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Alzheimer’s disease

Oct 24, 2018 | 0 comments

Oct 24, 2018 | Essays | 0 comments

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Impact of Alzheimer’s disease on pain perception: Causes and consequences

Introduction

Overview of Dementia

Dementia is a term used in genetics that describes the cognitive decline in the functioning of the brain. The condition is triggered by several conditions, including Alzheimer’s disease and injury to the head or brain. Alzheimer’s disease (AD) is the frequently testified form of dementia characterized brain generation leading to loss of memory or decline in cognitive function (Scherde & Manen 2005, p. 157). AD is most prevalent in populations over 65 years experiencing progressive memory decline, language, thinking, and learning capacity. However, it is significant to differentiate between AD and normal decline in cognitive function that comes with aging that is more steady and characterized with fewer disabilities. Alzheimer’s disease in its early stages promotes mild symptoms ending with severe damage to the brain. According to Summers (2006), “AD affects approximately 6 million American citizens and World Health Organization (WHO) has grouped it as the seventh prominent cause of death in the United States (US)” (p. 73). Alzheimer’s disease presents itself in two forms: Familial Alzheimer’s disease is more prevalent in people younger than 65 years, resulting in approximately 500,000 cases of AD in the US alone (Bethune 2). The remaining cases of AD affect adults aged 65 years and above, which is categorized as sporadic Alzheimer’s disease.

Effects on Pain Perception

Pain is a predominant challenge for the elderly population with approximately 80 percent of nursing homes and up to 50 percent of the community experiencing regular pain. Despite the technological and medical advances, pain remains a continuing predicament in the daily lives of the aging population (Beach 2014, 4). (I exclusively said only authentic papers which I will supply and by the way, this is from a dissertation, which is not acceptable) The progressive and increased prevalence of pain is associated with increased rates of chronic diseases in the senior population, particularly dementia and other health conditions. The prevalence of Alzheimer’s disease varies depending on various factors, including co-morbidities, age, level of education, and genetics. Currently, a definite diagnosis of AD entails performing an autopsy. However, there is no known cure for the disease, yet promising research and development in the medical field have enabled early detection and treatment that is underway.

Overview of Project Research

Previous studies have applied various techniques of investigation and tools of assessment to study and measure the effects of AD on emotional and cognitive dimensions of pain. A literature review has become an annual ritual for researchers handling various projects. Besides, a review of literature offers provides an insightful review of what had been done in the field and particularly to AD and its effects on pain. Therefore, this paper critically analyses literature from various studies reporting pain processing in AD from several databases, including PubMed, ScienceDirect, WebMed, and Nursing Center among others. As such, it provides a robust analysis of peer-reviewed articles and journals, alongside the mentioned websites. It also paper presents a research-based analysis of AD and its effects on pain based on the literature review. The main objective of the paper reflects on understanding pain processing and perception in AD by analyzing pharmaceutical, neuroimaging, electrophysiological and psychophysical explorations of pain processing in Alzheimer’s individuals on the reviewed literature.

Literature Review

Pain in AD

Chronic or acute pain presents one of the most prevalent medical complaints confronting medical experts. Persistent pain among the senior population leads to reduced mobility and decline in lower body strength, which causes depression, disability, falls, and disruptive behaviors. According to the International Association for the Study of Pain, “Pain as an unpleasant emotional as well as sensory feeling characterized with significant harm to the tissue.” (Beach 2014, p. 1), Thus, pain is a uniquely human condition since does not necessarily involve actual tissue damage. Meanwhile, increased morbidity makes patients with AD imperative regarding their assessment and proper treatment. In a study titled, “Pain in Alzheimer’s disease: A Study Of Behavior and Neural Correlates” by Beach (2014, 1), it is established that patients with AD often suffer steady and progressive loss in reasoning skills, cognition, and memory. In the meantime, the patients lose their functional autonomy and depend on professional caregivers. As the disease advances to its critical stages, these patients experience deterioration in memory, executive function, comprehension abilities, and language (McCarty 1993, p. 23). Patients suffering from AD become bed-bounded and risks contacting more painful conditions, including ulcers and pressure, according to Beach.

