Pathopysiology Of Diseases Essays Example

Type of paper: Essay

Topic: Migraines, Headache, Disorders, Brain, Autism, Syndrome, Theory, Nursing

Pages: 9

Words: 2475

Published: 2020/10/09

Abstract

Migraine is a complicated neurobiological syndrome that has been identified for quite a long time. A lot of studies exist on this subject matter. The main aspects of this disorder are throbbing and unilateral headache. It is commonly caused as a result of sensitivity to light and sound. It is considered as a vascular syndrome due to the pulsating aspect of the head. Nevertheless, the vascular alterations in the body do not fully support the pathophysiology of migraine symptoms. In fact, about 33% patients do not experience throbbing headache.
Migraine causes severe painful attacks of headache. As well, the hereditary susceptibility and exposure to ecological causes can impact people to invoke migraine genetic characteristics. Migraine Syndrome affects a large number of people in their daily lives. The identification of various biological processes that trigger migraine has been not easy to identify. It is because migraine does not have a clear pathology that could be identified by the contemporary technological tools. The modern theories explaining the identification of migraine have frequently concentrated on routine health methods involved in vascular and neurological premises. In addition, the migraine pathophysiology has been linked with the current data from imaging report and animal prototypes.
In fact, the occurrence of migraine bouts may range from once in the whole lifetime to almost every day. In order to clearly identify the migraine disorder, the research analyst should take into account both the features that impact the person’s susceptibility to view them to a migraine bout. As well, it should consider the ways that cause the migraine attacks and the related symptoms. In addition, the theories about pathophysiology should be based on the composition and makeup of the pain-generating structures within the brain.
As well, the hereditary aspect of migraine is studied critically through genome-wide related studies and case-management groups. Also, the research paper delves into pathophysiology and genetic roots of migraine with the application of most modern scientific data from genetics research.
Migraine is a well-known complex syndrome of the nervous system affecting a large segment of the population. It entails considerable economic cost on the contemporary society. The migraine is typified by extreme, persistent, one-sided intense headaches that commonly vomiting, sickness, photophobia and phonophobia. The prodrome usually takes place prior to the headache. The migraine patients experience modifications in their feelings or activities, extreme fatigue, frequent yawning and phonophobia. In addition, if the headache is successfully localized, it may still change between sides all over migraine attack. In accordance with the global headache criteria, the patients should face no less than five incidents meeting the above-stated standards prior to the identification of migraine could be done. Besides, the occurrence of migraine attacks, intensity of the ache and extent of the syndrome is different for each. However, a medium incidence is noted in one incident a month, and the usual period is just about a couple of days. Normally 15-30% of migraine people, an incidence of random symptoms last less than an hour just preceding the headache (Bigal et al., 2009). Consequently, the continued neurological occurrence known as “aura” usually consists of visual signs.

Causes of Headaches

The researchers believe that the primary reason of migraines is the preservation of toxins within the CNS. The irritant may create an over-reaction of brain tissues to other stimulants of the body. Rather than to state that migraine is the consequence of conflicting biological changes in the human body, it would be more correct to consider it as a pain and a symptom range that differs only in intensity of the symptoms.
Besides, a number of triggers may lead to the occurrence of the migraine. The common factors consist of the physical activities, alcohol use, sleeplessness, improper diet regimen or climatic changes. In addition, the diet containing high protein is usually considered to be a factor for chronic migraines. In fact, the breakdown of protein creates the creation of various toxins, particularly nitrogenous wastes that can exceed the blood-brain obstruction.
Also, some food sensitivities and allergies can cause migraine in several individuals. For instance, many salted foods are usually known as triggers. Also, it includes some nitrates and strong sweet foods (Hoffmann & Recober, 2013; Spierings et al., 2001; Martin & Seneviratne, 1997; Saracco et al., 2014; Wober & Wober-Bingol, 2010).
Yet, the most frequent triggers noted by health professionals for the rise of migraine are anxiety, changes in hormone level in the body and sleep disorders (Kerman, 2007).

