Tuesday 13 July 2010

Exercise and Mental Health: An Overview

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?

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.

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.

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”.”

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.]

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

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

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

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

Thursday 4 February 2010

Improvised Neuropsychological Assessment

Neuropsychological batteries and tests are usually reliably normed, conceptually well validated and thorough. However, they often take a long time to administer and are sometimes not at hand when assessment opportunities present themselves. Moreover, they are often not practicable or a client develops an adversity to testing.

Informal 'on-the-spot' testing using a magazine on a topic they are interested may provide a 'make shift' or improvised assessment opportunity.

Using Something as accessible and simple as a magazine can provide many assessment opportunities:

Memory- LTM can be assessed by using magazine features to trigger autobiographical memories; new memories can be assessed by asking the client to remember an item in the magazine for testing later; WM can be testing by asking a client to repeat back a short story or sentence.

Neglect- Look for missed words/pictures when asked to read/describe magazine.

Apraxias- Point to items, turn pages, match items in magazine to surroundings.

Praxis- can the client name items/objects in magazine.

Comprehension- understand the gist of article

Attention- can concentrate on magazine without distraction/fatigue.

Speech- any read aloud from magazine.

Colour agnosia- are colours recognised/matched?

Prosopagnosia- Are famous faces easily recognised?

Dyslexia- read part? Understand it?

Tuesday 26 January 2010

The Neuropsychology of Korsakoff's syndrome

Korsakoff's syndrome is a brain disorder caused by the lack of thiamine (vitamin B1) in the brain, often caused by heavy drinking restricting nutritional intake or through physical changes to the stomach lining restricting its ability to absorb thiamine. The syndrome is named after Sergei Korsakoff, the neuropsychiatrist who popularized the theory

Although often referred to as Korsakoff's psychosis or Korsakoff's dementia, in an attempt to describe its similar features to a dementia or to a psychotic episode, it is in fact best described as a syndrome or a ‘collection of symptoms’. This is because following the initial period of confabulatory/’psychotic-like’ features, cognitive functioning and orientation tends to be restored close to premorbid levels.


Physiology

On a physiological heavy levels of prolonged alcohol use (a neuro-toxic) create enduring changes of chemistry with the brain. Deficiency of thiamine along with prolonged neurotoxicity within the brain result in general cerebral and ventrical atrophy, damage to hippocampus, the medial thalamus and possibly to the mammillary bodies of the hypothalamus.


Neuropsychological Symptoms

Cerebral atrophy inherent in Korsakoff's syndrome presents like an accelerated ageing of the brain. Deficits in speed of information processing are most obvious, along with 6 other key features:

1. anterograde amnesia and
2. retrograde amnesia, severe memory loss
3. confabulation, that is, invented memories which are then taken as true due to gaps in memory sometimes associated with blackouts
4. meager content in conversation
5. lack of insight
6. apathy - the patients lose interest in things quickly and generally appear indifferent to change.

Wernicke's encephalopathy refers to the initial symptoms that often preclude Korsakoff’s syndrome (especially when left untreated). Wernicke's encephalopathy includes symptoms of: involuntary or jerky eye movements, paralysis of muscles, poor balance, staggering gait or inability to walk and drowsiness and confusion. Korsakoff’s syndrome is therefore on the more severe end of a spectrum, and sometimes this spectrum is referred to as: Wernicke-Korsakoff syndrome.


Treatment

Thiamine treatment is often successful in initiating the spontaneous phase of recovery. Longer term recovery focuses upon changes in lifestyle to include alcohol abstinence, regular exercise and a balanced diet.


Recovery

Recovery to premorbid levels of functioning has been repeatedly reported following five years of abstinence from alcohol, although may partly be explained by the ageing process ‘catching-up’ to put it crudely.

Monday 25 January 2010

The neuropsychology of Multiple Sclerosis (MS)


Multiple Sclerosis

People with Multiple sclerosis (MS) represent a core client group for the work of a Clinical Psychologist working in Neuropsychological rehabilitation. The first blog I’ve chosen to post is centred upon MS.

