The following is presentation of an overview of exercise in mental health which I recently gave. Although not specifically, neuropsychologically based nor neuro-rehab specific, some of the content is relevant in working therapeutically within neuro-rehab settings.
Intro to Sedentary Lifestyles
Society has become increase sedentary
Work, travel, domestic, leisure activities
Urbanisation
Labour saving devices
Changes to childhood
All creating a diversion from the physical role we evolved to do
Footnote:
Exercise is the purposeful application of physical activity
Both concepts have application to the promotion of mental health and wellbeing and both have been researched
Plan for Presentation
So….
We know generally we don’t get enough
But we know its society’s fault!!
We know its generally good for us
But…
What are the mechanisms/how does it work?
What are the specific psychological effects?
How effective exactly is it?
What about exercise and mental illness specifically?
How much do we need for an effect?
What are the current exercise dose recommendations?
What should we do with exercise as clinicians?
Mechanisms
Bio
Serotonin (Barchas & Friedman, 1963)
Endorphine/opioid system (Harber & Sutton, 1984).
Blood circulation/Cerebral blood flow (Dishman, 1995; Martinsen, 1987).
Realignment of circadian rhythm/sleep (Buxton et al., 2003; Youngstedt, 2005)
Psycho
Anxiolytic and mood enhancing qualities (see latter slides)
Accumulative mood improvements (Baekeland, 1970; Conboy, 1994; Mondin et al., 1996)
Increased tolerance to stress (Salmon, 2001)
Increase in self-esteem (Folkins & Sime, 1981; Fox, 2000)
Flow (Csikszentmihaly, 1990)
Distraction (Daley, 2002)
Control of negative thoughts (Morgan, 1985; 1987)
Improved retrieval of positive thoughts (Clark et al., 1983)
Positive rumination (Feldman et al., 2006)
Skill mastery (Lepore, 1997; Mynors-Wallis et al., 2000)
Spiritual/developmental theories
Social
Behavioural Activation/engagement (Jacobsen et al., 1996)
Socialisation (NHS, 2001; Priest, 2007)
Social inclusion (Taylor et al. 1999; DHSE, 1999)
Value of the group more than its constituent parts?
Drug and alcohol avoidance?
The Key Psychological Effects of Exercise:
Anxiolytic Effects
Low to moderate anxiety reducing effect (Long & van Stavel, 1995; McDonald & Hogdon, 1991; Petruzzello et al., 1991).
Exercise has an immediate anxiety reducing effect
Exercise training has been linked to trait measured reductions anxiety
Exercise sessions can reduce physiological reactivity and enhance recovery from psychosocial stressors
Main mechanism: it is believed that accumulative experiences of exercise protect people against physiological and cognitive stress and anxiety by reducing sympathoadrenal or pituitary-adrenal responses. Put another way, exercise presents an opportunity to habituate to similar symptoms to that of anxiety (Mills & Ward, 1986).
Antidepressant Effects
There is large scale, controlled, cross sectional support for a causal link between exercise and decreased depression (Steptoe and Butler, 1997 and Stephens, 1988)
Meta-analyses have estimated that Beck Depression Inventory (BDI) Scores decrease by between 0.3 and 1.3 of a standard deviation after exercise by controlled comparison (Craft & Landers, 1998; McDonald & Hogden, 1991; North et al., 1990; Lawlor & Hopker, 2001).
RCT studies have suggested that physical activity can be as successful at treating depression as psychotherapy or medication for mild and moderate levels (Klein, 1985; Mental Health Foundation, 2004; NICE, 2003).
Potential for treating comorbid depression (HIV, Dementia, CHF, cancer survivors, forensic)
Self-esteem
Exercise can promote physical self-worth and body image for males and females
The effect is strongest amongst children and middle-aged adults, and those with lowest self-esteem
Support for aerobic and resistance (latter acting quicker) (Fox, 2000)
Cognitive Function
Majority of cross sectional studies show that fit older adults display better cognitive task performance than less fit adults
Particularly in attention demanding and rapid tasks
Small improvement in cognitive functioning of older adults who experience improvement in fitness (Boutcher, 2000)
Slight beneficial & protective (Broe et al. 1990) effect in AD and other dementias but not VaD (Laurin et al. 2005)
Anecdotal evidence from physical training focus within non-physical sports (darts, snooker, golf)
Mental Illness
Inconsistent and poorly controlled evidence (Faulkner, 2005)
Significant impact upon negative symptoms
Mixed findings with positive symptoms (Helmsey, 1995)
Potential risks (esp. in mania (Moore 2010), eating disorders (Szasbo 2000) and poly-medication treated patients (Faulkner 2005
Exercise Routine
Exercise dependence is extremely rare
Mixed evidence to who benefits most: sedentary individuals with greater potential (Fasting & Gronningsaeter, 1986; Roth & Holmes, 1987; Simons & Birkimer, 1988; Williams & Lord, 1997) or more regular exercisers who value it higher (Steptoe et al. 1997)
Some evidence has shown that interruption of exercise routine in athletes/seasoned exercisers can lead to physical symptoms, including somatic anxiety and feelings of inability to cope (Loumidis & Wells, 1998).
Theories of stress may help explain this (Salmon, 2001 Gauvin & Szabo, 1992; Morris et al., 1990)
Single Dose Immediate Effect
15 minutes is enough to instigate an increase in positive mood, activation and valence, along with an energising effect whilst walking and a calming effect whilst recovering after walking (Ekkekakis et al., 1999; Ekkekakis & Petruzello, 1999; Thayer, 1987).
Approx. 65% of MHR but inter-individual difference in preference of intensity (Ekkekakis et al., 2005; Rocheleau et al., 2004).
