Welcome to Acorn Care Home

Our aim is to provide a professional, caring and sensitive haven at what can be a difficult time. We offer a relaxed, friendly and respectful approach to the care of your loved one in a comfortable, warm, peaceful setting.

Acorn is located in a spacious Victorian house, while homely, its layout affords space for our residents. It is set in landscaped spacious secured gardens, which gives our residents a sense of freedom to roam around whenever they wish, but with the peace of mind the area is safe and secure.

About us

We are a highly specialist unit offering care and support to 27 male residents aged between 18 and 70 years of age with a diagnosis of

  • Vascular dementia

  • Korsakoff dementia

  • Picks disease

  • Huntington’s disease

  • Creutzfeldt-Jakob disease (CJD)

We deliver person centred care built around the individual needs of our residents. Our highly trained, dedicated, dedicated staff team of professionals adopt a holistic approach to care. Our aim is to enhance the quality of life for all our residents and help them to achieve the best they can be, while ensuring their health, safety and wellbeing at the same time. Acorn is where quality and safety blend together and creates a caring, nurturing, innovative environment.

What is Dementia?

NICE defines dementia as; “…a progressive and largely irreversible syndrome that is characterised by a widespread impairment of mental function” (NICE & SCIE Dementia presentation September 2007).  So what does this mean? More than 800,000+ people suffer from dementia in the UK with 5% of over 65, rising to about 20% of over 80s and 50% for 95+.  It is associated with complex needs and high levels of dependency and morbidity, often with challenging behaviours.  When looking at dementia, Alzheimer’s disease has the largest prevalence, but in an academic perspective Alzheimer’s disease is not the same thing as Alzheimer’s dementia the difference being that Alzheimer’s disease is a pathological diagnosis where Alzheimer’s dementia is a clinical syndrome thought to be the underlying cause of Alzheimer’s disease (Ritchie C. 2009). In recent years many hospital beds are being blocked (delay discharged) by persons suffering from a range of dementias especially those with vascular and cognitive impairments, illnesses and disorders related to alcohol abuse.

There is a large body of research being carried out in how or why Alzheimer dementia happens and into understanding the role of Amyloid Plaque, Neurofibrillary Tangle, Neuritic Plaque.  One of the key discoveries over the last decade is the function of ‘tau’ proteins which bind and stabilise the microtubules in healthy neurons and the reason why proteins detach from the microtubules as we get older, making the transport of molecules along the neuron’s axon and dendrites impossible.

All very complicated, but once the process of dementia is clear the researchers can develop treatments to slow or prevent dementia happening, this time is now growing closer.  This is for the future, for now we are at the stage where we know that the disease and clinical changes are happening as invisible developments within the brain and it is only when signs of clinical changes (mostly in later life), often at a point where the individual cannot hid or deny the symptoms any more, go to the GP and complain of having problems with their memory.  This is often too late to allow drug treatments to provide their full potential but will allow some improvements and slow down the deterioration.  The research is now to the point where it is possible to detect those who will get Alzheimer disease before symptoms are detectable allowing the new drug regimes to work to gain the best results for each individual.

Normal ageing bring with it a degeneration of all the individuals’ major organs and functioning parts of the body.  You only have to think of how many heart beats or gallons of fluid that passes through the kidneys in a lifetime to realise the journey and the amount of punishment an individual place on their body throughout their lifetime. It is expected that at some time it will wear out (genetic timelines) or become damaged due to other factors i.e. cigarettes, alcohol, illicit drug use, disease or trauma.  We are also in the age of genetics and the predetermined instructions set out from the day of conception. This shapes our body, colour of hair, eye etc, but could it determine our life span and determine if we are going to get dementia given we live long enough?  These are the questions now being asked of the role of genetics, could they be manipulate and change the timelines of dementia.

It is good to ask questions about the future, but what is more important is what can we do now and how can we shape our future and improve the chance of not getting dementia?  In the last decade due to better treatment of disease, sanitation and better food the emphasis has had to change to take into account that people are now living longer which increases the chance of getting dementia.  Health services, although it has been known for some time, have still been caught on the hop in keeping pace with the change of needs for older people.  The money allocated for pensions are said not to meet the growing need, healthcare still using historical bureaucratic practices in both management and process that cannot adjust to meet future need, but the biggest tragedy of justice was the Labour Government was not ring-fencing £1.5b provided to fulfil the Dementia Strategy not use for solving some of the problems for dementia, but to find the PCT’s using the money to prop up their budget deficits and poorly functioning services in most Trusts.  The health service has now found themselves in a major crisis and unable to meet dementia service demand.