Literature Review

Pathophysiology of Migraine
The precise pathophysiology of the migraine syndrome is so far ambiguous. Although, it has been proposed the typical pathophysiology of the migraine syndrome is the cortical spreading depression (CSD) of neural tendencies from a vasoconstriction and after that by vasodilation. Nevertheless, it is improbable that vasoconstriction followed by vasodilation only explain the local oedema and focal ache usually noted the majority of migraine patients (Spierings, 2003; Vecchia & Pietrobon, 2012). In addition, Lashley explained the developmental feature of the visual aura in 1941 (Tfelt-Hansen, 2010). As well, Leao demonstrated the continuous depression in 1944 (Wolff, 1963). Milner related the developments in migraines in 1959 (Milner, 1958). In addition, the seminal work of Moskowitz and Olesen was useful for the present perception of spreading despair in the migraine syndrome (Moskowitz & Macfarlane, 1993; Reuter et al., 2000). However, the relationship of migraine with the arteries is still a vital aspect of the pathophysiology of migraine.
In the migraine patients, the spreading depression moves across nerve cells. It motivates the discharge of various endogenous matters that create pains and causes vasodilation (Dalkara et al., 2010; Sanchez-Del-Rio et al., 2006). In addition, there exist a couple of theories of migraine headaches, consisting of the vascular theory as well as neural theory.
The high inconsistency of medical factors of migraine and various biological irregularities have caused in the growth of several medical theories regarding the pathophysiology of migraine amongst the people. As well, the pathophysiological theories in the contemporary research have developed in particular health paradigms, remarkably the vascular, neurogenic, and hereditary/biological model (Tfelt-Hansen & Koehler, 2011). As a result of variable feature of migraine, it was considered a vascular health syndrome throughout the whole twentieth century (Graham & Wolff, 1938). Nevertheless, in the contemporary health environment a number of factors challenge the vascular theory of the source of migraine incident i.e. the vasoactive intestinal polypeptide is not the cause of migraine (Rahmann et al., 20087). However, the materials that do not create obstruction of the blood vessels may help in stopping a migraine occurrence.
However, there are several advocates of the neurogenic and neuro-transmitter premises who consider that the brain malfunction is the primary trigger of headaches (Akerman et al., 2011). In addition, the neuromodulatory organizations, locus coeruleus and nucleus raphe, control the spread of growing migraine pointers.
Functional brain imaging can show the dynamics of brain regions through the migraine attack. In addition, it can show an electrical spur that can trigger headaches like that of migraine.
At present, the majority of analysts approves and endorses the neurogenic inflammation theory of migraine, which presumes that the nervous system creates start of the meningeal blood vessels. It causes the pain and further motivates nerve dynamism (Goadsby, 2009). As well the analysts suggest that neural operation discharges vasoactive neuro-transmitters from these processes, which consequently incites inflammatory modifications in the brains blood arteries. Also, it is thought that the following procedures motivate the incidence of the migraine incidents:

“Cortical Spreading Depression (CSD)”

“Activation of the trigeminovascular system”
“Sensitization of peripheral and central brain areas.”
1. “Cortical Spreading Depression” in Migraine Aura
The earlier research showed s that “cortical spreading depression” is the essential aspect of migraine aura. The theory was first developed by Leão in 1944 (Leão, 1944). Besides, CSD is a progressive dispersal activity of constant neuronal depolarization that begins at the rear side of head lobe. It then develops over the outer layer of the brain. Later, it creates a high long-term neural avoidance. As well, the “Cortical Spreading Depression” concerns to the growth of the aura signs. Besides, it might also point out relationship of the aura and the migraine outcomes. Both of these may have affirmative and harmful results.
2. “Activation of Trigemonovascular System”
The “Activation Trigeminovascular System” consists of meningeal blood vessels that are in-enervated by the section of the trigeminal nerves (TN). These nerves are projected in the core part of brainstem that presents different estimations on a number of complex brain segments. In addition, the launch of the system motivates the discharge of neuro-peptides from the minor ends of the TN. It causes the vascular and provocative alterations linked to migraine pain.
As well, it is thought that the neuro-peptides contribute significantly in the creation of disinfected neuro-genically motivated irritation of the meningeal blood vessels wall and the maintenance of the migraine pain (Goadsby, 2009). The trigeminal strands send out distress signal using the brainstem to various brain points engaged in pain sensitivity. In fact, the headache is stopped when the “ipsilateral trigeminal denervation” is consisted only the evidence that TGVS creation is significant the occurrence of headache.
3. “Sensitization of Peripheral and Central Brain Areas”
It is usually thought that throbbing characteristics of migraine and the weakening of these symptoms through physical activities are generated by the peripheral sensitization process. However, another vital sign, which is typically noted in the migraine patients is the feeling caused by non-harmful stimulants. Accordingly, it is due to the procedure of central sensitization of the neurons in the nucleus that get the input signs from the skin. The primary sensitization contributes considerably in the later phases of migraine bouts and makes the brain excessively sensitive, i.e. “perpetuum migraine”.
As well, the central and peripheral sensitization causes the patients hyperexcitable of the cerebral cortex. In addition, the Neuro-physiological processes have lately showed that the chronic migraine patients have excitable somato-sensory and visual cortices. Also, it validates the viewpoints that the brain gets more impulsive and excited in the migraine patients in contrast to the non-migraine patients. In addition, the “migraine” brain is incapable of removing the sensory stimulants rapidly and entirely. Consequently, it results in “sensory overload” and the start of painful phase. Nevertheless, the sensitization procedure is believed to be one of the pathophysiological courses that lead to change of migraine bouts to severe recurring, and chronic form of migraine.

