Agnosia literally meaning “loss of knowledge” is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream
Alexia
Inability to recognize text.
Alexithymia
Whilst not strictly a form of agnosia, alexithymia may be difficult to distinguish from or co-occur with social-emotional agnosia. Alexithymia is deficiency in understanding, processing, or describing emotions common to around 85% of people on the autism spectrum. Alexithymia is believed to be due to an information processing delay in the combined processing of information in the left and right hemispheres, resulting in poor differentiation between body messages and emotions.
Amusia
Or receptive amusia is agnosia for music. It involves loss of the ability to recognize musical notes, rhythms, and intervals and the inability to experience music as musical.
Anosognosia
This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive agnosia
Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.
Apraxia
Is a form of motor (body) agnosia involving the neurological loss of ability to map out physical actions in order to repeat them in functional activities. It is a form of body-disconnectedness and takes several different forms; Speech-Apraxia in which ability to speak is impaired, Limb-Kinetic Apraxia in which there is a loss of hand or finger dexterity and can extend to the voluntary use of limbs, Ideomotor Apraxia in which the gestures of others can't be easily replicated and can't execute goal-directed movements, Ideational Apraxia in which one can't work out which actions to initiate and struggles to plan and discriminate between potential gestures, Apraxia of Gait in which co-ordination of leg actions is problematic such as kicking a ball, Constructional Apraxia in which a person can't co-ordinate the construction of objects or draw pictures or follow a design, Oculomotor Apraxia in which the ability to control visual tracking is impaired and Buccofacial Apraxia in which skilled use of the lips, mouth and tongue is impaired.
Associative agnosia
Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Auditory agnosia
With Auditory Agnosia there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal.
Autotopagnosia
Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Color agnosia
Refers to the inability to recognize a color, while being able to perceive or distinguish it.
Cortical deafness
Refers to people who do not perceive any auditory information but whose hearing is intact.
Finger agnosia
Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosia
Patients perceive only parts of details, not the whole object.
Integrative agnosia
This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Mirror agnosia
One of the symptoms of Hemispatial neglect. Patients with Hemispatial neglect were placed so that an object was in their neglected visual field but a mirror reflecting that object was visible in their non-neglected field. Patients could not acknowledge the existence of objects in the neglected field and so attempted to reach into the mirror to grasp the object.
Pain agnosia
Also referred to as Analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia
Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia
Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Semantic agnosia
Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning).
Simultanagnosia
Patients can recognize objects or details in their visual field, but only one at a time. They cannot make out the scene they belong to or make out a whole image out of the details. They literally "cannot see the forest for the trees." Simultanagnosia is a common symptom of Balint's syndrome.
Social emotional agnosia
Sometimes referred to as Expressive Agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Somatosensory agnosia
Or Astereognosia] is connected to tactile sense - that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Tactile agnosia
Impaired ability to recognize or identify objects by touch alone.
Time agnosia
Is the loss of comprehension of the succession and duration of events.
Topographical agnosia
This is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognise objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place
Verbal auditory agnosia
This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.[19]
Visual agnosia
Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.
Visual verbal agnosia
Difficulty comprehending the meaning of written words. The capacity to read is usually intact but comprehension is impaired.]
Monday, 8 March 2010
The Neuropsychology of ‘Brain Training’ and Cognitive Reserve
Many 'brain exercise' products have been marketed in recent years, promising to help people stay mentally fit as they age, and even help prevent dementia. However, a systematic review by Pap, Walsh and Snyder (2009) found no good evidence that brain training will either prevent or slow down mental deterioration in healthy older adults.
Mild memory problems are part and parcel of getting older, but more moderate and severe memory problems and cognitive dysfunction are often indicative of a dementia. Alzheimer's disease is the most common type of dementia, followed by vascular dementia. We know that unhealthy lifestyles including smoking, drinking and unbalanced high fat diets can increase our risk. We also know that genes play a role, and that neuro-traumatic events such as strokes or head injury can increase the risk of developing dementia. But many people wonder what they can do to lower their risk.
Pap, Walsh and Snyder (2009) found 10 good-quality studies that looked at cognitive training in healthy elderly people. When they pooled the studies' results, they found that training led to small improvements in specific tasks related to the training. However, they found no evidence that this prevented or slowed the onset of dementia. That's not to say that brain exercises don't have the potential to help, but researchers say that better-designed studies are needed to find out. Part of the problem with the studies so far is that they didn't assess people for very long. So they couldn't say what long-term effects the training might have had on people's risk of dementia. The studies also mainly looked at how well people performed tasks that were closely tied to their training and nothing else. To meaningfully explore the connection between brain training and dementia, studies would need to look at overall brain function as well as people's performance on tasks in everyday life.
Bold claims made by commercial computer games should be interpreted with an element of cynicism until better research is conducted. Scientists do know however, that there is clear evidence that physical exercise and a balanced diet can delay the progress of dementia significantly. Although the preventative effects of both of these factors is thought to be modest.