Salmon (2001) suggests one way exercise may improve mood is that each single dose has an accumulative effect, increasing the likelihood of triggering positive cognitive appraisals, behaviours and social interactions.
Exercise Guidance
Recommendations vary slightly according to different sources but most agree that greatest improvement to anxiety, depression and mood is caused by rhythmic, aerobic exercises, that use large muscle groups, such as walking, jogging, swimming, and cycling, of moderate and low intensity (between 50% and 75% of Vo2 max heart rate), conducted for 15 to 30 minutes and performed a minimum of three times a week in programs of 10-weeks or longer (Guszkowska, 2004; NICE 2003).
Exercise in this format is safe but initially aversive enough to present a challenge, whilst also remaining controllable and offering a sense of achievement on completion (Salmon, 2001).
Questions for the clinician?
How to we best get across the message?
How far do we push the message?
Is it our role?
How do we integrate exercise interventions into our therapeutic work?
How do we ensure longevity to the interventions?
How do we incorporate exercise into relapse prevention?
Should we and do we practice what we preach?
Tuesday, 13 July 2010
Friday, 25 June 2010
The Neuropsychology and Psychiatric Consequences of Anabolic-Androgenic Steroid Abuse (AAS)
AAS refers to the specific use of steriods to increase protein synthesis within cells, which results in the buildup of cellular tissue (anabolism), especially in muscles. More commmonly it is not athletes who seek this effect but recreational body builders. A number of key events in the evolution of this social concern are documented within Kanayama et al. (2008):
Psychiatric effects
In addition to several detrimental physiological consequences*, evidence points to several significant detrimental psychiatric effects of AAS:
1 Increased likelihood of aggression/violence
2 Increased likelihood of mania
3 Increased likelihood of psychosis and paranoia
4 Increased likelihood of mood disorder and depressive illness
5 AAS dependence
6 Increased progression to other illicit drug use
See http://en.wikipedia.org/wiki/Anabolic_steroid
And
http://www.archido.de/index.php?option=com_docman&task=doc_view&gid=2732
* Increased likelihood of hypertension, elavated cholesterol, heart problems, sexual dysfunction, testicular atrophy and infertility.
Neuropsychological Effects
Unfortunately no controlled studies have looked at long term neuropsychological effects of AAS; and this is partly down to the fact that the phenomena is relatively recent with participants at the very most, only passing into middel age now, and that participants are essentially hard to identify and recruit. However, some research has been conducted with animals into the neurophysiological mechanism of AAS. In an animal study male rats developed a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine antagonists, which suggests that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine, nicotine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, or benzodiazepines. The potential for androgen addiction remains to be determined.
The neuropsychological effects of AAS present an urgent opprtunity for clinical research.
Psychiatric effects
In addition to several detrimental physiological consequences*, evidence points to several significant detrimental psychiatric effects of AAS:
1 Increased likelihood of aggression/violence
2 Increased likelihood of mania
3 Increased likelihood of psychosis and paranoia
4 Increased likelihood of mood disorder and depressive illness
5 AAS dependence
6 Increased progression to other illicit drug use
See http://en.wikipedia.org/wiki/Anabolic_steroid
And
http://www.archido.de/index.php?option=com_docman&task=doc_view&gid=2732
* Increased likelihood of hypertension, elavated cholesterol, heart problems, sexual dysfunction, testicular atrophy and infertility.
Neuropsychological Effects
Unfortunately no controlled studies have looked at long term neuropsychological effects of AAS; and this is partly down to the fact that the phenomena is relatively recent with participants at the very most, only passing into middel age now, and that participants are essentially hard to identify and recruit. However, some research has been conducted with animals into the neurophysiological mechanism of AAS. In an animal study male rats developed a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine antagonists, which suggests that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine, nicotine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, or benzodiazepines. The potential for androgen addiction remains to be determined.
The neuropsychological effects of AAS present an urgent opprtunity for clinical research.
Tuesday, 20 April 2010
The Mental Capacity Act and the Deprivation of Liberty Safeguards
Mental capacity is an issue in neuropsychology/neuro-rehabilitation when a clients family and the clinical team providing care and treatment are trying to arrange what is in the best interests of the client, because the client may lack the mental function and capacity to make an informed decision. In 2005 a specific act, The Mental Capacity Act (2005) was created, in order to clear up a number of issues:
1. The assessment of a person's capacity and acts by carers and people working with those who lack capacity
2. The provisions whereby people can plan ahead for a time when they may lack capacity
3. Important safeguards
1 The Act makes it clear that any assessment of a person’s capacity must be ‘decision specific’. This means that:
• The assessment of capacity must be about the particular decision that has to be made at a particular time and is not about a range of decisions
• If someone cannot make complex decisions, this does not mean that he/she cannot make simple decisions
• You cannot decide that someone lacks capacity based upon his/her age, appearance, condition or behaviour
• People who have capacity have the right to make poor judgements/decisions- this is not a basis for lacking capacity.
People lacking capacity will include those with dementia, learning disability, mental health problems, brain damage, toxic confusional state and physical injury or illness. The mental incapacity may be permanent or temporary.
Key Principles
There are five important things to think about:
1. Start off by thinking that everyone can make their own decisions.
2. Give a person the support he/she needs to make decisions before concluding that he/she cannot make his/her own decisions.
3. Nobody should be stopped from making a decision just because others may think it is unwise or eccentric.
4. Anything done for, or on behalf of, a person without capacity must be in his/her “best interests” - a decision which is arrived at by working through a checklist.
5. When anything is done or decided for a person without capacity, it must be the least restrictive of his/her basic rights and freedoms.
What does the Act do?
• It aims to clarify a number of legal uncertainties.
• It reforms and updates the current law where decisions need to be made on behalf of others, incorporating good practice into statute and introducing a process.
