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The Nature and Occurrence of a Migraine

The Nature and Occurrence of a Migraine

Hello CRYSTAL,

Thank you for your post. The post was very educative; aside from explaining the nature and occurrence of migraine for a patient aged 20 years, you also stated common differences between it and cluster and tension headaches. I also think that migraine differs significantly from cluster and tension headaches because a migraine headache is characterized by acute agonizing discomfort or a pulsating feeling on the sides of the head, as well as nausea, vomiting, and increased reactivity to lights and noise. However, when a cluster phase begins, cluster headaches are not usually related to triggers such as meals, hormonal changes, or stress; nonetheless, drinking alcohol might immediately cause a splitting headache (Vollesen et al., 2018).

The main distinction is in the degree and location of pain, with a tension headache being likely moderate and treatable with nonsteroidal anti-inflammatory medicines. Still, a migraine headache is more intense and disruptive. I was also able to comprehend the phases of migraine and their manifestations, which help in differentiating them from other types of headaches. Migraine is known to result in mental changes within a patient, whereas tension headaches result from stress. For the specific case involving the patient, the classification of migraine would help identify the involvement of either the hypothalamic or parasympathetic system for the presented pathologies.

References

Vollesen, A. L., Benemei, S., Cortese, F., Labastida-Ramírez, A., Marchese, F., Pellesi, L., … & Lampl, C. (2018). Migraine and cluster headache–the shared link. The journal of headache and pain, 19(1), 1-15.

Hello KATHRYN,

Great post!! The post was very insightful; besides describing its occurrence and prevalence, you also enhanced my understanding of its pathology and etiology. The primary diagnosis established was Parkinson’s disease, which I would agree with. The condition is usually described as a disorder characterized by brain changes involving motor and non-motor neural functions. The prevalence of Parkinson’s disease is commonly witnessed among patients aged between 55 and 65 years, which indicates that its major risk factor is aging (Abbas et al., 2018).

I also agree with your mention of the two major pathological processes, including the loss of dopamine neurons at a premature age and the over-accumulation of Lewy bodies. The most preferred and successful management of this disorder involves therapies that aim at enhancing the quality of life for patients by eliminating cognitive impairment rather than slowing the progression of the disease. Bradykinesia is manifested by a complete loss of movements, which may present symptoms like loss of expressions and gestures. A lack of equilibrium characterizes postural instability but is hardly noticeable in patients since they are involuntary.

References

Abbas, M. M., Xu, Z., & Tan, L. C. (2018). Epidemiology of Parkinson’s disease—East versus West. Movement disorders clinical practice, 5(1), 14-28.

Length: A minimum of 250 words, not including references
Citations: At least one high-level scholarly reference in APA from within the last five years >2018

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Question 


The Nature and Occurrence of a Migraine

1. CRYSTAL

The patient in this case study is 20 years old and has received treatment for severe migraines for two years. We do not have information on the treatment. This discussion will explore the pathophysiology of migraine headaches and how to differentiate migraine headaches from tension and cluster headaches.
Dlugasch and Story define a migraine headache as a severe headache that includes various systemic clinical manifestations (2021). Migraines typically occur in phases, beginning with a prodromal phase in which the sufferer experiences symptoms that signal that a migraine is likely to occur in one to two days (Dlugasch & Story, 2021). The prodrome of a migraine usually includes fatigue, myalgia, light sensitivity, mood changes, and appetite changes, indicative of hypothalamus involvement (Dodick, 2018). Dodick further presents evidence from imaging studies showing increased connections between the hypothalamus, pain centers, and autonomic function centers in migraine sufferers’ brains compared to unaffected brains (2018). The hypothalamus involvement increases the parasympathetic brain nociceptors, which alter the body’s autonomic functions associated with the prodrome (Dodick, 2018).
Migraine headaches are unique in that their cause lies deep within the brain, where neuronal and glial depolarization create mental changes, activate trigeminal nerves, and upregulate matrix metalloproteinases, creating inflammation, tissue degradation, and pain (Dlugasch & Story, 2021). Many bodily changes can trigger a migraine, including other headaches. Tension headaches can be precursors to migraines and vice versa. Tension headaches are commonly caused by stress and, like migraines, are due to hypersensitive nerves (Dlugasch & Story, 2021). The central nervous system is hypersensitive, creating central and peripheral upset and deficient inhibition of trigeminal nerve descending pain pathways (Dlugasch & Story, 2021). In contrast to migraines, tension headaches are not familial, pain is usually mild, and most sufferers do not need pain treatment (Dlugasch & Story, 2021).
Trigeminal nerve and hypothalamus involvement are also identified in cluster headaches. Clusters are signified by short-term orbital pain that occurs throughout the day (Dlugasch & Story, 2021). Dlugasch and Story present that sets are linked to irritants and inflammation of the sinuses, which are linked to smoking (Dlugasch & Story, 2021). The pathophysiology behind cluster headaches also involves the hypothalamus and parasympathetic nervous system. The same symptoms in migraine prodrome are also clinical manifestations of cluster headaches (Dlugasch & Story, 2021).
When applied to our patient, her classification of migraine should alert us to hypothalamic and parasympathetic system involvement. She is likely to present unilateral throbbing pain associated with the trigeminal nerve and sensitivity to light, touch, and smells from nociceptor sensitivity (Dodick, 2018). Seeing as these are reoccurring, the patient is most likely able to anticipate her migraine arrivals due to prodromal changes in mood and activity; still, patient education should always include additional trigger avoidance to help decrease the severity and duration of the migraine (Dodick, 2018).

