Dementia powerpoint

DEMENTIA Milen Santiago Ramos PRACTITIONER IN CLINICAL PSYCHOLOGY AND NEUROSCIENCE

You Knew Me to the End YOU'RE TIRED AND CONFUSED TODAY YOU SEE THE MOMENT THROUGH A HAZE YOU BRAVELY SIT IN SHADOWS AS YOU LIVE YOUR FINAL DAYS AND I JUST WATCH YOU HELPLESSLY AS YOU DRIFT AWAY WHERE IS THE PASSION, THE HERO THE STRONG MAN WHO HELD MY HAND? MY COUNSELOR, MY FATHER AND FRIEND WHAT WILL I DO IF THE DAY COMES THAT YOU MAY FORGET MY FACE ANOTHER STEP CLOSER TO THE END I GAZE INTO YOUR SHINING EYES YOU HAVEN'T SPOKEN IN A WHILE BUT I BELIEVE THAT EVEN THOUGH YOUR WORDS ARE LOCKED AWAY I SEE YOUR LITTLE TEAR AND IT SAYS MORE THAN WORDS CAN SAY IT SAYS I'M STILL HERE, I LOVE YOU AND IF I COULD I'D HOLD YOUR HAND MY COMFORT, MY DAUGHTER AND FRIEND AND IF THE DAY COMES THAT I DON'T REMEMBER AND KNOW YOUR FACE YOU'LL BE IN MY HEART UNTIL THE END AND WHEN OUR VISIT'S OVER AND IT'S TIME TO SAY GOODBYE I PUT MY CHEEK SO CLOSE TO YOURS AND HEAR YOU SOFTLY SIGH YES YOU WERE STILL HERE, YOU LOVED ME AND IF YOU COULD YOU'D HOLD MY HAND MY FATHER MY HERO AND FRIEND THE FINAL GIFT THAT YOU GAVE ME I'LL ALWAYS TREASURE IN MY HEART WAS KNOWING YOU KNEW ME TO THE END WAS KNOWING YOU KNEW ME TO THE END Words and music by Geri Karlstrom. Copyright © 2006 Ger's Music. All Rights Reserved.

Beautiful poem about dementia Do not ask me to remember. Don't try to make me understand. Let me rest and know you're with me. Kiss my cheek and hold my hand. I'm confused beyond your concept. I am sad and sick and lost. All I know is that I need you To be with me at all cost. Do not lose your patience with me. Do not scold or curse or cry. I can't help the way I'm acting, Can't be different 'though I try. Just remember that I need you, That the best of me is gone. Please don't fail to stand beside me, Love me 'til my life is done. - Author Unknown

GET SET… READY? GO Below are four (4) questions and a bonus question. You have to answer them instantly. You can’t take your time, answer all of them immediately. OK? Let’s find out just how clever you really are…. Ready? GO!!!

First Question: You are participating in a race. You overtake the second person. What position are you in?

Answer : If you answered that you are first, then you are absolutely wrong! If you overtake the second person and you take his place, you are second!

Second Question : If you overtake the last person, then you are…?

Answer : If you answered that you are second to last, then you are wrong again. Tell me, how can you overtake the LAST Person?

Third Question : This must be done in your head only.Do NOT use paper and pencil or a calculator. Try it. Take 1000 and add 40 to it. Now add another 1000 . Now add 30. Add another 1000. Now add 20. Now add another 1000 Now add 10. What is the total?

Answer : Did you get 5000? The correct answer is actually 4100. If you don’t believe it, check it with a calculator!

Fourth Question: Mary’s father has five daughters: 1. Nana, 2. Nene, 3.Nini, 4. Nono. What is the name of the fifth daughter?

Answer : Did you Answer Nunu? NO! Of course it isn’t. Her name is Mary. Read the question again!

The bonus round: A mute person goes into a shop and wants to buy a toothbrush. By imitating the action of brushing his teeth he successfully expresses himself to the shopkeeper and! the purchase is done. Next, a blind man comes into the shop who wants to buy a pair of sunglasses; how does HE indicate what he wants?

Answer : He just has to open his mouth and ask… It’s really very simple….

