What Can Neuropsychology Contribute to the Identification and Treatment of Medically Unexplained Neurological Symptoms?
Medically Unexplained Symptoms (MUS) is an umbrella term for a broad collection of symptoms and syndromes that physical processes alone fails to explain. It has been criticised as type of 'non diagnosis' as it essentailly diagnoses what it is not rather than what it is. However, the term has gained popularity over other terms, such as cogniform disorder or somatisation because patients tend to view it as non-threatening, and because positive relationships to professionals (usually the GP) are a key correlate to positive outcome. Examples of MUS phenomena arguably include: inexplicable pain, inexplicable headache, fibromyalgia, chronic fatigue, and non epileptic attack disorder.
Up to one in five GP appointments is MUS related. It is important to statistically contextualise prevalency as sometimes medical experts are wrong and up to 5% of those diagnosed with MUS subsequently turn out to be medically explainable cases following long term follow-up. However, a mixture of factors including: a growth in civil prosecution, an increase in 'blame culture' and the advent of patient internet derived knowledge, has meant medics have approaches MUS with relentlessly fruitless further medical investigations. The costs and harms both physically, psychologically and financially of this trend is worrying and has attracted attention from psychologists and neuropsychologists alike.
The contribution clinical psychology and neuropsychology can make to MUS sufferers is at two levels: identification and treatment. Where complaints are made of a neurological nature symptom validity tests (SVTs) are routinely used in neuropsychological assessment to identify MUS. They are particular useful in questions over whether a patient has infact sustained a mild head injury or whether they are:
1 Completely malingering
2 or either consciousely or unconsciousely exaggerating symptoms
The BPS now advise routine use of SVTs even in clear cases of organic pathology, primarily to substantiate the reliability of test results and clinical interpretations. Each SVT has it's strengths and weaknesses. Each test aims to strike an appropriate balance between the likelihood of making type 1 versus type 2 error. Each test essentially aims to identify those who are making less than maximum effort. Similarly, 'forced choice' tests, tests that even when completed by random chance stand a 50% correct level, specifically aim to identify those who deliberately aim to mislead testers. Psychological assessments of personality and psychopathology can also be used as an adjunct in correctly identifying MUS. Subscales indicating anxiety, depression, somatisation, neuroticism and exaggeration of symptoms are often used as indicators of potential MUS. Unusual symptoms, symptoms out of context, long histories of attendance at A&E/GP are other indicators of increased MUS likelihood (see previous blog on DSM-IV indicators).
Most often psychological factors play a central explanatory role. It is believed approximately 70% of MUS patients share comorbidity with psychiatric symptoms, most often anxiety and depression, although the extrapolation of cause and effect complicate this simplistic statistic. At the level of treatment psychologists offer evidence based 'talking interventions' such as CBT and associated approaches. Such approaches focus upon: treating anxiety and depression symptoms, encouraging patients to acceptance their scenario and their symptoms, symptom management and dissemination of psychological formulation as an explanation of symptoms.
Psychologists have become increasingly interested in being involved at the primary care level. In Devon, Plymouth began a pilot project in 2008 focussing upon scripting GP messages on initial MUS diagnosis, specific risk assessment for MUS patients and approaches aimed at minimising unneccessary and potentially harmful medical investigations. Psychological approaches have identified the importance in 'getting in early'. Clinicians and researchers have identified a 6 month critical period for intervening (Bass/Stone/Halligan). Beyond this outcomes become increasingly pessimistic. MUS unsurprisingly fall into three crude groups, of which research is in process: 1. Those who are treatable; 2. Those who may become treatable; and 3. Those who will be highly resistant. Psychologists with considerable MUS experience will usually know which group a patient fits into following the first or second session.
Tuesday, 27 December 2011
Tuesday, 20 December 2011
A Neuropsychological Understanding of Anxiety
Anxiety is conceptually closely aligned with fear and stress responses and the concept of arousal level. As with most emotional topics concerning the brain the amygdala is implicated in all of the anxiety disorders (Etkin and Wager, 2007).
Within the lierature there is a lateralisation theory of the amygdala. The left amygdala is chiefly responsible for sustained emotional evaluation and the right short and rapid emotional stimuli detection (Phelps et al 2001; Baas et al. 2004). It is now believed past studies have neglected and dismissed right amygdala activation because of older technologies that used lower temporal resolution.
Stein et al. (2007) provides more up to date fMRI evidence for amygdala activation as described above in anxiety prone individuals versus controls. Further studies have noted gender differences, including increased left activation in war veterans with PTSD diagnoses (Shin et al. 2004). It is possible that this can be explained by gender differences in how emotional memories are constructed: language based-left-female; visual based-right-male.
The anterior cingulate cortex is responsible for motor control, cognition and arousal/drive state. Essentially it is involved in translating intentions into actions and in popular metaphor it is implicated in 'fight or flight' responses.
