PARKINSON’S DISEASE

Parkinson’s Disease, Linda Ronstadt.

Posted on

linda-ronstadt-600

Linda Ronstadt, Michael J. Fox

Soften ‘Cruel’ Hand of Parkinson’s Disease

That Linda Ronstadt would lose her powerful voice after a four-decade singing career is the ironic curse of Parkinson’s disease. The neurological degenerative condition affects more than 1 million Americans, robbing them of speech, mobility and their cognitive abilities.

“I am old enough to remember the beautiful vocalist and that is exactly the cruelty of what is taken away,” said Dr. James Bennett, director of the Parkinson’s Disease and Movement Disorders Center at Virginia Commonwealth University.

“Typically, people with Parkinson’s develop a softening of their voice, a loss of volume and even some slurring of their words,” he said.

In a 1977 Time magazine referred to Ronstadt as the queen of “torchy rock.”

The 67-year-old Grammy-winning singer revealed this week that she struggled with symptoms of the disease for nearly eight years before getting her diagnosis just months ago.

Ronstadt, half-German, half-Mexican, covered pop and folk with both sexiness and soul in the heyday of her career in the 1970s and ’80s. Perhaps her biggest claims to fame were relationships with both California Gov. Jerry Brown and Star Wars director George Lucas.

“I can’t sing a note,” she told AARP in a piece to be published next week. “I knew it was mechanical. I knew it had to do with the muscles, but I thought it might have also had something to do with the tick disease that I had. And it didn’t occur to me to go to a neurologist.”

See full text of AARP interview here.

Her celebrity status, as well as that of Michael J. Fox, who in 1991 was diagnosed with early-onset Parkinson’s at the age of 30, shines a spotlight on a disease that is still poorly understood and where little progress has been made beyond treating for symptoms. There is no cure and the prognosis for decline varies individually.

“I personally know many people with Parkinson’s who have great humor about their trials and tribulations in life.” – Joyce Oberdorf, National Parkinson Foundation

Today, at 52, Fox is starring in a new television series that aired for the first time this week and makes fun of his disease. He stars as Mike Henry, a New York news anchor who quits after a Parkinson’s diagnosis but goes back to work.

“I have challenges that come with Parkinson’s but my experience is to deal with things through humor,” he told People magazine. 

Linda Ronstadt acknowledged she struggled for years with symptoms.

Fox has said that his first symptom was a shaking pinky finger. Ronstadt said her hands shook, but she thought it was the result of shoulder surgery. Today, she walks with the aid of poles on uneven ground and uses a wheelchair when she travels.

An estimated 50,000 to 60,000 new cases of Parkinson’s disease are diagnosed each year in the United States, according to the Miami-based National Parkinson Foundation. The average age for onset is 62, but about 10 percent of all patients, like Fox, are under 40.

Man with early-onset Parkinson’s disease helped by deep brain stimulation.

Some have lived 20 years or more with the disease before getting a diagnosis.

By the time patients discover the classic shake, which happens when the finger or hand is at rest, the disease has progressed “significantly,” according to the foundation’s CEO, Joyce Oberdorf.

“Incidence increases as people age,” she said. “The brain is more vulnerable.”

The main symptom of Parkinson’s disease is a deficiency in dopamine, the “feel-good” chemical in the brain that affects mood and movement.

Dopamine relays messages between the substantia nigra and other parts of the brain to control coordinated muscle movement. When approximately 60 to 80 percent of the dopamine-producing cells are damaged, the motor symptoms of Parkinson’s disease appear. This process of impairment of brain cells is called neurodegeneration.

Some theories are that the earliest signs of the disease start in the olfactory bulb, affecting the sense of smell.

“The first signs can be very subtle,” said Oberdorf. “You might notice things like your handwriting is dramatically smaller, or notice a lack of smell or you are not sleeping as well at night. Or you feel stiff or rigid.”

Most often, a slight tremor in the hand or other body part, “shaking without any movement … all by itself,” sends a patient to the doctor, she said. “When we see the tremor, that is the tipping point.”

The disease can be highly variable. Those with tremor see a slower progression of the disease than those with rigidity, which is accompanied by more cognitive problems.