Current statistical research indicates that in current times,(this is not grammatically correct) approximately 5 million Americans suffer from AD, yet the number is projected to be higher in the future decades. It is also reported that these patients consume substantial healthcare resources as they entirely depend on caregivers as their lifespan before acceding to their medical conditions is estimated to be greater than ten years. Patients with AD suffer pain that is understood to be associated with both behavioral(preposition missing)motivator and sensory experience, creating a complex merger of emotion and sensation. The effects of AD include two distinct formalities in the brain: senile plaque and neurofibrillary tangles (Manukhina, Manukhina & Torshin et al. 2004, p. 391). However, the senile plaques (diffuse and neuritic) entail special structures surrounded by the abnormal amyloid protein found in the neocortex of the brain. As the tangles and plaques increases in numerical aspect, the healthy neurons become less functional. As a result, the patient gradually and progressively loses the ability to communicate because of the overall shrinking of the tissue. Besides, the death of the hippocampus neuron restricts the ability of a patient to form new memories leading to cognitive degeneration (Manukhina et al. 2004, p. 391). AD is highly correlated to cardiovascular health as having high levels of cholesterol or high blood pressure puts one at an increased risk of contracting AD. Therefore, AD causes pain to patients because it leads to damage of blood vessels in the brain and pain associated with cardiovascular diseases and Type 2 diabetes.

Influence of AD on Brain Functional Activity

Cole, Gavrilescu, Johnston, et al. (2010)(2011) investigated the influence of AD on the functional connectivity amid the brain activity sections causing primary pain perception. According to the investigative report, AD patients often get receive fewer(?????) analgesics for medication coupled with a decreased report of clinical pain as opposed to their cognitively-intact peers. The researchers used the concept of functional connectivity analysis to observe the influence of AD on the functioning of the brain in areas mediating cognitive, emotional, and sensory phases of pain. In the experiment, the researchers used 14 subjects suffering from AD alongside 15 controls (Cole et al. 2010). In the commencing psychological testing session, the researchers used a random staircase procedure to evaluate the sensitivity to noxious mechanical pressure on the thumbnail of the participants. Likewise, the researchers used 14 verbally communicative subjects with mild AD and further examined them by a professional neurologist, psychogeriatrician, and gerontologist. Researchers used the concept of the general linear model for analysis, which entails analysis of brain activity regional increment as well as functional connectivity analysis. The applied approaches evaluated the influence of AD concerning pain perceptions.

The figure of Functional magnetic resonance imaging results (Keightley, Saluja & Chen 2014, p. 438). (where about its being referred in the narrative i.e. this paper. It looks to me that the writer did not want to revise it at all that’s why he just cut and pasted random picture)

Cole, et al. (2010)(2011) used two different complementary procedures to functional connectivity analysis and identified regional networks of increased functional connectivity in AD patients. According to Cole and colleagues, the cognitive impairment in patients suffering from AD is at increased chances of experiencing pain. Besides, the dorsolateral prefrontal cortex (DLPFC) compound plays a significant function in pain modulation and cognitive function. It was reported that regions such as the hypothalamus, PAG(??? What’s the full form of this acronym), motor areas, and thalamus provides a convincing functional affiliation to DLPFC in AD patients. Cole, et al. (2010) established that pain is indeed an internally menacing experience. Particularly damages the essential tissues that must be sidestepped to uphold somatic integrity. Likewise, pain inception short of contextual factors leads to the generation of a defensive response that may get functioned at low neuraxis levels. Nonetheless, an unchallengeable response to pain cannot guarantee survival. The impacts of AD may change situations, and it causes life-threatening pain. Similarly, AD affects the nervous system that harbors the networks that connect and amplifies or diminishes the response to noxious events. The occurrence of modulating circuits offers an approach through which contextual-dependent responses get shaped (Cole et al. 2010, p. 568.e7).

