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.
Tuesday, 20 April 2010
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
Wednesday, 17 February 2010
Working with Challenging Behaviour in Neuro-Rehabilitation
Dealing with challenging behaviour is much the same in neuro-rehabilitation as it is in other care and therapeutic contexts. The following is the basis of a training workshop in progress aimed at increasing skills in dealing with challenging behaviour wihtin a neuro-rehab setting.
What do we mean by challenging behaviour?
Behaviours are actions that we can observe and record:
Hitting
Kicking
Biting
Spitting
Smearing
Self-harm
Swearing
Disinhibition
Sexualised actions
Verbal threats?
Stubborness?
Lack of insight?
Emerson’s definition
"culturally abnormal behaviour(s) of such intensity, frequency or duration that the physical safety of the person or others is placed in serious jeopardy, or behaviour which is likely to seriously limit or deny access to the use of ordinary community facilities"
How do we learn behaviours?
From reward (reinforcement)
Through association
From role modelling
From unique human ability of reflection on action/learning from mistakes?
How do we unlearn behaviours?
Through punishment?
Through negative reinforcement?
Through extinction?
Through rewarding alternative experiences
Why do challenging behaviours arise?
Behaviours or actions exist because they serve a function
Challenging behaviours are no different
Functions:
Get needs met
Communicate thoughts/feelings
Avoidance
Sensation
Maintaining and promoting rules & boundaries:
Don’t be afraid to say when CB is not appropriate- clearly describe to a client when behaviour unacceptable
Consistency is key
Maintaining equal/professional relationships
Promoting team approaches rather than split teams
Improved communication:
What is the behaviour trying to express?
Functional assessment/ABC analysis
Liaison with speech and language
Communication aids/development
Relationships
Proactive strategies and environmental changes:
Consistency is key: Follow nursing guidelines/plans
Observe and record what rewards apply to an individual
Assessment of Frequency-Intensity-Duration-Onset (FIDO)
Think about environment/places/people/promiximity etc
Make environment safe when addressing CB
Be aware of cognitive limitations when planning activities
Reactive strategies:
Consistency is key: following team nursing guidelines
Make sure people are safe
Firstly, state when behaviour is unacceptable
Secondly, guide toward alternative behaviours
Reward positive alternative behaviours
Team liaison
Try not to inadvertantly reinforce CB
Time out strategies only work if followed to the tee with no exceptions
Awareness of feelings/attributions:
Challenging behaviour can evoke strong feelings in us. Sometimes they create anger/sadness/guilt/dislike. Incidents can sometimes remind us of previous experiences, events or people.
The feelings are really important because:
They can influence how we respond and deal with the behaviour
Talking about CB to colleagues and learning from past events:
CB creates staff stress
Evidence says support/talking helps
Open culture of learning from mistakes
Psychology’s door is open if strong feelings arise
Responding to Challenging Behaviour Summary:
Maintaining and promoting rules & boundaries
Improved communication
Proactive strategies and environmental changes
Reactive strategies
Awareness of feelings/attributions
Talking about CB to colleagues and learning from past events
What do we mean by challenging behaviour?
Behaviours are actions that we can observe and record:
Hitting
Kicking
Biting
Spitting
Smearing
Self-harm
Swearing
Disinhibition
Sexualised actions
Verbal threats?
Stubborness?
Lack of insight?
Emerson’s definition
"culturally abnormal behaviour(s) of such intensity, frequency or duration that the physical safety of the person or others is placed in serious jeopardy, or behaviour which is likely to seriously limit or deny access to the use of ordinary community facilities"
How do we learn behaviours?
From reward (reinforcement)
Through association
From role modelling
From unique human ability of reflection on action/learning from mistakes?
How do we unlearn behaviours?
Through punishment?
Through negative reinforcement?
Through extinction?
Through rewarding alternative experiences
Why do challenging behaviours arise?
