Peer Responses – Male Patient with Parkinson’s Disease

Peer Responses – Male Patient with Parkinson’s Disease

Response 1

Hello,

This is a good discussion that captures all parts of the case study. As Parkinson’s disease is a chronic and progressive disease of the nervous system, it affects the parts of the body controlled by the nervous, negatively affecting their functioning. This leads to the presentation of motor and neurological symptoms. As you have noted, cardinal manifestations of Parkison’s disease include bradykinesia or slowed movement and progressively hesitated movements, muscle stiffness limiting range of motion and pain, and impairment of posture and body balance leading to stooping and increased risk of falling. Notably, most of these manifestations, which are cardinal during the diagnosis of Parkison’s, become notable mostly when major neurological damage has already occurred (Ball et al., 2019). Due to the late diagnosis, it is more likely that Parkinson’s disease will have advanced to chronic cognitive conditions such as memory loss and Parkinson’s disease dementia before interventions for care are implemented, further complicating the condition and the efficacy of the interventions.

The lack of a cure and current challenges in the treatment and management of Parkison’s disease is attributed to insufficient knowledge of reliable and sensitive biomarkers of disease progression (Jankovic & Tan, 2020). However, the knowledge of how regulation mechanisms such as the extrapyramidal system and the pyramidal tract in the management of voluntary and involuntary movements and influence the brain regions that control such movements can help in the treatment of Parkison’s disease. Further, understanding the types of nervous system cells and fibers and their efficacy in signal transmission can improve the efficacy of current management interventions for Parkison’s disease.

References

Ball, N., Teo, W. P., Chandra, S., & Chapman, J. (2019). Parkinson’s disease and the environment. Frontiers in Neurology, 10, 421551. https://doi.org/10.3389/FNEUR.2019.00218/BIBTEX

Jankovic, J., & Tan, E. K. (2020). Parkinson’s disease: Etiopathogenesis and treatment. Journal of Neurology, Neurosurgery & Psychiatry, 91(8), 795–808. https://doi.org/10.1136/JNNP-2019-322338

Response 2

Hello,

This is a great post. You have presented a comprehensive overview of the pathophysiology of migraines and a good comparison of cluster headaches with tension headaches. You have also provided good insights into the distinctions between migraines, tension, and headaches. The overall discussion presented in your post is detailed and informative. However, to help engage in a more meaningful discussion and simplify the information presented, it is important to note that the manifestation of early symptoms in the development of migraine might vary across individuals. However, the early symptoms may occur due to physical changes in neurons within various brain regions, such as the posterior-lateral hypothalamus and the midbrain tegmental area, as you have noted. These physical changes in neurons affect how the nerves in these regions get activated and sensitized. When the nerves within the hypothalamic and brainstem regions become too sensitized and activated, they become too sensitive to sensitive to pain than usual, initiating a migraine (Diamond & Natbony, 2021).

The sensitized hypothalamus during the initiation of the migraine impairs its ability to control daily physiological cycles and homeostasis, leading to accompanying symptoms such as higher urination rates, high appetite and cravings for food, mood changes, stiffness of the neck, and constipation. Migraines are majorly linked to genetic factors. However, there is a substantial interplay between the environment, physical and mental health factors, and lifestyle choices that can contribute to the development of migraines. Although pharmacologic treatments are the best in managing migraines, CBT (Cognitive Behavioral Therapy) can provide long-term management of episodic migraines, including effectively reducing the frequency, intensity, and duration of the migraine by employing self-management approaches, restructuring cognitive processes, and behavioral and lifestyle changes (Amatrudo et al., 2023). Notably, the diagnosis and treatment of headaches may be based on their pathophysiology and underlying factors.

References

Amatrudo, G., Kengetter, J., McCrea, S., & Amatrudo, M. (2023). Cognitive behavioral therapy for the management of episodic migraine. Current Pain and Headache Reports, 27(9), 471–477. https://doi.org/10.1007/S11916-023-01129-Y/METRICS

Diamond, J. A., & Natbony, L. R. (2021). Headache and sleep. Integrative Headache Medicine, 89–132. https://doi.org/10.1007/978-3-030-71513-7_6

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Male Patient with Parkinson’s Disease

Case Study: A 55-year-old male presents after a fall in his backyard.  His primary diagnosis is a 12-year battle with Parkinson’s Disease.

 Bradykinesia

 Bradykinesia is a condition characterized by a slowing down of movement and progressive hesitations or halts during continued movements. It is a major symptom of Parkinson’s disease and, in addition to either tremor or rigidity, is essential for a diagnosis of Parkinson’s disease (Parkinson’s Foundation,2023). Parkinson’s disease can present itself in various ways, resulting in a reduction of involuntary movements such as blinking or arm-swinging while walking. It can also result in challenges when commencing movements, such as rising from a seated position. Furthermore, physical actions may be slower, and facial expressions may appear unusually static or restricted (Parkinson’s Foundation,2023). Bradykinesia typically occurs in the advanced stages of Parkinson’s disease. As per a 2016 review published in Parkinson’s Disease, tremors are more likely to characterize the condition in individuals aged between 20s to 40s, whereas bradykinesia and rigidity are predominantly observed after the age of 60 (McNamara,2023).

