Parkinson’s disease (PD) is a neuro degenerative brain disorder that progresses slowly in most people. Most people’s symptoms take years to develop, and they live for years with the disease. In short, a person’s brain slowly stops producing a neurotransmitter called dopamine. With less and less dopamine, a person has less and less ability to regulate their movements, body and emotions.
Normal and Parkinson affected neuron
Idiopathic parkinson’s: Idiopathic Parkinson’s disease – or Parkinson’s – is the most common type of parkinsonism. Idiopathic means that the cause is unknown. The main symptoms of idiopathic Parkinson’s are tremor, rigidity (stiffness) and slowness of movement. Doctors may diagnose idiopathic Parkinson’s by seeing if there is a response to Parkinson’s medication. If symptoms improve, your specialist may confirm an idiopathic Parkinson’s diagnosis.
Vascular Parkinsonism: Vascular Parkinsonism (also known as arteriosclerotic Parkinsonism) affects people with restricted blood supply to the brain – usually older people who have health issues such as diabetes. Sometimes people who have had a mild stroke may experience this form of Parkinsonism. The common symptoms are walking difficulties, urinary incontinence and memory problems. The symptoms of vascular Parkinsonism are often the same as normal pressure hydrocephalus, which mainly affects the lower half of the body. Some people with vascular Parkinsonism may swing their arms less than those with Parkinson’s.
Drug-induced Parkinsonism: A small number (around 7%) of people diagnosed with Parkinsonism develop symptoms following treatment with particular medication. Neuroleptic drugs (used to treat schizophrenia and other psychotic disorders) which block the action of dopamine are thought to be the biggest cause of drug-induced Parkinsonism. The symptoms of drug-induced Parkinsonism tend to be static. Only in rare cases do they change in the manner that the symptoms of Parkinson’s do. Most people will recover within months, and often within hours or days, of stopping the drug that is the cause.
Parkinson’s is a condition that has been known about since ancient times. It is referred to in the ancient Indian medical system of Ayurveda under the name Kampavata. In Western medical literature it was described by the physician Galen as “shaking palsy” in AD 175. However it was not until 1817 that a detailed medical essay was published on the subject by London doctor James Parkinson
It was in the 1960s that that the chemical differences in the brains of Parkinson’s patients were identified. The low levels of dopamine cause the degeneration of nerve cells in part of the brain called the substantia nigra. It was this discovery that lead to the first effective medicinal treatment of the disease. In the 1960s the drug Levodopa was first administered to treat the symptoms and has since become the “gold standard” in medication.
Prevalence and incidence of AD
Crude prevalence of PD has been reported to vary from 15 (per 100,000 population) in China to 657 in Argentina in door-to-door surveys, and to vary from 100 to 250 in North America and Europe. Prevalence is easily affected by socioeconomic factors and factors that affect survival rate.
Incidence is a better estimate frequency, and it quantifies the number of new subjects with PD occurring in a given time period for a population of individuals at risk. It is relatively unaffected by factors affecting disease survival. During the last 4 decades, the crude annual incidence rates of PD ranged from 1.5 per 100,000 population in China in 1986 to 14.8 in Finland through 1968 to 1970. The variation may partly reflect study design differences, such as diagnostic criteria and methods of case ascertainment.
Although a primary cause for Parkinson’s disease is yet to be identified, a number of risk factors are clearly evident.
Advancing age- Although there is the occasional case of the disease being developed as a young adult, it generally manifests itself in the middle to late years of life. The risk continues to increase the older one gets. Some researchers assume that people with Parkinson’s have neural damage from genetic or environmental factors that get worse as they age.
Sex- Males are more likely to get Parkinson’s than females. Possible reasons for this may be that males have greater exposure to other risk factors such as toxin exposure or head trauma. It has been theorised that oestrogen may have neuro-protective effects. Or, in the case of genetic predisposition, a gene predisposing someone to Parkinson’s may be linked to the X chromosome.
Family history- Having one or more close relatives with the disease increases the likelihood that you will get it, but to a minimal degree. This lends support to the idea that there is a genetic link in developing Parkinson’s.
Declining oestrogen levels- Post menopausal who do not use hormone replacement therapy are at greater risk, as are those who have had hysterectomies.
Agricultural work- Exposure to an environmental toxin such as a pesticide or herbicide puts you at greater risk. Some of these toxins inhibit dopamine production and promote free radical damage. Those involved in farming and are therefore exposed to such toxins have a greater prevalence of Parkinson’s symptoms.
Genetic factors- A Mayo Clinic led international study revealed that the gene alpha-synuclein may play a role in the likelihood of developing the disease. Studies showed that individuals with a more active gene had a 1.5 times greater risk of developing Parkinson’s. These findings support the development of alpha-synuclein suppressing therapies, which may in the long run slow or even halt the disease.
Low levels of B vitamin folate- Researchers discovered that mice with a deficiency of this vitamin developed severe Parkinson’s symptoms, while those with normal levels did not.