Why is there such a problem? 

It is suggested, and predicted, that people are living longer placing an increased burden on healthcare. In the last decade, what little flexibility in older persons healthcare, has been outstripped by demand for services.  The world financial crisis has brought the spotlight on the health service structure as being very bureaucratic with a lot of duplication and wastage.  This has been addressed in the white paper from the Coalition Government “Equity and Excellence: Liberating the NHS” although not the complete answer (if anyone knows what that is) it does lay down the shape of things to come to meet the challenge of a fair healthcare for all no matter what you age.

For many years primary care for dementia has been provided by social service, providing packages of care to support both suffers of dementia and their carer’s in the community or the progression to residential care or nursing homes.  It was the role of mental health to provide secondary care or specialist care for those who had challenging behaviour or comorbid dementia and mental illness.  For some reason, possibly due to increasing costs, the lack of skilled practitioners as well as the increase of none trained staff in social services with the increase of need in the community, more is being asked of mental health services outside of its secondary care role as well as the General Hospitals Older person beds.  There is also an increase of presentations at A & E of families unable to look after the person with dementia because of the lack of support and the increasing costs now not meeting the care within Nursing or Care Home (there has not been an increase of fees to meet the increasing compulsory staff cost pension, wages etc).  It has also been noticeable that the age of people in general hospitals has risen and often 75% or more of occupancies of hospital beds are over the age of 70.

Adult Mental Health Services has also been slow to adjust services to meet need, especially in the older age group.  In developing the Mental Health Older Persons Services did not take into account the predicted increase of range of dementia care needs and has been seen as the poor relative to Adult or CAMHS Services when it came to service improvement.  There is a growing argument between Social services and Mental Health where the line should be drawn to who pays for what. In the last year discussions have been on the growing need to develop a cognitive impairment services as separate to functional mental illness in older people, as there service needs differ considerably.  Not only the growing literature but also the demand suggests urgency in developing major changes to the treatment of dementia.  Pressure from community systems and the introduction of the Dementia Strategy need both Social Services and Mental Health to look at how services will be provided to meet cognitive impairment.  It is estimated that up to about 90% of the new referrals coming to Older Persons Services are for cognitive impairment and not all of these are due to Alzheimer disease.  Due to the Age Discrimination Act the proposal to develop a cognitive impairment as a separate service and older persons with functional Mental Health issues continue to be treated within Adult Mental Health Services, until such time the cognitive impairment takes over as the bigger problem, seems to be the most logical answer, not only that, legislation makes it very clear that it is discriminatory to provide services due to age and must only determine by need.

Memory Clinics

Access to Memory Clinics can be gained through a referral from a local GP. The previous Government strongly suggested that all people over the age 18 should have access to “memory services” and memory services need to be developed in all of the trusts throughout the UK. The Royal College of Psychiatrists’ Centre for Quality Improvement has developed a; ‘Memory Services National Accreditation Programme (MSNAP), which has laid down the framework and standards for services to be assessed against.  A referral to a memory clinic that needs to have been accredited by MSNAP, starts a journey of investigation. First, a member of the initial assessment multidisciplinary team visits the referred person in their own home following an agreed day and time this is seen as best practice.  It is asked that the main carer and any other family or significant persons to be present.  The reason for the home visit is that so much more information can be gained from seeing the person in his/her own environment, not only that the individual may feel more relaxed in their own home.  A number of basic psychological tests are carried out to determine the base line memory states, MMSE, ACE-R, BADLS and Neuropsychiatric Inventory Questionnaire.  As well as assessing the person who was referred there is an assessment of the carers needs, because the success of maintaining health and wellbeing and achieving  quality outcomes is in providing care that meets both the service users and carer’s needs.

The Need for Assessment

The need to provide early intervention is as important within our ageing population as it is in the diagnosis of a mental illness within younger and adult populations. Understanding the ageing process allows assessments to provide effective treatment care pathways and care programmes. Early intervention sits within a holistic approach in providing appropriate and effective care especially in the evaluation of comorbid illnesses.  Comorbid illnesses often complicates, contribute to, or masks psychiatric disorders and on the other hand develop a psychiatric picture of confusion, anxiety or/and depression within normal or premature ageing.  A holistic approach provides a standard assessment process that looks at not only psychiatric symptoms but also the physical and psychological possibilities of being the primary or a comorbid disorder and provides an understanding of the individual’s presentation.