The voice is affected because it is controlled with muscular tissue. Patients often have trouble swallowing and breathing, as well. Most often those with Parkinson’s don’t realize their voices are softer, Oberdorf said.

“I am a huge fan of Linda Ronstadt,” she said. “There are voice therapists that help, but you have to keep practicing.”

Kathy Kiefer

Advertisements

MICHAEL J. FOX AND PARKINSON’S DISEASE

Posted on

back-to-the-future-before-after-1

MICHAEL J. FOX AND PARKINSON’S DISEASE

Michael J. Fox is a Canadian-American actor, author, producer, and advocate. With a film and television career spanning from the 1970s.   Fox was diagnosed with Parkinson’s disease in 1991 and disclosed his condition to the public in 1998. Fox semi-retired from acting in 2000 as the symptoms of his disease worsened. He has since become an advocate for research toward finding a cure; he created the Michael J. Fox Foundation, and on March 5, 2010, Sweden’s Karolinska Institutet gave him a honoris causa doctorate for his work in advocating a cure for Parkinson’s disease.   The neurological degenerative condition affects more than 1 million Americans, robbing them of speech, mobility and their cognitive abilities.

Fox started displaying symptoms of early-onset Parkinson’s disease in 1991 while shooting the movie Doc Hollywood, although he was not properly diagnosed until the next year. After his diagnosis, Fox began drinking more heavily than in the past; however, he sought help and stopped drinking altogether. In 1998, he decided to go public with his condition, and since then he has been a strong advocate of Parkinson’s disease research. His foundation, The Michael J Fox Foundation, was created to help advance every promising research path to curing Parkinson’s disease, including embryonic stem cell studies.

Fox manages the symptoms of his Parkinson’s disease with the drug Sinemet, and he also had a thalamotomy in 1998.

His first book, Lucky Man, focused on how, after seven years of denial of the disease, he set up the Michael J Fox Foundation, stopped drinking and began to be an advocate for Parkinson’s disease sufferers.   In Lucky Man, Fox wrote that he did not take his medication prior to his testimony before the Senate Appropriations Subcommittee in 1999;

I had made a deliberate choice to appear before the subcommittee without medication. It seemed to me that this occasion demanded that my testimony about the effects of the disease, and the urgency we as a community were feeling, be seen as well as heard. For people who had never observed me in this kind of shape, the transformation must have been startling

Michael J. Fox, Lucky Man”

In an interview with NPR in April 2002, Fox explained what he does when he becomes symptomatic during an interview;

Well, actually, I’ve been erring on the side of caution—I think “erring” is actually the right word—in that I’ve been medicating perhaps too much, in the sense [that] … the symptoms … people see in some of these interviews that [I] have been on are actually dyskinesia, which is a reaction to the medication. Because if I were purely symptomatic with Parkinson’s symptoms, a lot of times speaking is difficult. There’s a kind of a sluttering of speech and it’s very difficult to sit still, to sit in one place. You know, the symptoms are different, so I’d rather kind of suffer the symptoms of dyskinesia… this kind of weaving and this kind of continuous thing is much preferable, actually, than pure Parkinson’s symptoms. So that’s what I generally do… I haven’t had any, you know, problems with pure Parkinson’s symptoms in any of these interviews, because I’ll tend to just make sure that I have enough Sinemet in my system and, in some cases, too much. But to me, it’s preferable. It’s not representative of what I’m like in my everyday life. I get a lot of people with Parkinson’s coming up to me saying, “You take too much medication.” I say, Well, you sit across from Larry King and see if you want to tempt it.

Interview, April 30, 2002, Fresh Air, NPR

In 2006, Fox starred in a campaign ad for then State Auditor of Missouri Claire McCaskill (D) in her 2006 Senate campaign against incumbent Jim Talent (R), expressing her support for stem research. In the ad, he visibly showed the effects of his Parkinson’s disease;

As you might know, I care deeply about stem cell research. In Missouri, you can elect Claire McCaskill, who shares my hope for cures. Unfortunately, Senator Jim Talent opposes expanding stem cell research. Senator Talent even wanted to criminalize the science that gives us the chance for hope. They say all politics is local, but that’s not always the case. What you do in Missouri matters to millions of Americans, Americans like me.