NOW WHO IS DEMENTED? OLD FOLKS OR YOU

Dementia -What is it ? Dementia is an illness. It is the loss of powers of the mind, the ability to remember things, to think things out and to understand things. When someone has dementia their brain cells die off faster then they should. The person has gradual failure of the brain. At first the person may seem a bit forgetful but soon it may become obvious that they do not understand where they are, what day it is or who people are. The past may become more real to them than the present. The personality of the sufferer changes. They may behave oddly and become difficult. It is not unusual for them to get very anxious or aggressive. They may lose the ability to do everyday tasks. At first this may be things that require some thought, like writing a letter, but later they may not be able to tie their shoe-laces. In the end they cannot care for themselves. They depend completely on others.

ten warning signs of dementia • Memory loss that affects job skills • Diffi culty performing familiar tasks • Problems with language • Disorientation to time and place • Poor or decreased judgment • Problems with abstract thinking • Misplacing things • Changes in mood or behavior • Changes in personality • Loss of initiative

Apoptosis, or programmed cell death, is a highly regulated process that allows a cell to self-degrade in order for the body to eliminate unwanted or dysfunctional cells. During apoptosis, the genome of the cell will fracture, the cell will shrink and part of the cell will disintegrate into smaller apoptotic bodies. Unlike necrosis , where the cell dies by swelling and bursting its content in the area, which causes an inflammatory response, apoptosis is a very clean and controlled process where the content of the cell is kept strictly within the cell membrane as it is degraded [1]. The apoptotic cell will be phagocytosed by macrophages before the cell’s contents have a chance to leak into the neighbourhood [1]. Therefore, apoptosis can prevent unnecessary inflammatory response.

Apoptosis, or programmed cell death, is a highly regulated process that allows a cell to self-degrade in order for the body to eliminate unwanted or dysfunctional cells. During apoptosis, the genome of the cell will fracture, the cell will shrink and part of the cell will disintegrate into smaller apoptotic bodies.

STAGES OF NEURONAL DEATH IN ISCHEMIC ATTACK

Unlike necrosis , where the cell dies by swelling and bursting its content in the area, which causes an inflammatory response, apoptosis is a very clean and controlled process where the content of the cell is kept strictly within the cell membrane as it is degraded [1]. The apoptotic cell will be phagocytosed by macrophages before the cell’s contents have a chance to leak into the neighbourhood [1]. Therefore, apoptosis can prevent unnecessary inflammatory response.

Medical Conditions that May Cause Dementia HIV/AIDS Head Trauma Parkinson's Disease Huntington's Disease Pick's Disease Creutzfeldt-Jakob Disease (CJD) Wernicke-Korsakoff Syndrome Mixed Dementia

Dementia in the Young Cass Mann is one of the world's longest-term HIV-positive diagnosed gay men, now in his third decade of living with HIV , and the founder of UK's only gay men's HIV/AIDS charity Positively Healthy, which provides HIV services including education, support, and peer counselling. Here he talks about the terrible effects of AIDS dementia. People who don't respond to HAART or ARV are at risk of AIDS dementia. You can't distinguish AIDS dementia from syphilitic dementia. If you've seen AIDS dementia, you'll never again have unsafe sex. We do a disservice to gay men by ads showing healthy, buff young men. People don't show images of lipodystrophy or AIDS dementia because they are afraid of offending people. But if fear is OK for ad campaigns about drunk driving, why not for HIV? If we were honest about the image of clinical AIDS, people's vanity might motivate them to avoid contracting HIV.

HIV/AIDS HIV/AIDS is a disorder of the immune system (the part of the body that fights off disease and infection) caused by a virus that can also destroy brain tissue. Dementia due to HIV/AIDS is characterized by forgetfulness, slowness, and difficulties with concentration and problem solving. It can also include apathy (a lack of energy, interest, and/or emotion) and psychotic symptoms, such as delusions (fixed, false beliefs) and hallucinations (hearing, seeing, touching, tasting, or smelling things that are not truly present). Because HIV/AIDS affects people of all ages, dementia due to HIV/AIDS can occur in children as well as adults.

Head Trauma Dementia due to head trauma can result from a single major head injury (such as a blow to the head during a car accident) or from a repeated series of head injuries, such those sustained by football players or boxers (sometimes called dementia pugilistica). The degree and nature of cognitive impairment due to head trauma depends on the location and severity of the brain injury. People with this type of dementia often experience amnesia (an inability to learn and recall new information and/or remember previously learned information or past events), persistent memory loss, irritability, problems sustaining attention, depression, apathy, and other personality changes. This kind of dementia is most common among young men who engage in highly risky behaviors such as riding a motorcycle without a helmet and driving while intoxicated. For more information about closed head injuries, please read our Traumatic Brain Injury article .

Parkinson's Disease Parkinson's Disease is caused by a lack of cells that produce dopamine (a neurotransmitter, or chemical that transmits messages in the brain and nervous system). This disorder affects movement by creating tremors (shaking or trembling, sometimes limited to a certain part of the body such as arms or legs), rigidity, and other problems with balance and motor skills. About 20-60% of people with Parkinson's Disease also develop dementia. Dementia due to Parkinson's Disease causes difficulty retrieving memories, depression, and problems making decisions and carrying out daily tasks. Interestingly, the brains of people with dementia due to Parkinson's Disease often appear to have damage that is similar to the brains of people with Alzheimer's Disease or Lewy Body Disease when they are examined during an autopsy.

