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DEMENTIA AWARENESSCERTIFICATE COURSE

UNIT TWO

THE CONDITION: WHAT IS DEMENTIA?

Introduction

This Unit will explore the nature of dementia. In achieving this learning outcome you will explore your own perceptions and experiences of working with people with dementia, and compare these to research that has specifically addressed the nature of dementia. This will involve, firstly, exploring what is meant by the term dementia. Then, there is a need to consider its common manifestations in clinical contexts. Following on from this, there will be a need to examine proposed theories of causation, and their implications for practice. Finally, there is a need to explore possible differential diagnoses and explore the importance of correct diagnosis for the person and his or her family.

What is Dementia?

Let us begin with an activity to enable you to conceptualise your own understanding of dementia

ACTIVITY 2.1: QUESTION

A person tells you that their friend’s mother has just been diagnosed with dementia. They know you are a healthcare professional, and ask you what is dementia?

How would you respond?

Dementia is an English word derived from the Latin “de” (meaning apart) and “mentis” (meaning mind). However, this literal meaning of the word does not help in ascertaining what dementia is because, philosophically, there are difficulties defining what the mind is and, clinically, it is difficult to test if it is gone. The word is confusing in that it refers to both a group of illnesses that share common characteristics and specific types within that group of illnesses. For clarity, we shall consider dementia as a syndrome first, before moving on to consider its various types.

Dementia Awareness Certificate Course – Unit Two –

Dementia: The Syndrome

The standard conceptualisation of dementia from a clinical perspective is proposed by the World Health Organisation in 1992 in its International Classification of Diseases (at present in its tenth edition). This definition has been likened to an umbrella that encapsulates many types (to be considered later on).


Now find the definition of dementia proposed by the World Health Organisation (1992):

http://www.mentalhealth.com/icd/p22-or05.html

This offers a definition of dementia that is well recognised by clinicians within a European context.

When you have read this article, summarise what you have learned about dementia.

As mentioned above, within a European context, the standard medical classification system is the International Classification of Diseases, at present in its tenth edition (ICD-10) proposed by the World Health Organisation in 1992. This classification system defines dementia as follows:

Dementia is a syndrome due to disease of the brain, usually of a chronic or progressive nature, in which there is disturbance of multiple higher cortical functions, including memory, thinking, orientation, comprehension, calculation, learning capacity, language, and judgement. Consciousness is not clouded.

It will be useful to explore this definition in some detail so as to ascertain what the traditional view of dementia is.

Dementia is a syndrome

Dementia is defined, firstly, as a syndrome. A syndrome may be defined as:

A set of signs that occur together which often point towards a particular disease or condition

As such, it is important to ascertain what these signs and symptoms are which points towards dementia as the condition affecting the individual concerned.


http://www.mentalhealth.com/icd/p22-or05.html


List the signs and symptoms that you have seen in people diagnosed with dementia (of whatever type)

In the late nineteenth century, Kraeplin was a keen exponent of diagnosing based on this approach. He set out to list all the signs and symptoms that particular people with mental health problems experienced and, by a process of deduction, show that in order to be diagnosed with a particular illness the person needed to be experiencing these core signs and symptoms (Bentall 2003:13). The process is illustrated below (fig 2.1).

Figure 2.1: Process of Diagnosis


From Activity 2.3, you may have generated a list of symptoms such as the ones proposed by Jacques and Jackson (2000), Thomas (2008) and Rabin et al (2006):

Figure 2.2: What is Dementia?

This random array of symptoms can be classified as falling into one of five categories:

Impaired cognition Abnormal mental phenomena Problem behaviours Drive disturbances Impaired functioning

As can be seen, the dementia syndrome affects a vast array of functions.


Dementia is a disease of the brain

Dementia is a neuropsychiatric disorder that has, as its primary causation, a disease process that affects the brain. Depending on which part of the brain is affected, the manifestations will be different for each person. It may be useful to explore what the functions of the various parts of the brain are before discussing the abnormal manifestations present in the dementia syndrome.


Locate the following webpage:

http://www.waiting.com/brainanatomy.html#anchor2587568

Write what you have learnt about the brain

Complete the following table:

Lobe Function

Parietal

Occipital

Frontal

Temporal

Depending on which part of the brain is affected, this will dictate what symptoms the person with dementia will display. The dementias are sometimes defined in terms of being either cortical or subcortical. This refers to the part of the brain where the disease is present. The cortical dementias are those that affect the cortex of the brain. The subcortical dementias, in contrast, are those that affect the layers beneath the cortex. It is important to note that a person with dementia could experience disease processes in both parts of the brain.


Dementia is chronic or progressive in nature

At the present time, dementia is chronic and progressive in nature. This means that dementias are long in duration. At the present time, there is no known cure. Whilst some medications have been found to slow down the rate of deterioration, there is no means by which the dementing process can be permanently stopped or reversed. However, there are certain conditions that can present like dementia but do have a cure. As such, it is important that an accurate diagnosis is made early on.

Dementia is a disturbance of multiple higher cortical functions

The use of the word “cortical” refers to the cortex, the vast layer of nerve cells that covers nearly the whole surface of the brain (Anderson 2008). It amounts to almost two-thirds of the brain’s mass. It is often referred to as grey matter, primarily because it lacks insulation like other parts of the brain. This part of the brain is an important control centre for sensory information coming into the brain, and motor commands coming out of the brain. As such, when it experiences a disturbance in its ability to function, it results in a multitude of problems for the individual, including in the following spheres:

Memory Thinking Orientation Comprehension Calculation Learning Language Judgement


Considering your answers to Activity 2.4, which lobes are most affected by the dementia process?


Lobe Function Effects if Damaged

Parietal

Occipital

Frontal

Temporal

Check your answers by accessing the following webpage:

http://www.neuroskills.com/brain.shtml#map

Your answers to Activity 2.5 may have included some of the following (given in Table 2.1):


Table 2.1: Lobe – Function and Effects of Damage

Lobe Function Effects of Damage

Parietal SensationPerception

AnomiaAgraphiaAlexiaDyscalculiaApraxia

Occipital Centre of the visual-perceptual system

Visual hallucinationsVisual illusionsAlexiaAgraphia

Frontal LanguageEmotionsMovementProblem-solving skills

Emotional instabilityBalanceDysphasiaDyspraxiaImpaired problem-solving skillsPerseveration

Temporal MemoryDanger responseSenses (sound and smells)

Disturbed sensationsImpaired perceptionsImpaired organisation of verbal materialsDisturbed language comprehensionImpaired long-term memoryPersonality changesBehavioural changesAltered sexual behaviours(Kolb and Whishaw 1990)

Dementia occurs when consciousness is not clouded

All that has been stated so far indicates what dementia is. This is the only sentence in the definition of the dementia syndrome that explicitly states what it is not. As stated above, it is important to ascertain if the person is experiencing a true dementia-related illness from a curable condition that just mimics certain aspects of the dementia process. The fact that in dementia consciousness is not clouded is a useful diagnostic point that makes a clear distinction between dementia and delirium. In the latter, consciousness is clouded and is curable with correct diagnosis and intervention.