• It sets out a single test for assessing capacity which is a ‘decision specific test’ (covering emergency decisions; day to day decisions and significant, but not urgent, decisions – including where there are a series of minor decisions which together become significant).
• It covers a wide range of decisions, on personal welfare (including health care) as well as financial matters and substitute decision-making by attorneys or court appointed ‘deputies’. It also clarifies the position where no such formal process has been adopted.
• It includes new rules to govern research involving people who lack capacity and provides for new independent mental capacity advocates to represent and provide support to such people in relation to certain decisions.
• It provides recourse, where necessary and at the appropriate level, to a court with power to deal with all personal welfare (including health care) and financial decisions on behalf of adults who are lacking capacity.
• It replaces the current Court of Protection with a new Court of Protection which has more comprehensive powers.
What does the act mean?
It puts in place a code of practice to give guidance about the legislation. The code must be followed by those working in a professional capacity (e.g. doctors and social workers).
The Act offers appropriate protection for carers (both family members and unpaid carers), as well as health and social care professionals, to those who act in the reasonable belief that they are doing so in the person’s ‘best interests’ when the principles of the Act are followed.
2. The Act sets out provisions whereby people can plan ahead for a time when they may lack capacity
• Lasting Powers of Attorney (LPA)
the Act allows a person to appoint an Attorney to act on their behalf if they should lose capacity in the future. More information on Lasting Powers of Attorney is available.
• Advance decisions to refuse treatment
the Act makes it possible to make an advance decision to refuse treatment should they lack capacity in the future. The Act sets out clear safeguards for the making and application of advance decisions. Further guidance and explanation of advance decisions can found, in Chapter 9 of the Code of Practice.
3. The Act creates important safeguards
• A new Court of Protection
the new Court will have the power to make declarations about whether someone lacks capacity, make orders, or appoint Deputies to act and make decisions on behalf of someone who lacks capacity. More information on the Court of Protection and Deputies is available.
• A new Public Guardian
the Act creates a new public official called the Public Guardian. The Public Guardian will have several duties under the Act including registering Lasting Power of Attorney's (LPA's) and Deputies. The Public Guardian will be supported in his role by a new office called the Office of the Public Guardian (OPG). More information on the Public Guardian and OPG is available.
• Independent Mental Capacity Advocate (IMCA)
an IMCA is someone appointed to support a person who lacks capacity but has no one to speak for them, such as family or friends. They will only become involved when decisions about serious medical treatment or a change in the person's accommodation where it is provided by the NHS or a local authority. More information on the IMCA's can be found on the Department of Health website.
• Research involving people who lack capacity
the Act sets out clear guidelines for research involving people who lack capacity. The research must be approved by an appropriate body, who will also ensure that the research is safe and relates to the person's condition. They must also ensure that the research would not be as effective if they use people who have mental capacity. More information on research and its regulations can be found on the Department of Health website.
• New criminal offence
the Act introduces 2 new criminal offences of ill treatment and wilful neglect of a person who lacks capacity. A person found
The Mental Capacity Act Deprivation of Liberty Safeguard was introduced to specifically protect the freedom of people who cannot make decisions over their treatment and care because of a lack of mental capacity.
The Mental Capacity Act Deprivation of Liberty Safeguards is a new law, which came into force on 1st April 2009.
The safeguards are in response to the 2004 European Court of Human Rights judgement involving an autistic man who lacked the capacity to consent who was kept at Bournewood Hospital by doctors against the wishes of his carers. The court found that he had been deprived of his liberty unlawfully, and the Department of Health committed to introducing new legislation to close the 'Bournewood gap'.
These safeguards provide protection for a very vulnerable group of people who are cared for in hospitals or in care homes registered under the Care Standards Act 2000, in circumstances that deprive them of their liberty, and who are unable to consent (but who are not detained under the Mental Health Act 1983).
The safeguards are designed to protect the interests of an extremely vulnerable group of service users and to:
• ensure people can be given the care they need in the least restrictive regimes
• prevent arbitrary decisions that deprive vulnerable people of their liberty
• provide safeguards for vulnerable people
• provide them with rights of challenge against unlawful detention
• avoid unnecessary bureaucracy
What is a Deprivation of Liberty?
Deprivation of liberty has no clear definition. Many people in hospitals and care homes may have their liberty restricted but not all will be deprived of their liberty. The following factors need to be considered:
• Whether professionals have complete and effective control over assessment, care, treatment, contacts, movement and residence
• Whether the person will be under constant supervision and control and not free to leave
• Whether restraint is used including sedation
• Whether the person would be prevented from leaving if they attempted to do so
• Whether a request from carers for the person to be discharged into their care is likely to be agreed
• Whether the person can maintain social contacts
• Whether the person has choice about their life within the home or hospital
Who do the Deprivation of Liberty Safeguards apply to?
The safeguards apply to anyone:
• aged 18 and over
• who suffers from a mental disorder or disability of the mind – such as dementia or a profound learning disability
• who lacks the capacity to give informed consent to the arrangements made for their care and / or treatment and
• for whom deprivation of liberty (within the meaning of Article 5 of the ECHR) is considered after an independent assessment to be necessary in their best interests to protect them from harm
What are the authorities' duties under the Safeguards?
Hospitals and Care Homes (these are called Managing Authorities) have a duty to:
• provide care and treatment in ways that do not deprive a person of their liberty, or if this is impossible;
• apply to the Supervisory Body for authorisation of the deprivation of liberty.
The Council and the Primary Care Trust (these are called Supervisory Bodies) have a duty to:
• assess any person for whom the Managing Authorities request a deprivation of liberty;
• authorise a deprivation if it is necessary and in the best interests of a person to whom the Safeguards apply;
• set any necessary conditions to make sure the person's care/treatment meets their needs in their best interests;
• set a timescale for how long a deprivation can last;
• keep records of who is being deprived of their liberty.