Head Trauma- Recent research points to a link between damage to the head, neck, or upper cervical spine and Parkinson’s. A 2007 study of 60 patients showed that all of them showed evidence of trauma induced upper cervical damage. Some patients remembered a specific incident, others did not. In some cases Parkinson’s symptoms took decades to appear.
Parkinson’s disease is a rare and curious phenomenon, affecting approximately 1 in 300 people. Risk factors mentioned above influence its likelihood to only the tiniest of degrees. Most individuals will have one or more of the risk factors above and never experience any of the symptoms. The one risk factor we all possess is aging, which is a condition that is currently incurable! However, more and more is becoming understood as to how and why these various risk factors influence likelihood of Parkinson’s. As knowledge grows, so does the possibility of a cure.
- Primary symptoms include
- Impaired balance,
- And later on a shuffling gait.
- Some secondary symptoms include
- Depression, and
Symptoms of Parkinson’s
A substance called dopamine acts as a messenger between two brain areas – the substantia nigra and the corpus striatum – to produce smooth, controlled movements. Most of the movement-related symptoms of Parkinson’s disease are caused by a lack of dopamine due to the loss of dopamine-producing cells in the substantia nigra. When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired; the greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson’s disease.
Although it is well known that lack of dopamine causes the motor symptoms of Parkinson’s disease, it is not clear why the dopamine-producing brain cells deteriorate. Genetic and pathological studies have revealed that various dysfunctional cellular processes, inflammation, and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson’s disease. The function of these clumps in regards to Parkinson’s disease is not understood. In general, scientists suspect that dopamine loss is due to a combination of genetic and environmental factors.
Treatment and medications
Medications for Parkinson’s disease fall into three categories.
- The first category includes drugs that work directly or indirectly to increase the level of dopamine in the brain. The most common drugs for Parkinson’s disease are dopamine precursors – substances such as levodopa that cross the blood-brain barrier and are then changed into dopamine. Other drugs mimic dopamine or prevent or slow its breakdown.
- The second category of Parkinson’s disease drugs affects other neurotransmitters in the body in order to ease some of the symptoms of the disease. For example, anticholinergic drugs interfere with production or uptake of the neurotransmitter acetylcholine. These drugs help to reduce tremors and muscle stiffness, which can result from having more acetylcholine than dopamine.
- The third category of drugs prescribed for Parkinson’s disease includes medications that help control the non-motor symptoms of the disease, that is, the symptoms that don’t affect movement. For example, people with Parkinson’s disease-related depression may be prescribed antidepressants.
Levodopa: The cornerstone of therapy for Parkinson’s disease is the drug levodopa (Sinemet) (also called L-dopa). Levodopa (from the full name L-3,4-dihydroxyphenylalanine) is a simple chemical found naturally in plants and animals. Levodopa is the generic name used for this chemical when it is formulated for drug use in patients. Nerve cells can use levodopa to make dopamine and replenish the brain’s dwindling supply. People cannot simply take dopamine pills because dopamine does not easily pass through the blood-brain barrier, a lining of cells inside blood vessels that regulates the transport of oxygen, glucose, and other substances into the brain. Usually, patients are given levodopa combined with another substance called carbidopa. When added to levodopa, carbidopa delays the conversion of levodopa into dopamine until it reaches the brain, preventing or diminishing some of the side effects that often accompany levodopa therapy. Carbidopa also reduces the amount of levodopa needed.
Levodopa is very successful at reducing the tremors and other symptoms of Parkinson’s disease during the early stages of the disease. It allows the majority of people with Parkinson’s disease to extend the period of time in which they can lead relatively normal, productive lives.
Fortunately, physicians have other treatment choices for some symptoms and stages of Parkinson’s disease. These therapies include the following:
Dopamine agonists. These drugs, which include bromocriptine, apomorphine, pramipexole, and ropinirole, mimic the role of dopamine in the brain. They can be given alone or in conjunction with levodopa. They may be used in the early stages of the disease, or later on in order to lengthen the duration of response to levodopa in patients who experience wearing off or on-off effects. They are generally less effective than levodopa in controlling rigidity and bradykinesia. Many of the potential side effects are similar to those associated with the use of levodopa, including drowsiness, sudden sleep onset, hallucinations, confusion, dyskinesias, edema (swelling due to excess fluid in body tissues), nightmares, and vomiting. In rare cases, they can cause compulsive behavior, such as an uncontrollable desire to gamble, hypersexuality, or compulsive shopping. Bromocriptine can also cause fibrosis, or a buildup of fibrous tissue, in the heart valves or the chest cavity. Fibrosis usually goes away once the drugs are stopped.
