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
Wednesday, 17 February 2010
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
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?
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.
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.
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