Lesion studies have revealed arousal dysfunction in the absence of other neuropsychological dysfunction.
The dorsomedial prefrontal cortex has an anxiety inhibiting function when active. Kalisch et al. (2004) evidenced trait anxiety correlations to DmPfC function through animal studies and Etkin (2007) mirrored such findings in human lesion studies. Lesions in the DmPfC tend to flatten anxiety responses although findings are inconsistent and there are methodological limitations to the evidence base.
The ventromedial prefrontal cortex has a top down inhibitory effect upon the amygdala. fMRI evidence shows hypoactivation of VmPc when anxiety is high; thus there is a negative correlation to amygdala activity and PET studies have triangulated this finding (Ahs et al. 2009). In theory amydala lesion would necessitate a lower likelihood of developing anxiety and VmPfc lesion would predict an increased likelihood of anxiety development. However, the evidence base is somewhat contradictory, perhaps providing conceptual support for an emotional regulation model rather than a uni directional model of either excitation/inhibition.
Within the lierature there is a lateralisation theory of the amygdala. The left amygdala is chiefly responsible for sustained emotional evaluation and the right short and rapid emotional stimuli detection (Phelps et al 2001; Baas et al. 2004). It is now believed past studies have neglected and dismissed right amygdala activation because of older technologies that used lower temporal resolution.
Stein et al. (2007) provides more up to date fMRI evidence for amygdala activation as described above in anxiety prone individuals versus controls. Further studies have noted gender differences, including increased left activation in war veterans with PTSD diagnoses (Shin et al. 2004). It is possible that this can be explained by gender differences in how emotional memories are constructed: language based-left-female; visual based-right-male.
The anterior cingulate cortex is responsible for motor control, cognition and arousal/drive state. Essentially it is involved in translating intentions into actions and in popular metaphor it is implicated in 'fight or flight' responses.
Lesion studies have revealed arousal dysfunction in the absence of other neuropsychological dysfunction.
The dorsomedial prefrontal cortex has an anxiety inhibiting function when active. Kalisch et al. (2004) evidenced trait anxiety correlations to DmPfC function through animal studies and Etkin (2007) mirrored such findings in human lesion studies. Lesions in the DmPfC tend to flatten anxiety responses although findings are inconsistent and there are methodological limitations to the evidence base.
The ventromedial prefrontal cortex has a top down inhibitory effect upon the amygdala. fMRI evidence shows hypoactivation of VmPc when anxiety is high; thus there is a negative correlation to amygdala activity and PET studies have triangulated this finding (Ahs et al. 2009). In theory amydala lesion would necessitate a lower likelihood of developing anxiety and VmPfc lesion would predict an increased likelihood of anxiety development. However, the evidence base is somewhat contradictory, perhaps providing conceptual support for an emotional regulation model rather than a uni directional model of either excitation/inhibition.
Anger and the Brain/The Neuropsychology of Anger
Often the terms anger and aggression are used interchangeably; however this is somewhat of a faux pas as anger is a feeling and aggression is a behaviour. Central to the neuroanatomy of anger are the amydala, sitting deep with the medial temporal lobes. In cases of anger the amygdala proverbally hijack the prefrontal cortex, driving responses emotionally and impulsively rather than cognitively through reasoning. Biologists have correlated increased testosterone levels with increased amygdala activity.
The hypothalamus is also very important in a neuropsychological understanding of anger. So called 'sham' rage has been manufactured in animal studies where lesions have been introduced to the hypothalamus. More specific animal lesion studies have revealed lateral stimulation results anger with attack responses (Flynn, 1967). Obviousely, ethical criticisms are not the only limitations to these sort of studies as generalisability to humans is at best speculative.
The anterior cingulate cortex, in rather crude terms lies neatly between the affective and cognitive divisions of the brain. More animal experiments have implicated this area of the brain in anger emotional process (Kordidze and Oniani, 1972). But again one has to question whether we can measure the emotions of animals or are we at best merely studying behaviour?
Dougherty et al. (1999) has studied human anterior cingulate cortex activation through inducting anger through narrative scripts and measuring blood flow using PET techniques. Poor scanner accuraacy and high expense limits the value of these types of PET studies, however Denson et al. (2009) used fMRI to reaffirm PET evidence.
The orbito frontal cortex is implicated in impulse control. Bechara et al (1994) carried out lesion studies and ran gambling tasks. The researchers witnessed reckless behaviour in orbito frontal cortex lesion patients. Blair et al (1999) and his high profile psychopathy studies found increased orbito frontal cortex activation for angry faces but not sad or neutral.
The ventromedial cortex activation in anger has also been demonstrated through PET studies Dougherty et al. (2004) CT evidence (Grafmann et al. 1996) and fMRI studies (Lotze et al. 2007).
