of a screening paradigm for PD and other synucleinopathies.
One key question highlighted by this study is the timing of smell loss before motor PD. Not only did the RBD patients have olfactory loss comparable to the PD group, but they were also somewhat older with a duration of RBD of approximately 7 years (with a large standard deviation). If some of these RBD patients were indeed destined to develop PD, it would seem that smell loss occurs very early in the process. It would be interesting to follow the RBD patients to determine whether there is an association between degree of smell loss and risk of developing PD or DLBD. It may be that patients with hyposmia are different from those with anosmia but the numbers in this study are too small to make such a distinction. Moreover, it is not clear how well correlated the OSIT-J is with other more universal tests of olfactory function such as the University of Pennsylvania Smell Identification Test.
Finally, the pathologic correlates of olfactory loss need further study. It is possible that mesolimbic structures, the olfactory bulbs and other regions may affect odor identification but be differentially affected in RBD, PD and other disorders. Further, only a small percentage of patients with hyposmia develop neurodegenerative disease. What other factors contribute to olfactory dysfunction and predict either the development of PD, RBD or the transition from RBD to PD? These studies will prove critical in developing a screening paradigm for neurodegenerative diseases and ultimately diagnosing diseases at a time when neuropathologic changes are beginning and intervening with the disease process is more promising.
About Dr. Matthew B. Stern, MD
Dr. Stern is the Director of the Parkinson's Disease and Movement Disorders Center and is the Parker Family Professor of Neurology at the University of Pennsylvania, Philadelphia. Dr Stern also directs the Parkinson's Disease Research, Education, and Clinical Center at the Philadelphia Veteran's Hospital. Dr Stern received his medical degree from Duke University, Durham, North Carolina, and completed his neurology training at the University of Pennsylvania.
The Center at Penn is one of the largest of its type in the country and has a long track record of achievement in clinical trials and experimental therapeutics. Dr Stern has authored or co-authored numerous papers on Parkinson's disease (PD) and edited or co-edited 8 books. He has served on the executive committee of the American Academy of Neurology's Movement Disorders Section and is a member of the American Neurological Association. He has held several leadership positions in the international Movement Disorder Society and is currently Secretary-elect.
In addition to serving as institutional investigator for numerous clinical trials, Dr Stern has been the principal investigator or co-principal investigator of many studies related to PD. He serves on numerous consulting boards and has lectured throughout the world on PD and related disorders.