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Understanding the Process and Experience of Dementia

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Dementia – ‘generally accepted by clinical psychologist and psychiatrists is outlined in DSM-III-R (APA, 1987) and DSM-IV (APA, 1994). In summary, it states that for diagnosis of dementia, there should be demonstrable evidence of impairment in short-term and long-term memory. Impairment in short-term memory (inability to learn new information) may be indicated by an inability to remember three objects after five minutes. Long-term memory impairment (inability to remember information that was known in the past) maybe indicated by an inability to remember past personal information (for example, what happened yesterday, birth place, occupation) or facts or common knowledge (for example, past Prime Ministers, well known dates).’ (Thompson, 2006)

Question 1

(a) Alzheimer’s Disease

‘Alzheimer’s disease is the most common form of dementia affecting around 417,000 people in the UK. Alzheimer’s disease was first described by a German neurologist Dr Alois Alzheimer. Alzheimer’s disease is a physical disease of the brain. During the course of the disease plaques and tangles develop in the brain leading to the death of brain cells.’ (www.alzheimers.org.uk, 2011) Alzheimer’s disease affects the brain by nerve cell death and tissue loss. As time increases with this disease it causes the brain to shrink, affecting almost all its functions. In the early stages of Alzheimer’s, before symptoms can be detected plaques and tangles begin to form causing difficulty in learning, memory, thinking and planning.

In the moderate stages (stages of Alzheimer’s being diagnosed) the plaques ad tangles spread further around the brain causing difficulty in speaking and understanding speech and a sense of where you body is in relation to objects. In advanced Alzheimer’s the cortex is severely damaged. In the advanced stages of Alzheimer’s disease the cortex shrivels up, damaging areas involved in remembering, planning and thinking. There is severe shrinkage in the hippocampus (an area of the cortex that plays a key role in the formation of new memories). Also the Ventricles, which are fluid-filled spaces, grow larger.

Looking closely at the brain tissue of an Alzheimer’s patient, it can be seen that the brain has fewer nerve cells and synapse than a healthy brain. There is a build up of Plaques (abnormal clusters of protein fragments) between nerve cells. Plaques form when protein pieces called beta-amyloid are clumped together. Beta-amyloid is formed from a larger protein found in the fatty membrane surrounding nerve cells. The texture of the protein beta-amyloid is sticky, which helps the build up of the protein into plaques. Large groups of pieces, rather than plaques, cause more damage, as the small clumps block cell-to-cell signalling at synapses. They also active immune system cells that trigger devour disabled cells and inflammation.

There is also Tangles located in dead and dying nerve cells, which are made up of twisted strands of another protein. Tangles destroy important cell transport systems made of protein. In healthy areas the transport systems are organised straight parallel cells, the protein ‘tua’ helps keep the stands parallel. The strands get formed when tau collapses and tangles are formed, they then fall apart and disintegrate. Scientists are unsure what the cause of Alzheimer’s death and tissue loss in the brain is but they suspect the Plaques and Tangles to be the cause. There are many symptoms an individual suffering with Alzheimer’s mite experience. Memory loss that disrupts daily life is seen as the most common symptom.

An Alzheimer’s patient may forget recently learnt information. Challenges in planning or solving problems are a symptom of Alzheimer’s. They find it hard to work with a work plan and have difficulties dealing with numbers, for example, difficulty paying a monthly bill. Alzheimer’s patents find it difficult to complete familiar tasks at home, work and leisure times. For example, driving and play familiar games. An Alzheimer’s patent also has confusion with times and places and keeping track of time. They have trouble understanding visual images and spatial, for example, walking past the mirror and believing their own reflection is someone else.

Alzheimer’s patents have problems with words in speaking and writing, they may forget what they were talking about in the middle of a conversation. They also have difficulty in remembering where they have placed objects and lose the ability to retrace their steps. Alzheimer’s have poor judgement skills; this is most common when dealing with money for example. They also tend to withdraw themselves from work and/or social activities. There is a change in mood with Alzheimer’s patients, they become confused, suspicious, depressed, fearful or anxious. They may be easily upset at home or outside their comfort zone.