Michael J. Fox, Campaign Advertisement for Claire McCaskill.

In an ironic twist of fate, the wonderful singer Linda Ronstadt has also been diagnosed with Parkinson’s and as a result no longer     has the ability to sing.    Her celebrity status, as well as that of Michael J. Fox, who in 1991 was diagnosed with early-onset Parkinson’s at the age of 30, shines a spotlight on a disease that is still poorly understood and where little progress has been made beyond treating for symptoms. There is no cure and the prognosis for decline varies individually.

The former “Family Ties” actor explains that his positive outlook on the debilitating disease has a lot to do with his happiness being in “direct proportion” to his acceptance of having Parkinson’s.   “People look at me and have fear and sadness in their eyes, which they think they’re seeing reflected back at them,” he said. “They wouldn’t see what I’m really feeling, which is, ‘I’m OK!’ But people are afraid. … They’ll realize that this is just my life, the stuff I was given to deal with.”

Most often, a slight tremor in the hand or other body part, “shaking without any movement … all by itself,” sends a patient to the doctor. “When we see the tremor that is the tipping point.”

The disease can be highly variable. Those with tremor see a slower progression of the disease than those with rigidity, which is accompanied by more cognitive problems.

The voice is affected because it is controlled with muscular tissue. Patients often have trouble swallowing and breathing, as well. Most often those with Parkinson’s don’t realize their voices are softer.

Kathy Kiefer

 

HOW IS PARKINSON’S DISEASE TREATED

Posted on Updated on

parkinsons-disease

HOW IS PARKINSON’S DISEASE TREATED

Are there treatment options for Parkinson’s?

    Are they cost effective?

Or cost prohibitive?

Currently, there is no cure for Parkinson’s disease. Instead, therapy is directed at treating the symptoms that are most bothersome to an individual with Parkinson’s disease.  For this reason, there is no standard or “best” treatment for Parkinson’s disease that applies to every patient. Treatment approaches include medication and surgical therapy.  Other treatment approaches include general lifestyle modifications (rest and exercise), physical therapy, support groups, occupational therapy and speech therapy. In this section, you will become more familiar with the different types of medications commonly prescribed for PD, other alternative therapies, and surgical treatment options. Recent studies have implicated that a treatment is better than no treatment. In other words, medications and therapies may modify the progression of Parkinson’s disease.

Treatment for Parkinson’s Disease (PD), due to its chronic nature, requires broad-based management including patient and family education, support group services, general wellness maintenance, exercise, and nutrition. At present, there is no cure for PD, but medications or surgery can provide relief from the symptoms.   There are so many forms of therapy (or treatment) and medications for Parkinson’s, that I could make a small handbook from all the material available.   This is but a brief look to some treatments/therapies available and not meant to slight some others.

While many medications treat Parkinson’s, none actually reverse the effects of the disease or cure it. Furthermore, the gold standard treatment varies with the disease state. People with Parkinson’s therefore often must take a variety of medications to manage the disease’s symptoms. Several medications currently in development seek to better address motor fluctuations and non-motor symptoms of PD. However, none are yet on the market with specific approval to treat Parkinson’s.

The main families of drugs useful for treating motor symptoms are Levodopa (L-DOPA), dopamine agonists and MAO-B inhibitors. The most commonly used treatment approach varies depending on the disease stage. Two phases are usually distinguished: an initial phase in which the individual with PD has already developed some disability for which he needs pharmacological treatment, and a second stage in which the patient develops motor complications related to levodopa usage. Treatment in the initial state aims to attain an optimal tradeoff between good management of symptoms and side-effects resulting from enhancement of dopaminergic function. The start of L-DOPA treatment may be delayed by using other medications such as MAO-B inhibitors and dopamine agonists, in the hope of causing the onset of dyskinesia’s to be retarded. In the second stage the aim is to reduce symptoms while controlling fluctuations of the response to medication. Sudden withdrawals from medication, and overuse by some patients, also have to be controlled. When medications are not enough to control symptoms, surgical techniques such as deep brain stimulation can relieve the associated movement disorders.   L-DOPA has been the most widely used treatment for over 30 years. L-DOPA is transformed into dopamine in the dopaminergic neurons by dopa-decarboxylase. Since motor symptoms are produced by a lack of dopamine in the substantia nigra the administration of L-DOPA temporarily diminishes the motor symptomatology.

