Supplements Implications of Early Treatment for Parkinson’s Disease [CME/CPE]
Early Diagnosis of Parkinson's Disease: Recommendations From Diagnostic Clinical Guidelines
The frequency of olfactory impairment in PD provides an opportunity for differential diagnosis, although this particular dysfunction occurs to some extent in many parkinsonian patients. The AAN guidelines support consideration of olfactory testing for differentiation between PD and PSP, as well as PD and corticobasal degeneration, but not for differentiation of PD and MSA. Olfactory testing was associated with a diagnostic sensitivity of 77% and a specificity of 85%.19,29 The 2 UK guidelines recommend against olfactory testing in the clinical setting.20,21
Single Photon Emission Computed Tomography
Single photon emission computed tomography (SPECT) imaging uses a radiolabeled compound as a probe of dopamine transporters to study the progression of presynaptic dopaminergic degeneration. The AAN guidelines indicated that SPECT may be useful in differentiating PD from essential tremor but indicated that there was insufficient evidence to determine if SPECT is useful to differentiate various forms of parkinsonism.19 The NCCCC guidelines expressed ambivalence regarding the use of SPECT, but cited studies that support its use in differentiating essential tremor from dopaminergic deficiency in patients with upper limb postural or action tremor.21 The NCCCC further stated that SPECT may eventually be useful in distinguishing drug-induced and psychogenic parkinsonism from a state of dopaminergic deficiency. The SIGN guidelines support the use of SPECT to distinguish PD from nonneurodegenerative parkinsonism and tremor disorders, but not from neurodegenerative forms of parkinsonism.20
Magnetic Resonance Imaging
The AAN guidelines found magnetic resonance imaging (MRI) to possibly be useful in differentiating PD and MSA.19 The NCCCC guidelines regard structural MRI as potentially useful for differential diagnosis of PD from other forms of parkinsonism if conducted by an expert practitioner, but recommends against its diagnostic use otherwise.21 The SIGN guidelines recognize MRI as a useful tool for evaluating cerebrovascular disease to differentiate idiopathic PD from vascular parkinsonism. MRI is effective for measuring the extent of brain atrophy and to determine the presence of structural lesions that can be associated with parkinsonism, but SIGN advocates against the use of MRI for diagnosis of idiopathic PD.20
Transcranial sonography is not supported in the SIGN guidelines for differential diagnosis, whereas the AAN and NCCCC find insufficient data to make a recommendation.19-21
Positron Emission Tomography
None of the guidelines supports the use of positron emission tomography for differential diagnosis in PD.19-21
An early and accurate diagnosis of PD is critical to developing the most appropriate treatment strategy to maintain the best QOL for as long as possible. Unfortunately, the early recognition of PD can be challenging as there are other movement disorders, such as MSA, PSP, drug-induced parkinsonism, vascular parkinsonism, and essential tremor, which can initially appear very similar to PD. Several guidelines have been published to assist in the accurate diagnosis of PD. Studies have shown that these guidelines are often underutilized; however, when used, they do appear to improve diagnostic accuracy. As there are no definitive clinical tests to confirm PD at this time, the most accurate PD diagnosis has been shown to come from a neurologist specializing in movement disorders. Although the published guidelines are not in complete agreement, when used by a physician experienced in the diagnosis and treatment of PD, levodopa or apomorphine challenges, olfactory testing, and various neuroimaging techniques may have some utility in the diagnosis of PD. Improved awareness of the clinical features of PD and differential diagnosis, as well as knowledge of and appropriate application of diagnostic aids, will allow clinicians to more accurately diagnose and treat early PD.
Author Affiliation: Parkinson's Disease and Movement Disorder Center, University of Kansas Medical Center, Kansas City.
Funding Source: Financial support for this work was provided by Teva Neurosciences, Inc.
Author Disclosure: Drs Pahwa and Lyons report that they are consultants/ members of the advisory boards and have received honoraria from Teva.
Authorship Information: Concept and design (RP, KEL); acquisition of data/information (RP, KEL); analysis and interpretation of data/information (RP, KEL); and critical revision of the manuscript for important intellectual content (RP, KEL).
Address correspondence to: Kelly E. Lyons, PhD, University of Kansas Medical Center, 3599 Rainbow Blvd, Kansas City, KS 66160. E-mail: email@example.com.
1. Strickland D, Bertoni JM. Parkinson's prevalence estimated by a state registry. Mov Disord. 2004;19:318-323.
2. Twelves D, Perkins KS, Counsell C. Systematic review of incidence studies of Parkinson's disease. Mov Disord. 2003;18:19-31.
3. Dorsey ER, Constantinescu R, Thompson JP, et al. Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. Neurology. 2007;68(5):384-386.
4. Caslake R, Macleod A, Ives N, Stowe R, Counsell C. Monoamine oxidase B inhibitors versus other dopaminergic agents in early Parkinson's disease. Cochrane Database Syst Rev. 2009;(4):CD006661.