Cognitive reserve is valuable way of conceptualising one’s vulnerability to dementia and prognosis. The term cognitive reserve describes the mind's resilience to neuropathological damage of the brain. In the first study of its kind in Katzman et al. published findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease. This is to say that some participants whose brains had extensive Alzheimer’s disease pathology, clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears. Neuronoal density rather than brain size appear to be significant in high cognitive reserve individuals. Moreover, genetics again appear to play a part. Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition. However, cognitive reserve is somewhat of a double edged sword, as it is believed that people with high reserve go undiagnosed until neuronal damage is severe, then rapid decline ensues.
Reference
Pap KV, Walsh SJ, Snyder PJ. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia. 2009; 5: 50-60.
http://en.wikipedia.org/wiki/Cognitive_reserve
Mild memory problems are part and parcel of getting older, but more moderate and severe memory problems and cognitive dysfunction are often indicative of a dementia. Alzheimer's disease is the most common type of dementia, followed by vascular dementia. We know that unhealthy lifestyles including smoking, drinking and unbalanced high fat diets can increase our risk. We also know that genes play a role, and that neuro-traumatic events such as strokes or head injury can increase the risk of developing dementia. But many people wonder what they can do to lower their risk.
Pap, Walsh and Snyder (2009) found 10 good-quality studies that looked at cognitive training in healthy elderly people. When they pooled the studies' results, they found that training led to small improvements in specific tasks related to the training. However, they found no evidence that this prevented or slowed the onset of dementia. That's not to say that brain exercises don't have the potential to help, but researchers say that better-designed studies are needed to find out. Part of the problem with the studies so far is that they didn't assess people for very long. So they couldn't say what long-term effects the training might have had on people's risk of dementia. The studies also mainly looked at how well people performed tasks that were closely tied to their training and nothing else. To meaningfully explore the connection between brain training and dementia, studies would need to look at overall brain function as well as people's performance on tasks in everyday life.
Bold claims made by commercial computer games should be interpreted with an element of cynicism until better research is conducted. Scientists do know however, that there is clear evidence that physical exercise and a balanced diet can delay the progress of dementia significantly. Although the preventative effects of both of these factors is thought to be modest.
Cognitive reserve is valuable way of conceptualising one’s vulnerability to dementia and prognosis. The term cognitive reserve describes the mind's resilience to neuropathological damage of the brain. In the first study of its kind in Katzman et al. published findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease. This is to say that some participants whose brains had extensive Alzheimer’s disease pathology, clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears. Neuronoal density rather than brain size appear to be significant in high cognitive reserve individuals. Moreover, genetics again appear to play a part. Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition. However, cognitive reserve is somewhat of a double edged sword, as it is believed that people with high reserve go undiagnosed until neuronal damage is severe, then rapid decline ensues.
Reference
Pap KV, Walsh SJ, Snyder PJ. Immediate and delayed effects of cognitive interventions in healthy elderly: A review of current literature and future directions. Alzheimer's & Dementia. 2009; 5: 50-60.
http://en.wikipedia.org/wiki/Cognitive_reserve
Thursday, 4 March 2010
The Neuropsychology of Loss
Loss is a key process in adjustment to and acceptance of one's limitations following a neurological event such as a brain injury, stroke or neurological disorder. Loss refers to any concept of value that has been detrimented following a neurological event.
Common losses include: Independence; Mobility; Relationships; Ability to communicate; Career/Job; Friends; Memories; Self-awareness; Hobbies & interests; Driving; Freedom; Sex/sexual drive; Routine; Prospects etc.
Psychotherapists have often discussed the stages of loss that people tend to experience. However, these stages are not regularly experienced in a serial or linear fashion and therefore more recently psychotherapists and psychologists tend refer to the 'common feelings' of loss rather than the 'stages of loss'.
Although there is little scientific confirmation for the 'common feelings of loss', an overwheling majority of psychotherapists and psychologist agree, from many years clinical experience of providing therapy that there five 'common feelings' that appear to involved in loss.
1 Denial
* We deny that the loss has occurred or ignore the signs.
* We may use fiction or fantasy to deny the reality or make sense of confusing partial memories.
* We may withdraw believing we can avoid facing the loss and avoid those people who confront us with the truth.
* We may regress to being like a child who wants protecting from the loss.
2 Bargaining
* We may promise to do anything to make this loss go away.
* We may bargain or strike a deal with God, ourselves or others to make the loss go away.
* We lack confidence in our attempts to deal with the loss, looking elsewhere for answers or gamble on a miracle.
3 Anger
* Anger is a perfectly natural reaction to loss that passes with time.
* Anger can come from loss, grief, frustration and resentment and we can become angry with:
A Ourselves: ‘self blame’.
B Others: ‘kicking the cat’
C Our closest friends and family
4 Despair
*We become overwhelmed by the anguish, pain, sadness and hurt of our loss
*Our mood can be lowered and we might often cry
*We might wrongly convince ourselves that the loss was some sort or payback.
*We might begin feel despondent and to think things are utterly hopeless.
5 Acceptance
*We can identify losses and the common feelings of loss.