There are some indications that other drugs may be useful as treatment of motor symptoms in early and late PD, but since quality of evidence on efficacy is reduced they are not first choice treatments. In addition to motor PD is accompanied by an ample range of different symptoms. Different compounds are used to improve some of these problems.   A preliminary study indicates that taking the drug Aricept may help prevent falls in people with Parkinson’s. Donepezil boosts levels of the neurotransmitter acetylcholine, and is currently an approved therapy for the cognitive symptoms of Alzheimer’s disease. In the study, participants taking donepezil experienced falls half as often as those taking a placebo, and those who previously fell the most showed the most improvement.

Treating PD with surgery was once a common practice. But after the discovery of levodopa, surgery was restricted to only a few cases. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. Less than 10% of PD sufferers qualify as suitable candidates for a surgical response. There are three different mechanisms of surgical response for PD: ablative surgery, (the irreversible burning or freezing of brain tissue), stimulation surgery or deep brain stimulation (DBS), and transplantation or restorative surgery.

Neuroablative Lesion surgery (NAS) locates and destroys, by heat, the parts of the brain that are associated with producing Parkinsonian neurological symptoms. The procedures generally involve a thalamotomy and/or pallidotomy. Because it is difficult to accurately measure the amount of tissue to be destroyed, it is not uncommon for tremors to persist through multiple courses of surgery since tissue is irreversibly damaged and removed and it is safer to test smaller areas of tissue to prevent serious complications, such as a stroke or paralysis. This method has been generally replaced by deep brain surgery.

Deep brain stimulation (DBS) is presently the most used method of surgical treatment because it does not destroy brain tissue, it is reversible, and it can be tailored to each individual at their particular stage of disease. DBS employs three hardware components: a neuro-stimulator, also called an implanted pulse generator (IPG), which generates electrical impulses used to modulate neural activity, a lead wire which directs the impulses to a number of metallic electrodes towards the tip of the lead near the stimulation target, and an extension wire that connects the lead to the IPG. The IPG, which is battery-powered and encased in titanium, is traditionally implanted under the collarbone, and is connected by the subcutaneous extension to the lead, which extends from outside the skull under the scalp down into the brain to the target of stimulation. The entire three component system is sometimes referred to as a brain pacemaker, as the system operates on many of the same principles as medical cardiac pacing.

The pre-operative targeting of proper implantation sites can be accomplished via the indirect and direct methods.

Electrophysial functional mapping (EFM), a tool utilized in both methods in order to verify the target nuclei, has come under scrutiny due to its associated risks of hemorrhages, dysarthria or tetanic contractions.   DBS is recommended to PD patients without important neuropsychiatric contraindications who suffer motor fluctuations and tremor badly controlled by medication, or to those who are intolerant to medication.   DBS is effective in suppressing symptoms of PD, especially tremor. A recent clinical study led to recommendations on identifying which Parkinson’s patients are most likely to benefit from DBS.

Muscles and nerves that control the digestive process may be affected by PD, therefore, it is common to experience constipation and gastroparesis (food remaining in the stomach for a longer period of time than normal). A balanced diet is recommended to help improve digestion. Diet should include high-fiber foods and plenty of water. Levodopa and proteins use the same transportation system in the intestine and the blood–brain barrier, competing between them for access. When taken together the consequences of such competition is a reduced effectiveness of the drug. Therefore when levodopa is introduced excessive proteins are discouraged, while in advanced stages additional intake of low-protein products such as bread or pasta is recommended for similar reasons. To minimize interaction with proteins levodopa is recommended to be taken 30 minutes before meals. At the same time, regimens for PD restrict proteins during breakfast and lunch and are usually taken at dinner.

