Monday, 11 March 2013
Expert psychologist: Exploring quality
Research at the University of Central Lancashire has now been made available online detailing the wide variation in quality of expert psychologist reports. According to the research: "Results indicated wide variability in report quality with evidence of unqualified experts being instructed to provide psychological opinion. One fifth of instructed psychologists were not deemed qualified on the basis of their submitted Curriculum Vitae, even on the most basic of applied criteria. Only around one tenth of instructed experts maintained clinical practice external to the provision of expert witness work. Two thirds of the reports reviewed were rated as „poor‟ or „very poor‟, with one third between good and excellent (Ireland, Pinschoff and Trainor, 2012)". The full report, as a pdf, can be found at: http://www.uclan.ac.uk/news/files/FINALVERSIONFEB2012.pdf
Sunday, 17 February 2013
The Bell Curve and Standarised Scores
In order to assert clinical opinion toward a patients raw data test results from varying sources should be assimilated into a common metric (standardisation).
Percentiles tell us the rarity or abnormality of an individual's score. They are easily understandable and communicable but are not linear and so the difference between the 10-20th percentile in comparison to the 20-30th percentile is not necessarily the same.
Z scores on the other hand, are linear transformations. They indicate with positive and negative values how many standard deviations a score is away from its mean. However, working in negative can present communication problems and z scores tend to get lost in translation when communicating with non-neuropsychologists.
A common alternative is to use T scores (mean=50, SD=10) which offers a balanced level of incrementation. Others prefer index scales (mean 100, SD 15) which are often received with familiarity as they are used in the measurement if IQ. However, the fact that they are used in IQ can bring unwanted misconception when communicating interpretation and opinion.
Friday, 15 February 2013
Executive Function Brief Conceptualisation
Executive function is sometimes thought of as the functional equivalent of the frontal lobes. In 1982 Cummings proposed a fronto-straital circuits account of executive functioning and how it relates to structural circuits between the straitum located subcortically as part of the input to the basal ganglia, and the frontal lobes. In terms of executive function three specific areas are important within the fronto-straital circuits: the dorsolateral prefrontal cortex, which is typically concerned with tradional executive functions of planning, organisation and regulation. The orbitofrontal cortex (behind the orbits of the eye sockets) is more concenred with inhibition and decision making and social cogntion. Whilst the anterior cingulate is concerned with motivation. Dr Simon Gerhand of Bristol's Frenchay Brain Injury Rehabilitation Centre, practically summarises executive tests into the following:
Executive function test types.
Generativety: verbal fluency, design fluency. These are probably the only executive tests which lateralise.
Planning: Tower test, zoo map test, Key search test, SET.
Judgement: cognitive estimates, 20 questions, temporal judgement.
Inhibition: Stroop, Hayling.
Mental flexibility: Trails, Brixton, rule shift, WCST.
Social-emotional: Baron Cohen E-Q and faux pas (not standardised)
A way of remembering these dichotomies is: 'GP Jim's' model of executive function tests.
Friday, 5 October 2012
Psychological Assessments of Personal Injury
Psychological assessments of personal injury in South West England (Devon and surrounding areas). For more information contact Dr Moore at psychologyassessment@yahoo.co.uk
Tuesday, 10 January 2012
Orientating Around the Brain
The following technical terms are used to orientate around and within the brain and its structures:
Top=dorsal/superior
Bottom=ventral/inferior
Front=rostral/anterior
Back=caudral/posterior
Medial=mid-line
Lateral=away from mid-line
Contralateral=opposite side as
Ipsilateral=same side as
Unilateral=one side only
Bilateral=both sides
Proximal=close
Distal=distant
Top=dorsal/superior
Bottom=ventral/inferior
Front=rostral/anterior
Back=caudral/posterior
Medial=mid-line
Lateral=away from mid-line
Contralateral=opposite side as
Ipsilateral=same side as
Unilateral=one side only
Bilateral=both sides
Proximal=close
Distal=distant
Tuesday, 27 December 2011
MUS and Neuropsychology
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.
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, 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.
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