Postural Instability in Parkinson’s

Parkinson’s Postural Instability refers to the difficulty in maintaining balance caused by the loss of postural reflexes, including balance reaction, a flexed posture, and trunk rotation. These motor impairments result from dopaminergic neuronal deficits, comorbid white matter disease, and degeneration of the cholinergic system (Palakurthi & Burugupally, 2019).

Pyramidal vs. Extrapyramidal

The EPS (extrapyramidal system) is essential in maintaining posture and regulating involuntary motor functions. Therefore, EPS controls the automatic activities and influences voluntary motility through a tonic function. These regulation mechanisms involve processing centres in multiple brain regions, such as parts of the cerebral cortex, the cerebellum, the thalamus, the reticular substance, and several basal ganglia. Alterations affecting the various circuits play a crucial role in the pathogenesis of extrapyramidal motor disorders. A classic example of injury to the EPS is Parkinson’s disease  (Lee & Muzio,2022).

The pyramidal tract is a significant pathway that transmits signals for voluntary movement in the human body. If the pyramidal tract gets damaged, it can cause serious complications such as spasticity, hyperactive reflexes, weakness, and a Babinski sign where the big toe moves upwards upon stroking the sole of the foot. These symptoms are all indicative of an upper motor neuron lesion (Lohia & McKenzie,2023).

Myelinated and Unmyelinated fibres

 It is an established fact that the transmission speed of myelinated nerve fibres is significantly faster than that of unmyelinated fibres (Samanthi, 2018). Therefore, it is imperative to consider the type of nerve fibres one invests in to ensure optimal neural connectivity.  When a nerve fibre has a myelin sheath surrounding it, it is referred to as a myelinated nerve fibre or axon. This insulation allows for efficient and rapid transmission of nerve impulses. Nerve fibres that lack myelin sheaths are known as unmyelinated nerve fibres. Without this electrically insulating layer, their impulse transmission is slower than myelinated nerve fibres. Unmyelinated nerve fibres also appear grey in colour (Samanthi,2018).

PEER RESPONSE 2:

Pathophysiology of Migraines

What is the pathophysiology of the prodrome brought on by migraines? It is a neurological condition characterized by a throbbing headache on one side, nausea, vomiting, photophobia, and phonophobia. However, the occurrence of prodromal symptoms during the premonitory phase, such as symptoms before migraines, in the posterior-lateral hypothalamus as well as the midbrain tegmental area, periaqueductal gray, dorsal pons, and various cortical areas—the premonitory phase last 15 minutes to 2 days.

Additionally, prodrome syndromes cause the trigeminovascular system (the trigeminal nerve and axonal projection to the intracranial blood vessels of the dura mater) to become sensitized, which results in inflammation markers like the activity of calcitonin gene-related peptide (CGRP) and other neuropeptides that involve neurotransmission in the brainstem and upper spinal cord. Additionally, a migraine attack causes painfully dilated 5-HT1B and 5-HT1D serotonin receptors in the cranial arteries (Dodick, 2018; Do et al., 2023; “Genetics, Pathophysiology, Diagnosis, Treatment, Management, and Prevention of Migraine,” 2021).

Compare and contrast a cluster headache with a tension headache. Tension headaches are characterized by extracranial vasoconstriction, a band-like tightness around the head, and tenderness in the occipital region of the brain. They are caused by muscular contractions in the scalp, forehead, and neck muscles. It might only be mild to moderately severe and is simple to treat with NSAIDs. In addition, tension headaches trigger cluster headaches, which occur in groups or clusters and are linked to the hypothalamus, which produces hormones. Cluster headache attacks are intermittent and typically last one to three hours, and their frequency can range from several times per day. The pain is also very intense, and the remission period can last for months or even years (Dodick, 2018; Do et al., 2023; “Genetics, Pathophysiology, Diagnosis, Treatment, Management, and Prevention of Migraine,” 2021)

Furthermore, treating cluster headaches with high-dose oxygen therapy delivered via a face mask for 15-30 minutes or by having an FNP prescribe a selective serotonin receptor agonist like sumatriptan may help to lessen the pain by causing the blood vessels in the brain to constrict. Prednisone or a medication to relax blood vessels may be prescribed by the FNP to reduce swelling and inflammation (Dodick, 2018; Do et al., 2023; “Genetics, Pathophysiology, Diagnosis, Treatment, Management, and Prevention of Migraine,” 2021)

What are the pathophysiologic distinctions between tension and migraine headaches? The release of vasoactive neuropeptides, such as calcitonin gene-related peptide (CGRP), is what causes migraine headaches. Migraine headaches are the result of them being released from the trigeminal nerve’s fifth cranial nerve. This is in contrast to tension headaches, which are brought on by the trigeminal nerve becoming more sensitive and making the surrounding myofascial tissues more tender to the touch. Mechanoreceptor input is received by nociceptive neurons in the trigeminal nucleus in the interim. Since the central nervous system has become more sensitive, stimuli are more painful, leading to hyperalgesia (Dodick, 2018; Do et al., 2023; “Genetics, Pathophysiology, Diagnosis, Treatment, Management, and Prevention of Migraine,” 2021)