Relationship between Aura & Headache

The analysts believed that the procedure of cortical spreading depression is strongly related to aura and its development, while the trigemineovascular system creation causes the migraine problem. Nevertheless, the method in which Cortical Spreading Depression promotes the TGVS continues to be unambiguous. However, the tests carried out on various on animals have proved that Cortical Spreading Depression may cause trigeminal nociceptors as a result of the discharge of H-plus, K-plus and arachidonic in the extra-cellular gap of the neo-cortex. In addition, these means can create depolarization of perivascular TN endings and cause an anti-dromic activation of the trigeminal sensory routes.

Drawbacks of Neurovascular Theory

The holistic medical range of migraine syndromes is challenging to understand precisely the nature pathophysiology and molecular heredity. Accordingly, it is complicated to recognize a pathophysiological relationship between a headache and nausea or hypotension. Hence, Neurovascular Theory has couple of drawbacks namely 1) The explanation of the fact that the majority of migraine prone patients do not possess aura and 2) the modern notion of the migraine pathogens does not concentrate on the particular beginning of the migraine bout for the individuals (Bigal et al., 2009). Indeed, neither aura as well as headache implies the precise beginning of a migraine attack. However, the primary or contributory physiological occurrence for the migraine takes place throughout the prodromal stage. Specifically, it starts from the stimulants that cause headaches and the beginning of the prodrome symptoms. Hence, an important pathophysiological method causing migraine has to be determined. The migraine bouts take place throughout or following the nervous tension, and more commonly amongst women than in men. Thus, it appears rationale that the neuroendocrine system causes activation of the methods of vascular integrity and anti-nociception in migraine bouts. Hence, neurological and vascular genes are vital features in the pathophysiology of migraine and are the motivation of several contemporary experimental and fundamental analyzes.

Genetics & Migraine

In addition, one of the most significant features of the migraine pathophysiologies is that it is heritable normally. Indeed, the genetic aspect of migraine implies that several syndromes exist in the pathogens of migraine. So far, hereditary source or causal DNAs engaged in the migraine syndrome have not been recognized.
The universal types of migraine have been related to different kinds of genes. However, the application of genetic-wide study caused the identification of the first gene variant for the migraine syndrome. As well, the variant, that is situated on a particular gene and thus controls the appearance of the gene SLC1A2, which programs the main carrier in the brain.

Soon after that another variant related to migraine with aura was found.

In addition, the analyses for the patients experiencing family hemiplegic migraine symptoms have caused the detection of three variants that are engaged in ion and neuro-transmitter transfer in the brain. Hence, through the research from the hereditary outlook, it has been studied that migraine disorder could be called as a “channelopathy”. Also, the lab model was generated from a knock-in mouse similar to one of the well-known family migraine variants, and for this reason helped the methodical study of its pathophysiological results in various models regarding migraine disorder.
Presently, the majority of analysts think that the hereditary variety is the major pathogenic method of migraine symptoms (Schürks, 2012).