Overall, AD patients undergo are exposed to sporadic noxious pressure of thumbnail that is perceived as threatening. The heightened threat also promotes the onset of self-protective reactions, as well as autonomic responses, dorsal horn reaction descending modulation, and contemplating. The prominence of increased functional connectivity in AD patients, according to Cole et al. (2010), includes sensory, motor, and autonomic processing regions pipeline of school to prison. Ecenbarger (2012) believes that that evidence the notion of heightened arousal related to the unfriendly experience and less expected noxious events. AD patients also get associated with dampened autonomic response to hampering discomfort, and past studies verify that it affects the autonomic response to pain in AD. Meanwhile, it is established that loss of cognitive ability is a cardinal characteristic of cognitive impairment in patients with AD that has been used as a distinguishing feature with different dementia forms (Lukas, Schuler & Fischer et al. 2012, p. 48). The continued pain related to activation of the brain in AD patients shows the sustained attention to pain. This supports the notion that the lessened patient appraisal of the experimental environment of pain. Therefore, the pain experience in AD patients originates from changes related to diseases due to infection of brain regions (thalamus, hypothalamus, and motor activity regions) used in transmission and processing of noxious input.

Pharmaceutical Indications and Effects

Previous research on epidemiology has suggested that non-steroidal anti-inflammatory drugs (NSAID) promote crucial therapeutic effects in patients with AD. Particularly, researchers have reached a consensus that the use of Aβ-peptide (Aβ) to activate microglia can get influenced by NSAIDs. Accordingly, Alafuzoff, Overmyer, and Helisalmi et al. (2000) analyzed 42 clinically and histopathologically dementia patients confirmed with AD symptoms. Rendering to the scientists, consistent NSAID administering promotes a noteworthy impact on the Aβ-peptide loading. Moreover, it was established that regular NSAID application promotes a considerable decrease in the counts of astrocytes alongside subsequent tendency of lesser counts of activated microglia in brain tissue. Alafuzoff et al. (2000) write, “AD is described by the aggregation of Aβ-peptide (Aβ) in the brain tissue containing neurotic plaques/senile (SP/SP) as well as impaired helical filaments (PHF) constituents of neurofibrillary tangles (NFT)” (p. 37). (what is the refereeing to here? Which paper?) The subjects used in the research were members of continuing clinical studies and post-mortem material and were clinically diagnosed using the approach of NINCDS-ADRDA and the DSM-III-R. The methodology also included visualization of grey matter based on Aβ-protein aggregates, GFAP, and HLA DR that utilized an immunohistochemical approach. Finally, the GFAP and HLA DR quantification expression was conducted using Quantimet 570 Image Analysis System (Leica Cambridge Ltd, Cambridge, England) (Alafuzoff et al. 2000, p. 38).

The table below shows the clinical information of the patients. (He has not mentioned anything about the no of patients nor the gender and all of a sudden the reader is thrown a table like this? No relation at all)

  N Gender Age of Death Duration of Disease
No NSAID use 22 16/6 83 10.6
Regular NSAID use 20 19/1 79 7.6
All cases 42 35/7 81 9.2

(Alafuzoff et al. 2000, p. 39)

According to Alafuzoff et al. (2000), the recent contribution of astroglial and microglial activation in patients suffering from AD has been subjected to intense research. In the event, advanced GFAP immunoreactivity in the brain tissue and HLA DR on the surface of the cell markers expressed on microglia has been documented. It is identified that astrocytes are significant in the functioning of a neuron, prompting the debate that their dysfunction might be the real cause of AD. Besides, the microglia are known to respond to various stimuli, and once activated; its cell begins to secrete numerous inflammatory proteins. Microglia activation using Aβ-peptide thus supports the association between AD pathology and microglia. As a result, inflammatory proteins lead to neural damage witnessed in AD. Therefore, it has been found that anti-inflammatory income taxes and personal revenues. However, as much as the healthcare system in Canada is social and universal, the plan does not cater for drugs may have helping effects on AD patients. Particularly, Alafuzoff and colleagues report that experimental investigations reveal that activation of microglia by Aβ-protein can be affected by NSAID therapy. The study indicated that recurrent NSAID treatment is related to a considerable decrease in activated microglia counts in the brain tissue. Inflammation has been previously associated with excessive pain in the affected areas. Therefore, the fact that anti-anti-inflammatory drugs have been used in AD patients mainly prevents inflammation of the brain cells that would result in diseases causing severe pain.

