Excerpts reprinted with permission from the APDA Saint Louis Parkinson Newsletter, #1, 2006
The first-ever World Parkinson Congress (WPC, February 22-26, 2006) provided a unique international forum for sharing the latest scientific findings, medical practices and caregiver initiatives related to Parkinson's disease (PD). There were over 3000 participants who filled the new Washington D.C. Convention Center each day for this historic event. By bringing together Parkinson's researchers, health professionals, patients and caregivers, and some of the world's leading neuroscientists, a multi-layered dialogue was sparked between participants contributing their collective knowledge of PD.
Parallel sessions were divided into: a) Science sessions focusing on specific cutting-edge research; b) community sessions focusing on care delivery and quality of life topics; c) interactive sessions focusing on multidisciplinary approaches to care, advocacy and public policy issues. Each day was divided into a theme with an emphasis on how can knowledge be used to improve care delivery. Themes included: What causes PD?; How do brain cells lose their vitality in PD?; How can PD be identified before clinical onset? The final day was devoted to the needs of PD patients and families be met in relieving symptoms, improving quality of life and slowing progression.
Highlights for the Community and Integrative Sessions
Contributed by Deborah Dahlin Guyer, Speech and Language Pathologist
I tended to gravitate to the community sessions and interactive workshops. Here are some of the items that "stuck in my mind."
• A diminished sense of smell can be a precursor to PD.
• Gait problems arising from dysfunction of axial (midline) muscles and cognitive impairment are more likely to cause complications (morbidity) for patients with PD. These features are more common in older-onset patients and do not appear to be related to the overall duration of the illness.
• Non-motor features of PD include cognitive issues, visual hallucinations and depressed mood. These are under-reported, under-recognized (75% miss the diagnosis) and under- treated (94% not treated), yet they have a significant impact on the quality of life.
• Non-motor symptoms that are resistant to L-dopa can include cognitive decline, dementia, hallucinations, depression, choking, urinary incontinence, and hypotension. All add to the burden of disability.
• Apathy develops in 16-42% of persons with PD and contributes significantly to caregiver burden. This apathy is not just a simple reaction to disability. Its features include reduced emotion, diminished motivation, lack of initiative, difficulty sustaining activity, a seeming lack of concern and indifference. These individuals may stop reading the newspaper, no longer take part in family conversations, have difficulty articulating thoughts and prefer to sit around the house and take frequent naps. Apathy often co-exists with depression but can occur independently. Apathy is difficulty to differentiate from depression, but it is important to do so in terms of treatment. Apathy does not correlate with dementia. It is associated with impaired executive function (planning). It can co-exist with anxiety. It also fluctuates with motor function. Apathy is diminished when medication is working.
• Many PD patients suffer mild cognitive impairment, but this often does not clearly interfere with activities of daily living. Cognitive impairment increases with disease duration and in later stages. Current anti-PD medications have little effect on cognitive function. Rivastigmine (Exelon) may help mild cognitive impairment.
• Dementia occurs in 20-40% of PD patients. Associated features include visual hallucinations, confusion and daytime somnolence. The risk factor grows as the patient ages.
• Exercise promotes brain changes and is a legitimate therapeutic option. It slows the progression of the disease. It is a physiological tool to promote neuroplasticity. Use it or lose it! Use it and improve it! The BIG and LOUD approach combines physical exercise and speech exercises with great results and is being researched as a viable option for therapy.
• We must treat the patient, NOT the disease (patient-centered care vs. disease-centered model). One size does not fit all!
• An interdisciplinary team approach is needed. Interdisciplinary care favors quality of life issues. It is patient-centered and deals with symptom management, activity and functional improvement, education, patient and clinician adherence, awareness, prevention and risk reduction. Caregiver, community, society and the patient all take an active role. A wellness focus is not the same as focus on the disease.
Scientific Program Highlights
Contributed by: Dr. John L. Goudreau
The contributions of environmental and genetic causative factors in PD were vigorously discussed. While epidemiological studies on large populations cannot prove a cause-effect relationship, some occupations increase the risk of developing PD (e.g., farmers, teachers and health care workers), perhaps because and environmental exposure. Cigarette smoking and increased caffeine consumption has inverse associations with the developing PD; i.e., both significantly reduce the risk of developing PD. Genetic studies have identified 12 genes that are clearly involved with the development of familial PD. Both environmental factors make an important contributions to the cause of PD, aptly captured by the phrase "Genetics load the gun but environment pulls the trigger."