Kalbe et al. (2004) studied the dorsolateral prefrontal cortex and its role in anger. The researchers found when the dorsolateral prefrontal cortex was active the orbito frontal cortex is inhibited further inhibiting its affective cue processing. Alternatively, when its inhibited the OFC is active and aggressive behaviour is likely to be carried out.
In conclusion, although we now understand which areas of the brain appear to be involved in anger processing, nearly all research relies upon anger induction, often asking people to relive memories. Can we equate this with emotion or is it more similar to a cognition or a cognitised emotionally rich memory?
The hypothalamus is also very important in a neuropsychological understanding of anger. So called 'sham' rage has been manufactured in animal studies where lesions have been introduced to the hypothalamus. More specific animal lesion studies have revealed lateral stimulation results anger with attack responses (Flynn, 1967). Obviousely, ethical criticisms are not the only limitations to these sort of studies as generalisability to humans is at best speculative.
The anterior cingulate cortex, in rather crude terms lies neatly between the affective and cognitive divisions of the brain. More animal experiments have implicated this area of the brain in anger emotional process (Kordidze and Oniani, 1972). But again one has to question whether we can measure the emotions of animals or are we at best merely studying behaviour?
Dougherty et al. (1999) has studied human anterior cingulate cortex activation through inducting anger through narrative scripts and measuring blood flow using PET techniques. Poor scanner accuraacy and high expense limits the value of these types of PET studies, however Denson et al. (2009) used fMRI to reaffirm PET evidence.
The orbito frontal cortex is implicated in impulse control. Bechara et al (1994) carried out lesion studies and ran gambling tasks. The researchers witnessed reckless behaviour in orbito frontal cortex lesion patients. Blair et al (1999) and his high profile psychopathy studies found increased orbito frontal cortex activation for angry faces but not sad or neutral.
The ventromedial cortex activation in anger has also been demonstrated through PET studies Dougherty et al. (2004) CT evidence (Grafmann et al. 1996) and fMRI studies (Lotze et al. 2007).
Kalbe et al. (2004) studied the dorsolateral prefrontal cortex and its role in anger. The researchers found when the dorsolateral prefrontal cortex was active the orbito frontal cortex is inhibited further inhibiting its affective cue processing. Alternatively, when its inhibited the OFC is active and aggressive behaviour is likely to be carried out.
In conclusion, although we now understand which areas of the brain appear to be involved in anger processing, nearly all research relies upon anger induction, often asking people to relive memories. Can we equate this with emotion or is it more similar to a cognition or a cognitised emotionally rich memory?
Monday, 12 December 2011
Personal injury psychological assessment
For personal injury psychological assessment in the South West of England email: psychologyassessment@yahoo.co.uk or visit www.psychologyassessmentdevon.co.uk
Adjustment and Coping in Acquired Brain Injury
"People want something to do, somewhere to live and someone to love" (McColl et al. 1998).
Approximately 50% of people who acquire a brain injury will go on to develop chronic anxiety and/or depression (Anson & Ponsford, 2006). Thus there has been a focus on understanding this process in order to help. However, adjustment is a complex process. For a start Impairment does not linearly equate to disability, because disability has a social context, hence it is socially constructed (see Johnston, 1996). Therefore, the process of adjustment to brain injury is mitigated by internal and external, controllable and uncontrollable cognitive, emotional, social, and psychological factors.
The literature on adjustment diverts down many lines of enquiry. There is of course the founding theories of Kubler-Ross (1969) on the stages of grief. This model has undergone many updates moving away from a linear stage model of grief to an acceptance model describing the common feelings of loss in a wider context. This model has great therapeutic use in brain injury, but it still lacks the specificity in predicting positive adjustment and coping.
Of course brain injury carries with it an increased liklihood of specific cognitive factors that may affect coping. For example, reduced problem solving ability, mood dysregulation, lability, memory difficulties, reduced concentration and so on. However, researchers now believe the impact of this is less obvious than one might assume. For instance, although these cognitive dysfunctions are more prevalent in severe brain injuries, adjustment appears to be inversely correlated to severity self awareness and insight is not always a good thing (see Brown & Vandergoot, 1998 'quality of life' studies).
Poor adjustment has often been associated with self-blame, excessive worry, ruminative thoughts, wishful thinking, misuse of drugs and alcohol and general avoidance (Anson & Ponsford, 2006). In addition there appears to be a significant gender divide with females more likely to seek systemic support and males more likely to cope in isolation.
McColl et al. (1998) puts it simply: happier brain injury survivors want 'something to do, somewhere to live and someone to love'. In recent years reserachers have managed to specify positive predictors of adjustment. Some of these include:
-a problem solving approach
-low expectation of outcome and realistic hopes & goals
-internal locus of control
-healthy levels of self esteem
-Use of humour
-personal resilience
-high premorbid intelligence
-supportive families/home environments
Approximately 50% of people who acquire a brain injury will go on to develop chronic anxiety and/or depression (Anson & Ponsford, 2006). Thus there has been a focus on understanding this process in order to help. However, adjustment is a complex process. For a start Impairment does not linearly equate to disability, because disability has a social context, hence it is socially constructed (see Johnston, 1996). Therefore, the process of adjustment to brain injury is mitigated by internal and external, controllable and uncontrollable cognitive, emotional, social, and psychological factors.
