Relief Parkinson’s


Descriptions of Parkinson’s disease date back as far as 5000 BC. Around that time, an ancient Indian civilization called the disorder Kampavata and treated it with the seeds of a plant containing therapeutic levels of what is today known as levodopa. Parkinson’s disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in detail as “shaking palsy.”

Parkinson’s disease (PD) is a chronic, progressive neurodegenerative motor system disorders characterized by both motor and nonmotor features, which are the result of the loss of dopamine-producing brain cells. Parkinson’s is a progressive disease, which means that in most cases it will continue to gradually get worse. Many people who develop Parkinson’s will require nursing care. There is no cure for the disease and its exact cause is not known, but there are effective treatments that can relieve the symptoms.

Parkinson’s is the second most common age-related neurodegenerative disorder after Alzheimer’s disease, an estimated 10 million people worldwide have PD, with over 1 million people in US. The incidence of PD in the U.S. is approximately 20 cases per 100,000 people per year (60,000 per year), with the mean age of onset close to 60 years. The prevalence of PD ranges from 41 people per 100,000 in the fourth decade of life to more than 1,900 people per 100,000 among those 80 and older. Men are 1 1/2 times more likely to have Parkinson’s than women.

Idiopathic Parkinson’s (IDP)

Vascular Parkinsonism

Drug-Induced Parkinsonism

Drugs to avoid in Parkonism

These are some (but not all) of the drugs to avoid in Parkinson’s:

Multiple System Atrophy (MSA)

Progressive Supranuclear Palsy (PSP)

Progressive supranuclear palsy affects eye movement, balance, mobility, speech and swallowing. It is sometimes called Steele-Richardson-Olszewski syndrome.

Normal Pressure Hydrocephalus

Stages of Parkinson’s Disease

Stage 1

Stage 2

Stage 3

Stage 4

Stage 5

Signs and Symptoms

Risk Factors Associated With Parkinson’s Disease


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.

Mutations in the -synuclein gene (SNCA) in the Contursi kindred implicated this gene in Parkinson’s disease (PD). Subsequently, -synuclein was identified as the major component of Lewy bodies (cytoplasmic proteinaceous inclusions) in surviving dopaminergic neurons is the pathological hallmark of PD, and of glial cell cytoplasmic inclusions.

Genetic predisposing factors in combination with environmental factors are thought to be responsible for the cellular changes leading to progressive neuronal degeneration in which mitochondrial dysfunction, oxidative mechanisms and failure of the protein degradation machinery at the cellular level are probably involved. So far, five genes have been identified that are definitively associated with Parkinson’s disease.

  1. SNCA (synuclein, alpha non A4 component of amyloid precursor): SNCA makes the protein alpha-synuclein. In brain cells of individuals with Parkinson’s disease, this protein aggregates in clumps called Lewy bodies. Mutations in the SNCA gene are found in early-onset Parkinson’s disease.
  2. PARK2 (Parkinson’s disease autosomal recessive, juvenile 2): The PARK2 gene makes the protein parkin. Mutations of the PARK2 gene are mostly found in individuals with juvenile Parkinson’s disease. Parkin normally helps cells break down and recycle proteins.
  3. PARK7 (Parkinson’s disease autosomal recessive, early onset 7): PARK7 mutations are found in early-onset Parkinson’s disease. The PARK7 gene makes the DJ-1 protein, which may protect cells from oxidative stress.
  4. PINK1 (PTEN-induced putative kinase 1): Mutations of this gene are found in early-onset Parkinson’s disease. The exact function of the protein made by PINK1 is not known, but it may protect structures within the cell called mitochondria from stress.
  5. LRRK2 (leucine-rich repeat kinase 2): LRRK2 makes the protein dardarin. Mutations in the LRRK2 gene have been linked to late-onset Parkinson’s disease.

Several other chromosome regions and the genes GBA (glucosidase beta acid), SNCAIP (synuclein alpha interacting protein), and UCHL1 (ubiquitin carboxyl-terminal esterase L1) may also be linked to Parkinson’s disease.

Diagnosis of Parkinson’s Disease

Bradykinesia and at least one of the following:

Exclusion Criteria for PD

History of the following:

Features that Support a Diagnosis of PD

Three or more required for diagnosis of definite PD:

Treatment for Parkinson’s Disease

At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms.  Usually, affected individuals are given levodopa combined with carbidopa.  Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain.  Nerve cells can use levodopa to make dopamine and replenish the brain’s dwindling supply.  Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all.  Anticholinergics may help control tremor and rigidity.  Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine.  An antiviral drug, amantadine, also appears to reduce symptoms.  In May 2006, the FDA approved rasagiline to be used along with levodopa for patients with advanced PD or as a single-drug treatment for early PD.  In March 2017, the FDA approved safinamide tablets as an add-on treatment for individuals with PD how are currently taking levodopa/carbisopa and experiencing “off” episodes (when the person’s medicatins are not working well, causing an increase in PD symptoms).

In some cases, surgery may be appropriate if the disease doesn’t respond to drugs. A therapy called deep brain stimulation (DBS) has now been approved by the U.S. Food and Drug Administration. In DBS, electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for levodopa and related drugs, which in turn decreases the involuntary movements called dyskinesias that are a common side effect of levodopa. It also helps to alleviate fluctuations of symptoms and to reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device in order to work correctly.

Even if you experience symptoms common among people with PD, they may in fact be brought on by a different condition. Consult a doctor if you notice a change in your body with no obvious cause. While visiting the doctor, try to be as specific as possible when describing your symptoms. You may be referred to a movement disorders specialist; a neurologist with particular expertise in PD and other movement disorders.