Similarly, Akyol, Ugurcu, and Cakmak et al. (2014) based their research on evidence of the control aggressiveness by insulin and glucose in AD patients. The Western blot analysis enabled the medical scientist to show that ADAMTS5 protein handles the decrease in insulin-applied U87 cells. (if I am the reader I will be lost what he means by this term here. He needs to explain. I don’t want to hear his excuse that it’s a medical term. Fine if it is then explain it. In papers you get a footer where the term is explained) As such, high glucose application promotes a significant increase in levels of ADAMTS5 protein in cells, while application of low glucose resulted in a modest upsurge in ADAMTS5 protein levels (Akyol, Ugurcu, and Cakmak et al. 2014, p. 327). Akyol and colleagues concluded that both inflammation and aggrecanases mediators in AD patients were associated with pathophysiology aspects related to hyperglycemia and diabetes. Type 2 medical parishioners have credited social media for successful campaigns in chronic diseases. Diseases such as diabetes upturns the risk of developing AD (Akyol et al. 2014, 328). Therefore, diabetes mellitus and inflammation are common among patients diagnosed with AD. Moreover, the pathologic conditions associated with hyperinsulinemia and insulin resistance are also related to increased inflammation for AD. It is shown that insulin potentially promotes central nervous system (CNS) inflammation because the Aβ interrelates with inflammatory factors hence increasing pro-inflammatory cytokines (Akyol et al. 328). (which year? This is not Harvard referencing style) Subsequently, inflammatory cytokines production by various cells established in the CNS promotes complete inflammation response and affects the functioning of the risk of developing heart diseases. They contain saturated fats content that increase the cholesterol levels in the blood-brain barrier (BBB). The study suggests that inflammation is the main pain pathogenic factor concerning AD development. Overall, chronic pain is a direct consequence of an overzealous immune reaction in the brain that is associated with inflammation.

The growing number of investigations implies the relationship between pain and Ad among patients. Particularly, the participate actively in the product. According to the recent investigation of the connection between dementia, vitamin D, and depression have been conducted in older patients. It is verified that vitamin D promotes a proactive influence on the brain suggesting dementia because it has a beneficial effect on systemic vascular, such as cerebral vasculature that promotes individual neuron growths. The vascular disease of the brain incorporates more than 80 percent of all diseases, including AD. According to Cherniack (2011 p. 16), the etiology of AD involves mitochondrial dysfunction, hippocampal synaptic loss, genetic factors, amyloid plaque formation, and tau protein mutations. Previous research shows that an average of 80 percent of the vascular disease reported has an association with AD in brain autopsy. The heightened systemic inflammation comprising the metabolic syndrome is also allied to vascular disease and dementia. Particular characteristics of metabolic syndrome, including diabetes, hyperlipidemia, obesity, and hypertension are also associated with the presence of dementia (Cherniack 2011 p. 16). In fact, one of uncharacteristic metabolism and synthesis of amyloid precursor protein has been identified as one pathogenic feature of AD. The compound can act as a protein, which is a cytokine that stimulates inflammation of brain cells.