Huntington's Disease Huntington's Disease is a genetic (inherited) condition that affects cognition, emotion, and movement. It can start as early as 4 years of age or as late as 85 years of age, but most commonly affects people in their late 30s or early 40s. When Huntington's causes dementia, a primary symptom is difficulty retrieving memories. For instance, people with dementia due to Huntington's might have trouble remembering where they went to college or what they did on their last birthday. Other symptoms include problems with executive functioning (the ability to plan and carry out daily tasks), and impaired judgment. Memory deficits become more severe as the disease progresses, and some people experience delusions (fixed, false beliefs) and hallucinations (sensing things that are not truly present). Children of parents with Huntington's Disease have a 50% chance of developing the disease themselves.

Pick's Disease Pick's Disease is the most common of the frontotemporal dementias, a long word which simply means that the frontal (near the forehead) and temporal (side) portions of the brain are affected. Most commonly occurring in people who are between 50 and 60 years old, Pick's Disease is characterized by drastic personality changes, a deterioration of social skills, and emotional blunting (a lack of empathy and emotion). These signs usually occur before problems with memory and other symptoms emerge. In the advanced stages of the disease, people with Pick's Disease may become extremely apathetic or highly agitated, to the point that conducting a psychological assessment (for diagnostic purposes) is impossible because they cannot participate or focus on answering questions.

FRONTAL LOBE DEGENERATION A frontal dementia but without the typical changes seen on neuropathological examination in Pick’s disease (more on Pick's disease at the end of this page) although cell loss in the frontal lobes is apparent. The onset is usually slow with only changes in personality seen for some time. This is followed by changes in mood and behavioural disturbance. It may be sporadic or familial, and an as yet unidentified mutation on a gene on Chromosome 17 is believed to be the cause of some cases.

FRONTOTEMPORAL DEMENTIA This is a clinical term to describe patients with personality (frontal lobe) or language (temporal lobe) changes. It includes the specific diseases of Pick’s disease and frontal lobe degeneration amongst others.

Creutzfeldt-Jakob Disease (CJD) Sometimes referred to as "mad cow disease," CJD is caused by "slow viruses" called prions, which are folded proteins that interfere with the brain's ability to function. The disorder usually affects adults between 40 and 60 years of age, but can occur at any age. Anywhere from 5-15% of CJD cases have a genetic component; however, many people have no family history of the disorder. In individuals with no family history of CJD, the disease is often transmitted through infected medical equipment in procedures such as transplantation of the cornea of the eye. Dementia caused by CJD often progresses rapidly over several months and is characterized by problems with attention, concentration, appetite, vision, and coordination.

Normal Pressure Hydrocephalus Normal Pressure Hydrocephalus occurs when there is an abnormal increase in the level of cerebrospinal fluid (the fluid in and around the brain and spinal cord which serves a protective, nourishing function) in the brain's hollow spaces (called ventricles). This increased fluid level squeezes the brain, which can cause subsequent damage. In addition to dementia, people with this disorder often experience problems walking and controlling their bladder .

Parkinson’s in the Young- caused by INTAKE of ECSTACY

Wernicke-Korsakoff Syndrome Wernicke-Korsakoff Syndrome results from a deficiency in thiamine (Vitamin B1) and is often the result of chronic, severe alcoholism. This syndrome can also result from general malnutrition, severe eating disorders, or the effects of chemotherapy (often used in cancer treatment). Dementia due to Wernicke-Korsakoff Syndrome is characterized by confusion, apathy (a lack of energy, interest, and/or emotion), an inability to engage in meaningful conversation (i.e., impaired ability to discuss current events or one's outlook on life), hallucinations (sensing things that are not truly present), and severe memory impairment.

Mixed Dementia Dementia caused by multiple medical conditions is called Mixed Dementia or - in the DSM-IV - dementia due to "multiple etiologies." The most common form of Mixed Dementia is dementia due to both Alzheimer's and Vascular Disease, both of which we describe below.

Dementia can also be caused by the persisting effects of a substance (e.g., an illegal drug) over-the-counter or prescription medication toxin such as mercury, lead, or carbon monoxide.

In cases where a clear reason for the dementia cannot be determined, the dementia is referred to as Dementia NOS (not otherwise specified). There are a couple of reasons a diagnosis of Dementia NOS might be given. For example, a person may clearly show signs of dementia, but the clinician does not have enough information to make an accurate diagnosis. In this case, the NOS is a temporary diagnosis that will be changed once the clinician has gathered more information. In rare cases, every known cause of dementia is ruled out (e.g., found not to be a cause), so a diagnosis of Dementia NOS is given because the reason for the person's symptoms is truly unknown .