MAO-B inhibitors: These drugs inhibit the enzyme monoamine oxidase B, or MAO-B, which breaks down dopamine in the brain. MAO-B inhibitors cause dopamine to accumulate in surviving nerve cells and reduce the symptoms of Parkinson’s disease. Selegiline, also called deprenyl, is an MAO-B inhibitor that is commonly used to treat Parkinson’s disease. Studies supported by the NINDS have shown that selegiline can delay the need for levodopa therapy by up to a year or more. When selegiline is given with levodopa, it appears to enhance and prolong the response to levodopa and thus may reduce wearing-off fluctuations. Selegiline is usually well-tolerated, although side effects may include nausea, orthostatic hypotension, or insomnia. It should not be taken with the antidepressant fluoxetine (Prozac, Serafem) or the sedative meperidine, because combining selegiline with these drugs can be harmful. An NINDS-sponsored study of selegiline in the late 1980s suggested that it might help to slow the loss of nerve cells in Parkinson’s disease. However, follow-up studies cast doubt on this finding. Another MAO-B inhibitor, rasagiline, (Azilect) was approved by the FDA in May 2006 for use in treating Parkinson’s disease.
Diagnosis and tests
- No specific test exists to diagnose Parkinson’s disease. Your doctor trained in nervous system conditions (neurologist) will diagnose Parkinson’s disease based on your medical history, a review of your signs and symptoms, and a neurological and physical examination.
- Your doctor may order tests, such as blood tests, to rule out other conditions that may be causing your symptoms.
- Imaging tests such as MRI, ultrasound of the brain, SPECT and PET scans may also be used to help rule out other disorders. Imaging tests aren’t particularly helpful for diagnosing Parkinson’s disease.
- In addition to your examination, your doctor may give you carbidopa-levodopa, a Parkinson’s disease medication. You must be given a sufficient dose to show the benefit, as low doses for a day or two aren’t reliable. Significant improvement with this medication will often confirm your diagnosis of Parkinson’s disease.
- Sometimes it takes time to diagnose Parkinson’s disease. Doctors may recommend regular follow-up appointments with neurologists trained in movement disorders to evaluate your condition and symptoms over time and diagnose Parkinson’s disease.
According to Weinstock, preventing PD boils down to the following factors:
Genetics: Having a close relative with PD, does increase the risk of developing the disease. While you can’t change the genes you were born with, epigenetics research is proving that the life you live turns those genes on and off. Weinstock writes “Genetics loads the gun, but the environment pulls the trigger.”
Diet: Eating a healthy diet is a key element in an anti-PD lifestyle. As with the prevention of disease and promoting maximum health, an optimum diet for reducing the risk of Parkinson’s would include lots of greens, vegetables, and fruits, preferably organic, and foods high in protein, vitamins, antioxidants, minerals, and good fats, while being low in carbohydrates, chemicals, and foods causing inflammation.
Exercise: People who engage in moderate to vigorous physical activities have a significantly lower prevalence of PD. Unfortunately, once someone has developed Parkinson’s, there’s a strong likelihood that the benefits of exercise will not be fully realized due to lower levels of neurotransmitters in the body.
Sleep: Sleep is absolutely essential for your brain to work properly because during sleep your brain is busy processing information, consolidating memories, making connections, and clearing out toxins. When asleep, your brain does its housekeeping and not having adequate time to do this could potentially accelerate neurodegenerative diseases including Parkinson’s.
Stress Management: Chronic stress can upset the brain activity contributing to PD. Acute stress causes alterations in the protective function of the blood brain barrier, and long-term stress is toxic to the brain. It’s possible that repeated stress leads to the depletion of dopamine. Learn how you can break the cycle of stress here.
Avoiding Toxins: Exposure to certain toxins may be directly responsible for triggering Parkinson’s. In the book, Weinstock tells of Canadian study done in 2005 in which eleven people’s blood was tested, and an average of 44 chemicals were found present. Every one of us is a walking polluted reservoir of chemicals. From air pollution, bug and weed killers, solvents, metals, PCBs, to smoking, drug use, and radiation, you are immersed in and surrounded by known neurotoxins every day. Avoiding toxins will preserve your overall and brain health.
Managing Medical Problems: Poor general health management can lead to PD later in life. Obesity is linked to altered dopamine levels in the brain and in midlife, triples the risk of developing PD. Insulin resistance, high blood pressure, high triglycerides, low HDL, and inflammation may all contribute to the disease. Manage chronic physical pain, which is bad for your brain. Take care of your teeth and gums. Know the side effects of your medications and their interactions.
Preventing Head Injuries: The damage caused by a head injury may lead to developing PD years later. While it’s well-known that traumatic brain injuries can lead to short-term or permanent problems with memory, balance, and cognition, research is showing that repeated lower impact blows to the head also add up to take a toll. Having a brain injury resulting in the loss of consciousness, amnesia or hospitalization increases the risk of PD. Losing consciousness for five minutes or longer more than doubles a person’s chances, and the risk goes up with each occurrence. Within seconds, a head injury can set in motion a cascade of damaging pathological changes which can include the loss of dopamine producing molecules for months after the injury.