(b) Vascular Dementia

Vascular dementia is the second most common dementia, first being Alzheimer’s disease. Vascular dementia occurs when there is a problem with the supply of blood to the brain. The brain needs a good supply of oxygenated blood to remain healthy. The blood is delivered through a blood network of blood vessels called the vascular system. If the vascular system within the brain becomes damaged and blood cannot reach the brain cells, the cells will eventually die, this leads to vascular dementia. There are many conditions which cause or increase damage to the vascular system, these could be anything from high blood pressure, high cholesterol and diabetes. This means that it is important that these conditions are identified and treated at the earliest opportunity.

There are different types of vascular dementia. The two main types are: one caused by strokes and one caused by small vessels disease. A third type is a mixture of the two. Stroke related dementia – is permanent damage to the brain caused by an interruption in the supply of blood to specific parts of the brain. The symptoms of this vary because it depends of which part of the brain is damaged. For example, if the area in question is responsible for the movement of a limb, paralysis might occur. If it is responsible for speech, the person might have problems communicating.

Equally, damage to particular areas of the brain can cause the symptoms of dementia. When vascular dementia is caused by a single stroke, it is known as single-infarct dementia. If vascular dementia is caused by a series of small strokes, it is known as multi-infarct dementia. Small vessel disease related dementia – this type of dementia is also known as sub-cortical vascular dementia, in sever forms, Binswanger disease, this causes damage to tiny blood vessels that lie deep into the brain.

The symptoms develop more gradually and are often accompanied by walking problems. Vascular dementia and Alzheimer’s disease (mixed dementia) – this is formed when Alzheimer’s, as well as stroke or small vessel disease may cause damage to the brain. Vascular dementia can affect different people in different ways as does the speed of progression varies. Some symptoms of vascular dementia can be similar to other types of dementia. Typically people suffering with vascular dementia might experience:

* A problem concentrating and communicating.
* Depression accompanying the dementia.
* Symptoms of stroke, such as physical weakness and paralysis.
* Memory problems (although this may not be the first symptom).
* A ‘stepped’ progression, with symptoms remaining at a constant level and then suddenly deteriorating.
* Epileptic seizures.

* Periods of acute confusion.
Other symptoms may include:
* Hallucinations.
* Delusions.
* Walking about getting lost.
* Physical or verbal aggression.
* Restlessness.
* Incontinence.

(c) Dementia Syndrome or ‘Mixed Dementia’

‘The issue of mixed dementia is a challenge. Increasing evidence shows that the different vascular factors are related to Alzheimer’s disease, and frequently, Cerebrovascular coexists with Alzheimer’s disease.’ (Mohr, 2004) Mixed dementia is a coexistence of Alzheimer’s disease and vascular dementia. Mixed dementia caused by the blood flow in the brain compromised by the stroke. The causes of mixed dementia are:

* High blood pressure.
* High cholesterol caused to the small blood vessels in the brain can cause death of brain cells.
* Disease in the arteries.
* Heart rhythm abnormalities.

The symptoms of mixed dementia are:

* Memory loss.
* Confusion.
* Poor concentration.
* Unable to carry out daily tasks.
* Depression.

(d) Dementia with Lewy Bodies (DLB)

‘Dementia with Lewy bodies (DLB) is a form of dementia that shares characteristics with both Alzheimer’s and Parkinson’s diseases.’ (www.alzheimers.org.uk, 2011) Lewy bodies are spherical protein deposits found in the nerve cell. When present in the brain it disrupts the brain’s normal functioning, interrupting the action of important chemical messengers, including acetylcholine and dopamine. Lewy bodies are also found in the brain with people with Parkinson’s disease. Many people suffering with Parkinson’s disease later go on to developing a dementia closely related to DLB. The symptoms of dementia with Lewy bodies is a progressive disease. This means that the symptoms become worse over time. They typical symptoms are: * A person with DLB will usually have some of the symptoms of Alzheimer’s and Parkinson’s disease.

* They may experience problems with attention and alertness, often have spatial disorientation and experience difficulty with ‘executive function’, which includes difficulty in planning ahead and co-ordinating mental activities. Although memory is often affected, it is typically less so than in Alzheimer’s disease.

