Examine one interaction between cognition and physiology in terms of behaviour, (for example, agnosia, anosognosia, prosapagnosia, amnesia).

evaluate two relevant studies

Terms:
Cognition Physiology Prosopagnosia Fusiform Gyrus The mental process of knowing, including aspects such as awareness, perception, reasoning, and judgment. The physical bases of psychological processes A disorder of face perception where the ability to recognize faces is impaired Part of the brain responsible for the following localized functions: 1. processing of color information 2. face and body recognition 3. word recognition Consider an argument or concept in a way that uncovers the assumptions and interrelationships of the issue.

Examine

When cognitive functions and physiology interact with each other the reaction can take one of many forms. The brain is unpredictable and these reactions can be erratic, abnormal, subtle, or even psychotic.

Cognition

The functioning of your brain that determines the psychological reaction of our perception, learning, and how we reason. It is basically the inner workings of the brain that we can't feel or touch, but only study and record.

Physiology

The actual physical aspects of the brain and body that can have effects on behavior. This aspect of psychology is the part you can physically see, examine, and study. This also includes the actual functions that are a result of our physical make-up.

So How Do They Interact?

One such example could be the disorder Prosopagnosia or Face Blindness. This disorder impairs the ability for the brain to recognize faces. Depending on the severity of the physiological aspect of the disorder, it can determine the cognitive function of how your brain and memory work. When you are unable to remember faces it has a monumental effects on your behavior. Just think about your best friend or a loved one image not remembering their faces. The amount of people you associate your self with will not exist. Causes of Prosopagnosia: The causes of this disorder are either a tumor, surgery or damage in a particular area of the brain called the Fusiform Gyrus (acquired prosopagnosia), or may be inherited (developmental prosopagnosia).

Acquired Prosopagnosia
Acquired prosopagnosia may occur after brain damage from head injury, stroke, or neurodegenerative diseases. Individuals with this type had normal face recognition abilities in the past, but this has been impaired or lost due to brain injury.

Developmental Prosopagnosia
Prosopagnosia may be present from childhood and individuals with this type of prosopagnosia often do not realize until they are older that they are unable to recognize faces as well as other people do. Some researchers believe that developmental prosopagnosia may be inherited, since it appears to be present in more than one individual in some families. In 2005 German researchers found evidence of a genetic basis for the disorder by studying individuals with prosopagnosia in seven families. http://www.newscientist.com/article/dn7174 It is also thought that developmental prosopagnosia is present in children with autism and Asperger syndrome. Children with these disorders have impaired social development, and prosopagnosia might cause or contribute to their difficulty in relating to other people.

Two Research Studies

(1) Caldara et al. (2005) case study of acquired prosopagnosia (2) Joy & Brunsdon (2002) case study of developmental prosopagnosia

Caldara. R. et al. (2005) Does Prosopagnosia Take the Eyes Out of Face Representations? Evidence for a Defect in Representing Diagnostic Facial Information following Brain Damage. Journal of Cognitive Neuroscience, Volume 17, number 10, pages 1652-1666. Full paper
available: http://www.nefy.ucl.ac.be/facecatlab/PDF/RC_JoCN_05.pdf Abstract:

One of the most impressive disorders following brain damage to the ventral occipitotemporal cortex is prosopagno- sia, or the inability to recognize faces. Although acquired prosopagnosia with preserved general visual and memory functions is rare, several cases have been described in the neuropsychological literature and studied at the functional and neural level over the last decades. Here we tested a brain- damaged patient (PS) presenting a deficit restricted to the category of faces to clarify the nature of the missing and pre- served components of the face processing system when it is selectively damaged. Following learning to identify 10 neutral and happy faces through extensive training, we investigated patient PSs recognition of faces using Bubbles, a response classification technique that sampled facial information across the faces in different bandwidths of spatial frequencies [Gosselin, F., & Schyns, P. E., 2001]. Although PS gradually used less information (i.e., the number of bubbles) to identify faces over testing, the total information required was much larger than for normal controls and decreased less steeply with practice. Most importantly, the facial information used to identify individual faces differed between PS and controls. Specifically, in marked contrast to controls, PS did not use the optimal eye information to identify familiar faces, but instead the lower part of the face, including the mouth and the external contours, as normal observers typically do when processing unfamiliar faces. Together, the findings reported here suggest that damage to the face processing system is characterized by an inability to use the information that is optimal to judge identity, focusing instead on suboptimal information. Evaluation points for Caldara et al. (2005) (1) Method used to help our understanding of prosopagnosia. These type of studies on the neuro-functional basis of prosopagnosia provide clues about the reasons why PS' deficit is so specific. For example, while her main lesion in the right hemisphere destroyed part of the occipital cortex, the lesion spared other parts of the occipital cortex (the ventral and dorsal part as well as parahippocampal areas were preserved where recognition of non-face objects may take place). (2) Through these sorts of studies we have knowledge about the physiology of normal face processing. (3) Because this case study is not longitudinal, it is not clear whether other factors might contribute to this behavior.