The assessment of dementia covers common situations none of which are mutually exclusive to each other.  The most frequent is for the evaluation and diagnosis of cognitive disorder, also to determinate any differential diagnostic possibilities based on the individual’s behaviour.  It has been demonstrated over time the need to develop objective baseline for tracking changes where there is a need to establish deterioration or improvement within a treatment response. The use of neuropsychological assessment and the use of a laboratory diagnostic work up provide the information that guides clinical decisions, also necessary is the determination of the individuals capacity and competency to both physically and mental functions. Outside of adjusting imbalances within the individuals physical status there is a need to look at appropriate therapeutic interventions that identify cognitive strengths and weaknesses.  By applying the most appropriate rehabilitation treatment/care that meets the individuals’ physical and psychological needs will define their capacity to recover.

A comprehensive assessment must determine the individual level of function within ten competencies:

  1. Memory, is it degenerating slowly/rapidly, does it come and go and what is different now than the past, under what stress?
  2. Orientation, time, place, registration, attention, and recall
  3. Intellect, the ability to reason especially outside of the box
  4. Personality & Mood, has it changed recently, (pre-morbid), depression, mood variation and worthlessness
  5. Sensory & Motor, changes to physical functions and ability to rationalise
  6. Visual Perception, lost a level and ability to recognise – people, things and objects
  7. Attention & Concentration, Individual changes in ability, span and frustration
  8. Language, use of words, previous use of other languages other than the individuals native tongue
  9. Spatial Abilities, being able to judge distances, changes colour, visualising  step or other risks
  10. Executive Functions, impairments in planning, organisation, initiation, sequencing, working memory, behaviour adjustment in response to feedback, and safety/risk capacity or capacity to make legal or financial decisions.  Most of all the, the lack of insight into their behaviour, especially behaviour that offends people or breaches social norms.

Normal ageing of the nervous system is the most common cognitive changes after the age of 40 years.  Particularly vulnerable is the retention of memory, capacity of executive skills and divergent thinking such as short term memory use, retention/recall of information after 30 minutes and multitasking.

Alzheimer’s Dementia is the leading cause of dementia, especially in the population of 70 years and older.  It has an insidious onset, prominently memory impairment with progressive degenerative disorder that leads to rapid forgetfulness, diminished executive skills, impaired semantic fluency and naming of people, things and objects it also impairs the visual perceptual analysis.

Lewy Body Dementia, although rare, varies from Alzheimer’s by the presentation of mental illness symptoms like visual hallucinations, may not demonstrate excessive memory impairment in the beginning; signs of Parkinsonism like symptoms may lead to falls resulting from orthostatic hypotension.  This type of dementia is distinguished by its unique set of presenting symptoms of not only mental illness and cognitive defects but the neurological examination identifies rigidity, bradykinesia, strange postural changes and possible persistent grunting.

Pick’s Dementia is even rarer as it is often only diagnosed at post-mortem with the variable difference due to the site of change/damage within the frontal lobe.  The first signs may have nothing to do with the loss of memory, but the loss of executive functions, change in personality, may have the ability to follow instructions but unable to motivate or work out for themselves what needs to be done.

Vascular Dementia profiles differ in many respects from other types of dementia due to, in some cases, an absence of profound memory impairment.  The presentation varies according to the extent of the vascular damage in either physical or psychological function i.e. direct trauma, multi infarction, stroke, TIA, micro-vascular disease, cerebral hypo-perfusion, haemorrhage or any combination.  In this type of dementia the individual does not always display major loss of memory, and in time it can dramatically improve depending on the damage and the recovery programme engaged.  This suggests that the primary difficulty is in the retrieval rather than in the storage or consolidation of new information.

Other diseases that develop dementia are; Parkinson’s, Huntington’s Progressive Supranuclear gaze palsy, Hydrocephalus, and Creutzfeldt-Jakob Diseases.  All of the examples have cognitive syndromes and characteristics that provide a neuropsychological profile that defines each diseases and type of dementia.