HARD FACTS Dementia, including Alzheimer's Disease, is not infectious. Dementia is not usually inherited. Some families do have a tendency to have the disease. if a close relative has dementia you are only slightly more likely to get it than anyone else. Dementia is not caused by stress or a crisis. Sometimes at a time of crisis a person has to think clearly. This is when it is noticed that something is wrong- the person gets confused. Dementia is not caused by too much or too little mental activity. Dementia is not part of growing old. Most old people have very clear minds. But the older you get the more likely you are to get dementia Some younger people in their 40's and 50's get dementia. Dementia can't be cured at present. But treatment may be possible to relieve some of the symptoms .

TWO most common causes of dementia

The two most common causes of dementia include Alzheimer s disease Vascular dementia (dementia due to strokes ).

ALZHEIMER’S DISEASE 1 Alzheimer’s disease [AD] is characterized clinically by early memory impairment followed by language and perceptual problems. A key feature in the development of the disease is believed to be an abnormal protein b -amyloid which is deposed in the centre of the senile plaques. These can be seen together with neurofibrillary tangles under the microscope. AD may be sporadic or familial and the age of onset may vary enormously from around forty to over ninety, although it is predominantly a disease of old age. In familial cases, the age at onset within a family may be fairly constant. Several abnormalities in the genetic make up (gene mutations) have been identified in individuals with familial AD; the cause agent of the sporadic form of the illness is probably multifactorial.

ALZHEIMER’S DISEASE 2 The gene responsible for making the amyloid protein is on chromosome 21 and a mutation in this gene has been shown to cause AD in three families in Britain and about fifteen families world-wide. Many of the families that have a very young age of disease onset have been shown to have a mutation in a gene on chromosome 14 now called Presenilin 1. So far at least 25 different mutations have been described. Mutations in a similar gene, Presenilin 2, on Chromosome 1 have also been described; the age at onset in these families is later. In these families the inheritance is autosomal dominant. Late onset AD has been linked with chromosome 19 and type of Apolipoprotein. Although there is an increased predisposition to AD with the genotype Apolipoprotein 4 it is not conclusive and it is possible to have AD but not Type 4 and likewise to have Type 4 but not develop AD. Neuropathologically, the different forms of AD cannot yet be differentiated.

Stages of Alzeimer’s disease Barry Reisberg, MD and colleagues New York University Medical Center's Aging and Dementia Research Center Functional Assessment Staging (FAST) scale- allows professionals and caregivers to chart the decline of people with Alzheimer's disease. The FAST scale has 16 stages and sub-stages: FAST Scale Stage Characteristics 1... normal adultNo functional decline. 2... normal older adultPersonal awareness of some functional decline. 3... early Alzheimer's diseaseNoticeable deficits in demanding job situations. 4... mild Alzheimer'sRequires assistance in complicated tasks such as handling finances, planning parties, etc. 5... moderate Alzheimer'sRequires assistance in choosing proper attire. 6... moderately severe Alzheimer'sRequires assistance dressing, bathing, an toileting. Experiences urinary and fecal incontinence. 7... severe Alzheimer'sSpeech ability declines to about a half-dozen intelligibl words. Progressive loss of abilities to walk, sit up, smile, and hold head up.

Detailed Description of Each of the 7 Stages Stage 1 No cognitive decline . No subjective complaints of memory deficit. No memory deficit evident on clinical interviews.

Stage 2 (Forgetfulness) Very mild cognitive decline. Subjective complaints of memory deficit, most frequently in the following area: forgetting where one has placed familiar objects; forgetting names on formerly knew well. No objective evidence of memory deficit on clinical interview. No objective deficits in employment or social situations. Appropriate concern regarding symptoms.

Stage 3 (Early Confusional) Mild cognitive decline. Earliest clear-cut deficits. Manifestations in more than one of the following areas: _ patient may have gotten lost when traveling to an unfamiliar location ; co-workers become aware of patient's relatively low performance; word and name finding deficit becomes evident to intimates; patient may read a passage of a book and retain relatively little material; patient may demonstrate decreased facility in remembering names upon introduction to new people; patient may have lost or misplaced an object of value; concentration deficit may be evident on clinical testing. Objective evidence of memory deficit obtained only with an intensive interview. Denial begins to become manifest in patient. Mild to moderate anxiety accompanies symptoms.

Stage 4 (Late Confusional) Moderate cognitive decline . Clear-cut deficit on careful clinical interview . Deficit manifest in following areas: decreased knowledge of current and recent events; may exhibit some deficit in memory of one's personal history; concentration deficit elicited on serial subtractions; decreased ability to travel, handle finances, etc. Frequently no deficit in the following areas: orientation to time and person; recognition of familiar persons and faces; ability to travel to familiar locations. Inability to perform complex tasks. Denial is dominant defense mechanism. Flattening of affect and withdrawal from challenging situations occur.

