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
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