5. Hauser RA. New considerations in the medical management of early Parkinson's disease: impact of recent clinical trials on treatment strategy. Parkinsonism Relat Disord. 2009;15(suppl 3):S17-S21.
6. Olanow CW, Rascol O, Hauser R, et al. A double-blind, delayedstart trial of rasagiline in Parkinson's disease. N Engl J Med. 2009;361(13):1268-1278.
7. Olanow CW, Stern MB, Sethi K. The scientific and clinical basis for the treatment of Parkinson disease. Neurology. 2009;72(suppl 4):S1-S136.
8. Miyasaki JM, Martin W, Suchowersky O, Weiner WJ, Lang AE. Practice parameter: initiation of treatment for Parkinson's disease: an evidence-based review: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2002;58(1):11-17.
9. Pålhagen S, Heinonen EH, Hagglund J, et al. Selegiline delays the onset of disability in de novo parkinsonian patients. Swedish Parkinson Study Group. Neurology. 1998;51(2):520-525.
10. Parkinson Study Group. Effects of tocopherol and deprenyl on the progression of disability in early Parkinson's disease. N Engl J Med. 1993;328(3):176-183.
11. Ravina B, Camicioli R, Como PG, et al. The impact of depressive symptoms in early Parkinson disease. Neurology. 2007;69(4):342-347.
12. Haycox A, Armand C, Murteira S, Cochran J, François C. Cost effectiveness of rasagiline and pramipexole as treatment strategies in early Parkinson's disease in the UK setting: an economic Markov model evaluation. Drugs Aging. 2009;26(9):791-801.
13. Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry. 1992;55(3):181-184.
14. Schrag A, Ben-Shlomo Y, Quinn N. How valid is the clinical diagnosis of Parkinson's disease in the community? J Neurol Neurosurg Psychiatry. 2002;73(5):529-534.
15. Jankovic J, Rajput AH, McDermott MP, Perl DP. The evolution of diagnosis in early Parkinson disease. Parkinson Study Group. Arch Neurol. 2000;57(3):369-372.
16. Eggert K, Larisch A, Dodel R, Bormann C, Oertel WH. Awareness and knowledge of the clinical practice guideline on Parkinson's disease among German neurologists. Eur Neurol. 2009;61(4):216-222.
17. Larisch A, Oertel WH, Eggert K. Attitudes and barriers to clinical practice guidelines in general and to the guideline on Parkinson's disease. A national survey of German neurologists in private practice. J Neurol. 2009;256:1681-1688.
18. Swarztrauber K, Graf E. Nonphysicians' and physicians' knowledge and care preferences for Parkinson's disease. Mov Disord. 2007;22(5):704-707.
19. Suchowersky O, Reich S, Perlmutter J, et al. Practice parameter: diagnosis and prognosis of new onset Parkinson disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;66(7):968-975.
20. Scottish Intercollegiate Guidelines Network. Diagnosis and Pharmacological Management of Parkinson's Disease: a National Clinical Guideline. Edinburgh, Scotland: SIGN; 2010.
21. National Collaborating Centre for Chronic Conditions. Parkinson's Disease: National Clinical Guideline for Diagnosis and Management in Primary and Secondary Care. London, England: Royal College of Physicians; 2006.
22. Hughes AJ, Daniel SE, Lees AJ. Improved accuracy of clinical diagnosis of Lewy body Parkinson's disease. Neurology. 2001;57(8):1497-1499.
23. Gasser T. Update on the genetics of Parkinson's disease. Mov Disord. 2007;22(suppl 17):S343-S350.
24. Wenning GK, Ebersbach G, Verny M, et al. Progression of falls in postmortem-confirmed parkinsonian disorders. Mov Disord. 1999;14:947-950.
25. Wenning GK, Ben-Shlomo Y, Hughes A, Daniel SE, Lees A, Quinn NP. What clinical features are most useful to distinguish definite multiple system atrophy from Parkinson's disease? J Neurol Neurosurg Psychiatry. 2000;68:434-440.
26. Colosimo C, Albanese A, Hughes AJ, de Bruin VM, Lees AJ. Some specific clinical features differentiate multiple system atrophy (striatonigral variety) from Parkinson's disease. Arch Neurol. 1995;52:294-298.
27. Merello M, Nouzeilles MI, Arce GP, Leiguarda R. Accuracy of acute levodopa challenge for clinical prediction of sustained long-term levodopa response as a major criterion for idiopathic Parkinson's disease diagnosis. Mov Disord. 2002;17:795-798.
28. Rossi P, Colosimo C, Moro E, Tonali P, Albanese A. Acute challenge with apomorphine and levodopa in Parkinsonism. Eur Neurol. 2000;43:95-101.
29. Wenning GK, Shephard B, Hawkes C, Petruckevitch A, Lees A, Quinn N. Olfactory function in atypical parkinsonian syndromes. Acta Neurol Scand. 1995;91:247-250.