A Brief Definition

MS is a disease of the central nervous system (CNS) marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech, and bladder control. It is an autoimmune disease in which the body's immune system attacks myelin, a key substance that serves as a nerve insulator and helps in the transmission of nerve signals. The progress, severity and specific symptoms in MS are unpredictable. One never knows when attacks will occur, how long they will last, or how severe they will be. Most people with MS are between the ages of 20 and 40 at the time of diagnosis. The term "multiple" refers to the multiple places in the CNS that are affected and to the multiple relapses and remissions characteristic of MS.
MS causes demyelinization of the white matter of the brain, with this process sometimes extending into the gray matter. Demyelinization is loss of myelin, which is composed of lipids (fats) and protein. The white matter is the part of the brain which contains myelinated nerve fibers and appears white, whereas the gray matter is the cortex of the brain which contains nerve cell bodies and appears gray. When myelin is damaged in MS, nerve fiber conduction is faulty or absent. Impaired bodily functions or altered sensations associated with those demyelinated nerve fibers give rise to the symptoms of MS. Watch this clip on you tube for a quick run down on physiology:

http://www.youtube.com/watch?v=qgySDmRRzxY&feature=youtube_gdata

The understanding of the basic causes of the disease is notably incomplete. It is known that nerve cell death is part of the nervous system injury in MS. It is known, too, that in MS some types of blood cells, namely lymphocytes and monocytes, gain access to the central nervous system by breaking through the blood-brain barrier at sites of inflammation. The migration of these cells across the endothelium (lining of the blood vessels) and the activation of these immune cells depends on the cell surface molecule called integrin.
Ref: http://www.medterms.com/script/main/art.asp?articlekey=4457

Cognitive Deficits associated with MS

From a neuropsychological point of view MS often affects higher order cognitive functioning, typically causing deficits in speed of information processing and memory (cued and visual). In addition deficits in attention, executive function and verbal fluency are often reported and in some cases visuo-spatial problems. Cognitive deficits are one of the main symptoms of MS although they are often mitigated by stress and low mood. Intact abilities often include, rate of learning, liklihood of remembering a specific item based on when it was presented, identifying semantic characteristics of learned material, and incidental learning (learning without the need for significant attention). Recognition of these deficits is relevant both to the diagnosis and rehabilitation of this disorder.

Lazeron et al. (2006) looked at the neuropsychological profile of patients with MS. In the study thirty two patients with MS undertook MRI scans and thorough neuropsychological assessment.
Results indicated a decrease in the speed of processing and response speed stability, and a decrease in psychomotor accuracy and stability were clearly associated with less brain volume, and with higher lesion loads, in particular at frontal and occipital areas. Correlations with brain volume reduction were found for all domains, except for visuo-spatial processing. In particular, speed and speed fluctuation scores correlated with brain volume reduction, while accuracy of performance, in general, did not correlate. Only some test speed scores and speed fluctuation scores correlated with lesion load measurements. This study showed that, in MS patients, accuracy of processing is not compromised unless high working memory demands are involved. Problems in neurocognitive functioning in MS are mainly modulated by speed and stability of speed processing, in particular when attention-demanding controlled information processing is required. Abnormalities in these domains are most strongly associated with brain volume loss, confirming that pathology beyond focal lesions is important in MS.
Ref: http://msj.sagepub.com/cgi/content/abstract/12/6/760

Psychological support for MS

For people with MS the emotional aspects of living with a long-term condition can prove just as challenging as the physical aspects of the condition. MSis a major cause of neurological disability in young adults. There are at least five major factors of psychological adjustment to MS:

1. The personality of the patient
The first factor of psychological adjustment to multiple sclerosis is the personality of the patient. Some patients adapt quickly to new life whereas others are trapped in the stage of disbelief and continue to be depressed for a long time after the diagnosis.