Stage 5 (Early Dementia) Moderately severe cognitive decline. Patient can no longer survive without some assistance. Patient is unable during interview to recall a major relevant aspect of their current lives, e.g., an address or telephone number of many years, the names of close family members (such as grandchildren), the name of the high school or college from which they graduated. Frequently some disorientation to time (date, day of week, season, etc.) or to place. An educated person may have difficulty counting back from 40 by 4s or from 20 by 2s. Persons at this stage retain knowledge of many major facts regarding themselves and others. They invariably know their own names and generally know their spouse's and children's names. They require no assistance with toileting and eating, but may have some difficulty choosing the proper clothing to wear.

Stage 6 (Middl e Dementia) Severe cognitive decline . May occasionally forget the name of the spouse upon whom they are entirely dependent for survival. Will be largely unaware of all recent events and experiences in their lives. Retain some knowledge of their past lives but this is very sketchy. Generally unaware of their surroundings, the year, the season, etc. May have difficulty counting from 10, both backward and sometimes forward. Will require some assistance with activities of daily living, e.g., may become incontinent, will require travel assistance but occasionally will display ability to familiar locations. Diurnal rhythm frequently disturbed. Almost always recall their own name. Frequently continue to be able to distinguish familiar from unfamiliar persons in their environment. .

Personality and emotional changes occur. These are quite variable and include: delusional behavior, e.g., patients may accuse their spouse of being an impostor, may talk to imaginary figures in the environment, or to their own reflection in the mirror; obsessive symptoms, e.g., person may continually repeat simple cleaning activities; anxiety agitation, and even previously nonexistent violent behavior may occur; cognitive abulla, i.e., loss of willpower because an individual cannot carry a thought long enough to determine a purposeful course of action

Stage 7 (Late Dementia) Very severe cognitive decline . All verbal abilities are lost. Frequently there is no speech at all - only grunting. Incontinent of urine, requires assistance toileting and feeding. Lose basic psychomotor skills, e.g., ability to walk, sitting and head control. The brain appears to no longer be able to tell the body what to do. Generalized and cortical neurologic signs and symptoms are frequently present.

Alzheimer's Disease and Skill Abilities Dr Reisberg has also shown that the decline typical of Alzheimer's disease is the flip side of normal skill acquisition by infants, children, and young adults Ability Age of acquisition during Alzheimer's stage at which ability normal development is lost Hold a job. 12 years and older 3... early Alzheimer's disease Function independently in the world. Handle simple 8-12 years 4... mild Alzheimer's finances Select proper clothing. 5-7 years5... 5…moderate Alzheimer's

Multi-infarct dementia , also known as vascular dementia , is the second most common form of dementia after Alzheimer disease (AD) in older adults. The term refers to a group of syndromes caused by different mechanisms all resulting in vascular lesions in the brain. Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable .

This photo / picture shows mum, who suffered from advanced multi-infarct dementia, shortly before she died.

The main subtypes of this disease are: mild cognitive impairment multi-infarct dementia, vascular dementia due to a strategic single infarct (affecting the thalamus , the anterior cerebral artery , the parietal lobes or the cingulate gyrus ), vascular dementia due to hemorrhagic lesions, small vessel disease (which includes vascular dementia due to lacunar lesions and Binswanger's disease ), and mixed Alzheimer's and vascular dementia

Vascular lesions can be the result of DIFFUSE cerebrovascular disease or FOCAL lesions (or a COMBINATION OF BOTH, which is what is observed in the majority of cases) .

Symptoms The onset of multi-infarct dementia often goes unnoticed in the early stages, particularly if the strokes are minor. If the strokes are minor, symptoms caused by each stroke may include mild weakness in the limbs, slurred speech, dizziness and a slight impairment to the short-term memory, though these do not last for long. However, the cumulative effects of these strokes will eventually result in noticeable symptoms being displayed. These symptoms include: problems with recent memory wandering or getting lost in familiar places walking with rapid, shuffling steps disinhibition, including loss of bladder or bowel control emotional lability difficulty following instructions problems handling money

In terms of cognitive testing patients have patchy deficits. They tend to have better free recall and fewer recall intrusions compared with patients with Alzheimer's disease. As small vessel disease often affects the frontal lobes, apathy early in the disease is more suggestive of vascular dementia because it usually occurs in the later stages of 'Alzheimer's'. Consequently patients with vascular dementia perform worse than their Alzheimer's disease counterparts in frontal lobe tasks such as verbal fluency. They also tend to exhibit more perseverative behaviour. They may also present with general slowing of processing ability, difficulty shifting sets and impairment in abstract thinking. In the more severe patients or those patients affected by strategic infarcts in the Wernicke or Broca areas; dysarthrias , dysphasias and aphasias may be present.

Lateralizing signs such as hemiparesis , bradykinesia , hyperreflexia , extensor plantar reflexes , ataxia , pseudobulbar palsy , and gait and swallowing difficulties may be observed .