The literature on adjustment diverts down many lines of enquiry. There is of course the founding theories of Kubler-Ross (1969) on the stages of grief. This model has undergone many updates moving away from a linear stage model of grief to an acceptance model describing the common feelings of loss in a wider context. This model has great therapeutic use in brain injury, but it still lacks the specificity in predicting positive adjustment and coping.
Of course brain injury carries with it an increased liklihood of specific cognitive factors that may affect coping. For example, reduced problem solving ability, mood dysregulation, lability, memory difficulties, reduced concentration and so on. However, researchers now believe the impact of this is less obvious than one might assume. For instance, although these cognitive dysfunctions are more prevalent in severe brain injuries, adjustment appears to be inversely correlated to severity self awareness and insight is not always a good thing (see Brown & Vandergoot, 1998 'quality of life' studies).
Poor adjustment has often been associated with self-blame, excessive worry, ruminative thoughts, wishful thinking, misuse of drugs and alcohol and general avoidance (Anson & Ponsford, 2006). In addition there appears to be a significant gender divide with females more likely to seek systemic support and males more likely to cope in isolation.
McColl et al. (1998) puts it simply: happier brain injury survivors want 'something to do, somewhere to live and someone to love'. In recent years reserachers have managed to specify positive predictors of adjustment. Some of these include:
-a problem solving approach
-low expectation of outcome and realistic hopes & goals
-internal locus of control
-healthy levels of self esteem
-Use of humour
-personal resilience
-high premorbid intelligence
-supportive families/home environments
Sunday, 11 December 2011
I Feel what you Feel
The Functional Anatomy of Empathy
The main difficulty in understanding emapthy from a neuropsychological perspective is that it is a rather wooley concept, incorporating behaviours and cognitions, metacognitions and emotions. Essentially psychologists will define empathy as the ability for animals to recognise and act accordingly to the emotional state and perspective of others. The following summary of involved brain structures is, out of necessity, unfortunately bastardised. The amygdala is the most obvious place to start. The amygdala is located deep within the medial temporal lobes. It is in close proximity to limbic structures dealing with emotional related matters. Abnormality in the amygdala has been found in a number of clinical presentations, including autism, psychopathy, bipolar disorder and other mood disorders. Functionally the amygdala is involved in emotional learning, embuing memories with emotional significance and moderating their consolidation. It is also thought that it is involved in mitigating social distance and possibly important in sexual orientation (although this is obviously a sensitively politic). Patient SM had extensive damage to the amygdala in each hemisphere. She had no motor, sensory, or cognitive deficits but when asked to identify photographs of a series of facial expressions, SM could identify every expression but one, she could not recognize fear. Similarly, when asked to draw facial expressions, SM produced accomplished pictures of each emotion, but she could not reproduce the expression of fear. When asked about her drawings, she explained that 'she did not know what an afraid face would look like.'
Functional magnetic resonance imaging (fMRI) has been incredibly useful in our understanding of empathy. Recent studies have shown that observing another person's emotional state activates parts of the neuronal network involved in processing that same state in oneself, whether it is disgust, touch, or pain. Almost by accident, researchers Preston and Frans de Waal discovered that monkey's sensory cortices would fire whilst researchers were moving experimental stimuli. So called 'mirror neurons' are neurons that fire both when the creature watches another perform an action as well as when they themselves perform it. In their paper, they argued that attended perception of the object's state automatically activates neural representations, and that this activation automatically primes or generates the associated autonomic and somatic responses, unless inhibited. This mechanism is similar to the common coding theory between perception and action.
Autism often provides a 'case in point' for empathy dysfunction. Anatomically the autistic brain undergoes a statistically significant dvelopmentally governed overgrowth of white matter, with an impeded pruning process, leading to a relative underdevelopmental of grey matter in the frontal lobes especially. Frontal lobe function is incredibly important in attending to and intellectualising the emotional and cognitive states of others. It works in tandom with the aymygdala, the orbito frontal cortex, the medial cortex, the dorsolateral frontal cortex and the frontal gyrus.