Summary

As a result of what has been stated so far, the dementia syndrome has clear diagnostic features:

There are multiple cognitive deficits (of which memory must be one) There is also marked functional impairment Consciousness is clear The cognitive and functional deficits are a marked change from previous levels Symptoms have been experienced for a long duration (over six months)

Dementia: The Types

It has been noted that there are over two hundred types of dementia (Haan and Wallace 2004), although ninety-five percent of all dementias fall into one of four types (to be considered later).


What types of dementia have you heard of/worked with?

As stated earlier, Kraeplin envisaged a system of mental illness that comprises clearly defined symptoms linked to specific illnesses that are associated to specific aetiologies.


Reviewing your pre-generated list of symptoms from Activity 2.3, see if you can link the respective symptoms to particular types identified in Activity 2.6.

Depending on which part of the brain has been affected, this will determine how the dementing process manifests. If the classification system of cortical and subcortical dementias is employed, Rabins et al (2006:4) gives a methodology for differentiating between the two:


Table 2.2: Cortical and Subcortical Dementias

Cortical:The Four As

Subcortical:The Four Ds

AmnesiaApraxiaAphasiaAgnosia

DysmnesiaDelayDysexecutiveDepletion

Cortical dementias are defined by what Rabin et al (2006) refer to as the “Four As”. These are:

Amnesia: problems with memory Apraxia: problems with learned motor tasks Aphasia: problems with language Agnosia: problems with recognition

By contrast, subcortical dementias are defined by the “Four Ds”:

Dysmnesia: difficulties with memory Delay: slowed thinking and movement Dysexecutive: difficulties with decision-making Depletion: reduced complexity of thoughts

However, it is important to note that a person could experience both symptoms of cortical and subcortical dementias (i.e. mixed dementia).


Revisit your answers to Activity 2.6.

In light of the differentiation by Rabins et al (2006) of the two types of dementia, can you state whether each of the types of dementia you have noted are either cortical or subcortical dementias?

To assist you in this process, locating the information to complete the following table may be helpful.


Cortical Subcortical

Mental Status:LanguageMemoryCognitionPersonalityMood

Motor System:SpeechPostureGaitMotor speedMovement disorder

Anatomy:CortexBasal ganglia/ thalamus/ mesencephalon

One way to differentiate the clinical picture of the two types of dementia (cortical and subcortical) is to consider the effects they have on three distinct areas: mental status, motor system, and anatomy (Green 2000; Mendez and Cummings 2003; Miller and Morris 1994). Firstly, mental status comprises several distinct but interrelated areas. Language is a key symptom of cortical dementias, whereas it is not usually an issue for subcortical dementias. They both experience problems with memory. However, this is more noticeable in cortical than subcortical dementias. The same can also be said for cognition, with cortical dementias displaying more severe disturbance. Personality is affected in both types: a person with a cortical dementia will appear unconcerned or slightly euphoric; whereas a person with subcortical dementia appears more apathetic. Finally, in relation to mood, it is more common to see problems in this area in subcortical dementias than in cortical dementias.

Secondly, there are effects in the motor system that assist in differentiating between the two types. For cortical dementias, aspects of the motor system (such as speech, posture, gait and speed) are all normal. However, in subcortical dementias, there can be imperfections in speech (dysarthria), abnormalities in posture and gait, a reduction in motor speed; and, as a result, movement disorders are common.

Finally, when considering anatomical changes, there is a change in the cortex in cortical dementias and a change in the basal ganglia, thalamus and mesencephalon regions in subcortical dementias.


These clinical pictures are reflected in the types of dementia that are defined as either cortical or subcortical. Some examples of each are listed below:

Table 2.3: Dementia Types

Cortical Subcortical

Alzheimer’s DiseaseFrontotemporal DementiaDementia with Lewy Bodies

Vascular DementiaAIDS-related DementiaHuntington’s Disease

For older people (that is, those aged sixty-five years and older), the prevalence of dementias have been calculated in the “Dementia UK” report (AS 2007). It is important, however, to note that dementia has different prevalence rates depending on certain factors. For example, people aged under sixty-five have different prevalence rates (Harvey 1998). These are illustrated below:

Figure 2.3: Dementia Prevalence Rates

The four main types of dementia will now be considered.


Alzheimer’s Disease

Clinical Presentation


In your experience, what are the typical signs and symptoms of Alzheimer’s disease?

The World Health Organisation (1992) state that Alzheimer’s disease comprises the following:

Box 2.1 Alzheimer’s Disease: Diagnostic Criteria (ICD-10)

Fulfil the criteria for the dementia syndromeInsidious onsetGradual progressionNo focal neurological signsNo evidence of systemic/ brain disease that could cause dementia

However, this is not the only classification system that can be employed to diagnose Alzheimer’s disease.


Locate the NICE/SCIE (2007) guidelines on dementia.

They can be found at:

http://www.scie.org.uk/publications/misc/dementia/dementia-fullguideline.pdf

What diagnostic criteria does it recommend with regard to Alzheimer’s disease?

Compare and contrast these diagnostic criteria with those proposed by the World Health Organisation (1992)

What are the similarities? What are the differences? Which set of criteria most closely relates to your clients?

Alzheimer’s disease accounts for about sixty-two percent of all older people with a diagnosed dementia (AS 2007). According to NICE/SCIE (2007), the preferred diagnostic criteria are those proposed by NINCDS-ADRDA (McKhann et al 1984).


