Parkinson’s Disease is a progressive neurodegenerative disease that affects dopaminergic neurons in the substantia nigra of the brain. While the disease remains diverse in its symptoms, it primarily affects motor function. These symptoms (i.e. hand tremors, slowed movement, impaired posture and balance, etc.) begin gradually and worsen over time. While motor symptoms are the most common and prevalent symptom of Parkinson’s Disease, there are also many non-motor symptoms associated with the disease. The non-motor symptoms of the disease often occur before the onset of the motor symptoms and are carried out throughout the entire course of the disease (Bago et al). Parkinson’s Disease itself is not fatal, but complications of the disease are serious. Although there is no cure, various treatment options – such as medications and surgery – are available.
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The main cause of Parkinson’s Disease is the loss of nigrostriatal dopaminergic neurons. By activating the nigrostriatal projection, it causes the release of dopamine in the corpus striatum. This increases the responsiveness of the direct pathway to the corticostriatal input, while the responsiveness of the indirect pathway is decreased (). Normally, dopaminergic effects decrease the inhibitory outflow of the basal ganglia and increase upper motor neuron excitability. However, the inhibitory outflow of the basal ganglia is abnormally high and the timely thalamic activation of upper motor neurons in the motor cortex is less probable when the dopaminergic cells of the pars compacta are destroyed (). A failure of the disinhibition that is normally mediated by the basal ganglia, is the cause of many symptoms of Parkinson’s Disease. The rate of discharge of the inhibitory cells in the substantia nigra pars reticulata is increased with the disruption of the same circuits. As a result, there is an increase in tonic inhibition. This reduces upper motor neuron excitability in the superior colliculus which reduces the frequency and amplitude of saccades (Neuro Book).
The substantia nigra is a basal ganglia structure that consists of bilaterally symmetrical nuclei within the midbrain. It houses clusters of neurons that produce the neurotransmitter dopamine. Dopamine affects brain processes that control movement, emotional response, and the ability to experience pleasure and pain (Anatomy Book). A deficiency of this neurotransmitter prevents brain cells from performing their usual inhibitory functions within the cerebral nuclei (Anatomy Book).
Parkinson’s Disease increases in prevalence between the ages of 55 and 85 (Tonya et al). and most often occurs randomly – as it cannot be attributed to a specific genetic or environmental cause. Few people that are affected by the disease (between 5-10%) have a familial form with either an autosomal dominant or autosomal recessive pattern of inheritance (Tonya et al). The familial forms are characterized by an age of onset before 40 years old and get progressively worse over time. By the time symptoms of Parkinson’s Disease develop, 80-90% of the cells responsible for producing dopamine have been lost (Book).
Non-motor symptoms are more difficult to assess than the motor symptoms of Parkinson’s Disease and, as a result, are often left untreated. Some non-motor symptoms – such as autonomic dysfunction, REM sleep disorders, mood disorders, and olfactory dysfunction – can occur years before being diagnosed with the disease (Honglei et al). These non-motor symptoms have been identified as the cause of disability and deterioration in quality of life. Recognizing the non-motor symptoms of Parkinson’s Disease is important because these symptoms cause significant morbidity in the people affected by this disease.
Autonomic dysfunction of Parkinson’s Disease is the most common non-motor symptom of the disease and occurs in every stage (Sung et al). It consists of cardiovascular, gastrointestinal, and genitourinary dysfunction along with orthostatic hypotension. With cardiovascular dysfunction, cardiac sympathetic denervation occurs and contributes to orthostatic lightheadedness and hypotension, shortness of breath, and fatigue (Sung et al). Orthostatic hypotension results in cerebral hypoperfusion which impairs cognition (Sung et al). This can also lead to loss of consciousness and falls if severe enough. Gastrointestinal dysfunction consists of constipation, bowel incontinence, and incomplete bowel evacuation (Sung et al). Another gastrointestinal dysfunction that is caused by an increase in saliva production and decrease of involuntary swallowing is excessive drooling. Genitourinary dysfunction includes urinary urgency, frequency, and incontinence (Sung et al). It also includes sexual dysfunction, such as a decrease in drive and orgasm. In men, this manifests primarily as erectile dysfunction.
Cognitive dysfunction of Parkinson’s Disease includes slowed thinking and impairment of planning and goal-oriented behaviors (Sung et al). Once these symptoms reach a degree that they impair the day-to-day activities of living, they are classified as Parkinson’s Disease dementia. This symptom does not occur until after the onset of the motor symptoms involved with Parkinson’s (Sung et al).
REM sleep disorders associated with Parkinson’s Disease consist of restless leg syndrome, insomnia, periodic limb movements, and excessive daytime sleepiness (Sung et al). In more mild forms, these problems may be restricted to disruptions of nighttime sleep. REM sleep disorders proceed the motor symptoms of the disease and can be used as an indicator for the development of the Parkinson’s. Early recognition of this behavior is important for the onset of the disease. Sleep disorders associated with Parkinson’s Disease are characterized by recurrent dream enactment behavior, but without atonia on a polysomnography (Sung et al).