The main difficulty in understanding emapthy from a neuropsychological perspective is that it is a rather wooley concept, incorporating behaviours and cognitions, metacognitions and emotions. Essentially psychologists will define empathy as the ability for animals to recognise and act accordingly to the emotional state and perspective of others. The following summary of involved brain structures is, out of necessity, unfortunately bastardised. The amygdala is the most obvious place to start. The amygdala is located deep within the medial temporal lobes. It is in close proximity to limbic structures dealing with emotional related matters. Abnormality in the amygdala has been found in a number of clinical presentations, including autism, psychopathy, bipolar disorder and other mood disorders. Functionally the amygdala is involved in emotional learning, embuing memories with emotional significance and moderating their consolidation. It is also thought that it is involved in mitigating social distance and possibly important in sexual orientation (although this is obviously a sensitively politic). Patient SM had extensive damage to the amygdala in each hemisphere. She had no motor, sensory, or cognitive deficits but when asked to identify photographs of a series of facial expressions, SM could identify every expression but one, she could not recognize fear. Similarly, when asked to draw facial expressions, SM produced accomplished pictures of each emotion, but she could not reproduce the expression of fear. When asked about her drawings, she explained that 'she did not know what an afraid face would look like.'
Functional magnetic resonance imaging (fMRI) has been incredibly useful in our understanding of empathy. Recent studies have shown that observing another person's emotional state activates parts of the neuronal network involved in processing that same state in oneself, whether it is disgust, touch, or pain. Almost by accident, researchers Preston and Frans de Waal discovered that monkey's sensory cortices would fire whilst researchers were moving experimental stimuli. So called 'mirror neurons' are neurons that fire both when the creature watches another perform an action as well as when they themselves perform it. In their paper, they argued that attended perception of the object's state automatically activates neural representations, and that this activation automatically primes or generates the associated autonomic and somatic responses, unless inhibited. This mechanism is similar to the common coding theory between perception and action.
Autism often provides a 'case in point' for empathy dysfunction. Anatomically the autistic brain undergoes a statistically significant dvelopmentally governed overgrowth of white matter, with an impeded pruning process, leading to a relative underdevelopmental of grey matter in the frontal lobes especially. Frontal lobe function is incredibly important in attending to and intellectualising the emotional and cognitive states of others. It works in tandom with the aymygdala, the orbito frontal cortex, the medial cortex, the dorsolateral frontal cortex and the frontal gyrus.
The BPS Advised Neuropsychological Assessment Structure
As part of the process of QICN registration the BPS advise upon a structure for short case studies. It is perhaps a good idea in neuropsychology to practice this structure during assessment. The following titles are advised:
Reason for referral
Background
Brief rationale for Test Selection
Patients Behaviour during the Assessment
Assessment Results and Interpretation
Summary of Results
Recommendations
Appendices
For more information see:
http://exams.bps.org.uk/document-download-area/document-download$.cfm?file_uuid=0E8B11FE-B9C7-959C-E9C4-2B432CE6A7D9&ext=pdf
Reason for referral
Background
Brief rationale for Test Selection
Patients Behaviour during the Assessment
Assessment Results and Interpretation
Summary of Results
Recommendations
Appendices
For more information see:
http://exams.bps.org.uk/document-download-area/document-download$.cfm?file_uuid=0E8B11FE-B9C7-959C-E9C4-2B432CE6A7D9&ext=pdf
Saturday, 10 December 2011
The neuroanatomy of memory function in the brain
Much of the brain is involved in memory. Key areas are implicated but realistically these areas are reciprocally integrated in complex ways. But in an attempt to summarise, there are six main areas with more detailed divisions within these areas and new areas implicated by ongoing research all the time. The six areas are:
Prefrontal cortex- this areas is thought to be synonmous with working memory and acts as an attentional device for focusing on things to remember. Often memory recall problems are better conceptualised as attential deficits.
The hippocampus- this area of the limbic system is fundamentally synonymous with long term memory and its consolidation. This area is often affected in subcortial dementias. The landmark case on hippocampus lesion was the case of H.M., who displayed chronic amnesia relating to long term memory consolidation.
The medial temporal lobe is often adversly affected in temporal lobe epilepsy and its treatment sits behind the left ear, and is unsurprisingly related to verbal memory.
The amygdala is ancient in the evolutionary development of the human brain. It is involved in linking important powerful emotions to memory. Its dysfunction has been identified in psychopathy, autism and in PTSD.
The striatum is part of the basal ganglia and is involved in skill acquisition related memories.
The entorhinal cortex is thought to be involved in spatial memory process.
Prefrontal cortex- this areas is thought to be synonmous with working memory and acts as an attentional device for focusing on things to remember. Often memory recall problems are better conceptualised as attential deficits.
The hippocampus- this area of the limbic system is fundamentally synonymous with long term memory and its consolidation. This area is often affected in subcortial dementias. The landmark case on hippocampus lesion was the case of H.M., who displayed chronic amnesia relating to long term memory consolidation.
The medial temporal lobe is often adversly affected in temporal lobe epilepsy and its treatment sits behind the left ear, and is unsurprisingly related to verbal memory.
The amygdala is ancient in the evolutionary development of the human brain. It is involved in linking important powerful emotions to memory. Its dysfunction has been identified in psychopathy, autism and in PTSD.