Box 2.2 Probable Alzheimer’s Disease: Diagnostic Criteria (NINCDS-ADRDA)

Established by clinical examination (mental state/ neuropsychological tests)

Deficits in two or more cognitive domains (memory, language, visuospatial perception/construction, calculation, praxis, or executive function)

Progressive deterioration of memory/other cognitive domains

No disturbance of consciousness

Onset between 40-90 (most over 65)

Absence of systemic/brain diseases

The advantage of the NINCDS-ADRDA criteria model, is that it offers criteria for “possible” and “unlikely” Alzheimer’s disease, as well as “probable” and “definite”. “Possible” allows for an atypical onset, progression or presentation of the dementia. It also allows for the presence of a systemtic disease, although this is ruled out as being the cause of the dementia symptoms. In addition, it also allows for only one cognitive domain to be affected, so long as there is no known cause for the deterioration. “Unlikely” Alzheimer’s disease is one that presents with sudden onset, has focal neurological signs and the person experiences seizures or disturbances with gait in the early stages of the illness. However, a “definite” diagnosis can only be made based on histopathological evidence derived from autopsy or biopsy.

Thomas (2008) notes that the clinical presentation of Alzheimer’s disease is varied, with both cognitive and non-cognitive symptoms. As well as the cognitive disturbances already noted, he states some of the non-cognitive symptoms as (see Table 2.4 below):

Table 2.4 Alzheimer’s Disease: Non-Cognitive Symptoms

Psychotic: Mood: Behaviour:

DelusionsMisidentificationsHallucinations

DepressionEuphoriaAnxiety

ApathyAgitationAggression


Risk Factors


What are the risk factors most closely related to Alzheimer’s disease?

You may wish to compare your answer with those outlined in the factsheet on risk factors produced by the Alzheimer’s Society, which is available at:

http://www.alzheimers.org.uk/factsheet/450

The main established risk factor for having Alzheimer’s disease is age – the older you get, the greater the chance you have of getting dementia. This has been calculated as a 5% increase for every 5.1 years after 60 years of age. This equates to the frequently stated prevalence rates by age:

40-65 1 in 1000

65-70 1 in 50

70-80 1 in 20

80+ 1 in 5

However, there are other established risk factors that are important to consider. For example, there is family history, and the closely related genetic risk factors. The latter specifically relates to the presence of the apolipoprotein e4 allele and some autosomal dominant mutations. There are also certain conditions that increase the risk of developing Alzheimer’s disease (for example, Down’s Syndrome). However, it is important to note that these are risk factors, and not definitive factors that will lead to a person developing Alzheimer’s disease.

There are also other, less certain risk factors that may be important, although the evidence is inconclusive at the present time. These include probable risk factors such as: depression, a head injury, and/or hypertension. Others are: being female, low intelligence, smoking, diabetes and aluminium (Thomas 2008).


What are the implications of these risk factors with regard to health promotion advice for the person diagnosed with Alzheimer’s disease?

Prognosis

The onset is insidious and the progression of Alzheimer’s disease is gradual.


http://www.alzheimers.org.uk/factsheet/450

Figure 2.4: Progression of Alzheimer’s Disease

Once the symptoms have manifested, it has been estimated that the person will live, on average, for 10.1 years. However, the range can be as little as two years and as great as over twenty years (Mendez and Cummings 2003; Rabin et al 2006). This figure has not changed much over the last twenty years, when the mean was estimated at between 1-16 years (Knopman et al 1988).

Vascular Dementia



Consider a person with vascular dementia with whom you work. In what ways does s/he present differently from a person with Alzheimer’s disease?


The most common subcortical dementia is vascular dementia. Vascular dementia comprises a number of distinct subtypes which have differing aetiologies. For example, Mendez and Cummings (2003) note several subtypes: multi-infarct dementia, single strategic strokes, multiple subcortical lacunar strokes, Binswanger’s disease, post-ischaemic dementia, haemorrhagic dementia, genetic cerebrovascular disorders (eg CADASIL), and mixed Alzheimer’s and vascular dementia. However, they all experience similar symptoms.

There are several diagnostic criteria that have been proposed for vascular dementia (for example: ICD-10; DSM-IV-Tr). According to the NICE/SCIE (2007) guidelines, the preferred diagnostic criteria are those devised by the National Institute of Neurological Disorders and Stroke/Association Internationale pour la Recherche et l’Enseignement en Neurosciences (NINDS-AIREN) (Roman et al 1993).


Locate a copy of the NINDS-AIREN diagnostic criteria for vascular dementia.

You can find a copy of the criteria at:

http://www.strokecenter.org/trials/scales/ninds-airen.html

How do these criteria compare with ICD-10 and DSM-IV-Tr classification criteria?

The NINDS-AIREN model defines “probable” vascular dementia as requiring all of the following:

Dementia present: Impaired memory and two (or more) other cognitive domains

Cerebrovascular disease present: focal neurological signs present (e.g. hemiparesis)

A relationship of the aforementioned: manifested or inferred from one (or both) of the following:

o Onset of dementia within three months of experiencing a strokeo Abrupt deterioration in cognitive function, with step-wise deterioration noted


http://www.strokecenter.org/trials/scales/ninds-airen.html

There are slight differences between the varying diagnostic criteria:

Table 2.5 Vascular Dementia: different clinical criteria

NINDS-AIREN ICD-10 DSM-IV-Tr

Stepwise deterioration + – –

Patchy distribution – + –

Focal neurological signs + + +

Ischaemic strokes + – –

Significant CVD + + +

Aetiological relationship + + +

Temporal relationship of stroke with dementia

+ – –

There have been some concerns expressed about the usefulness of distinguishing vascular dementia as a separate entity from Alzheimer’s disease. This has been for several reasons:

Utilising “step-wise” and “gradual” deterioration as distinguishing features of the two dementia has been shown to be problematic (Fischer et al 1990)

They both share the same risk factors (Stewart 1998)

The high prevalence of “mixed” presentations (Holmes et al 1999)

There is also a complex interrelationship between the two types of dementia. For example, Altieri et al (2004) found that people with dementia exhibited Alzheimer’s disease features for the first couple of years, and then the clinical picture changed to one resembling vascular dementia over the next couple of years.