2. The quality of family support
The second factor of psychological adjustment to multiple sclerosis is the quality of support available to the patient within his family. All stakeholders should have an idea about the family dynamics before, during and after diagnosis. They should ask the following questions: Does the patient have a life together? What kind of relationship the patient has with his close relatives (children, spouse, and extended family)? The answers to these questions are important because the psychological suffering of a patient may result from tensions within his family (rejection, stigma, exclusion, indifference). Often a psychological maltreatment develops between the patient and his relatives; they feel unable to bear the daily progress of the disease.

3. The skills of social openness
The skills of social openness are the third factor of psychological adjustment to multiple sclerosis. They in fact correspond to how the patient is able to seek support and mental peace in his surroundings especially his family and friends. It helps the patient feel supported in the unhappy moments. Continuing his or her job helps the patient cope up with the new realities associated with the disease because continuing work lifts up the spirit of the patient and fills him with the feeling of productivity.

4. The quality of the relationship with the health professionals
The quality of the relationship of the patient with the health professionals (in the broadest sense, which also includes paramedical workers also) plays as a factor in psychological adjustment to multiple sclerosis. The patient has a high level of dependence on his doctor for psychological support as well as for the management of the disease.

5. The disease
The disease and its prognosis play an important role in the psychological adjustment of patients with multiple sclerosis. If the disease progresses slowly, the patient gets accustomed to his newly acquired disabilities gradually but if the disease has a rapid progression, the patient can not adjust and his life is compromised both physically and psychologically.

Ref;
http://ezinearticles.com/?The-5-Major-Factors-of-Psychological-Adjustment-to-Multiple-Sclerosis&id=2435238

What can a clinical psychologist contribute to an MS service? Boot et al. (2008) report the results of a team audit.

Figure 1. Psychological Symptoms on Assessment for MS Patients

What support was offered by the clinical psychologist?
The number of sessions offered was agreed between the clinical psychologist and the person with MS. People attended an average of three sessions, on a monthly basis. However, up to fifteen sessions were arranged, depending on individual requirements. A broad range of psychological interventions was provided. For some people, exploring options for change and being given self-help information about low mood, anxiety, falls and relationship difficulties was enough. Psychological therapy was used with people whose difficulties were more complex. Clinical psychologists learn a range of therapeutic approaches during their training. Different approaches were integrated in a way that best fit with the person and the problems they were experiencing. Partners and other family members were included at times so that they could discuss the best way of adjusting to the situation together. When problems with memory and thinking were identified, strategies to support these difficulties were developed. Some support over the telephone in conjunction with self-help information was occasionally provided for people who were unable to travel to the MS clinic.
According to Boot et al. (2008) psychological input can have benefits in the following areas:
• Managing their mood better
• Coping better
• Improved levels of daily activity
• Better understanding of their difficulties
• Improved relationships
• Less prone to feelings of suicide
• More confident about managing their future with MS.

Conclusions
This audit highlights the range and varying complexity of difficulties described by this group of people with MS, who were referred to a clinical psychologist. It shows how a number of different factors in people's lives can contribute to emotional difficulties. A flexible and individualised approach was used to provide psychological interventions that fit with the person and the problems they are experiencing at that time. The process facilitates individual management of emotional difficulties and encourages the individual to seek further support should they feel the need in future. These processes meet the government directives on managing long-term conditions, which promote self-care.

Ref: http://www.mstrust.org.uk/professionals/information/wayahead/articles/12042008_04.jsp

Support: http://www.mssociety.org.uk/

Sunday 24 January 2010

Defining neuropsychology

Neuropsychology or clinical neuropsychology concerns itself with the evaluation and treatment of functional consequences of neurological (especially cerebral) damage. It is a different way of looking at certain aspects of the brain-behavior relationship that may be helpful to physicians in all specialties. Over the next few posts I'll begin to introduce and discuss the neuropsychology and clinical implictions of various neurological disorders and brain injuries.

Neuropsychology blog begins