The striatum is part of the basal ganglia and is involved in skill acquisition related memories.
The entorhinal cortex is thought to be involved in spatial memory process.
Motor functions of the brain in a nutshell.
How does the brain control and execute movement? A rather crude summary of motor function would first describe the prefrontal cortex area of the brain as key to planning movement. Moving onward through the brain the premotor cortex prepares and organises the movement. The basal ganglia selects the appropriate movement, the cerebellum coordinates the timing of the movement and finally the primary motor cortex recruits the muscles to execute the movement.
http://www.google.co.uk/search?q=image+of+motor+brain+areas&hl=en&client=safari&tbo=u&tbm=isch&source=univ&sa=X&ei=qOnjTo3TBsHg8gOo8NGYBA&ved=0CDQQsAQ&biw=1024&bih=690
http://www.google.co.uk/search?q=image+of+motor+brain+areas&hl=en&client=safari&tbo=u&tbm=isch&source=univ&sa=X&ei=qOnjTo3TBsHg8gOo8NGYBA&ved=0CDQQsAQ&biw=1024&bih=690
Sunday, 18 September 2011
WWW.psychologyassessmentdevon.co.uk
WWW.psychologyassessmentdevon.co.uk
Based in Devon, UK 'Psychology Assessment in Devon' is a medico-legal psychology assessment service designed to provide expert witness assessment reports for instructing solicitors. All types of psychological assessment can be provided. Including cases involving: neuropsychological assessment of brain injury, psychological impact of injury including PTSD and depression, IQ/learning disability and criminal competence, depression and other mental illness and Disability Discrimination in the work place.
Contact psychologyassessment@yahoo.co.uk to make an enquiry.
Based in Devon, UK 'Psychology Assessment in Devon' is a medico-legal psychology assessment service designed to provide expert witness assessment reports for instructing solicitors. All types of psychological assessment can be provided. Including cases involving: neuropsychological assessment of brain injury, psychological impact of injury including PTSD and depression, IQ/learning disability and criminal competence, depression and other mental illness and Disability Discrimination in the work place.
Contact psychologyassessment@yahoo.co.uk to make an enquiry.
Monday, 23 May 2011
Brain injury assessment
For all types of private brain injury psychological assessment email psychologyassessment@yahoo.co.uk
Saturday, 14 May 2011
Tuesday, 15 February 2011
Assessing and defining mental disability under the disability discrimination act
Psychologists are sometimes instructed to assess a client's mental status for legal disputes involving the Disability Discrimination and Equality Act 2010.
Guidance to the DDA: http://www.equalityhumanrights.com/uploaded_files/guidance_on_matters_to_be_taken_into_account_in_determining_questions_relating_to_the_definition_of_disability.pdf
Guidance to the DDA: http://www.equalityhumanrights.com/uploaded_files/guidance_on_matters_to_be_taken_into_account_in_determining_questions_relating_to_the_definition_of_disability.pdf
Assessment of Capacity
There are five important things to think about when conducting an assessment of capacity:
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.
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.
Thursday, 3 February 2011
Malingering and the Expert Witness Psychologist (Devon/South West)
An overriding issue in psychology within a medico-legal arena is the issue of malingering. Malingering involves the exaggeration (fake bad) or underplay (fake good) of symptoms, either consciousely or unconsciousely for secondary gain (an ulterior motive). It differs from a number of other presentations, including somatization, health anxiety/hypocondriasis, and medically unexplained symptoms to name but a few. Psychologists should always bare the possibility of malingering in mind, especially during litigation because of monetary gains. The symptoms most commonly feigned include those associated with mild head injury, fibromyalgia, chronic fatigue syndrome, and chronic pain. Failure to detect actual cases of malingering imposes a substantial economic burden on the health care system, and false attribution of malingering imposes a substantial burden of suffering on a significant proportion of the patient population.
Diagnosis and detection
The DSM-IV-TR states that malingering is suspected if any combination of the following are observed:
1. Medicolegal context of presentation
2. Marked discrepancy between the person’s claimed stress of disability and the objective findings
3. Lack of cooperation during the diagnostic evaluation and in complying with prescribed treatment regimen
4. The presence of Antisocial Personality Disorder
However, these criteria have been found to be of little use in actually identifying individuals who are malingering.
