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Parkinson’s Disease: Neuroanatomy, Pathophysiology, Symptoms and Management
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Neuroanatomy and Pathophysiology of Parkinson’s Disease
Neuroanatomy and Pathophysiology of Parkinson’s Disease
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Neuroanatomy and Pathophysiology of Parkinson’s Disease
Overview
Parkinson’s Disease is a complex neurodegenerative disorder, characterized by bradykinesia, tremors, postural instability and rigidity (Kouli et al., 2018). Pathologically, the disease is characterized by the loss of nigrostriatal dopaminergic innervation and may also involve degeneration of neurons in other areas of the neural network (Kouli et al., 2018). Simply put, Parkinson’s disease is a neurodegenerative disease that occurs when the neurons or the nerve cells that innervate the area controlling movements die or get impaired (NIH, n.d.). The neurons normally, produce a brain chemical, dopamine, which is being produced in lesser amount when the neurons die or degenerate. Thus, lead to problems with body movement, called Parkinson’s disease or Parkinsonism (NIH, n.d.). The hallmark of Parkinson’s Disease is the aggregation of α-synuclein, also called as Lewy bodies or Lewy neurites (Kouli et al., 2018). Besides the loss of dopaminergic neurons, many people suffering from the disease may also lose nerve endings that produce norepinephrine, a chemical messenger of sympathetic nervous system controlling many systemic functions like blood pressure and heart rate. The impaired sympathetic nervous system can lead to many problems like fatigue, decreased mobility of food through the digestive tract causing constipation, irregular blood pressure, to name a few (NIH, n.d.). Although, the exact cause of the disease is not known, a number of genetic and environmental factors like smoking, pesticide exposure, and caffeine consumption have been attributed to the cause of Parkinson’s disease (Kouli et al., 2018).
Parkinson’s Disease is a chronic progressive condition that worsens over time (American Parkinson Disease Association, n.d.). The common symptoms of Parkinson’s Disease include, a triad of symptoms related to motor functions, namely, bradykinesia, rigidity and tremors that can further lead to speech and writing changes. It may also be associated with non-motor symptoms that may precede motor symptoms by over a decade or many years prior to developing full-fledged Parkinsonism (Kouli et al., 2018). A number of evidences reflect that the disease may start in the autonomic nervous system or the olfactory bulb and the pathology may then spread on to the central nervous system, including structures of the lower brain stem that involve substantia nigra (Kouli et al., 2018). Such an affection of the autonomic nervous system may explain the occurrence of non-motor symptoms like constipation, rapid eye movement and hyposmia, before the occurrence of motor symptoms. With progression of the disease, the severity of both motor and non-motor symptoms also worsens (Kouli et al., 2018). The non-motor symptoms include, pain, sleep disorders, fatigue, impaired olfactory ability and psychiatric, and cognitive disturbances (Kouli et al., 2018).
Neuroanatomical and Pathophysiological Changes
There are a number of neuroanatomical and pathophysiological changes associated with Parkinson’s disease. The motor signs appearing in Parkinsonism are a result of degeneration of dopaminergic neurons in basal ganglia (Galvan and Wichmann, 2008). Over the years, a lot many anatomical and physiological changes have been attributed to the loss of dopamine in the basal ganglia, and related areas of thalamus and cortex (Galvan and Wichmann, 2008). The Pathophysiology involved with Parkinsonism is complex and involves many electrophysiological changes associated with the disease, including, altered sensorimotor processing, incidences of burst firing, altered discharge rates, to name a few. It implies that there occurs abnormal neuronal activity in the basal ganglia, that affects the oscillatory activity, sensory responses, synchrony and excitability of the specific areas of the cerebral cortex that plan and execute body movements. They also affect limbic system and sensory functions also (Galvan and Wichmann, 2008). Neuroanatomically, Parkinson’s Disease involves changes in the basal ganglia, thalamus, cerebellum, hypothalamus, limbic system and glial cells that affect the cognition of the patient (Prakash et al., 2016).
Management, Prognosis and Complications
As Parkinson’s Disease is a chronic progressive degenerative disease, currently there is no cure available to treat the same. However, the symptoms can be managed and the quality of life can be maintained (NHS, n.d.).
Management of Parkinson’s Disease
The management of Parkinson’s Disease include Physiotherapy, medication and surgery. Physiotherapy relieves joint pain and muscle stiffness, helps the patients to move and walk and makes the body flexible. Medication in the form of levodopa, dopamine agonists and Beta-inhibitors are advised to patients suffering from Parkinson’s Disease. For some people, surgical intervention like Deep Brain Stimulation could also be advised (NHS, n.d.).
Prognosis and Complications
The prognosis of Parkinson’s Disease is such that the people with the disease have same life expectancy as people not affected with disease. However, in later stages, Parkinson’s Disease patients may stop responding to the drugs and may develop serious complications like pneumonia, choking and falls (NINDS, n.d.). Generally, women tend to be more affected than men and the usual onset of developing Parkinsonism is around 70 years (NINDS, n.d.). It has some genetic predisposition and the exposure to pesticides, especially in rural areas increase the risk of developing Parkinson’s Disease (NINDS, n.d.). The changes occurring in Parkinsonism are progressive and permanent but can be managed by drugs, supplement therapies and medication. There might also occur behavioral changes like Mood disorders, anxiety disorders, hallucination, psychosis, to name a few, as comorbidities of Parkinson’s Disease (Anderson, 2004).
Conclusion
Parkinson’s Disease is a complex, progressive neurodegenerative disease. The condition has associated neuroanatomical and pathophysiological changes that permanently affect the nervous system. The chief cause of Parkinson’s Disease is the depletion or degeneration of dopaminergic neurons in the basal ganglia and other parts of the central nervous system. The disease has some genetic predisposition and the associated risk factors include smoking, exposure to pesticides, to name a few. Women tend to develop Parkinson’s Disease more often than men. It involves both motor and non-motor symptoms. The triad of bradykinesia, rigidity and tremors make it called Parkinsonism. The management of the disease is possible by supplement therapies like physiotherapy, medication and surgery in some patients. As the cognitive functions are also affected by the disease, care of the patient needs to be taken to manage all the motor, non-motor and cognitive symptoms.
References
Anderson, K.E. (2004) Behavioral Disturbances in Parkinson’s Disease. Dialogues Clin
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American Parkinson Disease Association (n.d.) What is Parkinson’s Disease. [online] Available at https://www.apdaparkinson.org/what-is-parkinsons/
Galvan, A. & Wichmann, T. (2008) Pathophysiology of Parkinsonism. Clin Neurophysiol.
doi: 10.1016/j.clinph.2008.03.017. Available at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2467461/#:~:text=The%20earliest%20a nd%20most%20striking,)%2C%20and%20tremor%20at%20rest.
Kouli, A., Torsney, K.M. & Kuan, W.L. (2018) Chapter 1Parkinson’s Disease: Etiology,
Neuropathology, and Pathogenesis. Codon Publications. Available at
https://www.ncbi.nlm.nih.gov/books/NBK536722/
NIH (n.d.). Parkinson’s Disease. National Institute on Aging. Available at
NINDS (n.d.) Parkinson's Disease: Hope Through Research. National Institute of Neurological
Disorders and Stroke. Available at https://www.ninds.nih.gov/disorders/patient-caregiver-education/hope-through-research/parkinsons-disease-hope-through-research#prognosis
NHS (n.d.) Parkinson’s Disease Treatment. National Health Service. Available at
https://www.nhs.uk/conditions/parkinsons-disease/treatment/
Prakash, K.G. et al. (2016) Neuroanatomical changes in Parkinson's disease in relation to
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