What should I do if I feel a person is being deprived of their liberty?
Discuss the issue with the hospital or care home. They may be able to change a person's care or treatment to make sure the person is not being deprived of their liberty, or may be able to explain why a person is not actually deprived of their liberty.
Request that the Supervisory Body reviews the person to see whether they are being deprived of their liberty. This request can be by telephone, fax or email. There are standard letters available to use.
1. The assessment of a person's capacity and acts by carers and people working with those who lack capacity
2. The provisions whereby people can plan ahead for a time when they may lack capacity
3. Important safeguards
1 The Act makes it clear that any assessment of a person’s capacity must be ‘decision specific’. This means that:
• The assessment of capacity must be about the particular decision that has to be made at a particular time and is not about a range of decisions
• If someone cannot make complex decisions, this does not mean that he/she cannot make simple decisions
• You cannot decide that someone lacks capacity based upon his/her age, appearance, condition or behaviour
• People who have capacity have the right to make poor judgements/decisions- this is not a basis for lacking capacity.
People lacking capacity will include those with dementia, learning disability, mental health problems, brain damage, toxic confusional state and physical injury or illness. The mental incapacity may be permanent or temporary.
Key Principles
There are five important things to think about:
1. Start off by thinking that everyone can make their own decisions.
2. Give a person the support he/she needs to make decisions before concluding that he/she cannot make his/her own decisions.
3. Nobody should be stopped from making a decision just because others may think it is unwise or eccentric.
4. Anything done for, or on behalf of, a person without capacity must be in his/her “best interests” - a decision which is arrived at by working through a checklist.
5. When anything is done or decided for a person without capacity, it must be the least restrictive of his/her basic rights and freedoms.
What does the Act do?
• It aims to clarify a number of legal uncertainties.
• It reforms and updates the current law where decisions need to be made on behalf of others, incorporating good practice into statute and introducing a process.
• It sets out a single test for assessing capacity which is a ‘decision specific test’ (covering emergency decisions; day to day decisions and significant, but not urgent, decisions – including where there are a series of minor decisions which together become significant).
• It covers a wide range of decisions, on personal welfare (including health care) as well as financial matters and substitute decision-making by attorneys or court appointed ‘deputies’. It also clarifies the position where no such formal process has been adopted.
• It includes new rules to govern research involving people who lack capacity and provides for new independent mental capacity advocates to represent and provide support to such people in relation to certain decisions.
• It provides recourse, where necessary and at the appropriate level, to a court with power to deal with all personal welfare (including health care) and financial decisions on behalf of adults who are lacking capacity.
• It replaces the current Court of Protection with a new Court of Protection which has more comprehensive powers.
What does the act mean?
It puts in place a code of practice to give guidance about the legislation. The code must be followed by those working in a professional capacity (e.g. doctors and social workers).
The Act offers appropriate protection for carers (both family members and unpaid carers), as well as health and social care professionals, to those who act in the reasonable belief that they are doing so in the person’s ‘best interests’ when the principles of the Act are followed.
2. The Act sets out provisions whereby people can plan ahead for a time when they may lack capacity
• Lasting Powers of Attorney (LPA)
the Act allows a person to appoint an Attorney to act on their behalf if they should lose capacity in the future. More information on Lasting Powers of Attorney is available.
• Advance decisions to refuse treatment
the Act makes it possible to make an advance decision to refuse treatment should they lack capacity in the future. The Act sets out clear safeguards for the making and application of advance decisions. Further guidance and explanation of advance decisions can found, in Chapter 9 of the Code of Practice.
3. The Act creates important safeguards
• A new Court of Protection
the new Court will have the power to make declarations about whether someone lacks capacity, make orders, or appoint Deputies to act and make decisions on behalf of someone who lacks capacity. More information on the Court of Protection and Deputies is available.
• A new Public Guardian
the Act creates a new public official called the Public Guardian. The Public Guardian will have several duties under the Act including registering Lasting Power of Attorney's (LPA's) and Deputies. The Public Guardian will be supported in his role by a new office called the Office of the Public Guardian (OPG). More information on the Public Guardian and OPG is available.
• Independent Mental Capacity Advocate (IMCA)
an IMCA is someone appointed to support a person who lacks capacity but has no one to speak for them, such as family or friends. They will only become involved when decisions about serious medical treatment or a change in the person's accommodation where it is provided by the NHS or a local authority. More information on the IMCA's can be found on the Department of Health website.
• Research involving people who lack capacity
the Act sets out clear guidelines for research involving people who lack capacity. The research must be approved by an appropriate body, who will also ensure that the research is safe and relates to the person's condition. They must also ensure that the research would not be as effective if they use people who have mental capacity. More information on research and its regulations can be found on the Department of Health website.
• New criminal offence
the Act introduces 2 new criminal offences of ill treatment and wilful neglect of a person who lacks capacity. A person found
The Mental Capacity Act Deprivation of Liberty Safeguard was introduced to specifically protect the freedom of people who cannot make decisions over their treatment and care because of a lack of mental capacity.
The Mental Capacity Act Deprivation of Liberty Safeguards is a new law, which came into force on 1st April 2009.
The safeguards are in response to the 2004 European Court of Human Rights judgement involving an autistic man who lacked the capacity to consent who was kept at Bournewood Hospital by doctors against the wishes of his carers. The court found that he had been deprived of his liberty unlawfully, and the Department of Health committed to introducing new legislation to close the 'Bournewood gap'.
These safeguards provide protection for a very vulnerable group of people who are cared for in hospitals or in care homes registered under the Care Standards Act 2000, in circumstances that deprive them of their liberty, and who are unable to consent (but who are not detained under the Mental Health Act 1983).
