The likely diagnosis
The likely diagnosis is Parkinson’s disease. The disease is ranked among the most common of the main diseases that affect the motor system and impair movement. It is a chronic, progressive neurological condition with no known cure (McCance & Huether, 2014). The disease results from malfunction of the nervous system, which impairs communication between muscles and the brain.
Multiple clinical factors observed in Parkinson’s disease are present in the case. There are four major clinical signs associated with the disease, namely tremor, rigidity, bradykinesia, and impairment of posture and gait, which are noted in the patient (Dickson, 2012). Tremor in the fingers is the most common and easily noticeable by others. In fact, the resting tremor that is observed in the finger occurs when the patient is resting, but disappears with the movement. While tremor may be noticed in any part of the body, it is usually common in the fingers or thumbs. In addition, impassive flexion and extension of arms cause enhanced resistance that impairs and allows jerky, alternating, and the alleged cogweheeling rigidity in arms. A short gait associated with poor coordination and shuffling is noticed in patients. Difficult movement processes are noticed, and the patient may fall.
Underlying pathologic changes responsible for the clinical presentation
The disease has been associated with the steady neurodegenerative of cells found in different locations, but mainly in the substantia nigra of the brain. The neurodegenerative changes usually target some specific neuron classes found across the neuraxis, such as some sections of the cortex, brain stem, thalamus, and spinal cord (Korczyn & Hassin-Baer, 2015). In addition, the cell loss also affects sympathetic and parasympathetic ganglia. Acetylcholine, serotonin, glutamate, noradrenaline, and hydroxytryptaminc are some of the most affected neuromodulators and neurotransmitters during neuron degeneration. While notable complications are observed, the neuropathology for the disease is similar in all areas affected, showing that a general underlying pathogenic process is responsible. Once these cells are impaired, muscle activities fail due to deficiency of the dopamine, which is the chemical messenger responsible for signal transmission to the brain for coordination. Nerve cells become uncontrollable, leaving individuals affected with the difficulty of controlling or directing their movements.
As mentioned, the disease is progressive. Consequently, it gradually affects other parts of the nervous systems and the brain, leading to a more elaborate disorder in movements. It is also imperative to note that the precise factor responsible for cell loss is not clearly understood, but genetic and environmental factors, aging, and free radicals (unstable muscles) have been linked with the disease.
Some possible molecular mechanisms responsible for the pathologic changes
It is generally acknowledged that Parkinson’s disease, like other cell loss diseases, has a complicated pathogenesis accounting for various factors, each contributing marginally to the disease. Studies of involved neurons and genes observed in the progress of the disease have shown several possible molecular mechanisms responsible for the disease pathologic changes. They include mitochondrial dysfunction and oxidative stress; neuroinflammation and immune mechanisms; altered protein handling (including the ubiquitin–proteasome system); lysosomal dysfunction; and α-synuclein aggregation (Korczyn & Hassin-Baer, 2015).
A recent study focused on transglutaminase activity to show that the activity is engaged in molecular mechanisms responsible for both physiological and pathological processes (Gatta, Cammarota, Iannaccone, & Gentile, 2016), while the molecular mechanisms of viral infection and redox imbalance have also been proposed (Limongi & Baldelli, 2016). However, their progression during cell loss is not clearly understood.
References
Dickson, D. W. (2012). Parkinson’s Disease and Parkinsonism: Neuropathology. Cold Spring Harbor Perspectives in Medicine, 2(8), a009258. Web.
Gatta, N. G., Cammarota, G., Iannaccone, M., & Gentile, V. (2016). Transglutaminase Activity as a Possible Molecular Mechanism in the Etiopathogenesis of Neurodegenerative Diseases. Journal of Biochemistry and Molecular Biology Research, 2(1), 157-165.
Korczyn, A. D., & Hassin-Baer, S. (2015). Can the Disease Course in Parkinson’s Disease be Slowed? BMC Medicine, 13, 295. Web.
Limongi, D., & Baldelli, S. (2016). Redox Imbalance and Viral Infections in Neurodegenerative Diseases. Oxidative Medicine and Cellular Longevity, 2016, 6547248. Web.
McCance, K. L., & Huether, S. E. (2014). Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed.). St. Louis, Missouri: Elsevier.