There is partial evidence that speech or mobility problems can improve with rehabilitation although studies are scarce and of low quality. Regular physical exercise and/or therapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. Exercise may also improve constipation. Exercise interventions have been shown to benefit patients with Parkinson’s disease in regards to physical functioning, health-related quality of life, balance and fall risk. In a review of 14 studies examining the effects of exercise on persons with Parkinson’s disease, no adverse events or side-effects occurred following any of the exercise interventions. There are five proposed mechanisms by which exercise enhances neuroplasticity. 1) intensive activity maximizes synaptic plasticity; 2) complex activities promote greater structural adaptation; 3) activities that are rewarding increase dopamine levels and therefore promote learning/relearning; 4) dopaminergic neurons are highly responsive to exercise and inactivity (“use it or lose it”); 5) where exercise is introduced at an early stage of the disease, progression can be slowed. Occupational therapy (OT) aims to promote health and quality of life by helping people with the disease to participate in as many activities of their daily living as possible. There have been few studies on the effectiveness of OT and their quality is poor, although there is some indication that it may improve motor skills and quality of life for the duration of the therapy.

Palliative care is often required in the final stages of the disease, often when dopaminergic treatments have become ineffective. The aim of palliative care is to achieve the maximum quality of life for the person with the disease and those surrounding him or her. Some central issues of palliative are; caring for patients at home while adequate care can be given there; reducing or withdrawing dopaminergic drug intake to reduce drug side effects and complications; preventing pressure ulcers by management of pressure areas of inactive patients; facilitating the patient’s end of life decisions for the patient as well as involved friends and relatives.

Present treatments of Parkinson disease provide satisfactory disease control for most early stages patients. However, present gold standard treatment of Parkinson disease using Levodopa, is associated with motor complications, and does not prevent disease progression. More effective and long term treatment of Parkinson disease are urgently needed to control the progression of the disease. In vivo gene therapy is a new approach for treatment of Parkinson disease. The use of somatic-cell gene transfer to alter gene expression in brain neurochemical systems is a novel alternative conventional treatment.

Gene therapy is currently under investigation. It involves the use of a non-infectious virus to shuttle a gene into a part of the brain. The gene used leads to the production of an enzyme which helps to manage PD symptoms or protects the brain from further damage.

One of the gene therapy based approach involves gene delivery of neurturin and gilial-cell-derived nuerotrophic factor (GDNF) to the putamen in patients with advanced Parkinson’s disease. GDNF protects dopamine neurons in vitro and animal models of parkinsonism; neurturin is a structural and functional analogue of GDNF that protected dopamine neuron in animal model of the disease. Despite the open-label trials have shown benefits of continuous infusion of GDNF, the results were not confirmed in double-blind studies. This may be due to the distribution factor; the trophic factor was not distributed sufficiently throughout the target place.

Investigations on neuro-protection are at the forefront of PD research. Currently, there are no proven neuro-protective agents or treatments available for Parkinson Disease. While still theoretical, neuro-protective therapy is based on the idea that certain neurons that produces dopamine and are susceptible to premature degeneration and cell death can be protected by the introduction of neuro-protective pharmaceuticals. This protection can occur before any symptoms manifest based on genetic risk, and also during early or late-stage PD when other treatments have ceased their impact due to the progression of the disease. Accordingly, neuro-protective therapy seeks to delay the introduction of levodopa.

Kathy Kiefer

WHAT IS PARKINSON’S DISEASE?

Posted on

493x335_parkinsons_disease_overview_slideshow

WHAT IS PARKINSON’S DISEASE?

Is everyone at risk for the development of Parkinson’s?   Who is affected by this neurological disorder? How is it diagnosed?   What are the treatments available?   Is there a cure for Parkinson’s?

I am very well aware of the effects that Parkinson’s has not only the patient, but on the family   as a whole.   My mother was diagnosed with Parkinson’s about 15 years ago, when she had mild tremors which got worse over time.   She became a candidate for Deep Brain Stimulation (DBS) surgery which was successful and controlled the tremors, plus daily medication. Some of the side effects of Parkinson’s that mom dealt with was the worsening of her beautiful handwriting and her speech. There were times it was so difficult to understand what mom was saying, but with patience and understanding you could figure out what she was saying. There are other side effects that have to be dealt with as well. Not every patient with Parkinson’s is eligible for this type of treatment and surgery. It is not easy on the caregiver or the family to see a loved one deteriorate, but it must be dealt with.   Unfortunately, for our family mom passed away a few months ago, but I know that she is more at peace now, and can relax.