The safeguards are designed to protect the interests of an extremely vulnerable group of service users and to:
• ensure people can be given the care they need in the least restrictive regimes
• prevent arbitrary decisions that deprive vulnerable people of their liberty
• provide safeguards for vulnerable people
• provide them with rights of challenge against unlawful detention
• avoid unnecessary bureaucracy
What is a Deprivation of Liberty?
Deprivation of liberty has no clear definition. Many people in hospitals and care homes may have their liberty restricted but not all will be deprived of their liberty. The following factors need to be considered:
• Whether professionals have complete and effective control over assessment, care, treatment, contacts, movement and residence
• Whether the person will be under constant supervision and control and not free to leave
• Whether restraint is used including sedation
• Whether the person would be prevented from leaving if they attempted to do so
• Whether a request from carers for the person to be discharged into their care is likely to be agreed
• Whether the person can maintain social contacts
• Whether the person has choice about their life within the home or hospital
Who do the Deprivation of Liberty Safeguards apply to?
The safeguards apply to anyone:
• aged 18 and over
• who suffers from a mental disorder or disability of the mind – such as dementia or a profound learning disability
• who lacks the capacity to give informed consent to the arrangements made for their care and / or treatment and
• for whom deprivation of liberty (within the meaning of Article 5 of the ECHR) is considered after an independent assessment to be necessary in their best interests to protect them from harm
What are the authorities' duties under the Safeguards?
Hospitals and Care Homes (these are called Managing Authorities) have a duty to:
• provide care and treatment in ways that do not deprive a person of their liberty, or if this is impossible;
• apply to the Supervisory Body for authorisation of the deprivation of liberty.
The Council and the Primary Care Trust (these are called Supervisory Bodies) have a duty to:
• assess any person for whom the Managing Authorities request a deprivation of liberty;
• authorise a deprivation if it is necessary and in the best interests of a person to whom the Safeguards apply;
• set any necessary conditions to make sure the person's care/treatment meets their needs in their best interests;
• set a timescale for how long a deprivation can last;
• keep records of who is being deprived of their liberty.
What should I do if I feel a person is being deprived of their liberty?
Discuss the issue with the hospital or care home. They may be able to change a person's care or treatment to make sure the person is not being deprived of their liberty, or may be able to explain why a person is not actually deprived of their liberty.
Request that the Supervisory Body reviews the person to see whether they are being deprived of their liberty. This request can be by telephone, fax or email. There are standard letters available to use.
Tuesday, 13 April 2010
Wernicke’s Aphasia
Wernicke’s aphasia (AKA fluent aphasia/receptive aphasia) is characterised by inappropriate words and the inability to understand spoken language. Speech is preserved with normal rhythm, but language content is incorrect. This may vary from the insertion of a few incorrect or nonexistent words to a profuse outpouring of jargon. Grammar, syntax, rate, intonation and stress are normal. Substitutions of one word for another (paraphasias, e.g. “telephone” for “television”) are common. Comprehension and repetition are poor.
It is often a result of damage to Wernicke’s area, a left laterised focal area in 97% of people (including the majority of left handers). The major deficit of Wernicke’s aphasia can be understood as an inability synchronising objects and ideas with the words that signify them. Patients who recover from Wernicke’s aphasia report that, while aphasic, they found the speech of others to be unintelligible and, despite being cognizant of that fact that they were speaking, they could neither stop themselves nor understand their own words. Contrast this to Broca’s aphasia which is typified by non-fluent speech lacking in grammer.
An example of Broca’s aphasia:
“I am a sig… no… man… uh…., well,…again.”
(These words were emitted slowly and with great effort. The sounds were not clearly articulated and each syllable was uttered harshly, explosively and in a throaty voice. Moreover, Broca’s aphasia is often accompanied by right hemiparesis).
An example of Wernicke’s aphasia:
“Ive done a lot well, I impose a lot, while, on the other hand, you know what I mean, I have to run around, look it over, ?trebbin? and all that sort of stuff”.”
It is often a result of damage to Wernicke’s area, a left laterised focal area in 97% of people (including the majority of left handers). The major deficit of Wernicke’s aphasia can be understood as an inability synchronising objects and ideas with the words that signify them. Patients who recover from Wernicke’s aphasia report that, while aphasic, they found the speech of others to be unintelligible and, despite being cognizant of that fact that they were speaking, they could neither stop themselves nor understand their own words. Contrast this to Broca’s aphasia which is typified by non-fluent speech lacking in grammer.
An example of Broca’s aphasia:
“I am a sig… no… man… uh…., well,…again.”
(These words were emitted slowly and with great effort. The sounds were not clearly articulated and each syllable was uttered harshly, explosively and in a throaty voice. Moreover, Broca’s aphasia is often accompanied by right hemiparesis).
An example of Wernicke’s aphasia:
“Ive done a lot well, I impose a lot, while, on the other hand, you know what I mean, I have to run around, look it over, ?trebbin? and all that sort of stuff”.”
Monday, 8 March 2010
Types of Agnosias
Agnosia literally meaning “loss of knowledge” is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream
Alexia
Inability to recognize text.
Alexithymia
Whilst not strictly a form of agnosia, alexithymia may be difficult to distinguish from or co-occur with social-emotional agnosia. Alexithymia is deficiency in understanding, processing, or describing emotions common to around 85% of people on the autism spectrum. Alexithymia is believed to be due to an information processing delay in the combined processing of information in the left and right hemispheres, resulting in poor differentiation between body messages and emotions.
Amusia
Or receptive amusia is agnosia for music. It involves loss of the ability to recognize musical notes, rhythms, and intervals and the inability to experience music as musical.
Anosognosia
This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive agnosia
Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.