*We can describe the details of our loss and the details of the rehabilitation.
* We can get through each day, cope somehow and keep sight of some level of hope.
* We are now aware when we dip back into stages or common feelings of loss and know what to do to help.
* Adapt and drive toward our potential.
Acceptance presents the final and most adaptive phase of feeling associated with loss. Therapeutic aims are often based upon experiencing more feelings associated with acceptance.
There is a growing collection of evidence that loss has neurological consequences. fMRI scans of women from whom loss and grief was elicited about the death of a mother or a sister in the past 5 years found it produced a local inflammation response as measured by salivary concentrations of pro-inflammatory cytokines. These were correlated with activation in the anterior cingulate cortex and orbitofrontal cortex. These activation also correlated with free recall of grief-related word stimuli. This suggests that grief can cause stress, and that this is linked to the emotional processing parts of the frontal lobe.
Among those bereaved within the last three months, those who report many intrusive thoughts about the deceased show ventral amygdala and rostral anterior cingulate cortex hyperactivity to reminders of their loss. In the case of the amygdala, this links to their sadness intensity. In those who avoid such thoughts, there is a related opposite type of pattern in which there is a decrease in the activation of the dorsal amgydala and the dorsolateral prefrontal cortex.
In those not so emotionally affected by reminders of their loss, fMRI finds the existence of a high functional connectivity between the dorsolateral prefrontal cortex and amygdala activity, suggesting the former regulates activity in the latter. In those who had greater intensity of sadness, there was a low functional connection between the rostal anterior cingulate cortex and amygdala activity, suggesting a lack of regulation of the former part of the brain upon the latter
Common losses include: Independence; Mobility; Relationships; Ability to communicate; Career/Job; Friends; Memories; Self-awareness; Hobbies & interests; Driving; Freedom; Sex/sexual drive; Routine; Prospects etc.
Psychotherapists have often discussed the stages of loss that people tend to experience. However, these stages are not regularly experienced in a serial or linear fashion and therefore more recently psychotherapists and psychologists tend refer to the 'common feelings' of loss rather than the 'stages of loss'.
Although there is little scientific confirmation for the 'common feelings of loss', an overwheling majority of psychotherapists and psychologist agree, from many years clinical experience of providing therapy that there five 'common feelings' that appear to involved in loss.
1 Denial
* We deny that the loss has occurred or ignore the signs.
* We may use fiction or fantasy to deny the reality or make sense of confusing partial memories.
* We may withdraw believing we can avoid facing the loss and avoid those people who confront us with the truth.
* We may regress to being like a child who wants protecting from the loss.
2 Bargaining
* We may promise to do anything to make this loss go away.
* We may bargain or strike a deal with God, ourselves or others to make the loss go away.
* We lack confidence in our attempts to deal with the loss, looking elsewhere for answers or gamble on a miracle.
3 Anger
* Anger is a perfectly natural reaction to loss that passes with time.
* Anger can come from loss, grief, frustration and resentment and we can become angry with:
A Ourselves: ‘self blame’.
B Others: ‘kicking the cat’
C Our closest friends and family
4 Despair
*We become overwhelmed by the anguish, pain, sadness and hurt of our loss
*Our mood can be lowered and we might often cry
*We might wrongly convince ourselves that the loss was some sort or payback.
*We might begin feel despondent and to think things are utterly hopeless.
5 Acceptance
*We can identify losses and the common feelings of loss.
*We can describe the details of our loss and the details of the rehabilitation.
* We can get through each day, cope somehow and keep sight of some level of hope.
* We are now aware when we dip back into stages or common feelings of loss and know what to do to help.
* Adapt and drive toward our potential.
Acceptance presents the final and most adaptive phase of feeling associated with loss. Therapeutic aims are often based upon experiencing more feelings associated with acceptance.
There is a growing collection of evidence that loss has neurological consequences. fMRI scans of women from whom loss and grief was elicited about the death of a mother or a sister in the past 5 years found it produced a local inflammation response as measured by salivary concentrations of pro-inflammatory cytokines. These were correlated with activation in the anterior cingulate cortex and orbitofrontal cortex. These activation also correlated with free recall of grief-related word stimuli. This suggests that grief can cause stress, and that this is linked to the emotional processing parts of the frontal lobe.
Among those bereaved within the last three months, those who report many intrusive thoughts about the deceased show ventral amygdala and rostral anterior cingulate cortex hyperactivity to reminders of their loss. In the case of the amygdala, this links to their sadness intensity. In those who avoid such thoughts, there is a related opposite type of pattern in which there is a decrease in the activation of the dorsal amgydala and the dorsolateral prefrontal cortex.
In those not so emotionally affected by reminders of their loss, fMRI finds the existence of a high functional connectivity between the dorsolateral prefrontal cortex and amygdala activity, suggesting the former regulates activity in the latter. In those who had greater intensity of sadness, there was a low functional connection between the rostal anterior cingulate cortex and amygdala activity, suggesting a lack of regulation of the former part of the brain upon the latter
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