One of the predominant symptoms in the early onset of dementia is a level of depression, but at the same time it could be the depression symptoms which may appear as a dementia.  Depression could in its self be the predominate driver or at the same time mask other symptoms that could be progressing dementia characteristics of memory loss, anxiety, panic and behaviours associated with dementia.  The role that depression might play needs to be clearly evaluated as it can result in serious mood changes with disabling cognitive impairment or what has become known as the ‘dementia of depression’ or “pseudo-dementia”.  Depression also frequently co-occurs in the context of arrange of medical disorders and often complicates the diagnosis and can exacerbate the functional loss associated with each disorder on its own or in combination especially in the older person.  Previous drug abuse, alcohol or illicit or a combination of each could have dramatic affect on cognitive ability in prolonged use into older adults, the other area of concern is in some people the loss of memory after a general anaesthetics.

Many treatments for depression are successful in improving cognitive impairments, but not all.  Those who respond poorly to oral medication, who are treatment intolerant, or the concerns of the interaction with concurrent treatments may benefit from Electroconvulsive Therapy (ECT).  Improvements in anaesthetics and the ability to titrate levels of the current, in some cases the frail elderly can achieve better outcomes than younger service users.
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Korsakoff syndrome; Alcohol Related Dementia

Heavy alcohol use (is indicated when the liver does not have time to remove the alcohol from body before the next period of drinking) can interfere with the breakdown of thiamine (B1) even if an individual maintains a well-balanced diet, as most of the thiamine is not absorbed.  When the deficiency reduces to a certain level the individual may well develop Wernicke encephalopathy and when memory is affected can develop Korsakoff syndrome.  The age of onset for developing Wernicke-Korsakoff syndrome can be at any age following many years of alcohol abuse could be as young as young 25 – 30 years of age this is unusual, but it is common in people in their early 40’s. Wernicke-Korsakoff syndrome is seen in about 4 to 1 males to females.

Thiamine deficiency (vitamin B1): Thiamine deficiency can be found within two neurological disorders, beriberi and Wernicke-Korsakoff syndrome. Beriberi is caused by lack of dietary thiamine and can cause myocardial failure where Wernicke-Korsakoff syndrome is defined by an acute encephalopathy manly due to alcohol abuse, which causes cognitive impairment effecting impairment of short-term memory being stored into long term memory. Wernicke-Korsakoff syndrome is most commonly observed in people with chronic alcohol abuse suggesting that it affect the systems of absorption of nutrients from the digestive system. This has also been seen in people with eating disorders who are malnourished with dietary deficiencies also brain trauma or stroke causing neurological damage from a lack of oxygen to the brain, prolonged vomiting, starvation, uraemia that builds up toxins from the waste in the urine, prolonged kidney dialysis, prolonged intravenous therapy, gastric bypass or stapling, and has been reported by sufferers of tuberculosis, other drug abuse and side-effects of chemotherapy medications have also been indicated.

Thiamine is used in the production of connections necessary for neurons function, poor levels of thiamine can lead to damage or death of neurons in different regions of the brain, particularly the thalamus and the mammillary bodies, this disrupts the formation and storage of memories.  Damage to the nervous system in the brain and spinal cord and the peripheral (external) systems throughout the body may be caused by alcohol withdrawal.

Signs and Symptoms at the beginning of Thiamine deficiency the symptoms are nonspecific and are difficult to differentiate, they may include fatigue, irritability, poor memory, sleep disturbances, pericardial (heart) pain, anorexia, and a range of non-specific discomfort. Other defining symptoms of encephalopathy are mental confusion, eye twitching, poor balance and lack of coordination.  Symptoms may resemble the effects of severe alcohol intoxication but on carrying out a blood alcohol test found to be negative.  In the acute phase treatment with thiamine will help some individuals to recover without memory deficits, particularly if they are treated quickly.  The untreated phase or chronic stage is called Korsakoff syndrome and is distinguished by no recovery and persistent anterograde amnesia where the individual cannot transfer new memories into long-term memories.  Untreated individuals with Wernicke’s encephalopathy nearly always will develop this severe memory disorder, which affects all aspects of life and relationships especially those that need executive decisions.  Symptoms of Korsakoff syndrome has been reported to spontaneously develop in persons who have not suffered Wernicke’s encephalopathy this thought to come about due to long term use of alcohol on a daily bases over many years (20 or more). Once patients develop Korsakoff amnesia, full recovery is unlikely, but when treated in a specialist unit a reasonable quality of life may be able to be reached.  In some persons with Korsakoff syndrome suffer retrograde amnesia with memory loss of past events in addition to anterograde amnesia, with most being able to recall most long term memories of the distant past.