* They may also develop the symptoms of Parkinson’s disease, including slowness, muscle stiffness, trembling of the limbs, a tendency to shuffle when walking, loss of facial expression, and changes in the strength and tone of voice. There are also symptoms that are particular to dementia with Lewy Bodies. In addition to the symptoms above, a person with DLB may: * Experience detailing and convincing visual hallucinations, often of people or animals. * Find that their abilities fluctuate daily, or even hourly. * Fall asleep very easily by day, and have restless nights with confusion, nightmares and hallucinations. * Experience depression.

* Faint, fall, or have ‘funny turns’.

(e) Pick’s disease (Fronto-temporal)

Pick’s disease is a ‘Premature abnormal aging of the brain within the scope of degenerative neurologic disease with behavioural changes and dementia.’ (Ursus-Nikolaus, 2004) Pick’s disease named after Arnold Pick, who first described the disease in 1892, was the irreversible decline in a person’s functioning over a period of years. Pick’s disease is a rare disorder that causes the frontal and temporal lobes of the brain, which controls speech and personality. It is therefore classed as ‘frontotemporal dementia’. (www.helpguide.org, 2010) Pick’s disease usually occurs from the age range of 35-75 and is more common in individuals with a positive family history of dementia. The rate of progression of pick’s disease dementia varies enormously, ranging from less than two years to over ten years. Pick’s disease is the result of a build up of protein in affected areas of the brain.

The accumulation of abnormal brain cells, know as Pick’s bodies, eventually builds up to a change in character, poor decision making, inappropriate behaviour and progressing towards severe impairment of speech, intellect and memory. The first sign of Pick’s disease usually involves a personality change or a decline in basic functioning. The progression of Pick’s disease is fortunately slow, symptoms do worsen over time. Behavioural signs and symptoms of Pick’s disease involve: impulsive and poor judgment, extreme restlessness, over eating and drinking, lack of personal hygiene, sexual exhibitionism, withdrawal from hobbies and daily activities, decline in function at home or work and repetitive or obsessive behaviour.

Emotional signs and symptoms of Pick’s disease involve: abrupt mood changes, apathy, lack of concern/warmth/empathy, rudeness, aggression, easily distracted and being unaware of behavioural changes. Language signs and symptoms of Pick’s disease involve: loss of vocabulary, trouble finding the right words, repetitive, weak and uncoordinated speech sounds, decrease in the ability to read and write and eventually a complete loss in speech. Physical signs and symptoms of Pick’s disease involve: increase in muscle rigidity and stiffness, difficulty to move about, lack of coordination, general weakness, memory loss and urinary incontinence.

(f) HIV – associated dementia

HIV Dementia is clinically defined as ‘a disabling cognitive or motor dysfunction interfering with the patent’s occupation or activities of daily living, or loss of behavioural development milestones in the absence of a concurrent illness or condition.’ (Clive, 2007) It is not know exactly how the HIV virus damages the brain. Aids dementia complex is caused by the virus itself. HIV affects the brains in several ways. Viral proteins damage cells directly or by infecting inflammatory cells in the brain and spinal cord.

HIV may then induce these cells to damage and disable nerve cells. At first the symptoms of AIDS Dementia complex are subtle and may be over looked, but they soon become troublesome. The symptoms vary widely from person to person. The symptoms may involve: poor concentration, mental slowness, reduced productivity at work, behaviour changes, difficulty learning new things, confusion, decrease libido, forgetfulness, apathy, confusion, withdrawal from social activities, depression, speech problems, vision problems, bladder control and balance control.

Other symptoms may include: psychosis (severe mental and behavioural disorder), sleep disturbance, mania (extreme restlessness) and seizures. Without HAART (drug cocktail: a combination of protease inhibitors taken with reverse transcriptase inhibitors; used in treating AIDS and HIV), these symptoms gradually get worse causing patent’s to go into a vegetative state.

