Parkinson’s disease (PD) impacts people in different ways. Not everyone will experience all the symptoms of PD; even if people do, they won’t necessarily experience the symptoms in quite the same order or at the same intensity.
While symptoms and disease progression are unique to each person, knowing the typical stages of Parkinson’s can help you cope with changes as they occur. Some people experience the changes over 20 years or more. Others find the disease progresses more quickly.
It is difficult to accurately predict the progression of Parkinson’s. Following a diagnosis, many people experience a good response to medications, such as levodopa. This optimal timeframe can last many years and varies for everyone.
However, as the disease progresses, people with Parkinson’s often need to work alongside their doctor to adjust levodopa dosages. In this timeframe, they may experience new or worsening movement symptoms and fluctuations, levodopa-induced dyskinesia, swallowing problems, freezing of gait, falls and imbalance.
People with young-onset PD are more prone to levodopa-induced dyskinesia and changes in movement (called motor fluctuations), while those diagnosed later in age may experience more cognitive changes and non-movement symptoms.
Motor fluctuations can become an issue five to 10 years after diagnosis. Postural instability (trouble with balance and falls) typically occurs after about 10 years.
Recently, the Movement Disorder Task Force also recognized three stages in early PD.
The degeneration of the dopamine producing neurons has already begun, but no clinical symptom is evident yet.
Some symptoms are present, but they are insufficient for the clinician to make a diagnosis of PD.
Parkinsonian symptoms have manifested and are clearly recognizable.
Theory of PD Progression: Braak’s Hypothesis
Researchers believe a combination of genetic and environmental factors cause Parkinson’s. In 2003, Heiko Braak, MD, hypothesized that an unknown pathogen (a bacteria, virus or other microorganism that causes disease) in the gut could be the cause of PD.
This was followed by a more extensive hypothesis, stating that PD starts in two places: the neurons of the nasal cavity and the neurons in the gut. This is now known as Braak’s hypothesis. In this theory, the pathogen enters the body via the nose and/or gets swallowed and reaches the gut. The pathogenic products thus come into contact with the olfactory (smell) and/or enteric (gut) neurons, triggering the aggregation of an abnormal protein called α-Synuclein. The aggregated α-Synuclein (called Lewy body) then spreads toward the central nervous system (namely the brain), and eventually arriving in and causing the degeneration of the dopaminergic neurons in the area of the brain called the substantia nigra.
This theory is supported by evidence that non-movement symptoms, such as a loss of sense of smell, sleep disorders and constipation, may appear several years ahead of movement symptoms. For this reason, researchers focus on these non-motor symptoms to detect PD as early as possible and to look for ways to stop its progression.
Page reviewed by Dr. Jun Yu, Movement Disorders Fellow at the University of Florida, a Parkinson’s Foundation Center of Excellence.
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