Conclusion & Recommendations

Migraine is a neurological health syndrome that significantly affects the central nervous system (CNS). It causes severe painful attacks of headache. As well, the hereditary susceptibility and experience to ecological causes can impact people to invoke migraine genetic characteristics. Migraine Syndrome affects a large number of people in their daily lives. The identification of various biological processes that trigger migraine has been not easy to identify. It is because migraine does not have a clear pathology that could be identified by the contemporary technological tools. The modern theories explaining the identification of migraine have frequently concentrated on routine health methods involved in vascular and neurological premises. In addition, the migraine pathophysiology has been linked with the current data from imaging report and animal prototypes.
In fact, the occurrence of migraine bouts may range from once in the whole lifetime to almost every day. In order to clearly identify the migraine disorder, the research analyst should take into account both the features that impact the person’s susceptibility to view them to a migraine bout. As well, it should consider the ways that cause the migraine attacks and the related symptoms. In addition, the theories about pathophysiology should be based on the composition and makeup of the pain-generating structures within the brain.
Migraine is a complicated neurobiological syndrome that has been identified for quite a long time. A lot of studies exist in the subject matter. The main aspects of this disorder are throbbing and unilateral headache. It is usually caused as a result of sensitivity to light and sound.
Migraine is considered as a vascular syndrome due to the pulsating aspect of the head. Nevertheless, the vascular alterations in the body do not fully support the pathophysiology of migraine symptoms.
There exist various scientific theories regarding the pathophysiological causes of the migraine syndrome. However, the apparent underlying algorithms of pathophysiology of the migraine syndrome are the typically the condition of hyper-excitability of sterilized neurovascular irritation of meninges blood vessels, the activation of TGVS and sensitization.
Over a couple of decades, there has been a major growth in the knowledge of various significant features of migraine pathophysiology. As well, the growing data of hereditary heterogeneity stress migraine, together with the extensive experimental variations noted in the migraine syndromes.

References

Akerman, S., Holland, P.R., Goadsby, P.J. (2011). Diencephalic and brainstem mechanisms in migraine. Nat Rev Neurosci; 12(10):570-84.
Bigal, M.E., Ferrari, M., Silberstein, S.D., Lipton, R.B., & Goadsby, P.J. (2009). Migraine in the triptan era: lessons from epidemiology, pathophysiology, and clinical science. Headache; 49 (Supll 1):S21-33.
Graham, J.R., & Wolff, H.G. (1938). Mechanism of migraine headache and action of ergotamine tartarate. Arch Neurol Psychiatry; 39:737-63.
Hoffmann, J., & Recober, A. (2013). Migraine and triggers: post hoc ergo propter hoc? Curr Pain Headache Rep 17:370.
Kelman, L. (2007). The triggers or precipitants of the acute migraine attack. Cephalalgia; 27(5):394-402.
Martin, P.R., & Seneviratne, H.M. (1997). Effects of food deprivation and a stressor on head pain. Health Psychol 16:310-318.
Rahmann, A., Wienecke, T., Hansen, J.M., Fahrenkrug, J., Olesen, J., Ashina, M. (2008). Vasoactive intestinal peptide causes arked cephalic vasodilation, but does not induce migraine. Cephalalgia; 28:226-36.
Saracco, M.G., Calabrese, G., Cavallini, M., et al. (2014). Relationship between primary headache and nutrition: a questionnaire about dietary habits of patients with headache. Neurol Sci 35 Suppl 1:159-161
Schürks, M. (2012). Genetics of migraine in the age of genome-wide association studies. J Headache Pain; 13(1):1-9.
Spierings, E.L., Ranke, A.H., & Honkoop, P.C. (2001). Precipitating and aggravating factors of migraine versus tension-type headache. Headache 41:554-558.
Tfelt-Hansen, P.C., & Koehler, P.J. (2011). One hundred years of migraine research: major clinical and scientific observations from 1910 to 2010. Headache; 51:752-78.
Goadsby, P.J. (2009). Pathophysiology of migraine. Neurol Clin; 27(2):335-60.
Wober, C., & Wober-Bingol, C. (2010). Triggers of migraine and tension-type headache. Handb Clin Neurol 97:161-172.

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