(g) Huntington’ disease (HD)

‘Huntington’s disease is chronic, progressive, hereditary disease affecting the central nervous system, stemming from damage to the basal ganglia within the brain.’ (Waller, 2002) Huntington’s disease is caused by a genetic defect on chromosome #4. The defect causes a part of the DNA, called a CAG repeat, to occur many more times than it is supposed to. For a normal person it usually repeated about 10-35 times, but with someone suffering from Huntington’s disease it’s about 36-120 times. As the gene passes from one generation to another the number of CAG’s tends to get larger. The larger number of repeats means the larger chance of gaining the symptoms at an earlier age. Huntington’s Disease is caused by cell death in specific regions of the brain.

Patients of Huntington’s disease are born with mutated versions of the protein huntingtin (Htt), which is thought to cause these toxic effects. Researchers know that HD results from a single mutated protein, no one seems to know what it does and why it does not cause symptoms till later on in life, or why it kills a specific set of brain cells, even though Htt is found in every single cell in the human body.

Physical symptoms of Huntington’s disease can occur at any age even from infancy. It is most common to occur in middle age. Death usually occurs 15 to 20 years after the first symptoms, as a result in the general decline in health, or more specific the inability of swallowing. The symptoms of Huntington’s disease resemble those of Parkinson’s disease with rigidity, slow movements and tremor. The symptoms of Huntington’s disease involve: behaviour changes, abnormal and unusual movements, Dementia that slowly gets worse.

(h) Creutzfelt-Jacobs disease (CJD)

Creutzfelt-Jacobs disease is ‘a progressive, fatal, dementing illness caused by an infectious agent known as a prion.’ (Ferri, 2008) Prions ‘are infectious disease-causing agents that consist of a modified protein (unlike bacteria, for example, which are more complex whole cells). In some unique way, which isn’t understood, prion proteins cause degenerative diseases of the nervous tissues (for example, brain, spinal cord and nerves), which are usually fatal.’ (BBC Health, 2011) Prion proteins occur in a normal form (harmless proteins found in the body’s cells and infectious forms (which cause diseases).

The normal prions are in the same sequence of amino acids, but the infectious prions take a different folded shape. Once they appear, the abnormal prion proteins clump together. This leads to neurone loss and brain damage. CJD may have been passed to humans through infected beef products, but there are several types of CJD and infections and it is not clear how it is gained, it may be inherited, infectious or unknown origin. Creutzfelt-Jacobs disease is a very rare affecting every one in a million.

The symptoms usually occur from the age of 60 onwards. Early symptoms include: memory loss, mood changes and a loss of interest in life. It is then followed by slurred speech, clumsiness, confusion and unsteadiness. As the weeks passes the movements become jerky, the limbs become stiff and incontinence also occurs, until they lose awareness of their surroundings. Death usually occurs within 6 months to a year, although the progression of the disease can be slower. The problem with CJD is that it has a very long incubation period, a person maybe infected for a long period of time without knowing.

Question 2

Dementia causes the brain to gradually lose its mental ability, including problems with memory, understanding, judgement, thinking and language. Memory is information which is stored in the brain. The three stages required to remember are: registering memories, storing memories and retrieving memories. Short term memory is the ability to remember things which have occurred recently, although it also recalls something that happened many years ago. Memories are often thought as like an onion. The long term memories are at its core and the short term are on the outside, damages always occur from the outside first causing people with dementia to lose their short term memories first. It is difficult to give new information to a dementia patient as they don’t seem to store recent memories.

The outside cells of the brain are the first to die; this is the reason for short term memory loss. Damages to the nerves to the brain to deliver information, neuron transmitters, are the cause of information not being processed. The 100 billion neurons are divided in two halves, the right side puts the information together and the left analysis it. People with the left side of the brain damage find it difficult to put information together and will see things but are not able to make connection as to what they are.

People with neuron damage to the left side of the brain tend to suffer from dementia; they also have organisational problems and also problems with speech. Dementia sufferers are able to recall memories from a long time in their past. This is because these memories are stored in the core of the brain and have not been damaged yet. The memories that tend to stick in their mind are memories of good times and bad times in their past.

