Parkinson’s Disease (PD) is a neurological disorder that manifests itself in abnormal movements and posture. It’s more frequently seen in patients over the age of 60 and is one of the most common neurological disorders of this age group. The prevalence of this progressive disorder is close to 1% of the geriatric population. Estimates are that at least a million people in America live or suffer with PD, and there are approximately 50,000 new cases reported each year. While this disease has certainly been around for thousands of years, it was first brought to the attention of Western doctors in 1817 when a British physician named James Parkinson wrote about the condition in An Essay on the Shaking Palsy. The same physical signs and symptoms appeared throughout Ayurvedic texts in India some 5,000 B.C. and also in the 2,500-year-old Chinese medicine text: Huangdi Neijing. PD is usually a slow, progressive disorder that once diagnosed can be stalled with medical therapy, but not halted or cured. The neuropathology in this disorder is the loss of dopaminergic neurons of the substantia nigra pars compacta, a primitive part of the brain that is responsible for movement. On evaluation of this brain tissue at autopsy, the pathologist would confirm the diagnosis by finding a loss in the dark pigmentation (neuromelanin) of the cells that produce the neurotransmitter dopamine. Within the substantia nigra and locus ceruleus surviving neurons oft en contain the histological presence eosinophilic intracytoplasmic inclusion bodies named Lewy bodies and Lewy neuritis, considered the hallmark findings of classical Parkinson’s. Destruction of dopamine production heralds the onset of symptoms. There’s also concomitant hyperactivity of the cholinergic neurons in the brain as well.
Research demonstrates that anywhere between 60 to 80% of the substantia nigra dopamine producing cells must die before neurological symptoms of PD even appear. It’s highly debated as to what actually causes PD. While widely known familial predisposition occurs and this disorder is inherited, there are also contributing environmental factors. During a 1900s fl u epidemic a severe form of the influenza virus left many with a Parkinson’s-like disorder. Parkinsonian features were also diagnosed when several people in the 1980s took an illegal designer-drug contaminated with MPTP. So very likely there’s genetic predisposition that is triggered by environmental factors. A locus on the short arm of the chromosome 4 gene has been implicated as the genetic site of involvement. Some recent research has shed light on biomarkers that may in the future be helpful in assessing risk. One study showed that individuals with two copies of the L-form of CYP2D6 on their chromosomes have over a fi ve-fold increased risk of developing PD. Aberrancies in the mitochondrial complex I respiratory enzymes (ubiquinone oxidoreductase), the monoamine oxidase B (MAO B) enzyme and the cytochrome P450 enzyme system have also been implicated.
Signs and symptoms of this disorder usually start with a tremor. This is most often the first sign; it can be subtle and transient initially, worsening with time. Usually found asymmetrically and at rest (hence the term resting tremor), this shaking seems to be confined to the upper extremity. One description of this resting tremor is called pill-rolling, as the subject appears to make a rolling movement with their fingers that is nonvoluntary. Another sign is a subtle decrease in dexterity and a reduction in the arm swing (normally accompanying walking) on the involved side where the tremor is first observed. Noteworthy is the softening of the voice, and oftentimes the flattened affect or decrease in facial expression. Some will remark about the decreased sense of smell and sleep disturbances that occur with rapid eye movement behavior disorder (RBD). In this condition, there is a loss of atonia or paralysis during REM sleep. Symptoms of autonomic dysfunction such as constipation, abnormal sweating, seborrheic dermatitis and sexual dysfunction can follow. There is the slowing of thinking and cognitive impairment also known as Parkinson dementia, and a general feeling of weakness, malaise, depression, anhedonia and lassitude.
With the progression of PD, the patient will often experience bradykinesia or slow movements with rigidity (sometimes noted as cogwheeling of the upper extremities when another tries to move the limb in a passive way). Patients can eventually succumb to gait disturbance, which puts them in danger of falling. Falls in the elderly have a high morbidity and mortality rate, so any means of protecting the PD sufferer from falling will add to their longevity. Further progression shows in the gait, as the patient will tend to become more flexed or stooped forward when walking with shortening of their stride. Balance impairment following this gait disturbance is usually a later phenomenon.
The diagnosis is made by the astute clinician who picks up on the resting tremor and patient’s exhibiting rigidity and slow movements (bradykinesia). A tremor is not always necessary to make a diagnosis as it occurs in about 70% of patients afflicted with this disorder. So other signs and symptoms must also be recognized to catch it promptly. Early detection resulting in immediate drug therapy intervention can reduce the speed of progression. There are no readily available clinical blood biomarkers, but at least four spinal fluid (CSF) tests are under investigation. MRI and CT scans are not effective as a diagnostic tool, but can rule out other disorders that may mimic PD. Positron emission tomography (PET) or SPECT scans may show findings consistent with PD but they are not routinely performed. Serum or CSF ceruloplasmin levels can be checked to rule out other causes such as Wilson’s disease (a copper metabolism disorder), which can mimic PD in presentation. Regarding young-onset PD, dystonia may be the first common symptom seen in those under age 40. This usually involves the involuntary turning in and down of the foot, dorsiflexion of the great toe, and abduction of the arm and elbow making the hands rest in front of the abdomen. Dystonia with associated fatigue can flair and abate. Another feature in progressive PD is micrographia, where the handwriting becomes very small and writing itself requires great effort. Helpful in confirming a diagnosis of PD is the response to dopamine agonists (levodopa) as other non-PD conditions don’t usually have the same symptom-reversing effect.