Behaviours or actions exist because they serve a function
Challenging behaviours are no different
Functions:
Get needs met
Communicate thoughts/feelings
Avoidance
Sensation
Maintaining and promoting rules & boundaries:
Don’t be afraid to say when CB is not appropriate- clearly describe to a client when behaviour unacceptable
Consistency is key
Maintaining equal/professional relationships
Promoting team approaches rather than split teams
Improved communication:
What is the behaviour trying to express?
Functional assessment/ABC analysis
Liaison with speech and language
Communication aids/development
Relationships
Proactive strategies and environmental changes:
Consistency is key: Follow nursing guidelines/plans
Observe and record what rewards apply to an individual
Assessment of Frequency-Intensity-Duration-Onset (FIDO)
Think about environment/places/people/promiximity etc
Make environment safe when addressing CB
Be aware of cognitive limitations when planning activities
Reactive strategies:
Consistency is key: following team nursing guidelines
Make sure people are safe
Firstly, state when behaviour is unacceptable
Secondly, guide toward alternative behaviours
Reward positive alternative behaviours
Team liaison
Try not to inadvertantly reinforce CB
Time out strategies only work if followed to the tee with no exceptions
Awareness of feelings/attributions:
Challenging behaviour can evoke strong feelings in us. Sometimes they create anger/sadness/guilt/dislike. Incidents can sometimes remind us of previous experiences, events or people.
The feelings are really important because:
They can influence how we respond and deal with the behaviour
Talking about CB to colleagues and learning from past events:
CB creates staff stress
Evidence says support/talking helps
Open culture of learning from mistakes
Psychology’s door is open if strong feelings arise
Responding to Challenging Behaviour Summary:
Maintaining and promoting rules & boundaries
Improved communication
Proactive strategies and environmental changes
Reactive strategies
Awareness of feelings/attributions
Talking about CB to colleagues and learning from past events
Tuesday, 9 February 2010
Accelerated Forgetting and the Neuropsychological Assessment of Memory in Epilepsy
Patients with epilepsy frequently complain of memory difficulties yet often perform normally on standard neuropsychological tests of memory. It has been suggested that this may be due to an impairment of very long-term memory consolidation processes, beyond those normally assessed in the neuropsychological clinic.
Blake et al. (2000) found despite normal learning and retention over 30 min, patients with epileptic foci in the left temporal lobe performed disproportionately poorly on the long-term test compared with both patients with epileptic foci in the right temporal lobe and controls. Findings provide evidence for an extended period of memory consolidation and point to the critical region for this process, at least for verbal material, in the left temporal lobe.
Zeman et al. 1998 studied the concept of transient epileptic amnesia (TEA). TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to “remember not being able to remember”. The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. He hypothesises that post ictal states (5-30 mintues following seizure) may be responsible for disrupting the consolidation of long term memories, thus explaining accelerated forgetting. Direct links between temporal lobe epilepsy and memory difficulties is complicated by a number of confounding variables:
• Anti-convulsent medication side effects
• Age of epilepsy onset
• Seizure frequency
• Structural damage arising from epileptic activity
See Butler and Zeman for a comprehensive and up to date review of the issues
http://brain.oxfordjournals.org/cgi/reprint/131/9/2243
Blake et al. (2000) found despite normal learning and retention over 30 min, patients with epileptic foci in the left temporal lobe performed disproportionately poorly on the long-term test compared with both patients with epileptic foci in the right temporal lobe and controls. Findings provide evidence for an extended period of memory consolidation and point to the critical region for this process, at least for verbal material, in the left temporal lobe.
Zeman et al. 1998 studied the concept of transient epileptic amnesia (TEA). TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to “remember not being able to remember”. The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. He hypothesises that post ictal states (5-30 mintues following seizure) may be responsible for disrupting the consolidation of long term memories, thus explaining accelerated forgetting. Direct links between temporal lobe epilepsy and memory difficulties is complicated by a number of confounding variables:
• Anti-convulsent medication side effects
• Age of epilepsy onset
• Seizure frequency
• Structural damage arising from epileptic activity
See Butler and Zeman for a comprehensive and up to date review of the issues
http://brain.oxfordjournals.org/cgi/reprint/131/9/2243
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