In order to distinguish between Alzheimer’s disease and vascular dementia, the usual tool employed is the “Hachinski Scale” (Hachinski et al 1975). This is a 13-item scale that attaches either a score of 1 or 2 to each. A score of four or less means that it is probably Alzheimer’s, whereas a score of seven or more means that it is vascular dementia. Common differences are summarised in the table below (Table 2.6 below):

Table 2.6

Vascular Dementia Alzheimer’s Disease

Onset Abrupt onset Gradual onset

Risk Factors Vascular Family History

Mental Status Complex attentional deficits Word-finding difficulties

Findings Frontal executive dysfunction Visuo-spatial decline

Memory Poor retrieval and procedural memory

Poor recognition and cuing

Language Verbal fluency for letters less than verbal fluency for categories

Verbal fluency for categories less than verbal fluency for letters

Behaviour Apathy, depression, emotional lability

Delusions and loss of insight

Neurological Examination

Focal abnormalities Non-focal abnormalities

Risk Factors

As has been noted earlier, vascular dementia shares similar risk factors within Alzheimer’s disease (Mendez and Cummings 2003; Stewart 2008):

Demographics: for example, age (the older you are, the increased risk) and gender (more men than women are diagnosed with vascular dementia)

Physical health: for example, hypertension, and type-two diabetes

Vascular risk factors: for example, strokes, ischaemia, and atherosclerosis

Lifestyle: for example, smoking, diet (particularly an atherogenic diet) and obesity


Prognosis

Although there has been some discussion around the nature of the rate of deterioration, the usual pattern for vascular dementia (as defined by NINCDS-AIREN) is of the “step-wise” form.

Figure 2.5: Progression of Vascular Dementia

Due to the numerous subtypes, there are no definitive factors which assist in predicting the rate of decline for a person with vascular dementia. Wolfson et al (2001) estimated that the median survival rate for a person with vascular dementia was 3.3 years, which was slightly better than those with “probable” Alzheimer’s disease (3.1 years) and slightly less than those with “possible” Alzheimer’s disease (3.5 years). However, the differences are negligible.


Dementia with Lewy Bodies



Consider a person you have worked with who was diagnosed with dementia with Lewy bodies.

In what ways were they similar in presentation to either Alzheimer’s disease or vascular dementia?

In what ways were they distinct?

Dementia with Lewy Bodies (DLB) accounts for about five percent of people with dementia who are sixty-five years or older. However, its underlying pathology is more prevalent than this. For example, Hamilton (2000) has noted that 20% of brains of people who had dementia have Lewy bodies present in their brainstems. DLB is a relatively recent type of dementia that has been identified. Its first reports were in Japan in the 1960s and, in only a couple of decades, there was an agreed consensus on what criteria needed to be met for a clinical diagnosis (McKeith et al 1996). A decade later, an agreement was made on the neuropathological criteria as well (McKeith et al 2005). However, DLB is not without some debate. For example, its close relationship with Parkinson’s disease has led to issues around the nature of the distinction between Parkinson’s disease dementia and DLB. The discussion is similar to that surrounding the issue of when does mild cognitive impairment become dementia?

The NICE/SCIE (2007) guidelines recommend the use of the international consensus diagnostic criteria proposed by McKeith et al (2005)


Box 2.3: Dementia with Lewy Bodies: Diagnostic Criteria

Two of the following:

Fluctuating cognition with pronounced variations in attention and alertness

Recurrent visual hallucinations (typically well formed and detailed)

Spontaneous features of Parkinsonism

Or one of the above plus one of the following:

REM sleep behaviour disorder Severe neuroleptic sensitivity Low dopaminine transporter uptake in basal ganglia (seen

in SPECT/PET imaging)

As the diagnostic criteria above illustrate, the core features of DLB are:

Fluctuating cognition Visual hallucinations (70%) Parkinsonism (50%) REM sleep behaviour disorder Neuroleptic sensitivity Dopaminergic imaging

The consensus criteria also included other features of DLB which, whilst not being necessary for a diagnosis, are strongly supportive of a diagnosis (Gauthier and McKeith 2006). These include:

Repeated falls and syncope (40% of people with DLB) Transient loss of consciousness Severe autonomic dysfunction (eg orthostatic hypotension) Auditory Hallucinations (15% of people with DLB) Paranoid delusions (70% of people with DLB) Depression (40% of people with DLB) Relative preservation of temporal lobe structures (seen by CT/MRI imaging) Prominent slow wave activity on EEG


Risk Factors

Mendez and Cummings (2003:241) note that:

“Except in rare familial cases, little is known about specific risk factors or the aetiology of DLB”

However, age is clearly a risk factor (as it is with all forms of dementia). For DLB, the risk is higher if Parkinson’s Disease occurs after the age of 60. Its close association with Parkinson’s disease also hints at another possible risk factor, namely, familial history. It has been estimated that the prevalence rates are two- to three-times higher in families with PD than those without (Gasser 1998). Other possible risk factors have been identified, such as low educational attainment and increased severity of movement disorders, especially bradykinesia (that is, slowness of movement).


What are the implications of these risk factors with regard to health advice you would give to the person with DLB and their family?

Prognosis

As the diagnostic criteria note, the progression of DLB shows a fluctuating picture.


Figure 2.6: Progression of Dementia with Lewy

Jellinger et al (2007) estimate that the mean age of onset for DLB is 67 years, and the median survival rate from onset is five years. Gallasko (2003) states the mean survival rate to be between two and twelve years.


When compared to Alzheimer’s disease, DLB is shown to have the following similarities and differences (Table 2.7 below):

Table 2.7

Dementia with Lewy Bodies Alzheimer’s Disease

Onset Progression fluctuates Gradual progression

Mental Speed

Abnormal (slow) Normal

Attention Abnormal (sustained and divided)

Normal

Speech Abnormal (dysarthric) Normal

Language Normal Impaired comprehension

Memory Retrieval deficit; better recognition

Amnesia; impaired recognition

Affect Abnormal (apathy; depressed) Abnormal (apathy; depressed)

Movement Abnormal (Parkinsonism) Normal (parkinsonism can appear later on)

Frontotemporal Dementia


Consider people you work with who have been diagnosed with frontotemporal dementia.

How do they present?