PHASES OF PD PROGRESSION
Parkinson’s disease can be categorized into five stages. They range from mild, subtle symptoms and signs usually noticed by family and friends (Stage 1) to severe, debilitating symptoms of Stage 5 that require constant one-on-one nursing care. Dementia can occur with PD in upwards of 40% of cases, and one typically finds onset of cognitive dysfunction about eight years or more after the onset of the tremor or motor derangement. There is an atypical Parkinsonism disorder called PPS (Parkinson’s Plus Syndromes) that typifies the same symptoms and signs but is more rapidly progressive and resistant to the usual treatments. One of the most common PPS is called Progressive Supranuclear Palsy (PSP) and the youngest documented case reported was a patient in their early 40s (www.nhs.uk/conditions/progressive-supranuclearpalsy/ pages/Introduction.aspx).
For a better prognosis with better quality of life (QoL), early diagnosis is imperative and prompt implementation of therapeutics is required. Drug therapy usually favors levodopa and carbidopa. MAO inhibitors come with warnings yet are beneficial and do improve long-term QoL indicators. Sometimes drugs such as catechol-o-methyltransferase inhibitors (COMT-inh) are used to bolster the effects of levodopa. Dopamine agonists including ropinirole and pramipexole are helpful as well. Surgical options include the implantation of deep brain stimulation devices (DBS), which is replacing neuroablative lesion procedures. Methylphenidate can help with fatigue, and modafinil for those with excessive daytime somnolence. Gene therapy is still under investigation and likely wholesale clinical application is years away.
PREVENTION AND TREATMENT
Because the exact cause of PD is not known, proven preventive methods are still a bit of a mystery. However, some research has shown that caffeine in coffee, tea and other beverages may reduce the risk of PD. Green tea may also decrease the risk. It has been noted that heavy coffee drinkers and smokers have a lower incidence of PD. Flavonoids and anthocyanins in berries may have a positive effect. Chocolate (cocoa) has had some mixed reviews, but researchers in Dresden, Germany are actively studying the effects of dark chocolate. In the early 1990s vitamins C (ascorbic acid) and E showed a little promise in reducing progression of PD. Some have reasoned that antioxidants and anti-inflammatory agents may be helpful in prevention and slowing of progression.
Scientists indicate that regular aerobic exercise may reduce the risk of Parkinson’s disease. Advocates for alternative medicine feel that CAM therapies may be beneficial. Co-Enzyme Q10 in high doses appears helpful in some small studies. Manual therapy (therapeutic massage) can be useful with muscle tension and posture. Also, acupuncture may assist with symptom reduction and reduce pain. T’ai Chi can improve flexibility, balance and help prevent falls. Practiced by folks of all ages, T’ai Chi appears to be safe and in at least one study helped improve balance in mild to moderate stage PD more than stretching and resistance training. Zumba® is all the rage these days, and apparently has a place with PD clients. Yoga can certainly help with flexibility and balance, while the Alexander technique can aid with posture, balance and how one is to use his or her muscles. Meditation is recommended to help with the psychological aspects of PD. Music and art therapy can also improve walking, speech and emotional health.
PHYSICAL ACTIVITY AND PARKINSON’S DISEASE
Studies have found that people with PD who exercise have improved strength, cardiovascular fitness, balance, flexibility and gait. Even though PD is a neurodegenerative disease, the downstream effects are on motor behavior. There is a link between neurological impairments of PD (rigidity, tremors, motor planning) and musculoskeletal impairments (stooped, flexed posture; loss of spinal and peripheral flexibility) where both contribute to bradykinesia and loss of balance. Exercise also seems to protect against the dementia associated with PD. Dementia is a non-motor symptom that 83% of PD sufferers will develop about 20 years following their diagnosis. Another aspect of PD is that patients have a fear of falling and general loss of interest in physical activity since they cannot perform tasks very well, so they stop being active. This lack of physical activity leads to loss of strength and endurance that are not directly caused by their Parkinson’s. Falling can be largely avoided with proper training.
When designing an exercise program be sure to include strength training, aerobic exercise, low-intensity aerobic exercise, flexibility and balance training. It’s not necessary to introduce all these elements at once, but to start where the individual is most comfortable and interested, then progress.