Furthermore, adipocytes are important elements in the development of systemic inflammation. The adipocytes handle the discharge of specific substances that promote vascular growth observed in vascular disease. Also, adipocytes regulate adipocytes-related hormone as well as insulin, including leptin, resistin, and retinal binding protein. In particular, resistin induces macrophages that lead to the production of tumor necrosis factor and cytokines that promotes brain cell inflammation (Cherniack 2011 p. 17). Likewise, leptin inhibits intake of food and can also act on macrophages enhancing discharge of cytokines leading to the reactive oxygen species generation inside the vascular endothelium. The rationale of the research was based on the principle that vitamin D can encounter inflammatory effects on adipocytes. Also, the polymorphisms found in vitamin D receptors show an association with depressive and cognitive symptoms. Cherniack (2011 p. 17) hints that vitamin D increases gene art and involves employing reason and intellectual in art work. Romanticism stressed on the expression for tyrosine hydroxylase found in productive animals. Therefore, there is an established connection between vitamin D and depression. The correlation of levels of vitamin D with the manifestation of depressive symptoms in the senior population alongside related health complications results in pain for patients with AD.

Effects of Physical Activity on AD

It has been established that physical exercise alleviates debilities of AD as well as normal aging. Physical exercise, according to Archer (2010, p. 221(2011)), endorses harnessing inherent biological features that respond to the putative interventional effects in laboratory, clinical, or institutional settings. In the meantime, the neurodegenerative and pathophysiologic progressions responsible for constituting AD have indicated the presence of various putative mechanisms. Archer indicates that adherence to routine physical fitness facilitates the longevity and efficacy of cognitive performances in the senior population. However, similar mechanisms and moderating dynamics demonstrate the benefits of exercise beginning in times of adolescents upheld throughout adulthood. As noted, neurogenesis, angiogenesis neurotrophic factors, and depression among the aging population promote the palliative physical activity effects upon cognition. The proliferation of an adult cell is regulated in dissimilar mechanisms through genetic and epigenetic factors. Physical exercise has also been time-honored to regulate neurogenesis in the brain of an aging individual. Therefore, age-related neuroinflammation is a direct consequence of reduced neurogenesis resulting from aging. Likewise, AD pathophysiology ways out in the brain regions close to the hippocampus, hence promoting the destruction of healthy brain regions (2010, p. 222(what is being referred here) which paper, which author)). Besides, the decline in neurocognition is linked to limbic stages as AD advances via the neocortical Braak stages. The proof that exercise improves balance and creates severity in AD uncovers the relationship between AD and pain.

Pain Improvement in AD

In a report on pain improvement in AD patients prepared by Corbett, Achterberg, and Huseboet al. (2014), it is provided that pain is a dominant sensation in demented population with a consequently challenging identification. Therefore, pain assessment tools, including observation of behaviors related to pain, facial expressions, and vocalizations were used to investigate pain in cognitively impaired patients. Approximately 80 percent of individuals suffering from dementia experience pain regularly. However, according to Corbett and Associates, little evidence supports the effects of dementia on pain. Similarly, little research supports the concept of altered pain pathways resulting from dementia pathology. Previous studies have reported the threshold of pain tolerance in AD patients. While conflicting reports have been presented, pain in dementia is consistent with musculoskeletal, cardiac, and gastrointestinal conditions (Corbett, 2014, p. 5). Demented individuals experienced neuropathic pain resulting from a CNS dysfunction, especially in vascular dementia (VaD) patients. Pain among AD patients is often rampant, yet patients are lack communication ability(grammatically incorrect), especially in mild stages making them lack the insight to provide precise reports on their pain.

Corbett (2014, p. 5) compiled a report on pain assessment tools based on such reviews. However, expert opinion shows that none of the pain assessment tools has shown appropriate or complete clinical utility regarding the consensus process and inclusion criteria. Despite the predicaments, most of the existing pain assessment tools that have been identified offer a significant item collection necessary in the construction of a combined meta-tool. The development of reliable and validated pain assessment tools alongside nearer collaboration with professionals in healthcare would promote clinical advantage for early-stage AD diagnosis. Challenges indeed exist; however, the present unprecedented mythological tools of pain assessment based on empirical as opposed to theoretical have demonstrated universally recognized utility. The instrument that is currently in the testing field has been used in pain evaluation in AD patients during rest, eating, and drinking as well as oral care. Therefore, it has shown effectiveness in back pain evaluation as well as that of neuropathic pain, yet there are severe difficulties in the detection of neuropathic pain in cognitively impaired patients.