Question 3

There are a number of other conditions which cause changes to an individual with dementia. Brain injury, such as an external trauma, blow to the head or an internal one such as a stroke. The injuries for this may be mild or severe depending on the condition; the results of this could either be short-term, long-term or permanent. Drug and alcohol misuse also cause memory loss as they damage neurons. Diet makes a difference; vitamin C and sugars can have an effect on memory. Brain tumour can be benign or malignant, which cause great affects on memory loss. Myalgic Ecephalomyelitis causes neurological disorder – this causes persistent fatigue and muscle pain. Medication can also cause some side effects of memory loss.

Encephalitis, which is the inflammation of the brain, caused by a viral infection, causes memory loss. Stress and insomnia affect the memory. The day to day aspects of an individual with dementia change over time. As time goes on conditions worsen, but that depends on the severity of the dementia as it varies from person to person. Individuals tend to have good days and bad days depending on their mood and environment they are in. In a normal environment the signs and symptoms of a dementia patient are hard to see, but taking a dementia patient out their comfort zone may cause them to have confusion.

Question 4

(a) Providing up to date care plans are vital for patients suffering with dementia. Dementia is a deteriorating condition and the speed of the decline in health varies from person to person. This means that care plans must be updated and looked at on a weekly basis. A clients needs may change, which causes a change in care planning. Person centred care is very important as it is ensuring that the person receiving the care is at the centre of everything you do. The person centred approach can help in reducing agitation with the person with dementia. It is good to discuss the care plans with the carer, patient, family, friends and/or next of kin.

This way you are able to give the individual care in accordance to their needs, wishes, beliefs and preference. Taking daily records of the client will help in showing the changes of condition over time. This will also show the deteriorating rate of the dementia. If the carer changes an activity, for example, keeping bread in the fridge rather than cupboard, this may confuse and agitate the client.

The bread will be kept uneaten because the client is not used to seeing it in the fridge. Documenting mood changes in the client may show give some sort of indication that something has changed to make the clients mood change. When a client changes it carer, it would be very beneficial for the new carer to read the old carers daily routines and care plans to get a good inside to the history of the client.

(b) Reporting signs of dementia must be done in the daily routine paper work of the carer. The carer must note down at every single visit of any changes in the mood or activity of the client. If the signs of a client’s needs change dramatically, the carer must consult the care manager. The care manager should re-assess the care plan with the family/friends/medical staff.

There may be a call to change medication or even moving out their private home to more of a protected environment. The most important thing is the client’s safety and well-being. The clients own preferences should come first and it is up to the carers to provide a care plan around the needs of the client. Documents should be kept at each visit and on a weekly basis the care manager should read the weekly activities and decide on ways, if needed, on how to improve the standard of care.

Alzheimer’s Society. (2011). Alzheimer’s disease. Available: http://www.alzheimers.org.uk/site/scripts/services_info.php?serviceID=7. Last accessed 3rd May 2011. Alzheimer’s Society. (2011). What is dementia with Lewy bodies (DLB)?. Available: http://alzheimers.org.uk/site/scripts/documents_info.php?documentID=113. Last accessed 7th May 2011. BBC Health. (2011). Creutzfeldt-Jakob Disease (CJD). Available: http://www.bbc.co.uk/health/physical_health/conditions/cjd1.shtml. Last accessed 9th May 2011. Clive, E (2007). Primary HIV/AIDS Care: A Practical Guide for Primary Care Personnel in a Clinical and Supportive Setting. Malaysia: Jacana Ferri, F. (2008). Ferri’s color atlas and text of clinical medicine. China: Elsevier Health Sciences. p196. Jocelyn Block, M.A., Segal, J.. (2010). Pick’s Disease Signs, Symptoms, Treatment, and Support. Available: http://www.helpguide.org/elder/picks_disease.htm. Last accessed 8th May 2011. Mohr, J (2004). Stroke: pathophysiology, diagnosis, and management. 4th ed. USA: Churchill Livingstone. p655. Thompson, S (2006). Dementia and memory: a handbook for students and professionals. Hampshire: Ashgate Publishing Ltd. 19. Ursus-Nikolaus, R. Werner M. (2004). Color atlas of pathology: pathologic principles, associated diseases, sequela. Germany: Thieme. Waller, D. (2002). Arts therapies and progressive illness:
nameless dread. USA: Psychology Press. P56.

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