Keep in mind, many individuals with PD routinely see a physiotherapist who focuses on gait, balance training and flexibility, so be aware of this redundancy. Make sure you communicate with other healthcare providers to optimize program design.
Individuals with PD have fluctuating symptoms from day to day and even hour to hour, so close monitoring is important. Poor regulation of body temperature, altered heart rate and blood pressure responses during exercise are common. These fluctuations are due to autonomic nervous system dysfunction. To avert undesirable outcomes include precautions such as a proper climate-controlled exercise area, heart rate monitor and a blood pressure cuff with stethoscope.
It is also imperative to keep in mind that fear of falling and loss of self-efficacy are barriers to physical activity, so introducing exercises slowly and incrementally is important to a long-term commitment. Begin with activities that afford the individual the feeling of safety and require the least effort with the greatest reward. In some individuals this may be upper body strength training, in others walking may be more suitable.
It is largely unnecessary to do formal strength and cardiovascular testing. Instead, progress can be tracked by charting improvements during the evolution of the program. More meaningful assessments in evaluation of PD patients are the 6-minute walk, 10-meter comfortable pace, 10-meter fast pace and 15-meter fast pace.
The individual with PD walks back and forth on a 30-meter long flat course marked by orange cones for 6 minutes. The distance is recorded; the farther they go the better.
Ten-meter comfortable pace, 10-meter fast pace and 15-meter fast pace
Individuals walk either at a pace they feel comfortable for 10 meters (10-meter comfortable pace test), or at a fast pace where they push themselves to walk as fast as possible for either 10 or 15 meters (10-meter and 15-meter fast pace test). All tests are performed on a fl at course without obstacles and the distance is marked. Shorter times recorded during the program with each test indicate improvement.
FORMAL METABOLIC TESTING
If any metabolic testing is required, it’s recommended to be done on a cycle ergometer or arm crank ergometer rather than a treadmill to limit risk of falling. Another option is to have a treadmill harness for any treadmill testing. An additional consideration to keep in mind is the use of a breathing mask rather than a mouthpiece for metabolic gas collection, as those with PD have difficulty maintaining the seal on a mouthpiece.
TYPES OF EXERCISE AND PARKINSON’S DISEASE
People with PD show improvements in their physical performance specific to the type of exercise prescription and how far their PD has progressed. Resistance training improves strength; higher intensity aerobic training improves walking speed; low intensity or endurance training improves gait.
Nearly all types of exercise have the added benefit of improving brain function. Aerobic, resistance, dance and T’ai Chi boost cognitive function—that includes memory, language, complex visuospatial processing and executive function (PD individuals use this function when planning, organizing, strategizing, paying attention to and remembering details, and managing time and space).
SUGGESTED EXERCISE PRESCRIPTION
Aerobic: Start at 40 to 60% maximal heart rate reserve for 15 minutes and every two weeks add 5 minutes and 0.2 km/hr (0.1 mph) and 1% incline until client gets to 70 or 80% maximal heart rate reserve for 30 minutes. Each week there should be three aerobic sessions between 30 to 60 minutes per session. Alternatives to treadmill walking are stationary bicycles and walking in a waist- to chest-deep swimming pool. Walking patterns are preferred since it challenges balance and is specific to gait dysfunction.
Light Aerobic: Walking up to individual capability; four to six sessions per day, 20 to 30 minutes duration. An alternative is walking in a waist- to chest-deep swimming pool. Walking patterns are preferred since they challenge balance and are specifi c to gait dysfunction.
Strength: Light weights, three sessions per week, one to two sets of 8 to 12 repetitions using closed kinetic chain activities and the major muscle groups (for example dead lift s, dips, planks, pull-ups, push-ups and squats). Progression should be encouraged, but start with the activities having the least balance requirement.
Flexibility and Balance: One to three sessions per week. T’ai Chi and dancing have been shown to increase balance in individuals with PD. The recent surge in Zumba movement classes offers some advantages, as published accounts show this type of activity offers benefits to PD suffers.
BARRIERS TO EXERCISE
While care needs to be taken to minimize risk of falling and monitoring body temperature, heart rate and blood pressure, many individuals with early and moderate levels of PD have perceived barriers to exercise that need to be overcome. Such barriers include fear of falling, lack of time and low outcome expectations. Fear of falling and prevention can be addressed with proper exercise prescription (proper progression, use of cycle ergometers and harnesses on treadmills). Perceived lack of time and low confidence in the ability of exercise to work for them is not unique to PD clients and can be overcome with adequate encouragement and confidence-building approaches. AF
YUSUF (J.P.) SALEEBY, MD, is a contributing writer for American Fitness magazine. He practices preventive integrative medicine in Murrells Inlet, S.C. Dr. Saleeby is regional director of a direct access testing site that offers analysis of inflammatory biomarkers. He can be reached at www.PriorityHealthSC.com or by e-mail at email@example.com.