Frontotemporal Dementia (FTD) has become the umbrella term for a group of dementias which display signs of degeneration in the frontal and temporal lobes over time. Rabins et al (2006) defines four types of FTD:

Table 2.8

Type Features Duration

Frontal Lobe Type Early stages: Disinhibition and lack of insight; Middle stages: Memory loss, rigidity and dysarthria; Latter stages: Withdrawal, apathy, aphasia and lack of spontaneity

5-7 years

Thalamostriatal type (e.g. PSP)

Personality changes and extrapyramidal motor symptoms (eg rigidity; slowness); visuospatial problems (sometimes); disinhibition (rarely)

7-10 years

Motor neuron type (eg ALS)

Language and memory problems appear early

2-4 years

Asymmetric Type Similar to frontal lobe typeSymptoms based on dominant hemisphere (left = language problems; right = visuospatial problems)

2-4 years

The NICE/SCIE (2007) guidelines do not state preferred diagnostic criteria for FTD. However, they state two:

LUND-Manchester criteria (Neary et al 1998) NINDS working group on FTD (McKhann et al 2001)


Pasquier et al (2008), in their review of FTD, note that the LUND-Manchester criteria show good inter-rater reliability and good validity. These diagnostic criteria differentiates three types of FTD:

Frontotemporal lobar degeneration (FTLD) Progressive non-fluent aphasia (PNFA) Semantic dementia (SD) (i.e. fluent aphasia and associative agnosia)

Box 2.4 Frontotemporal Dementia: LUND-Manchester Core Criteria

FTD PNFA SD

Insidious onsetGradual progressionEarly decline in social interpersonal conductEarly impairment in regulation in social conductEarly emotional bluntingEarly loss of insight

Insidious onsetGradual progressionNon-fluent spontaneous speech with either: AgrammatismPhonemic paraphasiasAnomia

Insidious onset and gradual progressionLanguage disorder (progressive/fluent/empty spontaneous speech; loss of word meaning; semantic paraphasia)Perceptual disorder (prosopagnosia; agnosia associative)Preserved perceptual matchingPreserved single-word repetitionPreserved ability to read aloud/write

Distinct from other types of dementia, the main clinical presentations for people with frontotemporal dementias, according to Pasquier et al (2008) and Mendez and Cummings (2003) are:

Personality changes: for example, invading others’ personal space and disinhibition

Emotional changes: for example, lacking empathy and appearing emotionally shallow and indifferent

Executive functions: for example, deficits in insight, planning, abstraction and problem-solving are common

Compulsive behaviours: for example, repetitive acts (checking, washing)


Language: for example, decreased verbal output leading to mutism

Memory: for example, memory is inefficient, patchy and inconsistent (rather than the typical amnesic picture of the aforementioned dementia types)

Perception: for example, largely remains intact (as opposed to other types of dementia)


Consider your answer to Activity 2.17.

In what ways do the people you considered there reflect any of these particular subtypes?

Risk Factors

This has proven difficult to ascertain due to the many possible variants. In some cases heredity has been shown to be a risk factor (for example, chromosome 17). There have also been studies that show a family history (40% in one study) (Munoz and Kertesz 2003). Age may be a risk factor although, due to it being more common in people under the age of sixty-five years, it is different from the previous dementias.

Prognosis

Mendez and Cummings (2003) state that the duration of frontotemporal dementia is about eight to eleven years. However, there are variations depending on the subtype (see Rabins et al (2006) classification above). It follows a course similar to Alzheimer’s disease (insidious onset and gradual progression).


Figure 2.7: Progression of Frontal Lobe

As a consequence, it is often misdiagnosed. For example, in one study, eighteen out of twenty-one people had been given a diagnosis of Alzheimer’s disease when, in actual fact, they had Pick’s disease, a form of primary progressive aphasia (a subtype of frontal lobe dementia) (Mendes et al 1993). Some of the similarities and differences are noted below (Table 2.9):


Table 2.9

Frontal Temporal Dementia

Alzheimer’s Disease

OnsetInsidious onset and gradual progression

Insidious onset and gradual progression

NumeracyAcalculia relatively spared early on

Acalculia prominent early on

Mental StatusVisuospatial disturbance late

Visuospatial disturbance early

PersonalityPersonality changes occur early

Personality changes occur late

Memory Amnesia late Amnesia early

Language Stereotyped speech Word-finding difficulty

Behaviour Emotional blunting early Emotional blunting late

Neuro Exam Frontotemporal atrophy Widespread atrophy

Others

There are many more types of dementia than the four discussed so far. Indeed, Haan and Wallace (2004) state that there are over 200 types of dementia. However, the four discussed so far account for over 90% of all the people who have dementia at the present time. Some of the other types of dementia result from:

Head injury Trauma Bacterial/viral infections Toxic/endocrine/metabolic disorders Anoxia


There are also “reversible” dementias. These are conditions that appear to meet diagnostic criteria for dementia, but are treatable. These include:

Thyroid problems Vitamin B12 deficiency Abnormal calcium levels Intracranial space-occupying lesions

As such, it is important that a correct diagnosis is made in order to ensure that the person gets the correct treatment.

Summary


Summarise your understanding of the four main types of dementia by completing the following table:

AD VaD DLB FTD

Clinical Features

Risk Factors

Prognosis

Dementia: The Conceptual Frameworks

“The term dementia was used to describe patients whose mental disability was secondary to some form of acquired brain damage – usually degenerative and occurring in old age” (McKeith and Farbairn 2001:8)


Ever since Marce described signs of cortical atrophy, enlarged ventricles and “softening” of the brain tissue in people with dementia in the nineteenth century, dementia has been synonymous with a conceptualisation that is based on the “disease model” (Tyrer and Steinberg 2005). However, Kitwood (1997) has pointed out that to understand dementia, neurological impairment is only one facet that needs to be considered. He devised an equation to conceptualise dementia, which states that:

Dementia = NI + P + B + H + SP

Where:

NI = Neurological ImpairmentP = PersonalityB = BiographyH = Physical HealthSP = Social Psychology

To gain a holistic view of dementia, the various conceptualisations will be considered under the three headings of:

Biological Psychological Social

Biological View of Dementia

The biological view of dementia stresses the importance of understanding the illness as a neurological impairment. As such, the main focus is on understanding what changes occur in the brain during the dementing process, and ascertaining reasons for these changes. This has been the view since the nineteenth century (Berrios 1990). Since then, there has been much work that has been carried out that has detailed many of the physiological changes associated with dementia. These include neurobiology (Arendt 2004), neuropathology (Nagy and Hubbard 2008) and genetics (Holmes 2008). Mendez and Cummings (2003) provide details of the nature of these neurological changes with reference to the various types of dementia.