Detection
Some features at presentation which are unusual in genuine cases include:
1. Dramatic or atypical presentation
2. Vague and inconsistent details, although possibly plausible on the surface
3. Long medical record with multiple admissions at various hospitals in different cities
4. Knowledge of textbook descriptions of illness
5. Admission circumstances that do not conform to an identifiable medical or mental disorder
6. An unusual grasp of medical terminology
7. Employment in a medically related field
8. Pseudologia fantastica (i.e., patients' uncontrollable lying characterized by the fantastic description of false events in their lives)
9. Presentation in the emergency department during times when obtaining old medical records is hampered or when experienced staff are less likely to be present (e.g., holidays, late Friday afternoons)
10. A patient who has few visitors despite giving a history of holding an important or prestigious job or a history that casts the patient in a heroic role
11. Acceptance, with equanimity, of the discomfort and risk of diagnostic procedures
12. Acceptance, with equanimity, of the discomfort and risk of surgery
13. Substance abuse, especially of prescribed analgesics and sedatives
14. Symptoms or behaviors only present when the patient knows he is being observed
15. Controlling, hostile, angry, disruptive, or attention-seeking behavior during hospitalization
16. Reporting of wild psychological symptoms, and silly wrong answers on questionaires, not likely in patients with similar but real conditions.
17. Fluctuating clinical course, including rapid development of complications or a new pathology if the initial workup findings prove negative
18. Coinciding indigence or homelessness of the patient, with impending cold weather and a need for indoor lodgings.
19. Giving approximate answers to questions, usually occurring in factitious disorder with predominantly psychological signs and symptoms (see Ganser Syndrome)
20. Eagerly endorsing symptoms suggested by a clinician, but not mentioned by the patient, though they would have been prominent and obvious had they been real.
21. A test for factitious mental disorders presents symptoms which are extremely improbable. Endorsing these symptoms which almost never occur can raise doubt of the person's sincerity.
If a psychologist suspects malingering in a case of possible brain damage (i.e. caused by head trauma or stroke), they may look for a discrepancy between the patient's reported functions of daily living and their performance on neuropsychological tests. In theory, any neuropsychological test could be used in this way, depending on the context. No one test, administered by itself, can proffer a diagnosis of malingering, so a neuropsychological examination typically consists of a battery of tests. Two tests commonly used to determine malingering are:
• Minnesota Multiphasic Personality Inventory (MMPI) (see Validity scales)
• The Test of Memory Malingering (TOMM)
The psychiatrist or neuropsychologist may use these tests, and use the DSM-IV TR criteria while adding a "dimensional analysis" to assist in diagnosis and treatment. Dimensional analysis consists of learning the patient’s history, information about similar cases, and the context of the illness, which could help differentiate cases of malingering from factitious disorders. Tests are rarely conclusive but often need to be triangulated and weighed against other forms of information, including presentation and self reported symtpoms as mentioned before.
Diagnosis and detection
The DSM-IV-TR states that malingering is suspected if any combination of the following are observed:
1. Medicolegal context of presentation
2. Marked discrepancy between the person’s claimed stress of disability and the objective findings
3. Lack of cooperation during the diagnostic evaluation and in complying with prescribed treatment regimen
4. The presence of Antisocial Personality Disorder
However, these criteria have been found to be of little use in actually identifying individuals who are malingering.
Detection
Some features at presentation which are unusual in genuine cases include:
1. Dramatic or atypical presentation
2. Vague and inconsistent details, although possibly plausible on the surface
3. Long medical record with multiple admissions at various hospitals in different cities
4. Knowledge of textbook descriptions of illness
5. Admission circumstances that do not conform to an identifiable medical or mental disorder
6. An unusual grasp of medical terminology
7. Employment in a medically related field
8. Pseudologia fantastica (i.e., patients' uncontrollable lying characterized by the fantastic description of false events in their lives)
9. Presentation in the emergency department during times when obtaining old medical records is hampered or when experienced staff are less likely to be present (e.g., holidays, late Friday afternoons)
10. A patient who has few visitors despite giving a history of holding an important or prestigious job or a history that casts the patient in a heroic role
11. Acceptance, with equanimity, of the discomfort and risk of diagnostic procedures
12. Acceptance, with equanimity, of the discomfort and risk of surgery
13. Substance abuse, especially of prescribed analgesics and sedatives
14. Symptoms or behaviors only present when the patient knows he is being observed
15. Controlling, hostile, angry, disruptive, or attention-seeking behavior during hospitalization
16. Reporting of wild psychological symptoms, and silly wrong answers on questionaires, not likely in patients with similar but real conditions.
17. Fluctuating clinical course, including rapid development of complications or a new pathology if the initial workup findings prove negative
18. Coinciding indigence or homelessness of the patient, with impending cold weather and a need for indoor lodgings.
19. Giving approximate answers to questions, usually occurring in factitious disorder with predominantly psychological signs and symptoms (see Ganser Syndrome)
20. Eagerly endorsing symptoms suggested by a clinician, but not mentioned by the patient, though they would have been prominent and obvious had they been real.
21. A test for factitious mental disorders presents symptoms which are extremely improbable. Endorsing these symptoms which almost never occur can raise doubt of the person's sincerity.