Mood disorders are another non-motor symptom of Parkinson’s Disease. This primarily includes depression and anxiety, but other disorders – such as psychosis and apathy – can occur. Depression in Parkinson’s is thought to be related more to primary neuropathology that is selective to the disease state, rather than a secondary reaction to motor deficits because it shows higher dysphoria and irritability, but less guilt and a lower incidence of suicide (Sung et al). Anxiety disorders of Parkinson’s Disease can include generalized anxiety disorder, agoraphobia, panic disorder, and social phobia (Sung et al).
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Some non-motor symptoms may not be the direct result of Parkinson’s Disease itself but may occur as a result of medical treatment by means of drugs. The non-motor symptoms of Parkinson’s vary between periods of “on” and “off” (Buck et al). “On” periods are characterized by the use of medication which minimize the symptoms, while “off” periods are when the symptoms return. These are known as fluctuating symptoms. As Parkinson’s Disease progresses, the non-motor symptoms become worse for patients with fluctuating symptoms (Buck et al). Impulse control disorders – such as compulsive shopping, eating, or gambling – occur more frequently in people with Parkinson’s Disease. These symptoms are important to recognize because of their known link to treatment, especially dopamine agonists (Sung et al). Another result of dopamine-replacement therapy are vivid dreams and frank psychosis. Most commonly, hallucinations, delusions, and illusions occur as psychotic symptoms (Sung et al). Hallucinations are usually nonthreatening and often include seeing people or small animals.
While the exact pathophysiology of the non-motor symptoms of Parkinson’s Disease is unknown, it is insufficient to say that these symptoms are caused purely by a dopamine deficiency beginning in the substantia nigra. The pathology of the disease reflects abnormalities in multiple neurotransmitters – from the cortex to the brainstem, and to the outside of the central nervous system (Sung et al). Parkinson’s Disease has been linked to the depigmentation of the midbrain substantia nigra, with surviving neurons in this nucleus containing Lewy bodies. These cytoplasmic inclusions are known for providing dopamine to the striatum (Sung et al).
Stage One of Parkinson’s Disease is characterized by degeneration in the caudal brainstem or olfactory bulbs. This degeneration is clinically apparent as the non-motor symptoms of olfactory loss that has been implicated in the preclinical stage of Parkinson’s (Sung et al). Stage Two of the disease involves the progression of neurodegeneration to the lower brainstem. This area is where non-dopamine nuclei are found. Noradrenaline producing cells in the locus coeruleus of the dorsal pons and the reticular formation of the medulla oblongata have been shown to be degenerated in patients with Parkinson’s Disease (Sung et al). These nuclei are implicated in the pathogenesis of the non-motor symptoms of autonomic dysfunction and are important in central autonomic control (Sung et al). Raphe nuclei that produce serotonin are also degenerated at this stage. As a result, the degeneration of the noradrenaline and serotonin systems are the cause of the mood disorder symptoms of Parkinson’s Disease (Sung et al).
Stages Three and Four of the disease are a progression of degeneration to the midbrain, especially the substantia nigra, where loss of dopamine cells has been linked to the motor symptoms of Parkinson’s (Sung et al). However, dopamine loss also influences non-motor symptoms to some extent as well. Dopamine plays a role in modulating the sleep-wake cycle and controls limb movement and REM sleep atonia in sleep disorders of patients with Parkinson’s. Although dopamine and non-dopamine producing nuclei influence the non-motor symptoms of Parkinson’s Disease, these nuclei have complex interconnections and are linked to higher cortical regulation (Sung et al). In the final stages of Parkinson’s Disease (Stages Five and Six) there is progression to the limbic structures and cortex. The presence of Lewy bodies is a primary cause of the cognitive dysfunction associated with the disease. Decreased activity of choline acetyltransferase – the synthetic enzyme responsible for acetylcholine production – also contributes to cognitive dysfunction (Sung et al). Mood disorders and psychosis are also a result of the spread to the limbic system.
The pathology of Parkinson’s Disease is far more extensive than the nigrostriatal dopamine pathways. The non-motor symptoms of the disease occur as a result of underlying Lewy pathogenesis at olfactory bulb, enteric nerves, and the lower brainstem before invading the substantia nigra (Honglei et al). The symptoms of the disease are the more commonly known and seen motor symptoms, but many non-motor symptoms occur as well that are not always seen and are often ignored. Not only do non-motor symptoms affect the persons quality of life, but they decrease life expectancy and prolong the duration of hospitalization. The severity of non-motor symptoms is directly associated with the severity and duration of the disease (Liu et al). These non-motor symptoms greatly impact the quality of life for the people affected by the disease. Early recognition of these symptoms can help with the diagnosis and treatment of Parkinson’s Disease and may, one day, help to prevent the disease in at-risk patients (Adler et al).
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