What is the pathology of the four main types of dementia discussed above?

a. Alzheimer’s diseaseb. Vascular dementiac. Dementia with Lewy bodiesd. Frontotemporal lobe dementia

The most common form of dementia, Alzheimer’s disease, has the most well known pathology of all the dementias. When Alzheimer (1906, 1907) detailed the case of Auguste D, a 51 year old female, and his post-mortem revealed changes in her brain pathology. These included:

Brain atrophy Arteriosclerotic changes Senile plaques Neurofibrillary tangles

The latter two have become synonymous with the disease that bears his name. There are two main theories that have been proposed for the creation of these “plaques and tangles”: the amyloid cascade hypothesis and the tau hypothesis (Mohandas et al 2009). The first states that the neuritic placques (which are amyloid fibils that appear in dense formations outside neurons in the brain) are the result of excess levels of the amyloid beta protein. There is some evidence for this in that the amyloid precursor protein (APP) gene is located on chromosome 21, and this chromosome, which is duplicated in people with Down’s syndrome, almost universally display the symptoms of Alzheimer’s disease by the time they reach forty years of age (Nistor et al 2007).

The tau hypothesis states that the neurofibrillary tangles are formed as the result of an accumulation of the tau protein in the cytoskeleton of the neurons in the brain. Evidence for this theory derives from the observation that the deposition of amyloid placques do not necessarily correlate with the loss of neurons (Schmidt et al 2004).

Similar neurological understandings have been noted with the other forms of dementia. For example:

Vascular dementia: single ischaemic or thromboembolic infarcts in the brain (Grutzendler et al 2006)

Dementia with Lewy bodies: noted for the presence of Lewy bodies (that is, round shaped protein that develop inside nerve cells) located in the neocortex and/or substantia nigra (Mendez and Cummings 2003)


Frontotemporal lobe dementia: for example, Pick’s bodies (that is, silver staining spherical aggregations of tau protein in neurons) located in the brain of people with the primary progressive aphasia subtype (Kertesz et al 2005)

Such a conceptualisation of dementia as a neurological impairment lends itself to three distinct implications:

If the cause is biological, then the treatment will be biological in nature. Research will thus focus on finding out the precise mechanism of causation

The person’s behaviours will be seen in terms of symptoms to be managed

If there is no cure, then a paternalistic attitude to care may ensue

Psychological View of Dementia

Kitwood (1997) argued that dementia is not just about neurological impairment, but that the way in which we interact with the person with dementia can either enhance their quality of life or be detrimental to them. He termed this “malignant social psychology”. When we adopt “malignant positioning” (Sabat 2001), we can have a detrimental effect on the person with dementia. As such, Kitwood and Bredin (1992) note that dementia is the outcome of two related factors:

Neurological impairment The individual psychology of the person and the psychosocial context the person is in

As a consequence, there is a need to consider what constitutes these other factors that have an effect on the outcome of the dementing process for the individual. Kitwood (1997) has identified the need to consider four other factors: firstly, the person’s personality: this refers to the repertoire of experiences that help to form the individual’s ability to act in situations – whether the person learns to see situations as challenges to be overcome, or to avoid situations due to the stress they cause; secondly, the person’s biography: this refers to the life story of the person – their childhood, occupation, hobbies and interests – that helps to know something of the person we are working with; thirdly, the person’s health: some degree of confusion can be the result of physical health problems (for example, sensory deficits, metabolic problems etc) and these need to be considered and addressed; and, finally, social psychology: Kitwood (1996:273) states that:

“each individual is viewed as a creative agent: one who attempts to define situations, to make sense of what others are doing, and to put out appropriate actions in a context of meaning.”



What are the implications of this understanding of dementia for your work with people with dementia?

Understanding and dealing with aspects of malignant social psychology will be discussed in Unit Three. However, it is clear that there is a need to ascertain as much information as possible about the person with dementia.


If you already utilise a “Getting to Know You” type form as part of your assessment process, evaluate its usefulness:

What factors are considered? What factors are not considered?

If you do not already utilise such a form, devise a “Getting to Know You” form. Consider carefully what factors are essential to help you know relevant information about the person.

One example is the “Personal History Profile” that forms part of the “Pool Activity Level Instrument for Occupational Profiling” devised by Pool (2002). This asks questions about the individual’s:

Childhood Adolescence Adulthood Retirement Likes and dislikes How he/she likes to do things

Kitwood (1996) stresses the need to consider especially any losses that have been experienced by the person.

The implications for care are numerous. Firstly, if the dementia is a result of an interplay between neurological impairment, the person’s own psychology, and the social and psychological context that the person inhabits, then there is a need to consider more than just the person’s neurological deficits. Secondly, there is a need to get to know the person – their personality, their life story, etc. Finally, there is a need to consider carefully how we interact with the person with dementia as the psychosocial context we create may be detrimental to them. This will be discussed more fully in Unit Three.


Social View of Dementia

A third conceptualisation of dementia is that of the social model of dementia. This has been argued by people such as Marshall (2004), Gilliard et al (2005) and Harding and Palfrey (1997). In simple terms, this model sees dementia as a disability and, hence, just as societies have adapted to other disabilities in order to assist those affected to function more fully, so, it is argued, society needs to change in order to assist people with dementia to function. There are several advantages of this model, according to Marshall (2000, cited in Gilliard et al 2005). Firstly, the social model focuses on a person’s remaining abilities, rather than their losses. NICE/SCIE (2007:165) refer to the advantages of this in both assessment and planning of care:

“it should not be assumed that the person with dementia does not retain abilities to perform an activity. Individualised and creative ways need to be explored to maximise the use of an individual’s strengths”

Secondly, the social model recognises how people with dementia are marginalised and discriminated against. The idea of social exclusion has been conceptualised by Burden and Hamm (2000) as when a person lacks one or more of the following:

Accepted levels of material well-being and social benefits Commonly held legal and civil rights A positive estimation of social status and identity

With regard to dementia, these factors are pertinent:

Are family carers of people with dementia adequately recompensed for the care they give in financial terms?

Are people with dementia still having their civil rights violated by not being allowed out (due to inability to operate confusion locks on the doors) even though they are not detained formally under the Mental Health Act?

Are people with dementia valued within our society?


Another advantage of the social model is that it notes the importance of listening to the personal, subjective experience of having dementia. As NICE/SCIE (2007:70-71) notes:

“While the clinical model of dementia presented above describes the changes occurring within the brain, the way that dementia affects a person in day-to-day life will vary from one individual to the next.”