LEWY BODY DEMENTIA 1 Lewy Body dementia has been increasingly recognised over the past 5-10 years. Lewy bodies are areas of abnormal staining (distinct from Pick bodies and neurofibrillary tangles) found within brain cells. They are found in a particular area of the brain stem, the substantia nigra, in Parkinson’s disease. In Lewy body dementia they are found in the cerebral cortex, either alone or in combination with the senile plaques of Alzheimer’s disease. Lewy body dementia may present as: late onset Parkinson’s disease followed months or years later by visual hallucinations, episodes of confusion, memory loss and then global dementia, or cognitive or psychiatric symptoms followed by milder Parkinsonian features later in the course of the disease.

LEWY BODY DEMENTIA 2 Main pointers to a diagnosis of Lewy Body disease include: fluctuating cognitive performance with episodes of confusion hallucinations and/or paranoid delusions early gait disturbance any combination of rigidity, bradykinesia, tremor and flexed posture temporoparietal dementia with inattention in a patient with Parkinson’s disease

LEWY BODY DEMENTIA 3 People with Lewy Body dementia may also have problems with their short term memory, word finding difficulties, difficulty sustaining a line of thought and problems locating objects in space. They may also experience symptoms of anxiety and depression. Anybody can develop Lewy Body disease. Studies which have looked at the brains of people with dementia after they have died suggest that it is relatively common although prevalence figures do vary. It appears to affect men and women alike. As yet it is impossible to identify risk factors for developing the disease. However, rare ‘familial’ cases of Lewy Body disease have been described. Although there is no cure for Lewy Body disease it is sometimes possible to treat some of the symptoms of this disease. The depression which accompanies this disease for example will usually respond to antidepressant therapy.

PICK’S DISEASE 1 In 1892, Arnold Pick, a German neurologist, described a man who had presented in life with progressive loss of language. After death the patient’s brain was shown to have asymmetric atrophy as opposed to Alzheimer’s disease where the atrophy is more general. In Pick’s disease the frontal and temporal lobes are most affected. In addition, brain cells in these areas are sometimes found to be abnormal and swollen . These abnormal cells (Pick cells) together with the presence of abnormal staining within cells (Pick bodies) are the hallmark of the disease.

PICK’S DISEASE 2 When these typical features are not seen on post mortem examination but the same areas of the brain are affected by cell death, the case may be described as Pick’s syndrome or frontotemporal Dementia. Pick’s disease varies in the way it affects individuals. There are however, a common core of symptoms. Some or all of these may be present at different stages of the disease.

PICK’S DISEASE 3 The more common symptoms include: personality change: loss of inhibitions/rudeness/impatience/inappropriate behaviour failure to recognise objects using objects wrongly development of routines speech problems, echolalia (repeating what is said to the patient) overeating, changes in dietary preference, obsessional cravings for certain types of food attention problems changes in sexual behaviour Anybody can develop Pick’s disease. It affects men and women alike. Although it typically affects people in their 50s and 60s it has been diagnosed in people from the ages of 20 to 80. It does exist as a familial disease [autosomal dominant] in some families, but the majority of cases are sporadic. The rate of progression varies enormously ranging from a duration of less than 2 years to well over 10 years.

The role of the clinical psychologist in the assessment, diagnosis and Management of patients with dementia

Guidelines for the Evaluation of Dementia and Age-related Cognitive Decline

General Guidelines: Familiarity with Nomenclature and Diagnostic Criteria 1 . Psychologists performing evaluations of dementia and age-related cognitive decline should be familiar with the prevailing diagnostic nomenclature and specific diagnostic criteria. II. General Guidelines: Ethical Considerations 2 . Psychologists attempt to obtain informed consent. 3. Psychologists gain specialized competence. 4 . Psychologists seek and provide appropriate consultation 5. Psychologists are aware of personal and societal biases and engage in nondiscriminatory practice.

III. Procedural Guidelines: Conducting Evaluations of Dementia and Age-Related Cognitive Decline 6. Psychologists conduct a clinical interview as part of the evaluation. 7. Psychologists are aware that standardized psychological and neuropsychological tests are important tools in the assessment of dementia and age-related cognitive decline. 8. When measuring cognitive changes in individuals, psychologists attempt to estimate premorbid abilities. 9. Psychologists are sensitive to the limitations and sources of variability and error in psychometric performance. 10. Psychologists recognize that providing constructive feedback, support, and education, as well as maintaining a therapeutic alliance, can be important parts of the evaluation process.

Key points . Psychological assessment can make a useful contribution in the diagnosis of dementia, but like other methods for detecting dementia is not wholly accurate, and so evidence from psychological assessments needs to be considered in the context of other possible indicators. . Within psychological forms of assessment, tests of memory offer the best single indicator of the presence of dementia. . Psychological assessment is not very useful for discriminating between different forms of dementia.

