Located at the base of the brain, the basal ganglia are a group of nuclei that include the substantia nigra, globus pallidus, and striatum. These nuclei have connections to the cerebral cortex, thalamus, and other areas of the brain. They are responsible for a variety of functions, including voluntary motor control, procedural learning, motivation, and executive function. Dopamine deficiency in the striatum of the basal ganglia leads to changes in many complex circuits, ultimately resulting in excessive inhibition of the motor systems (see Figure 1).
Figure 1: Basal Ganglia Pathways in Parkinson’s Disease
Changes in the basal ganglia pathways as compared to normal. Note . From Western Schools, 2018.
Etiology and risk factors Idiopathic PD involves degeneration of the dopaminergic neurons of the substantia nigra of the basal ganglia and leads to loss of dopamine in the striatum of the basal ganglia. The basal ganglia nuclei are a part of the autonomic motor pathway. In PD, a protein called alpha-synuclein binds to a substance called ubiquitin and accumulates in the neural cells of the substantia nigra, in which it forms inclusions called Lewy bodies . It is not yet known how Lewy bodies lead to dysfunction – only that their presence is correlated with damage that results in diseases such as PD. The cellular damage then disrupts the motor circuits, which results in the cardinal motor signs of PD: resting tremor, bradykinesia, rigidity, and postural reflex impairment – as well as other symptoms such as difficulties with the autonomic system, attention and learning, and loss of the sense of smell (Armstrong & Okun, 2020). The underlying causal mechanism of PD is unknown. Research has not yet fully explained the role of Lewy bodies and their formation in PD and other diseases. In addition, newer studies have revealed that the mechanisms of cell death that contribute to neuronal cell loss in PD include mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory changes (Poewe et al., 2017). The underlying mechanism that Symptoms PD has systemic effects that impact not only the motor systems but also the autonomic nervous system and cognition. Motor deficits have a profound impact on function and quality of life and are a primary focus of treatment by the physical therapist. To provide truly safe and effective care for the individual with PD, however, one must consider the impact of the disease in its entirety, including motor problems, autonomic problems, and cognitive changes associated with idiopathic PD. Cardinal motor signs of Parkinson’s disease As a movement disorder, PD is characterized by early onset of motor problems. Individuals are typically diagnosed based on the appearance of motor symptoms that lead to difficulty in walking, maintaining balance, and performing higher-level functional activities. As PD progresses, autonomic nervous system-related disorders and cognitive issues become more prevalent. The motor problems observed in PD include difficulty in initiating movement and, once initiated, the tendency toward slow, smaller amplitude movements. Diagnosis of PD is based on the presence of at least two of the four cardinal motor signs of PD: (1) bradykinesia, (2) resting tremor, (3) rigidity, and (4) postural instability: 1. Bradykinesia: Is defined as slowness of movement. Other terms typically grouped with bradykinesia include hypokinesia , which refers to small movements, and akinesia , which refers to a lack of movement and is typically associated with the inability to initiate movement, or “freezing.” Hypokinesia is believed to be one of the primary causes of
triggers this cascade of events is still unknown and is the subject of ongoing research. Genetics play a role in 5 to 10% of cases (Poewe et al., 2017). Environmental factors have been shown to be associated with PD, but these associations may be due to reverse causation or have not yet been well defined through prospective studies (Bellou et al., 2016; Dorsey et al., 2018). There is some limited evidence that exposure to pesticides may increase the risk of developing PD and that the use of tobacco and caffeine lower the risk of developing PD (Dorsey et al., 2018). The underlying mechanisms for these findings have yet to be discovered. Although these new findings will likely lead to more effective treatments for PD in the future, symptomatic management with the medication levodopa (Sinemet ® ) remains the mainstay of current treatment. Age is the one factor that most strongly correlates with the onset of PD. The mean age of onset of PD is between the ages of 58 and 62. Five to 10% of cases occur before age 40, but most cases occur between the ages of 50 and 79. Men have a slightly higher prevalence than women, and ethnicity has previously been tied to incidence, but societal rather than biological causes might underlie race-specific findings (Poewe et al., 2017). reduced walking velocity because of the reduction in step length. In addition, slowness and reduction in movement prolong the amount of time needed to complete activities of daily living (ADLs) and may also impair reflex movements such as blinking or postural reflexes. The typical parkinsonian gait pattern is described as a “shuffling gait” in which the individual takes small steps that fail to consistently clear the floor, and the trunk is usually in a flexed posture (see Figure 2). Figure 2. Normal Gait Pattern Compared to Gait Pattern of an Individual with Parkinson’s Disease
The top gait pattern reflects the walking pattern of an older adult with no neurologic diagnosis; notice the longer stride lengths. The bottom gait pattern reflects the walking pattern of an individual with PD. Note. From Western Schools, 2018 .
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