Parkinsons Disease Treatment

Diagnosis of Parkinson’s Disease

Patients with suspected Parkinson’s disease are generally referred to a consultant neurologist who specializes in disorders of the central nervous system. The neurologist will first obtain a detailed history of the symptoms, including information on any close relatives who may also have symptoms of the disease or who have been diagnosed with PD. The consultant will then perform a routine clinical examination to establish the extent of the symptoms.

Methods of Diagnosis for Parkinson’s Disease

A neurologist will use a number of tools during the diagnostic process.

SPECT and PET Brain-Imaging: Tools for quantifying the level of dopamine neuron degeneration in the mid-brain may include specialized neuro-imaging brain scans called SPECT (single positron emission computed tomography) or PET (positron emission tomography) scans. Using a metabolically active tracer, PET scans produce three-dimensional images of abnormalities in the brain, such as dopamine deficiency. SPECT scans are less expensive and more routinely available for the diagnosis of Parkinson’s disease than PET scans.

The DaTSCAN: A new generation brain scan DaTSCAN (also called I123-FP-CIT), first launched in Europe in 2002, has been shown to diagnose PD with greater accuracy (up to 98 percent accuracy) compared with conventional scanning methods in patients exhibiting no PD symptoms other than tremors. According to a study outlined at the December 2002 Annual Meeting of the Radiological Society of North America (RSNA), DaTSCAN is particularly effective at distinguishing between Parkinson’s disease and a less severe type of neurological disorder called essential tremor. In the words of David J. Tuite, MD: “Until the advent of DaTSCAN, the diagnosis of Parkinson’s disease was primarily based upon clinical assessment…which has only an eighty percent accuracy rate.” Although currently not widely available, DaTSCAN is an important advancement in the area of PD diagnosis.

Genetic Testing: Genetic testing is another method used for the diagnosis and prognosis of Parkinson’s disease. However, the complex nature of the genetic mutations and various combinations of mutations, involved in the progression of PD, can be difficult to identify using currently available screening techniques.

Recent developments in the field of genetic testing for Parkinson’s disease (The Lancet, January 2005) revealed that three separate studies in the US, UK and Netherlands had succeeded in isolating the LRRK2 gene mutation associated with approximately five percent of inherited cases of PD. According to Dr Tatiana Foroud, Associate Professor at Indiana University School of Medicine, Indianapolis, these findings indicate that the LRRK2 gene mutation is “the most common cause of Parkinson’s disease identified to date.”

Parkinson’s Disease Treatments, Medications and Therapies

Currently no treatments or therapies can cure, retard or reverse Parkinson’s disease. Existing treatments, drugs and therapies all focus on alleviating the debilitating symptoms of PD. Surgery or alternative therapies are usually only recommended as a last resort for those patients who fail to respond to the standard treatments for Parkinson’s disease.

Drug Therapy: Levodopa, a dopamine precursor, is the most widely used drug treatment for managing the symptoms of Parkinson’s disease. L-DOPA is administered orally and is converted to dopamine in the mid-brain. Other drugs for PD include Ropinirole, Pramipexole and Pergolide, all of which help reduce the common symptoms of tremor, muscle rigidity and lack of co-ordination.

In May 2006 the FDA approved Azilect® (rasagiline), a monoamine oxidase type-B (MAO-B) inhibitor, as a single drug therapy for early Parkinson’s disease and for use in combination with levodopa in more advanced disease. Compared with participants taking a placebo, patients with early Parkinson’s disease taking Azilect experienced a slower decline of mental and motor skills. Patients with advanced Parkinson’s taking Azilect and levodopa experienced fewer hours of reduced function and mobility each day.

To prevent a hypertensive crisis, people taking Azilect need to avoid foods and beverages containing tyramine and medicines and supplements containing amines. Azilect, levodopa and other Parkinson’s drugs may be associated with dyskinesia, hallucination and lowered blood pressure.

In June 2006 the FDA approved the use of the Alzheimer’s drug Exelon® (rivastigmine tartrate) for mild to moderate Parkinson’s dementia. Exelon is currently the only drug that specifically treats Parkinson’s dementia, which affects an estimated 0.2 to 0.5 percent of people over 65 years of age. While Exelon does not have the same side effects as other Parkinson’s drugs, it is associated with nausea, vomiting, upset stomach, loss of appetite and loss of strength.

What is Tardive Dyskinesia?

The word “tardive” derives from the Latin word meaning “late onset” and dyskinesia from the Greek word meaning “abnormality in performing involuntary muscle movements.” Common symptoms of tardive dyskinesia include repetitive involuntary movements such as chewing, grimacing, tongue pulling, lip smacking, humming, grunting, body rocking and feet stamping.

Tardive dyskinesia may result from the long-term use of the drug Levodopa and chronic exposure to similar drugs that block the dopamine receptors in the brain.

The Role of Exercise: Physiotherapy and physical activity involving exercises for strengthening the muscles are generally recommended as an adjunct to drug therapy in Parkinson’s disease treatment.

Deep Brain Stimulation (DBS): DBS therapy has been shown to reduce tremors, decrease involuntary movements (dyskinesias) and improve general coordination in chronic sufferers of Parkinson’s disease. DBS treatment may also help patients reduce the level of drugs required to manage their symptoms. Deep brain stimulation is FDA approved.

Fetal Tissue Transplantation: The use of fetal stem cell transplantation to treat Parkinson’s disease is not widely available and research is in its infancy. Medical and ethical opinion is strongly divided over the issue of using fetal tissue to stimulate the dopaminergic neurons in patients suffering from PD.

Research and studies into the benefits of fetal stem cell transplantation have produced mixed results. A number of experiments have shown that grafted cells can survive and function effectively in the mid-brain regions of the recipients, while also improving movement initiation and rigidity. Findings from other studies are less optimistic citing side-effects such as tardive dyskinesia in up to fifty percent of PD patients undergoing fetal tissue transplantation.

Resources

Associated Neurologists (2002). Research update: Neuroimaging. Parkinson’s Disease News IV(2), 1.

Freed, C.R., Greene, P.E., Breeze, R.E., Tsai, W-Y., DuMouchel, W., Kao, R., Dillon, S., et al. (2001). Transplantation of embryonic dopamine neurons for severe Parkinson’s disease. New England Journal of Medicine 344(10), 710-719.

Hotton, G.