Joy, P & Brunsdon, R. (2002). Visual Agnosia and Prosopagnosia in Childhood: A Prospective Case Study. Child Neuropsychology. Volume. 8 No. 1, pages 1-15. Report the case of patient A.L. a child with developmental prosopagnosia. Abstract available:
http://www.ncbi.nlm.nih.gov/pubmed/12610772 Abstract: Selective impairments in visual processing are well documented in adults but rarely reported in children. The few childhood cases reported are mostly retrospective accounts with little attention paid to developmental, assessment or management issues. We report a prospective case study of a boy with prosopagnosia and visual processing deficits of presumed developmental origin. At the age of 4 years, AL presented with a range of cognitive and visual recognition deficits. Subsequent assessments revealed an evolving pattern in visual recognition and dissociations between developing skills. At the age of 7 AL has impairments in early perceptual analysis, visual organisation and in complex visual processing. Although he can identify facial features and match faces he is unable to recognise familiar faces. His reading and spelling are developing normally. The nature of his deficits and his progress are discussed within a cognitive neuropsychological framework.

Evaluation points for Joy & Brunsdon (2002)

(1) Like the previous study, this study highlights the interaction between cognition and physiology. (2) Although there is cause for some optimism with this particular case, the result is still inconclusive about whether our neuroplasticity is powerful enough to completely heal this cognitive disorder. (3) This study suggests there is a complex interaction between age, physiology and neuroplasticity, which is another factor to consider when trying to make generalisations.

Evaluation points for both research studies:

Methodology Consistency Clinical Case Studies: since different methods are not possible, case study method provide valuable insight into this disabling condition. Although this condition is rare, both studies highlight the relationship between cognition and physiology suggesting the importance of specific functioning of the brain and the impact on face processing. Both cases provide establish a link by illustrating the effect of the disorder prosopagnosia has on social interaction These research studies concerned suggests that specific processes involved in face recognition is localized (to the Fusiform Gyrus for face recognition). However, it is important to remember that these case studies cannot be generalize for all the patients with prosopagnosia because it may be that the damage to the fusiform gyrus can have different effects on different patients due to the variability of neuroplasticity. However, the implications of neuroplasticity itself suggests that it might be possible for the brain to repair itself and function can be more plastic. Strengths

General Implications

It is important to realise that patients who have this cognitive disorder are extremely rare, therefore a larger sample size is not possible. Therefore the

case study research method allow for in-depth analysis, which helps us understand prosopagnosia. Limitations

These case studies are limited to specific clinical cases, that are not crosscultural, therefore it is not clear whether other factors might contribute to this behavior. It should be kept in mind that this research provides a reductionist approach exposing the causes of this disorder but findings are restricted to very particular and limited examples.

References:

Bakalar, N. (2006) Just Another Face in the Crowd. Indistinguishable Even it Its Your Own. New York Times: http://www.nytimes.com/2006/07/18/health/psychology/18face.html PDF:
http://www.cnbc.cmu.edu/~behrmann/dlpapers/newscientist.pdf

Grueter, M., Grueter, T., Bell, Vlk Horst, J., Laskowski, W., Sperling, K., Halligan, P.W., Ellis, H.D., & Kennerkrnecht, I. (2007) Hereditary prosopagnosia: the first case series. Cortex, Volume 43, number 6 pages 734-749. Abstract:
http://www.researchgate.net/publication/6128766_Hereditary_prosopagnosia_the_first_case_series Prosopagnosia is defined as a specific type of visual agnosia characterised by a discernible impairment in the capacity to recognise familiar people by their faces. We present seven family pedigrees with 38 cases in two to four generations of suspected hereditary prosopagnosia, detected using a screening questionnaire. Men and women are impaired and the anomaly is regularly transmitted from generation to generation in all pedigrees studied. Segregation is best explained by a simple autosomal dominant mode of inheritance, suggesting that loss of human face recognition can occur by the mutation of a single gene. Eight of the 38 affected persons were tested on the Warrington Recognition Memory Test for Faces (RMF; Warrington, 1984), famous and family faces tests, learning tests for internal and external facial features and a measure of mental imagery for face and non-face images. As a group, the eight participants scored significantly below an age- and education-matched comparison group on the most relevant test of face recognition; and all were impaired on at least one of the tests. The results provide compelling evidence for significant genetic contribution to face recognition skills and contribute to the promise offered by the emerging field of cognitive neurogenetics.

http://prosopagnosiaresearch.org/index/information accessed September, 2012