Figure showing Response to acute pain behavior in mouse models of AD

(Corbett, A. et al. 2012)(2014)

Epidemiological studies have described and reported pain reduction and lower consumption of analgesics in AD patients. Besides, AD patients report incidences of painless frequently compared to their healthy peers. Jensen-Dahm, Werne, and Dahl et al. (2014), (2012)researched “quantitative sensory testing and pain tolerance in patients” confirmed with mild to moderate AD compared to healthy individuals. It is suggested that pain reporting or perception is already disturbed in the initial stages of AD development. Previous study findings have increased debate as to whether AD promotes an alteration in the experience of pain resulting from changes in process of pain connected to neurodegenerative changes (Jensen-Dahm, Werne and Dahl et al. 2014, p. 1439). According to the conclusive remarks of the researchers, patients suffering from mild to moderate AD have the ability to show collaboration with standardized mechanical and tests of thermal pain sensitivity. Using three different sensory quantitative assessments, it was reported that pain thresholds are no different from controls patients. Because the assessment tool guaranteed good data reproducibility, that is, agreement and reliability, depressed mechanical pain tolerance was common among AD patients compared to their control group counterparts. While there is a reduced pain verbal report among AD patients, it may be difficult to explain considering consequences of impaired mechanical and thermal stimuli, weakened network of communication of low latency. The I2P network was designed largely to enhance anonymous communication, anosognosia, and memory lapses associated with AD.

Similarly, Scherder (2005) studied pain in AD among 20 patients with the condition using the Coloured Analogue Scale important pain intensity assessment and Pain effect. It was observed that patients’ pain overestimation hints at an association with AD since the condition is characterized by an ailment in the pain experience. Also, both experimental and clinical pain investigations suggest that it is prominent and intense despite a lack of reporting in AD patients (Scherder, Herr, and Gibson et al. 2009, p. 277). The consequence of AD on the dispensation of pain, however, diverges in quality and direction depending on the type and intensity of pain, stage of dementia, and neuropathology (Scherder, Herr, and Gibson et al. 2009, p. 277). Overall, pain is associated with dementia, and Scherder and colleagues warn of an increased risk of undertreatment, especially, in patients with language and communication challenges.

Discussion

Cole, Farrell, Duff, et al. (2006( 2011), p. 2960) pronounces Alzheimer’s disease as a gradually progressive degenerative brain illness characterized by loss of memory leading to reasoning, planning, language, and acuity problems. The assumption that AD patients may never feel pain might seem obvious, the research provides powerful evidence that AD patients feel pain as their normally aging peers, if not more so. The processing and perception of pain are less increased in AD, thereby hovering questions over the present-day inadequate treatment of paint in the significantly vulnerable and dependent AD patients. (this one looks as if two different sentences were combined but it doesn’t make sense) Cole et al. indicate, “the brain has the power to tell what patients may not be able to tell” (p. 2959). Studies that involve testing in which a device is used(which device is he talking here?) to press the thumbs of patients until they fully notice the pain of different levels has proved the perception of pain in AD patients. Meanwhile, epidemiological studies employed a real-time brain scan, that is functional magnetic resonance imagine (fMRI) to observe the brain activities in major pain pathways. It is established that pain activity in the brain among AD patients is as powerful as those healthy individuals, even lasting longer in AD patients (Cole, Farrell, Duff, et al. 2006, p. 2960). Present literature suggests that brain pain activity in AD patients is real, yet the patients lack the ability to report compared to their healthy counterparts. Patients ailing from Alzheimer’s disease have symptoms of communication difficulty that makes it challenging for them to report pain, besides they may be mystifying in more severely affected AD, patients. The experience of pain, according to Cole et al., is very stressful for a patient with AD owing to the account that they have suffered from an inability to report the experience of painful sensation accurately. Pain is indeed a predicament among AD patients, yet these patients lack the verbal ability that breeds the perception of less pain(????). AD patients have the capacity for relevant pain that deserves proper diagnosis, evaluation, and treatment. Reviewed literature hints that, fortunately, pain diagnosis is possible even when an individual is not able to testify about it (Pieper, Dalen-Kok & Francke et al. 2013, p. 1050). Pain assessment tools such as, colored analog scale (CAS), Pain and Discomfort Scale (PADS), verbal descriptor scale (VAS) and faces pain scales (FPSs), used for pain assessment based on body movements and facial expressions have been used to validate effects of pain among AD patients. Besides, preceding research that involves watching of body movements and facial expressions of AD patients when not in pain during waking hours and sleep proves a strong relationship between AD and pain. Using such baseline principles, researchers suggest, one can be able to tell when the patient looks agitated, where there is grimacing suggesting discomfort, or where eye contact is altered (Castanho & Santos 2014, p. 323). (Where is the caption for this figure and wherein the paper it is referred to? Could you show me maybe I need glasses)