This is important not only in understanding the effects of the illness on the individual, but their experiences of services as well. Goldsmith (1996:167) notes in his “consultative discussion paper” on people with dementia that the first key area to consider is that communication is possible. He states that:

“If communication is possible, then it must be possible for them to communicate about services … Not to pursue the task of eliciting such views is tantamount to saying either that they are unable to communicate or that their views are irrelevant”

Finally, the influence of the physical and social environment on enhancing or disabling the person with dementia is emphasised in the social model. The means by which Kitwood’s (1997) malignant social psychology can work to disable people with dementia will be considered in Unit Three. Alzheimer’s Australia (2003) notes the following with regard to quality care for people with dementia in relation to the environment:

People receiving care should feel secure and comfortable in their surroundings The care environment should be designed and developed to support the person The care environment should enrich the person’s life and provide appropriate stimulation


Reflect on your own practice in working with people with dementia in light of the four factors listed above:

How can you enhance your work to be more strengths-based instead of deficits-based?

In what ways are people with dementia marginalised and discriminated against in your locale?

In what ways do you enable the person with dementia to “tell their story”?

How do the physical and social environments where you work enhance and/or disable the person with dementia?


The implications of the social model of dementia are outlined in NICE/SCIE (2007:70-71). They note that:

The illness is not the fault of the individual (as such, not all their behaviours should be seen solely in light of the dementing process)

The focus is on the skills retained rather than the losses incurred (as such, a more positive, empowering approach to care is advocated)

The individual can be fully understood (as such, there is a need to know as much about the person as possible)

The influence of a supportive environment is important (as such, the social environment should be as supportive as possible for the person with dementia to function in)

The key value of communication is endorsed (as such, communication is possible and should be encouraged)

Opportunities should be taken for rehabilitation and re-enablement (as such, dementia services should be proactive and not just a “warehouse” that advocates a paternalistic approach to care)

The responsibility to reach out to people with dementia lies with those who do not have dementia (as such, the onus is on us to support, enable, and equip people with dementia to function as valued members of society)

Summary

By way of your own understanding of what has been discussed so far, complete the following table to summarise your knowledge of the respective approaches to the conceptualisation of dementia.


What are the implications to caring for a person with dementia depending on which theory of dementia one accepts?

Biological Psychological Social


Dementia: Differential Diagnoses

It is important to differentiate “true” dementia from conditions that may be mistaken for dementia, but are not. The main differential diagnoses are known as the “three Ds”:

Decline in old age (also known as minor cognitive impairment or age associated memory impairment)

Delirium (or toxic confusional state)

Depression (or pseudodementia)

Each will be considered in turn.

Decline in Old Age (MCI/AAMI)


Locate the following article on Mild Cognitive Impairment.

Hodson R and Keady J (2008) Mild cognitive impairment: a review and nursing implications British Journal of Nursing 17(6): 368-373

Make notes on what you understand by the concept.


Mild Cognitive Impairment is categorised by the person experiencing problems with memory, but not experiencing functional problems that are more consistent with a dementia-type illness. Such a concept can be dated back to Kral’s (1962) attempts at defining what he termed “benign senescent forgetfulness”. This referred to people in a nursing home who experienced subjective problems with memory, but with no objective evidence of impairment. However, this lacked clear diagnostic criteria. Other attempts have been made when considering Age Associated Memory Impairment (AAMI) (Crook et al 1987), Age Associated Cognitive Decline (Levy 1994), and Cognitive Impairment Not Dementia (Graham et al 1997). However, the more preferred term to date is Mild Cognitive Impairment. Although not officially recognised in diagnostic criteria such as DSM-IV-Tr (APA 2000) and ICD-10 (WHO 1992), work by Petersen (2004) has devised the following diagnostic criteria for MCI:

Box 2.5 Mild Cognitive Impairment: Diagnostic Criteria (Petersen 2004)

Memory complaint (preferably corroborated by an informant)

Memory impairment relative to age-matched and educationally-matched healthy people

Essentially preserved general cognitive function

Largely intact activities of daily living

Not clinically demented

Often, an assessment scale such as the Clinical Dementia Rating Scale (Hughes et al 1982) is used because it gives a category of “questionable dementia” that could be linked to the concept of MCI. However, as O’Brien (2008) notes, it could equably be linked to early Alzheimer’s disease as well.


The debate around this concept lies in where it stands on the normal ageing versus dementia spectrum. Is it a normal part of the ageing process? Or is it a pre-clinical syndrome that leads to dementia? Petersen et al (1999), in a study that followed 220 people with MCI over three to six years, found that the rate at which these people went from MCI to dementia was 12% per year. O’Brien (2008) states the following as predictors of this change:

Severity of baseline cognitive performance (especially in episodic memory according to Rabins et al 2006)

Older age

Possession of APOE e4

Presence of functional impairment

Changes in volume loss in hippocampus and entorhinal cortex

Increased rates of whole brain atrophy

Hypometabolism and hypoperfusion on functional imaging

But O’Brien (2008:413) notes:

“However, all of these predictors, whilst highly significant, cannot predict with much certainty whether or not an individual with MCI will develop dementia”

Delirium

It is important to differentiate whether a person has got a dementia-type illness or is experiencing delirium because the former is irreversible but the latter is not. Often these can be mistaken by merely considering the clinical manifestations. Primarily this is because both disorders will manifest confusion. However, there are clear differences between the two types. For example, the diagnostic criteria from the DSM-IV-Tr (APA 2000) (listed below) show differences between delirium and dementia.


Box 2.6 Delirium: Diagnostic Criteria (DSM-IV-Tr, APA 2000)

A. Disturbance of consciousness

B. A change in cognition (not better accounted for by dementia)

C. Disturbance developed over a short period of time (hours to days) and fluctuates during the course of the day

D. There is evidence from history, physical examination or laboratory findings, that the condition has a physiological cause

The causes of delirium are multifactorial. However, they can be considered using the mnemonic DELIRIUMS:

Drugs – particularly as a result of their toxicity and/or side effectsElectrolytes and/or endocrine problemsLack of drugs (that is, withdrawal)Infections (for example, pneumonia and urinary tract infections)Retention of urine and faecal impactionIntracranial (for example, strokes and epilepsy)Under-nutrition and dehydrationMyocardial causes (for example, ischaemia, infarcts and arrhythmias)Subdural haematoma

All of these possible causes have the propensity to be treated and, thus, improve the quality of life for the individual experiencing them. However, Hogg (2008:512) notes that:

“the evidence overwhelmingly points to delirium being a marker for physical and cognitive decline and increased mortality”

As such, it is important to ascertain if the cause of the confusion is a result of delirium, dementia, or both.