If a psychologist suspects malingering in a case of possible brain damage (i.e. caused by head trauma or stroke), they may look for a discrepancy between the patient's reported functions of daily living and their performance on neuropsychological tests. In theory, any neuropsychological test could be used in this way, depending on the context. No one test, administered by itself, can proffer a diagnosis of malingering, so a neuropsychological examination typically consists of a battery of tests. Two tests commonly used to determine malingering are:
• Minnesota Multiphasic Personality Inventory (MMPI) (see Validity scales)
• The Test of Memory Malingering (TOMM)
The psychiatrist or neuropsychologist may use these tests, and use the DSM-IV TR criteria while adding a "dimensional analysis" to assist in diagnosis and treatment. Dimensional analysis consists of learning the patient’s history, information about similar cases, and the context of the illness, which could help differentiate cases of malingering from factitious disorders. Tests are rarely conclusive but often need to be triangulated and weighed against other forms of information, including presentation and self reported symtpoms as mentioned before.
Monday, 24 January 2011
Private Neuropsychology Assessment in Devon, Somerset and Cornwall (South West)
Private Neuropsychology Assessment
Private neuropsychological assessment shares many similarities to the work done within the NHS. Private work is often conducted by an experienced psychologist to provide an expert assessment and report that outlines the nature and extent of any genuine cognitive impairment following a neurological event/insult. Often this is in cases of personal injury, but sometimes clinical negligence. Neurological events most relevant to legal work include various types of brain injury (severe/moderate/mild/open/closed/anoxic/diffuse/focal). In recent years post concussion syndrome has caused much debate within neuropsychology and related arenas, as to its validity and suitability for assessment and diagnosis. As the quality of assessments increases through time and experience, the professional concensus is one of better understanding and clearer identification of this syndrome.
More time is spent in private work assessing possible malingering, exaggeration or falsification of symptoms. Treatments are usually recommended following an assessment and report, but are usually carried out by another practioner. Individual psychologists or psychologist consortiums offer private services. Most of these psychologists will work within the NHS and conduct private work part-time or in their spare time. The South West, including Devon, Cornwall and Somerset is a huge geographical area with a restricted number of suitable psychologists available to conduct private neuropsychological assessments.
Private neuropsychological assessment shares many similarities to the work done within the NHS. Private work is often conducted by an experienced psychologist to provide an expert assessment and report that outlines the nature and extent of any genuine cognitive impairment following a neurological event/insult. Often this is in cases of personal injury, but sometimes clinical negligence. Neurological events most relevant to legal work include various types of brain injury (severe/moderate/mild/open/closed/anoxic/diffuse/focal). In recent years post concussion syndrome has caused much debate within neuropsychology and related arenas, as to its validity and suitability for assessment and diagnosis. As the quality of assessments increases through time and experience, the professional concensus is one of better understanding and clearer identification of this syndrome.
More time is spent in private work assessing possible malingering, exaggeration or falsification of symptoms. Treatments are usually recommended following an assessment and report, but are usually carried out by another practioner. Individual psychologists or psychologist consortiums offer private services. Most of these psychologists will work within the NHS and conduct private work part-time or in their spare time. The South West, including Devon, Cornwall and Somerset is a huge geographical area with a restricted number of suitable psychologists available to conduct private neuropsychological assessments.
Tuesday, 11 January 2011
Demystifying Psychology in Neuro-Rehabilitation: Emotional Support
The following is a presentation to neuro-rehabilitation multi-disciplinary staff explaining the role of the clinical psychologist when supporting patients with emotional distress.
The Core Roles of a Clinical Psychologist
To work as part of the MDT
To conduct cognitive assessments and to make recommendations
To provide emotional support and psychological treatments to patients who require them…. This is the focus of this presentation.
Common Emotional Symptoms in Neuro-Rehabilitation
Anxiety
Panic
Depression and low mood
Low mood
Trauma
Stress
The Need for Addressing Emotional Symptoms
Primary reason is to address the ongoing personal distress of the patient.
However, emotional symptoms are also addressed because they are:
To the detriment of the rehab potential
Have a negative impact upon family and friends
Increase the risk of suicide/harm
What does emotional support really mean?
Different from full-on therapy
Patient needs to be onboard
Timing has to be right
Sometimes the goals is an improvement in mood, sometimes it preserves mood and ‘gets people through’ a difficult spell.
Other Key Factors of the Patient
Personal history
Personality before the event
Style that they were parented in/early experiences
Psychiatric history (previous mental illness)
Relevance of any neurological deficits
Triggers
Level of support from others
Level of personal resilience and coping style
Interests
A Psychologist Basic Tools: Listening Skills
To provide a safe/private place to talk
To clarify what they mean and to summarise
To listen and resist offering too much opinion or direction
To consider that some behaviours may be ‘attempted solutions’ to a problem
To guide the patient in discovering their own solutions
More Advanced Psychological Techniques
Formulation
Behavioural Experiments
Challenging negative thoughts
Relaxation
Identity work
Stress management
Assertiveness work
Empty chair work
Therapeutic letters
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