There is good evidence that even people with quite marked levels of dementia are sensitive to environmental influences. For example, even such simple things as the arrangement of furniture can have an effect on the amount of verbal interaction between residents in a residential unit.

A number of specially designed forms of intervention for use with those suffering from dementia have been devised. The best known and best validated of these is reality orientation , but even here the gains are limited and short-lived after the programme has been discontinued. Special forms of intervention, such as reality orientation and reminiscence therapy, tend to assume that all those suffering from dementia share a single key disability or feature. This assumption may not be entirely true and the use of more specific forms of psychological intervention of the kinds used with other client groups should be considered in order to address the specific problems of individuals.

Sharing with you my own clinical experience

A CONDITION THAT RESEMBLES DEMENTIA BUT IS ACTUALLY DUE TO DEPRESSION . IN PSEUDODEMENTIA, A PERSON MAY APPEAR CONFUSED, EXHIBIT DEPRESSIVE SYMPTOMS SUCH AS SLEEP DISTURBANCE, AND COMPLAIN OF MEMORY IMPAIRMENT AND OTHER COGNITIVE PROBLEMS. HOWEVER, UPON CAREFUL TESTING, MEMORY AND LANGUAGE FUNCTIONING ARE INTACT. PEOPLE WITH PSEUDODEMENTIA OFTEN RESPOND TO ANTIDEPRESSANT MEDICATIONS. When dealing with a demented patient make sure that you yourself is not demented - DO NOT FORGET THE WORD PSEUDODEMENTIA

NEUROPSYCHOLOGICAL ASSESSMENT TOOLS

CANTAB HALSTEAD REITAN MURIEL LEZAK’S TOOL LURIA NEBRASKA AVAILABLE NEUROPSYCHOLOGICAL TOOLS

The Cambridge Neuropsychological Test Automated Battery (CANTAB) is a battery of neuropsychological tests, administered to subjects using a touch screen computer. The 22 tests in CANTAB examine various areas of cognitive function , including: general memory and learning, working memory and executive function , visual memory, attention and reaction time (RT), semantic/verbal memory , and decision making and response control.

The CANTAB endeavours to import the accuracy and rigour of computerised psychological testing whilst retaining the wide range of ability measures demanded of a neuropsychological battery. It is suitable for young and old subjects, and aims to be culture and language independent through the use of non-verbal stimuli in the majority of the tests

Halstead-Reitan Battery Definition The Halstead-Reitan Neuropsychological Test Battery is a fixed set of eight tests used to evaluate brain and nervous system functioning in individuals aged 15 years and older. Children's versions are the Halstead Neuropsychological Test Battery for Older Children (ages nine to 14) and the Reitan Indiana Neuropsychological Test Battery (ages five to eight).

Purpose Neuropsychological functioning refers to the ability of the nervous system and brain to process and interpret information received through the senses. The Halstead-Reitan evaluates a wide range of nervous system and brain functions, including: visual, auditory, and tactual input; verbal communication; spatial and sequential perception; the ability to analyze information, form mental concepts, and make judgments; motor output; and attention, concentration, and memory. The Halstead-Reitan is typically used to evaluate individuals with suspected brain damage. The battery also provides useful information regarding the cause of damage (for example, closed head injury, alcohol abuse, Alzheimer's disorder, stroke ), which part of the brain was damaged, whether the damage occurred during childhood development, and whether the damage is getting worse, staying the same, or getting better. Information regarding the severity of impairment and areas of personal strengths can be used to develop plans for rehabilitation or care.

Muriel Deutsch Lezak is an American neuropsychologist best known for her book "Neuropsychological Assessment", widely accepted as the standard in the field. She holds bachelor's and master's degrees from the University of Chicago, and earned a Ph.D. (Clinical Psychology) from the University of Portland in 1960. Her work has centred on research into, assessment and rehabilitation of brain injury. Muriel Lezak

Alexander Romanovich Luria ( Russian : Алекса́ ндр Рома ́ нович Лу ́ ри я ; July 16 , 1902 – August 14 , 1977 ) was a famous Soviet neuropsychologist and developmental psychologist . He was one of the founders of cultural-historical psychology and psychological activity theory . Luria-Nebraska Neuropsychological Test The Luria-Nebraska is a standardized test based on the theories of Luria regarding neuropsychological functioning. There are 14 scales: motor functions, rhythm, tactile functions, visual functions, receptive speech, expressive speech, writing, reading, arithmetic, memory, intellectual processes, pathognomic, left hemisphere and right hemisphere. It is used with people who are 15 years or older; however, it may be used with adolescents down to 12 years old. Part of A.R. Luria's legacy was the premium that he placed on the observation of a patient completing a task; intraindividual differences. The modern practice of standardized testing tends to neglect this aspect of psychology. The Luria-Nebraska Neuropsychological Battery (now in its third iteration) attempts to create an alloy of standardized testing and idiosyncratic observation by allowing comparison to the normative sample, and at the same time giving the test administrator flexibility in the administration