Investigations of pain in AD are still underway; however, investigations approve that demented patients, particularly those with AD, have regular pain sensitivity. Nevertheless, the component of an emotion that depends on the structures of their brain is often abolished or reduced. Therefore, AD patients present insignificant pain protests that decline as the condition progresses to its mild stages. Likewise, numerous reviewed researchers support that patients with preceding osteoarticular pathology with AD reports less subjective pain. Most importantly, there is a declaration of conflicting interests in the research of AD and pain association. Therefore, the process of pain evaluation in AD patients should consider using reliable and appropriate scales rather than wholly contingent on caregivers’ reports. As noted, pain medication considerably reduces pain in control groups, indicating that such drugs; acetaminophen, for instance, improves all day long activity (Plooij, Spek & Scherder 2012, p. 380). Moreover, untreated pain provokes sleep disturbances and affects social interaction, hence reducing life quality. However, existing AD literature lacks diverse randomized controlled trials (RCT) investigations with pain sensitivity as the major outcome. Current research focusing on large pain intervention studies relies on improved pain intensity as the main outcome (Sandvik, Selbaek & Seifert et al. 2014, p. 1495). The lack of data concerning the impact of pain intensity partly challenges accurate pain identification.

Alzheimer’s disease promotes brain changes that begin at the microscopic level long before the development of memory loss signs. The brain contains 100 billion nerve cells that connect to many others to constitute a communications network. Additionally, the brain includes specialized cells that support and nourish other cells (Anchez, Moghadam & Naik et al. 2011, p. 34). Groups of nerve cells perform different functions, as some are involved in learning, thinking, and memory. The tiny brain cells operate like factories based on the premise that they receive supplies, construct equipment, generate energy, and get rid of waste. Likewise, cells process and store information and communication. Medical scientists have found that AD prevents parts of the brain “factory” from normal operation. The brain has plaques and tangles that develop in most people as they age, however, in AD patients, autopsy studies show that they tend to develop faster. Scientists suggest that plaques and tangles are responsible for the blockage of communication in nerve cells and disrupt cellular processes. Therefore, the disruption and death of nerve cells cause memory failure leading to AD (Richards a& Tsai 2006, p. 92). People with AD experience physical pain for a similar reason to any healthy individual. Nevertheless, because of their declined brain abilities and functioning, patients are less able to communicate to their carers that they experience pain. Experiencing physical pain is very individual, and people feel pain because signals are sent from the affected part of the body to particular areas of the brain (Richards a& Tsai 2006, p. 92).

Research is conflicting as to whether the changes that occur in the brain due to AD causes pain. However, scientists have agreed that AD patients are at increased risk of contracting pain due to exposure to various medical conditions that cause pain. According to (Richards & Tsai 2006), “Previously, AD patients were perceived not to feel pain because the brain damage prevents them from feeling any pain (p. 93). (again which paper???) However, it is interesting to know that reviewed literature shows people with AD have pain-related activities in the brain region similar to healthy people.