Apraxia
Is a form of motor (body) agnosia involving the neurological loss of ability to map out physical actions in order to repeat them in functional activities. It is a form of body-disconnectedness and takes several different forms; Speech-Apraxia in which ability to speak is impaired, Limb-Kinetic Apraxia in which there is a loss of hand or finger dexterity and can extend to the voluntary use of limbs, Ideomotor Apraxia in which the gestures of others can't be easily replicated and can't execute goal-directed movements, Ideational Apraxia in which one can't work out which actions to initiate and struggles to plan and discriminate between potential gestures, Apraxia of Gait in which co-ordination of leg actions is problematic such as kicking a ball, Constructional Apraxia in which a person can't co-ordinate the construction of objects or draw pictures or follow a design, Oculomotor Apraxia in which the ability to control visual tracking is impaired and Buccofacial Apraxia in which skilled use of the lips, mouth and tongue is impaired.
Associative agnosia
Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Auditory agnosia
With Auditory Agnosia there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal.
Autotopagnosia
Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Color agnosia
Refers to the inability to recognize a color, while being able to perceive or distinguish it.
Cortical deafness
Refers to people who do not perceive any auditory information but whose hearing is intact.
Finger agnosia
Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosia
Patients perceive only parts of details, not the whole object.
Integrative agnosia
This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Mirror agnosia
One of the symptoms of Hemispatial neglect. Patients with Hemispatial neglect were placed so that an object was in their neglected visual field but a mirror reflecting that object was visible in their non-neglected field. Patients could not acknowledge the existence of objects in the neglected field and so attempted to reach into the mirror to grasp the object.
Pain agnosia
Also referred to as Analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia
Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia
Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Semantic agnosia
Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).
Simultanagnosia
Patients can recognize objects or details in their visual field, but only one at a time. They cannot make out the scene they belong to or make out a whole image out of the details. They literally "cannot see the forest for the trees." Simultanagnosia is a common symptom of Balint's syndrome.
Social emotional agnosia
Sometimes referred to as Expressive Agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Somatosensory agnosia
Or Astereognosia] is connected to tactile sense - that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Tactile agnosia
Impaired ability to recognize or identify objects by touch alone.
Time agnosia
Is the loss of comprehension of the succession and duration of events.
Topographical agnosia
This is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognise objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place
Verbal auditory agnosia
This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.[19]
Visual agnosia
Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.
Visual verbal agnosia
Difficulty comprehending the meaning of written words. The capacity to read is usually intact but comprehension is impaired.]
Alexia
Inability to recognize text.
Alexithymia
Whilst not strictly a form of agnosia, alexithymia may be difficult to distinguish from or co-occur with social-emotional agnosia. Alexithymia is deficiency in understanding, processing, or describing emotions common to around 85% of people on the autism spectrum. Alexithymia is believed to be due to an information processing delay in the combined processing of information in the left and right hemispheres, resulting in poor differentiation between body messages and emotions.
Amusia
Or receptive amusia is agnosia for music. It involves loss of the ability to recognize musical notes, rhythms, and intervals and the inability to experience music as musical.
Anosognosia
This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive agnosia
Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.
Apraxia
Is a form of motor (body) agnosia involving the neurological loss of ability to map out physical actions in order to repeat them in functional activities. It is a form of body-disconnectedness and takes several different forms; Speech-Apraxia in which ability to speak is impaired, Limb-Kinetic Apraxia in which there is a loss of hand or finger dexterity and can extend to the voluntary use of limbs, Ideomotor Apraxia in which the gestures of others can't be easily replicated and can't execute goal-directed movements, Ideational Apraxia in which one can't work out which actions to initiate and struggles to plan and discriminate between potential gestures, Apraxia of Gait in which co-ordination of leg actions is problematic such as kicking a ball, Constructional Apraxia in which a person can't co-ordinate the construction of objects or draw pictures or follow a design, Oculomotor Apraxia in which the ability to control visual tracking is impaired and Buccofacial Apraxia in which skilled use of the lips, mouth and tongue is impaired.
Associative agnosia
Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Auditory agnosia
With Auditory Agnosia there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal.
Autotopagnosia
Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Color agnosia
Refers to the inability to recognize a color, while being able to perceive or distinguish it.
Cortical deafness
Refers to people who do not perceive any auditory information but whose hearing is intact.
Finger agnosia
Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosia
Patients perceive only parts of details, not the whole object.
Integrative agnosia
This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Mirror agnosia
One of the symptoms of Hemispatial neglect. Patients with Hemispatial neglect were placed so that an object was in their neglected visual field but a mirror reflecting that object was visible in their non-neglected field. Patients could not acknowledge the existence of objects in the neglected field and so attempted to reach into the mirror to grasp the object.
Pain agnosia
Also referred to as Analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia
Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia
Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Semantic agnosia
Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).
Simultanagnosia
Patients can recognize objects or details in their visual field, but only one at a time. They cannot make out the scene they belong to or make out a whole image out of the details. They literally "cannot see the forest for the trees." Simultanagnosia is a common symptom of Balint's syndrome.
Social emotional agnosia
Sometimes referred to as Expressive Agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Somatosensory agnosia
Or Astereognosia] is connected to tactile sense - that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Tactile agnosia
Impaired ability to recognize or identify objects by touch alone.
Time agnosia
Is the loss of comprehension of the succession and duration of events.
Topographical agnosia
This is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognise objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place
Verbal auditory agnosia
This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.[19]
Visual agnosia
Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.
Visual verbal agnosia
Difficulty comprehending the meaning of written words. The capacity to read is usually intact but comprehension is impaired.]
The Neuropsychology of ‘Brain Training’ and Cognitive Reserve
Many 'brain exercise' products have been marketed in recent years, promising to help people stay mentally fit as they age, and even help prevent dementia. However, a systematic review by Pap, Walsh and Snyder (2009) found no good evidence that brain training will either prevent or slow down mental deterioration in healthy older adults.