Luria-Nebraska Neuropsychological Test

LURIA NEBRASKA SCALES 2.1 Critical Level (as based from age years and completed educational exposure of 10 years ) 2.2 Clinical Scales Scales beyond the critical limit of are deviant scores 2.3 Summary Scales S1 Pathognomonic S2 Left hemisphere S3 Right hemisphere S4 Profile Elevation S5 Impairment 2.4 Localization scales L1 Right Frontal L2 Right Sensorimotor L3 Right Parieto –Occipital L4 Right Temporal L5 Left frontal L6 Left Sensorimotor L7 Left parietal-occipital L8 Left Temporal

2.5 Factor Scales C1 Motor functions C2 Rhythm Functions C3 Tactile Functions C4 Visual Functions C5 Receptive Speech C6 Expressive speech C7 Writing C8 Reading C9 Arithmetic C10 Memory C11 Intellectual Processes

SIMPLEST NEUROPSYCHOLOGICAL TEST

WECHSLER DETERIORATION RATIO HOLD TEST – DON’T HOLD TEST HOLD TEST x 100 10 PERCENT - POSSIBLE 20 PERCENT – TRUE DETERIORATION 30 PERCENT – SEVERE DETERIORATION

Sa Aking Pagtanda ... Sa aking pagtanda, unawain mo sana ako at pagpasensyahan. Kapag dala ng kalabuan ng mata ay nakabasag ako ng pinggan o nakatapon ng sabaw sa hapag kainan, huwag mo sana akong kagagalitan. Maramdamin ang isang matanda. Nagse-self-pity ako tuwing sisigawan mo ako. Kapag mahina na ang teynga ko at hindi ko maintindihan ang sinasabi mo, huwag mo naman sana akong sabihan ng ?binge!? paki- ulit na lang ang sinabi mo o pakisulat na lang. Pasensya ka na, anak. Matanda na talaga ako. Kapag mahina na ang tuhod ko, pagtiyagaan mo sana akong tulungang tumayo, katulad ng pag-aalalay ko sa iyo noong nag-aaral ka pa lamang lumakad. Pagpasensiyahan mo sana ako kung ako man ay nagiging makulit at paulit ulit na parang sirang plaka. Basta pakinggan mo na lang ako. Huwag mo sana akong pagtatawanan o pagsasawaang pakinggan. Natatandaan mo anak noong bata ka pa? kapag gusto mo ng lobo,paulit-ulit mo ?yong sasabihin, maghapon kang mangungulit hangga?t hindi mo nakukuha ang gusto mo. Pinagtyagaan ko ang kakulitan mo.

Pagpasensiyahan mo na rin sana ang aking amoy. Amoy matanda, amoy lupa. Huwag mo sana akong piliting maligo. Mahina na ang katawan ko. Madaling magkasakit kapag nalamigan, huwag mo sana akong pandirihan. Natatandaan mo noong bata ka pa? Pinagtiyagaan kitang habulin sa ilalim ng kama kapag ayaw mong maligo. Pagpasensiyahan mo sana kung madalas, ako?y masungit, dala na marahil ito ng katandaan. Pagtanda mo, maiintindihan mo rin. Kapag may konti kang panahon, magkwentohan naman tayo, kahit sandali lang. inip na ako sa bahay, maghapong nag-iisa. Walang kausap. Alam kong busy ka sa trabaho, subalit nais kong malaman mo na sabik na sabik na akong makakwentuhan ka, kahit alam kong hindi ka interesado sa mga kwento ko. Natatandaan mo anak, noong bata ka pa? Pinagtiyagaan kong pakinggan at intindihin ang pautal-utal mong kwento tungkol sa iyong teddy bear. At kapag dumating ang sandali na ako?y magkakasakit at maratay sa banig ng karamdaman, huwag mo sana akong pagsawaang alagaan. Pagpasensiyahan mo na sana kung ako man ay maihi o madumi sa higaan, pagtiyagaan mo sana akong alagaan sa mga huling sandali ng aking buhay. Tutal hindi na naman ako magtatagal. Kapa g dumating ang sandali ng aking pagpanaw, hawakan mo sana ang aking mga kamay at bigyan mo ako ng lakas ng loob na harapin ang kamatayan. At huwag kang mag-alala, kapag kaharap ko na ang Diyos na lumikha, ibubulong ko sa kanya na pagpalain ka sana ? dahil naging mapagmahal ka sa iyong mga magulang. Ang iyong Ama or Ina

Dementia powerpoint

More Related Content

What's hot

Viewers also liked

Similar to Dementia powerpoint

More from Milen Ramos

Recently uploaded

Dementia powerpoint