Some of the difficulty in identifying causes of PD stems from how one defines the disease; i.e., by brain pathology or by responsiveness to dopaminergic medication. Accuracy of the clinical diagnosis of PD was reviewed: about 10% of rigorously classified PD are not found to be PD when examined pathologically. When pathological diagnosis is used, about 6% of autopsy proven cases of PD have atypical symptoms. Up to 5% of patients in a movement disorders subspecialty clinic are incorrectly classified. There may be clinical subtypes of PD that include a tremor-dominant, postural instability gait difficulty (PIGD), akinetic/rigid and mixed forms of PD. The etiology, pathology and evolution of these subtypes may be distinct.
"Evil proteins and their mischief " were explored as underlying features of PD pathogenesis. Modifications in a-synuclein that promote protein aggregation contribute to disease pathogenesis and are targets for neuroprotective therapies. A new protein, LRRK 2 or dardarin, has been identified through genetic studies and may explain a significant portion of cases as inherited PD. The function of this protein is currently unknown, but discovering the normal and pathological function of LRRK-2 has great promise for providing new targets for PD therapies. Inflammation following initial injury appears to be an important mechanism in sustaining neurodegeneration in PD and anti-inflammatory medications can slow this process. Finally, proteosomal proteins involved in removing "mischievous" proteins may be dysfunctional in PD and this pathway also provides a compelling target for therapy development.
Neuroimaging studies are being refined for use as biomarker of PD and progression. For example, "PD related pattern" of changes on PET scanning may provide a method for confirming the diagnosis of PD and following the course of the disease, both essential to accelerate the development of new therapies. Neuroimaging may be effectively combined with other approaches such as smell testing to identify early PD. A "bionomics" approach to identifying important core biochemical features of PD was proposed that included a global evaluation of all genes and how they are translated into cell proteins in patients with Parkinson disease. Cutting edge tools are rapidly being developed to accomplish this goal.
Advanced approaches to patient care were reviewed. While dopaminergic treatments liberate patients from the grasp of rigidity and bradykinesia, they can cause involuntary movements (dyskinesias) and fluctuating responses to dopaminergic medications (short duration reponses). Dyskinesias developed in 13%, 35-40% and 100% of patients having PD for 0-5, 6-9 and >10 yrs, respectively. The frequency of dyskinesias may be declining as treatment strategies have changed over the last decade and dyskinesias appear to have little impact on quality of life. The classification and treatment of dyskinesias were reviewed; they all may be a form of stereotypic movement. Adjustments in dopaminergic drugs and amantadine are the current treatments; sarizotan and NR2b glutamate and A2A adenosine blockers are future treatments being developed. New treatments under development by pharmaceutical companies are: sublingual selegiline, new MAO-B inhibitors (rasagiline), istradephylline and other adenosine blockers, dopamine agonist patch (rotigitine). Cutting-edge therapies on the horizon were discussed including: manipulating synuclein expression, modification or removal; gene therapies to deliver or nerve growth factors enzymes that produce dopamine or GABA; transplanting stem cells or encapsulated cells producing growth factors. Early clinical (Phase I) studies are beginning with some of these new and exciting approaches and provide a ray of hope for those living with PD. A unique component of the WPC was the emphasis on Creativity. The following is an excerpt from the newly developed website,wwwcreativity.pdf.org, where you can also view the web gallery, featuring works displayed during the Congress. A Committee has been created to further study the phenomenon that many people with PD develop creative abilities. Many people living with Parkinson's disease have found ways to rise above its impact to produce truly beautiful works of art, including visual arts, music, writing, drama, dance, craft, and web design. The therapeutic value of creativity was evident throughout the program. A component of the WPC, Creativity & Parkinson's - an exhibition of artwork made solely by people diagnosed with Parkinson's - provided a rich, comprehensive and inspirational message to the participants and gave tangible evidence that creativity can have an impact on one's quality of life. "The impact of the artwork and the artists' statements will hopefully fuel further study on the creative process and the therapeutic value of creativity."