Parkinson’s disease (PD) is a neurodegenerative brain disorder that progresses slowly in most people. What this means is that individuals with PD will be living with PD for twenty years or more from the time of diagnosis. While Parkinson’s disease itself is not fatal, the Center for Disease Control rated complications from the disease as the 14th top cause of death in the United States. There is currently no cure for Parkinson’s; however, your doctors will be focused and dedicated to finding treatments that help control the symptoms of PD and have a good quality of life.

Normally, there are brain cells (neurons) in the human brain that produce dopamine. These neurons concentrate in a particular area of the brain, called the substantia nigra. Dopamine is a chemical that relays messages between the substantia nigra and other parts of the brain to control movements of the human body. Dopamine helps humans to have smooth coordinated muscle movements. When approximately 60 to 80% of the dopamine-producing cells are damaged, and do not produce enough dopamine, the motor symptoms of Parkinson’s disease appear. This process of impairment of brain cells is called neurodegeneration.  Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, tremors, rigidity, slowness of movement and difficulty with walking and gait. Later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease, whereas depression is the most common psychiatric symptom. Other symptoms include sensory, sleep and emotional problems. Parkinson’s disease is more common in older people, with most cases occurring after the age of 50.

The main motor symptoms are collectively called parkinsonism, or a “parkinsonian syndrome”. Parkinson’s disease is often defined as a parkinsonian syndrome that is idiopathic (having no known cause), although some atypical cases have a genetic origin. Many risk and protective factors have been investigated: the clearest evidence is for an increased risk of PD in people exposed to certain pesticides and a reduced risk in tobacco smokers. The pathology of the disease is characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons, and from insufficient formation and activity of dopamine produced in certain neurons within parts of the midbrain. Lewy bodies are the pathological hallmark of the idiopathic disorder, and the distribution of the Lewy bodies throughout the Parkinsonian brain varies from one individual to another. The anatomical distribution of the Lewy bodies is often directly related to the expression and degree of the clinical symptoms of each individual. Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used for confirmation.

Modern treatments are effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists. As the disease progresses and dopaminergic neurons continue to be lost, these drugs eventually become ineffective at treating the symptoms and at the same time produce a complication called dyskinesia, marked by involuntary writhing movements. Diet and some forms of rehabilitation have shown some effectiveness at alleviating symptoms. Surgery and deep brain stimulation have been used to reduce motor symptoms as a last resort in severe cases where drugs are ineffective. Research directions include investigations into new animal models of the disease and of the potential usefulness of gene therapy, stem cell transplants and neuro-protective agents. Medications to treat non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, also exist.

The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy in 1817. Several major organizations promote research and improvement of quality of life of those with the disease and their families. Public awareness campaigns include Parkinson’s disease day (April 11th) and the use of a red tulip as the symbol of the disease. People with parkinsonism who have increased the public’s awareness of the condition include actor Michael J. Fox, Olympic cyclist Davis Phinney, and professional boxer Muhammad Ali. Parkinson’s not only affects humans, but other primates as well, which have often been used in researching the disease and testing approaches to its treatment.

The term parkinsonism is used for a motor syndrome whose main symptoms are tremor at rest, stiffness, slowing of movement and postural instability. Parkinsonian syndromes can be divided into four subtypes according to their origin: primary or idiopathic, secondary or acquired, hereditary parkinsonism, and parkionson plus syndromes or multiple system degeneration. Parkinson’s disease is the most common form of parkinsonism and is usually defined as “primary” parkinsonism, meaning parkinsonism with no external identifiable cause. In recent years several genes that are directly related to some cases of Parkinson’s disease have been discovered. As much as this conflicts with the definition of Parkinson’s disease as an idiopathic illness, genetic parkinsonism disorders with a similar clinical course to PD are generally included under the Parkinson’s disease label. The terms “familial Parkinson’s disease” and “sporadic Parkinson’s disease” can be used to differentiate genetic from truly idiopathic forms of the disease.