Mild memory problems are part and parcel of getting older, but more moderate and severe memory problems and cognitive dysfunction are often indicative of a dementia. Alzheimer's disease is the most common type of dementia, followed by vascular dementia. We know that unhealthy lifestyles including smoking, drinking and unbalanced high fat diets can increase our risk. We also know that genes play a role, and that neuro-traumatic events such as strokes or head injury can increase the risk of developing dementia. But many people wonder what they can do to lower their risk.
Pap, Walsh and Snyder (2009) found 10 good-quality studies that looked at cognitive training in healthy elderly people. When they pooled the studies' results, they found that training led to small improvements in specific tasks related to the training. However, they found no evidence that this prevented or slowed the onset of dementia. That's not to say that brain exercises don't have the potential to help, but researchers say that better-designed studies are needed to find out. Part of the problem with the studies so far is that they didn't assess people for very long. So they couldn't say what long-term effects the training might have had on people's risk of dementia. The studies also mainly looked at how well people performed tasks that were closely tied to their training and nothing else. To meaningfully explore the connection between brain training and dementia, studies would need to look at overall brain function as well as people's performance on tasks in everyday life.
Bold claims made by commercial computer games should be interpreted with an element of cynicism until better research is conducted. Scientists do know however, that there is clear evidence that physical exercise and a balanced diet can delay the progress of dementia significantly. Although the preventative effects of both of these factors is thought to be modest.
Cognitive reserve is valuable way of conceptualising one’s vulnerability to dementia and prognosis. The term cognitive reserve describes the mind's resilience to neuropathological damage of the brain. In the first study of its kind in Katzman et al. published findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease. This is to say that some participants whose brains had extensive Alzheimer’s disease pathology, clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears. Neuronoal density rather than brain size appear to be significant in high cognitive reserve individuals. Moreover, genetics again appear to play a part. Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition. However, cognitive reserve is somewhat of a double edged sword, as it is believed that people with high reserve go undiagnosed until neuronal damage is severe, then rapid decline ensues.
Reference
Pap KV, Walsh SJ, Snyder PJ. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia. 2009; 5: 50-60.
http://en.wikipedia.org/wiki/Cognitive_reserve
Mild memory problems are part and parcel of getting older, but more moderate and severe memory problems and cognitive dysfunction are often indicative of a dementia. Alzheimer's disease is the most common type of dementia, followed by vascular dementia. We know that unhealthy lifestyles including smoking, drinking and unbalanced high fat diets can increase our risk. We also know that genes play a role, and that neuro-traumatic events such as strokes or head injury can increase the risk of developing dementia. But many people wonder what they can do to lower their risk.
Pap, Walsh and Snyder (2009) found 10 good-quality studies that looked at cognitive training in healthy elderly people. When they pooled the studies' results, they found that training led to small improvements in specific tasks related to the training. However, they found no evidence that this prevented or slowed the onset of dementia. That's not to say that brain exercises don't have the potential to help, but researchers say that better-designed studies are needed to find out. Part of the problem with the studies so far is that they didn't assess people for very long. So they couldn't say what long-term effects the training might have had on people's risk of dementia. The studies also mainly looked at how well people performed tasks that were closely tied to their training and nothing else. To meaningfully explore the connection between brain training and dementia, studies would need to look at overall brain function as well as people's performance on tasks in everyday life.
Bold claims made by commercial computer games should be interpreted with an element of cynicism until better research is conducted. Scientists do know however, that there is clear evidence that physical exercise and a balanced diet can delay the progress of dementia significantly. Although the preventative effects of both of these factors is thought to be modest.
Cognitive reserve is valuable way of conceptualising one’s vulnerability to dementia and prognosis. The term cognitive reserve describes the mind's resilience to neuropathological damage of the brain. In the first study of its kind in Katzman et al. published findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease. This is to say that some participants whose brains had extensive Alzheimer’s disease pathology, clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears. Neuronoal density rather than brain size appear to be significant in high cognitive reserve individuals. Moreover, genetics again appear to play a part. Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition. However, cognitive reserve is somewhat of a double edged sword, as it is believed that people with high reserve go undiagnosed until neuronal damage is severe, then rapid decline ensues.
Reference
Pap KV, Walsh SJ, Snyder PJ. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia. 2009; 5: 50-60.
http://en.wikipedia.org/wiki/Cognitive_reserve
Thursday, 4 March 2010
The Neuropsychology of Loss
Loss is a key process in adjustment to and acceptance of one's limitations following a neurological event such as a brain injury, stroke or neurological disorder. Loss refers to any concept of value that has been detrimented following a neurological event.
Common losses include: Independence; Mobility; Relationships; Ability to communicate; Career/Job; Friends; Memories; Self-awareness; Hobbies & interests; Driving; Freedom; Sex/sexual drive; Routine; Prospects etc.
Psychotherapists have often discussed the stages of loss that people tend to experience. However, these stages are not regularly experienced in a serial or linear fashion and therefore more recently psychotherapists and psychologists tend refer to the 'common feelings' of loss rather than the 'stages of loss'.
Although there is little scientific confirmation for the 'common feelings of loss', an overwheling majority of psychotherapists and psychologist agree, from many years clinical experience of providing therapy that there five 'common feelings' that appear to involved in loss.
1 Denial
* We deny that the loss has occurred or ignore the signs.
* We may use fiction or fantasy to deny the reality or make sense of confusing partial memories.
* We may withdraw believing we can avoid facing the loss and avoid those people who confront us with the truth.
* We may regress to being like a child who wants protecting from the loss.
2 Bargaining
* We may promise to do anything to make this loss go away.