2. KATHRYN

A 55-year-old male presents after a fall in his backyard. His primary diagnosis is a 12-year battle with Parkinson’s Disease.
Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. Parkinson’s disease typically develops between the ages of 55 and 65 years of age. Parkinson’s disease is a neurodegenerative syndrome involving multiple motor and nonmotor neural circuits (Rizek et al., 2018). There are two major pathologic processes: (a) premature selective loss of dopamine neurons; (b) the accumulation of Lewy bodies, composed of α-synuclein, which become misfolded and accumulate in multiple systems of patients with Parkinson’s disease (Rizek et al., 2018). When motor symptoms become evident, there is 30–70% cell loss apparent in the substantia nigra on a pathologic examination The goal of therapy aims to replace dopamine with dopaminergic medications and modulate the dysfunctional circuit (Rizek et al., 2018). Cognitive dysfunction, mood disorders, and impulse control disorders are related to deficits of dopamine outside the basal ganglia or in serotonergic and noradrenergic systems. Autonomic dysfunction has been linked to pathologies outside the brain, including the spinal cord and peripheral autonomic nervous system. Parkinson’s disease can affect every aspect of one’s life.

How does Bradykinesia manifest?

Bradykinesia shows up early in the disease as motor slowness, which develops into a complete loss of spontaneous movements (akinesia). This can result in loss of facial expressions, reduced gesturing, impaired swallowing, reduced blinking, loss of words, and loss of arm swing while walking (Hess & Hallett, 2017).

What causes postural instability in this patient?

Postural instability is the inability to maintain equilibrium under dynamic and static conditions, such as the preparation of movements, perturbations, and quiet stances (Appeadu & Gupta, 2021). Posture balance control is a multifactorial activity dependent on integrating motor, sensory, visual, cognitive, and vestibular neural networks. A disruption in any of these processes can lead to postural instability. The specific etiology of postural instability is complex to identify because it is a heterogeneous disorder, and there is much ground left to uncover regarding knowledge of the pathogenesis of the disease (Appeadu & Gupta, 2021).
Compare and contrast pyramidal vs. extrapyramidal.
Extrapyramidal motor activities result in automatic movement and static, postural movement activities that are not noticeable. The extrapyramidal system includes theorized connections within the basal ganglia and other central nervous system structures that regulate movement, including related brainstem nuclei and the cerebellum (Lee & Muzio, 2021). Extrapyramidal symptoms are involuntary. The pyramidal system controls voluntary actions through precise anatomic pathways from the cortex to the muscle. Voluntary activities through the pyramidal procedures are visible (Lee & Muzio, 2021). An example of a classic disorder of the pyramidal system is a stroke, resulting in paralysis of an extremity.

Compare and contrast myelinated and unmyelinated fibers.

The main difference between myelinated and unmyelinated nerve fibers is that myelinated nerve fibers contain myelin insulation, whereas unmyelinated nerve fibers do not contain myeline insulation (Metzger et al., 2021). Myelinated nerve fibers appear white and unmyelinated Gragrayger et al., 2021). About Parkinson’s disease, unmyelinated fibers are more vulnerable to degeneration than myelinated fibers of the cardiac nerve because α-synuclein aggregates accumulate much more abundantly in unmyelinated fibers (Metzger et al., 2021).

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