Depression

The third condition that needs to be differentiated from dementia is depression. This is another condition that could be mistaken for dementia due to the clinical presentations of the person. This is compounded by the fact that as many as half of all people with dementia will also experience depression (Starkstein et al 2005). When one considers some of the symptoms of depression, the association with dementia is obvious.

Box 2.7 Depression: Symptoms

a sad, hopeless or irritable mood for much of the time

increased anxiety

a loss of interest or pleasure in activities that were once enjoyed

feelings of low self esteem, worthlessness or undue guilt

feelings of isolation and of being cut off from other people

sleep disturbance, such as early waking

problems with remembering, concentrating or making simple decisions

slowing down in mind and body, or increased agitation and restlessness

eating too little or too much, and weight loss or gain

aches and pains that appear to have no physical cause

thoughts of death and suicide.

NICE (2007) state that depression can be treated with either the use of a selective serotonin reuptake inhibitor and/or cognitive behavioural therapy. As such, it is important to get an accurate diagnosis so that the correct treatment can be prescribed.



Locate the following document:

RNAO (2003) Screening for Delirium, Depression and Dementia in Older Adults which is available online at: http://www.rnao.org/Storage/12/645_BPG_DDD.pdf

Make notes on what constitutes best practice according to this report.

Reflect on how your practice equates with this report’s findings.

Summary

It is important to ascertain a correct diagnosis so as to ensure the best care is given. However, it is also important to note that these conditions are not necessarily mutually exclusive. For example, a person with dementia can also experience periods of depression. They could also have an infection from time to time that may lead to delirious episodes. It is also possible that an individual could have all three at the same time! Therefore, a thorough assessment is essential to ascertain the extent of the problems that the person is experiencing.

Assessment


Consider the people you work with who have a diagnosis of dementia.

What types of assessment were conducted to reach a clinical diagnosis of dementia (of whatever type)?


Throughout all that has been discussed so far, it is clear that an accurate diagnosis is essential for the person. It has been estimated that only a third of all people with dementia receive a diagnosis (NAO 2007). In light of some of the problems with accurate diagnosis that have been highlighted in this Unit, coupled with the ability to treat some conditions that mimic dementia symptoms, there is a need for good quality and accurate assessment of the person to ascertain precisely what they are experiencing: Is it dementia? Depression? Delirium? Or a combination of these three? Because delirium has a physical cause, it is important to assess the possible physiological causes that may mean that the confusion is more accurately attributable to delirium than dementia. Thomas (2008:426) recommends the following physical assessments:

Full Blood Count Erythrocyte Sedimentation Rate Urea & Electrolytes Liver Function Test Thyroid Function Test Vitamin B12 and Folate CT/MRI/SPET

Syphilis serology Blood Glucose Cholesterol Mid-stream specimen of Urine Chest X-Ray ECG EEG


When conducting a cognitive assessment, Kipps and Hodges (2008) provide possible means of assessing the various aspects of cognition (Table 2.10):

Table 2.10

Cognition Assessment

Orientation:TimePlacePerson

Ask them the day and dateAsk them where they areAsk them their name, DOB, age

Attention Spell WORLD backwardsSerial 7s: take away 7 from 100 five times

Memory:EpisodicWorkingSemantic

Have they forgotten recent events?Have they forgotten common telephone numbers?Do they forget the word for something (usually saying “thing” instead)

Language:NamingComprehensionRepetitionReadingWritingAcalculia

Addenbrooke’s Cognitive Examination (Mioshi et al 2006)Say a word and get the person to point to that itemAsk them to define words such as “hippopotamus” and “perimeter”Repeat well-known phrase (eg.“No ifs, ands or buts”)Read and obey the following statement: “Close your eyes”Ask them to write a sentence (must contain an object, subject and a verb)Ask the person to write numbers you say, copy numbers, and read numbers aloud

Executive function:Letter fluencyCategory functionImpulsivity Perseveration Behaviour

State as many words as possible starting with the letter “A” “F” or “S”List as many animals as you can in one minuteGo-No-Go task: ask person to tap once in response to a single tap, and not to tap in response to two tapsCopy a short sequence of alternating squares and triangles and then continue across the pageNeuropsychiatric InventoryCambridge Behavioural InventoryFrontal Behavioural Inventory

Apraxia Imitate a gesture (eg wave)Ask: Stick out your tongue and brush your hairLuria three-step command (fist, edge, palm)

Visuospatial ability:Neglect DressingConstructional apraxiaVisual agnosiasProsopagnosia

Ask the person to bisect lines of variable lengthAsk the person to put on clothing that is inside outCopy two bisecting pentagons Ask the person to name objects, and identify objects from descriptionsDo they recognise familiar faces


However, the most common assessment tool used in clinical practice is the “Mini-Mental State Examination” (Folstein et al 1975).


Find a copy of the MMSE.

What are its strengths and limitations?

The MMSE is a simple cognitive assessment tool that can be easily employed in clinical practice, only taking about ten minutes to complete. It has been shown to have good reliability and validity (Tombaugh and McIntyre 1992). However, there are known variations depending on the age and educational level of the person being assessed (Crum et al 1993). The test also relies heavily on the person being able to read, write and communicate verbally. If any of these abilities are impaired, then the test may give inaccurate results (Kurlowicz and Wallace 1999). Although it should never replace a thorough clinical assessment (as outlined by Kipps and Hodges 2008, above), it is useful for distinguishing cognitive impairment from non-cognitive impairment, and may be used frequently so as to ascertain the clinical effectiveness of interventions utilised.

Unit Summary

This Unit has considered the nature of dementia, arguing that a truly holistic conceptualisation of the illness needs to consider the biological, psychological and social aspects of the illness. It has also considered the importance of differentiating “true” dementia from other illnesses that mimic some of its symptoms.

Further Reading

NICE/SCIE (2007) Dementia: a NICE-SCIE guideline on supporting people with dementia and their carers in health and social care (especially sections 4 and 6)

Sabat SR (2008) A bio-psycho-social approach to dementia In: Downs M and Bowers B (eds) Excellence in Dementia Care: Research into practice Open University Press: Maidenhead

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http://www.who.int/classifications/icd/en/bluebook.pdf (accessed: 26-11-08)

TUTOR TALK: Congratulations on coming to the end of this unit. Move on and answer the questions then return your completed test paper to the College for marking. Good luck and well done.

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