Summary and Conclusion

Age has been described as the highest risk factor for Alzheimer’s disease and its role and consequences pain. (It don’t make sense ) The aging population across the continent is on the rise and the percentage of the high-ranked population with dementia experiencing pain will significantly upturn. Alzheimer’s disease and pain are complicated singularities because of the numerous ways the pain may express itself. Scientists show that AD causes pain that presents in various forms, including neuropathic pain, nociceptive pain, and central pain. Clinical and Experimental Studies also show that there is a significant trend in the undertreatment of pain perhaps because they are no longer reported. The consequence of AD on the processing of pain varies in terms of quality and direction, type of pain, stage of AD, and neuropathology (Morrison & Siu 2000, p. 34). The potential causes of pain in AD include constipation and urinary tract infections, pressure sores, diabetes alongside other medical conditions related to dementia and aging.

The assessment of pain has proved complex and challenging as there is no simple measure of an individual’s pain. Previously, reports from patients have been used in the measurement of pain by being asked to rate their pain o a scale of 1 to 10. Difficulty in communication, however, makes patients with AD vulnerable to pain because they cannot communicate. Therefore, observational assessment tools have been developed for recording and scoring pain among dementia patients. Findings on pain threshold and tolerance among AD patients show that pain is altered and depends on effective and cognitive factors (Do Carmo & Cuello 2013, p. 8). However, a sensory-discriminative component of pain is often maintained in AD patients. As such, tolerance of pain is strongly associated with the severity of AD disease according to assessment tools that work on the principle, the more severe changes in pain assessment tools, the higher and the tolerance to pain. It is understood that patients with AD get administered inadequate analgesics and report a reduced amount of pain than their peers without cognitive problems. AD patients also show higher tolerances to pain in both experimental and clinical results when equated with their healthy peers, according to Scherder, Oosterman & Swaab 2005, p. 463). However, it is still uncertain whether the reported pain disparity results from blocked pain communication and memory networks or whether the experience and perception of pain get altered because of the subcortical and cortical gradual deterioration associated with the processing and transmission of nociceptive information (Monroe, Gore, Chen, et al. 2012, p. 248).

Strong theoretical and practical research supports the expectation of altered transmission and processing of pain among AD patients. The dissociation between affective-motivational and sensory-discriminative pain aspects has been found that patients indicate analogous thresholds for pain detection, yet inclined tolerance to severe pain. Existing literature shows that the pain patterns-associated brain activity as in fMRI supports that the nociceptive information central dispensation cannot be weakened in patients with AD.

To be precise, pain experienced is more distressing for AD patients owing to their compromised ability to precisely weigh up the unfriendly sensation alongside its imminent implications (Torre 2012 p. 79). Therefore, the reviewed literature of the present study has clinically and experimentally significant implications and raise concerns on the present insufficient pain assessment and treatment of the dependent and vulnerable AD patients in the society. While previous research is diverse, little has demonstrated a direct response to this study objective. Overall scarcity of existing literature has provided a limited understanding of pain processing and perception in AD because little has been analyzed on electrophysiological pain processing.

Therefore, future research is needed to enable the prevention of pain using sensible precautions. Also, treatment and necessary precautions should be adopted to eliminate conditions that are associated with pain; including pressure sores, infections, and fractures especially when caring for demented patients. Lastly, persistent use of medication should be implemented to control continuous pain in individuals suffering from chronic conditions.

References

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Alafuzoff, I., Overmyer, M. & Helisalmi, S. et al. (2000). Lower counts of astroglia and activated microglia in patients with Alzheimer’s disease with regular use of non-steroidal anti-inflammatory drugs. Journal of Alzheimer’s disease 2, 37.46.

Anchez, M., Moghadam, S., & Naik, P. et al. (2011). Hippocampal network alterations in Alzheimer’s disease and Down syndrome: From structure to therapy. Journal of Alzheimer’s Disease 26, 29–47.

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