Short term memory up to a few minutes may not affected and can repeat a sequence of numbers or objects soon after hearing them, but will be forgotten 10 to 20 minutes later. Because immediate memory remains intact in individuals can interact with others, respond to questions, and function within small groups and follow simple instructions but often confabulate during discussions by making up stories to compensate for an inability to remember often confusing the past and present.

Individuals may also show signs of indifference with what is going on around them and have poor insight or emotional response.  Self-harm, is unlikely although part of their delirium may injure them self. This sudden confusion due to changes in brain function can be associated with hallucinations and hyperactivity, which does not respond to normal interaction.  Individuals going through detoxification will start with a varying degree of withdrawal, in long term abusers you may see delirium tremens (DTs) with very vivid hallucinations or epileptic fits, withdraws may include sweats, tremors, irritability, confusion, stupor, and depersonalised episodes.

Diagnosis Wernicke’s encephalopathy is suspected when individuals seeking medical attention present with signs of mental confusion, eye movement (nystagmus) disorders, and lack of coordination.  It will have thought to become Korsakoff syndrome when there is loss of memory of present events, a history of long-term heavy drinking, or possibility of malnutrition could suggest a diagnosis of Korsakoff syndrome. When Korsakoff follows a previous diagnosis of Wernicke’s it would be appropriate to have the diagnosis of Wernicke-Korsakoff syndrome.  The diagnosis can be confirmed by neuro-imaging (brain imaging) or an autopsy after death with findings that show degeneration of parts of the brain including the thalamus and mammillary bodies, along with loss of brain volume in the area surrounding the fourth ventricle (a fluid-filled cavity near the brainstem).

Mental status: Mental status changes are commonly present and appear in various forms from being withdrawn to presenting with major challenging behaviour.  Memory impairment will significantly inhibit an individual’s ability to perform normal activities and functions and present as a decline from a previous level of testing and can affect executive functions where individuals capacity to make decisions for themselves, even at the simple level very difficult.  It is not unusual once the memory has been affected for the individual to feel that everyone has gang up on him/her because of the loss of memory live in a world of the past capabilities which are now not possible especially around their ability to drink alcohol.  Will often not understand why they end up in a mental health institution due to the individual’s behaviour while intoxicated by alcohol.  This will/can end up with repeated challenging behaviour.

Physical Condition: Physical examination of the nervous/muscular systems may show decreased reflexes and impaired gait and coordination. Muscles may be weak and may show atrophy (loss of tissue mass). Examination of the eyes may show abnormalities of eye movement. Blood pressure and body temperature measurement may be low. Pulse (heart rate) may be rapid.  Vertical and horizontal nystagmus that cause involuntary eye movements, ptosis causing drooping eyelids, weakness or paralysis of muscles in the eye, non-reacting miotic causing constricted pupils, or complete loss of ocular movements in degenerative cases.

Blood Tests: Blood tests used to check an individual’s nutrition status include serum B1 (thiamine) levels, along with liver function. Blood or urine alcohol levels and liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), are usually tested and may be high if the individual has a history of chronic (long-term) alcohol abuse. Blood tests may include electrolytes (including sodium, potassium, and chloride).
Blood tests may also be done to rule out other chronic conditions that may cause thiamine deficiency including acquired immunodeficiency syndrome (AIDS), hyperemesis gravidarum (continuous nausea and vomiting during pregnancy), thyrotoxicosis (very high thyroid hormone levels), cancers that have metastasized (spread), long-term dialysis in kidney problems, and congestive heart failure (CHF, or the inability of the heart to pump the blood) when treated with long-term diuretic therapy.

Neuro-Imaging: Computerized tomography (CT) scans may help in rapid assessment to rule out haemorrhaging, oedema (swelling), and sub-acute stroke (neurological damage due to lack of oxygen to the brain). A brain magnetic resonance imaging (MRI) study rarely shows changes in the tissue of the brain indicating Wernicke-Korsakoff syndrome. However, MRIs can detect acute lesions of Wernicke-Korsakoff syndrome in regions of the brain.

Poor Diet/Malnutrition: Eating processed foods (such as packaged meats and canned foods), food that contains too many refined carbohydrates (such as white breads, sweets, and other foods containing refined sugars), and white rice can cause thiamine deficiencies. Thiamine deficiency may result in the development of Wernicke-Korsakoff syndrome, although this is now rare and is caused mostly by alcohol abuse. Most developed nations add thiamine to some foods, such as flour and white rice.