Usually classified as a movement disorder, PD also gives rise to several non-motor types of symptoms such as sensory deficits, cognitive difficulties or sleep problems. Parkinson plus diseases are primary parkinsonisms which present additional features. They include multiple system atrophy, progressive supra-nuclear palsy, corti-co-basal degeneration and dementia with Lewy bodies.

Postural instability is typical in the late stages of the disease, leading to impaired balance and frequent falls, and secondarily to bone fractures. Instability is often absent in the initial stages, especially in younger people. Up to 40% may experience falls and around 10% may have falls weekly, with number of falls being related to the severity of PD. Other recognized motor signs and symptoms include gait and posture disturbances such as rapid shuffling steps and a forward-flexed posture when walking, speech and swallowing disturbances including voice disorders, mask-like face expressions or small hand writing, although the range of possible motor problems that can appear is large.

Parkinson’s disease in most people is idiopathic (having no specific known cause). However, a small proportion of cases can be attributed to known genetic factors. Other factors have been associated with the risk of developing PD, but no causal relationships have been proven.   A number of environmental factors have been associated with an increased risk of Parkinson’s including: pesticide exposure, head injuries, and living in the country or farming. Rural environments and the drinking of well water may be risks as they are indirect measures of exposure to pesticides.   Implicated agents include insecticides, primarily chlorpyrifos and organochlorides and pesticides, such as rotenone or paraquat, and herbicides, such as Agent Orange.   Heavy meals exposure has been proposed to be a risk factor; however, studies on the issue have been inconclusive.

A physician will diagnose Parkinson’s disease from the medical history and a neurological examination. There is no lab test that will clearly identify the disease, but brain scans are sometimes used to rule out disorders that could give rise to similar symptoms. People may be given levodopa and resulting relief of motor impairment tends to confirm diagnosis. The finding of Lewy bodies in the midbrain on autopsy is usually considered proof that the person had Parkinson’s disease. The progress of the illness over time may reveal it is not Parkinson’s disease, and some authorities recommend that the diagnosis be periodically reviewed

There is some evidence that speech or mobility problems can improve with rehabilitation, although studies are scarce and of low quality. Regular physical exercise with or without physiotherapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. However, when an exercise program is performed under the supervision of a physiotherapist, there are more improvements in motor symptoms, mental and emotional functions, daily living activities, and quality of life compared to a self-supervised exercise program at home. As for gait and addressing the challenges associated with the disease such as hypokinesia (slowness of movement), shuffling and decreased arm swing; physiotherapists have a variety of strategies to improve functional mobility and safety. Areas of interest with respect to gait during rehabilitation programs focus on but are not limited to improving gait speed, base of support, stride length, trunk and arm swing movement. Strategies include utilizing assistive equipment (pole walking and treadmill walking), verbal cueing (manual, visual and auditory), exercises (marching and PNF patterns) and altering environments (surfaces, inputs, open vs. closed). Strengthening exercises have shown improvements in strength and motor function for people with primary muscular weakness and weakness related to inactivity with mild to moderate Parkinson’s disease. However, reports show a significant interaction between strength and the time the medications was taken. Therefore, it is recommended that people with PD should perform exercises 45 minutes to one hour after medications, when they are at their best. Also, due to the forward flexed posture, and respiratory dysfunctions in advanced Parkinson’s disease, deep diaphragmatic breathing exercises are beneficial in improving chest wall mobility and vital capacity.   Other patients prefer less invasive forms of therapy like tai chi.

There is no cure for Parkinson’s disease, but medications, surgery and multidisciplinary management can provide relief from the symptoms.

The U.S. Food and Drug Administration approved deep brain stimulation, which is also used to treat depression, to reduce symptoms in Parkinson’s patients. Electrodes are implanted into the brain and connected to a small device, (similar to a pacemaker) that emits programmed pulses to help control movement.   Deep brain stimulation (DBS) is the most commonly used surgical treatment. It involves the implantation of a medical device called a brain pacemaker, which sends electrical impulses to specific parts of the brain. DBS is recommended for people who have PD with motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems.

Kathy Kiefer