* We may bargain or strike a deal with God, ourselves or others to make the loss go away.
* We lack confidence in our attempts to deal with the loss, looking elsewhere for answers or gamble on a miracle.
3 Anger
* Anger is a perfectly natural reaction to loss that passes with time.
* Anger can come from loss, grief, frustration and resentment and we can become angry with:
A Ourselves: ‘self blame’.
B Others: ‘kicking the cat’
C Our closest friends and family
4 Despair
*We become overwhelmed by the anguish, pain, sadness and hurt of our loss
*Our mood can be lowered and we might often cry
*We might wrongly convince ourselves that the loss was some sort or payback.
*We might begin feel despondent and to think things are utterly hopeless.
5 Acceptance
*We can identify losses and the common feelings of loss.
*We can describe the details of our loss and the details of the rehabilitation.
* We can get through each day, cope somehow and keep sight of some level of hope.
* We are now aware when we dip back into stages or common feelings of loss and know what to do to help.
* Adapt and drive toward our potential.
Acceptance presents the final and most adaptive phase of feeling associated with loss. Therapeutic aims are often based upon experiencing more feelings associated with acceptance.
There is a growing collection of evidence that loss has neurological consequences. fMRI scans of women from whom loss and grief was elicited about the death of a mother or a sister in the past 5 years found it produced a local inflammation response as measured by salivary concentrations of pro-inflammatory cytokines. These were correlated with activation in the anterior cingulate cortex and orbitofrontal cortex. These activation also correlated with free recall of grief-related word stimuli. This suggests that grief can cause stress, and that this is linked to the emotional processing parts of the frontal lobe.
Among those bereaved within the last three months, those who report many intrusive thoughts about the deceased show ventral amygdala and rostral anterior cingulate cortex hyperactivity to reminders of their loss. In the case of the amygdala, this links to their sadness intensity. In those who avoid such thoughts, there is a related opposite type of pattern in which there is a decrease in the activation of the dorsal amgydala and the dorsolateral prefrontal cortex.
In those not so emotionally affected by reminders of their loss, fMRI finds the existence of a high functional connectivity between the dorsolateral prefrontal cortex and amygdala activity, suggesting the former regulates activity in the latter. In those who had greater intensity of sadness, there was a low functional connection between the rostal anterior cingulate cortex and amygdala activity, suggesting a lack of regulation of the former part of the brain upon the latter
Common losses include: Independence; Mobility; Relationships; Ability to communicate; Career/Job; Friends; Memories; Self-awareness; Hobbies & interests; Driving; Freedom; Sex/sexual drive; Routine; Prospects etc.
Psychotherapists have often discussed the stages of loss that people tend to experience. However, these stages are not regularly experienced in a serial or linear fashion and therefore more recently psychotherapists and psychologists tend refer to the 'common feelings' of loss rather than the 'stages of loss'.
Although there is little scientific confirmation for the 'common feelings of loss', an overwheling majority of psychotherapists and psychologist agree, from many years clinical experience of providing therapy that there five 'common feelings' that appear to involved in loss.
1 Denial
* We deny that the loss has occurred or ignore the signs.
* We may use fiction or fantasy to deny the reality or make sense of confusing partial memories.
* We may withdraw believing we can avoid facing the loss and avoid those people who confront us with the truth.
* We may regress to being like a child who wants protecting from the loss.
2 Bargaining
* We may promise to do anything to make this loss go away.
* We may bargain or strike a deal with God, ourselves or others to make the loss go away.
* We lack confidence in our attempts to deal with the loss, looking elsewhere for answers or gamble on a miracle.
3 Anger
* Anger is a perfectly natural reaction to loss that passes with time.
* Anger can come from loss, grief, frustration and resentment and we can become angry with:
A Ourselves: ‘self blame’.
B Others: ‘kicking the cat’
C Our closest friends and family
4 Despair
*We become overwhelmed by the anguish, pain, sadness and hurt of our loss
*Our mood can be lowered and we might often cry
*We might wrongly convince ourselves that the loss was some sort or payback.
*We might begin feel despondent and to think things are utterly hopeless.
5 Acceptance
*We can identify losses and the common feelings of loss.
*We can describe the details of our loss and the details of the rehabilitation.
* We can get through each day, cope somehow and keep sight of some level of hope.
* We are now aware when we dip back into stages or common feelings of loss and know what to do to help.
* Adapt and drive toward our potential.
Acceptance presents the final and most adaptive phase of feeling associated with loss. Therapeutic aims are often based upon experiencing more feelings associated with acceptance.
There is a growing collection of evidence that loss has neurological consequences. fMRI scans of women from whom loss and grief was elicited about the death of a mother or a sister in the past 5 years found it produced a local inflammation response as measured by salivary concentrations of pro-inflammatory cytokines. These were correlated with activation in the anterior cingulate cortex and orbitofrontal cortex. These activation also correlated with free recall of grief-related word stimuli. This suggests that grief can cause stress, and that this is linked to the emotional processing parts of the frontal lobe.
Among those bereaved within the last three months, those who report many intrusive thoughts about the deceased show ventral amygdala and rostral anterior cingulate cortex hyperactivity to reminders of their loss. In the case of the amygdala, this links to their sadness intensity. In those who avoid such thoughts, there is a related opposite type of pattern in which there is a decrease in the activation of the dorsal amgydala and the dorsolateral prefrontal cortex.
In those not so emotionally affected by reminders of their loss, fMRI finds the existence of a high functional connectivity between the dorsolateral prefrontal cortex and amygdala activity, suggesting the former regulates activity in the latter. In those who had greater intensity of sadness, there was a low functional connection between the rostal anterior cingulate cortex and amygdala activity, suggesting a lack of regulation of the former part of the brain upon the latter
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