The Mysteries of Autism Spectrum Disorder: Phenomena that Confounds Cognitive Neuropsychology - Essay Example

Running head: AUTISM The Mysteries of Autism Spectrum Disorder: Phenomena that Confounds Cognitive Neuropsychology [date] Abstract The population afflicted with an Autism Spectrum Disorder (ASD) consists of an unusually diverse group of individuals with equally distinct symptoms and levels of severities in each case. Cognitive neuropsychology struggles to understand the complexities of this disorder, as well as the higher psychological functions which show the most noticeable impairments. Some of the higher psychological functions include the ability to process facial expressions, understand the difference between one’s own personal state of mind and another’s, and inability to interpret emotions. In this respect, the discipline of cognitive neuropsychology cannot find explanations for the brain’s deficits of how, where and even why such cognitive anomalies occur. Several studies of Autism and Asperger’s Disorder provide stark proof that cognitive neuropsychology remains at a standstill in terms of progress made in the understanding of higher psychological functions. Outline I. Introduction A. Neuropsychology and cognitive neuropsychology: determining the brain’s role in psychological functions. B. Cognitive neuropsychology’s strengths. C. Cognitive neuropsychology’s weaknesses. Thesis: The mysteries of ASD continue to confound the field of cognitive neuropsychology in its attempt to progress in understanding higher order psychological functions. II. Autism Spectrum Disorders (ASD) and Asperger’s Syndrome A. Diverse symptoms lead to difficulties for neuropsychologists to pinpoint dysfunctional areas of the brain. B. Undetermined biological causes and locations of ASD contribute to confusion for neuropsychologists. C. Various proposed causes for the detriments in higher functioning psychological processes leave cognitive neuropsychology with numerous possibilities but few concrete answers. a. Levels of Serotonin in cerebellum b. Dissipation of data traveling through brain c. Other hypothetical possibilities III. Conclusions A. What intensive imaging of the brain has revealed to cognitive neuropsychologists about ASD. B. Remaining mysteries of higher function psychological processes. The Mysteries of Autism Spectrum Disorder: Phenomena that Confounds Cognitive Neuropsychology Neuropsychology has traveled a long intriguing road of study. The results of this scientific field continue giving humans a great deal of knowledge about the processes of the brain, and how that mysterious organ plays an important role in our concept of the mind. Cognitive neuropsychology aims to connect the mind-body experience, suggesting that specific areas of our brain contribute directly to our mind’s perception of the world around us. Head trauma victims, and those suffering from lesions or cancerous tumors in the cerebral cortex often report that their experiences concur with this idea. Upon sustaining their injuries, they note serious differences in how they can perceive various types of stimuli, as well as changes in their personal range of thoughts and feelings. Further scientific and medical examination, including MRI imaging has allowed researchers to observe the different parts of the brain responsible for assorted psychological functions. Correspondingly, the strengths of cognitive neuropsychology lie in its ability to help researchers determine some of the locations of different psychological functions. This information in turn offers some enlightenment on the biological causes for psychological disorders. For example, when aphasia in Broca’s and Wernickes area of the brain occur, a cognitive disorder or learning disability usually ensues (Berndt (Caramazza, 1990, p. 123). Cognitive neuropsychologists determine that these two areas of the brain play an important role in grammar and sentence comprehension, thus damage or aphasia to such would then likely cause the aforementioned impairments. However, processes such as grammar and sentence interpretation reveal only primary psychological functions. While complex, they still only require exposure to and absorption of the textual stimulus. Higher psychological functions such as understanding and reflecting upon one’s existence in relation to an object, person or stimulus tends to confound the progress of cognitive neuropsychology. The vast range of symptoms found in Autistic Spectrum Disorders (ASD) attests to cognitive neuropsychology’s weaknesses to explain why individuals with the disorder have no concept of their thoughts and the state of their mind opposed to another, why they cannot interpret facial expressions, and why there appears no one specific brain anomaly to account for the psychological detriments presented. Such high order psychological problems of ASD result in the following characteristics noted by Lord and Volkmar (2002). ASD affects the acquisition of social relationships, difficulties do not lie in typical measures of attachment (e.g., strange situation). Rather, they [deficits] are found in very basic social-communicative behaviors, such as use of gaze and facial expression. [Also] in specific contexts in which the coordination of these behaviors results in a “social-cognitive event,” such as pointing to express interest in something (e.g., “protodeclarative pointing”) And [finally deficits occur] in reciprocal relationships, most easily seen in the absence of friendships with peers. (Journal of the American Academy of Child and Adolescent Psychiatry, pp. 1134-1136). Overall, the mysteries of ASD continue to confound the field of cognitive neuropsychology in its attempt to progress in understanding higher order psychological functions. Autism Spectrum Disorder and Asperger’s Disorder have striking similarities, but often just as many differences. This creates a difficult scenario for cognitive neuropsychologists who try to specify a distinct area of dysfunction in the brain. Autism consists of several cognitive deficits, most notable of which include an individual’s inability to process the facial expressions, feelings and emotions of those around them, along with troubles in language acquisition and communication. Lord and Volkmar (2002) tell readers that, autistic spectrum disorders (ASD) involve severe difficulties in basic aspects of social behavior and communication, such as eye contact, facial expressions, and the development of spontaneous, reciprocal language, which, for reasons not well understood, are associated with behaviors characterized by repetition and restriction, ranging from finger-flicking to compulsive touching to complex preoccupations with electrical appliances or highly circumscribed interests such as names of radio stations or Scottish clans (Journal of the American Academy of Child and Adolescent Psychiatry, pp. 1134-1136). Individuals with ASD may also show signs of mental retardation, seizures, and developmental problems (Lord & Volkmar, 2002). Asperger’s falls into its own specific category under the umbrella of ASD, and as of 1994, has a separate listing in the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (Autism Society of America, 2006). Asperger’s Disorder characteristically defines individuals who show some autistic traits but have high functioning capabilities in both language and cognition. The problems that ASD poses for cognitive neuropsychology first revolve around trying to determine when, where, how, and why the symptoms occur biologically. Secondly, in terms of mind theory, more difficult problems arise when cognitive neuropsychologists attempt to discover the reasons for the lack of high functioning psychological processes. A brief overview of the biological anomalies of autism will help to further understand why cognitive neuropsychology finds itself with so many unanswerable questions. Autism and its biological cause has been an issue of debate for several years. For some time there existed a rumor of mercury induced poisoning coming from infant inoculations. Heavy metals in water supplies, fish products and other sources gleaned a good portion of blame for the cognitive abnormalities. Likewise, prenatal difficulties, viral infection and genetics all have played key roles in trying to determine the onset of the disorder (Lord & Volkmar, 2002). Asperger’s syndrome has a predominantly genetic cause, as described by Nunley (2006), who quotes Gillberg, C. & Cederlund, M. (2005), “Most of the time Asperger syndrome has a genetic component (55% of all cases).  It tends to follow paternal blood lines as about half of all people with Asperger syndrome have some type of autism spectrum disorder in their fathers family line” (Journal of Autism & Developmental Disorders, 2005).  With time, autopsy reports revealed several abnormalities in the autistic brain, rather than one distinct area with atrophy or irregularity. (Bauman & Kemper, 2003). The causes of such cerebral cortex oddities in so many different locations still remain a mystery (Frith, 2003). The present variety of information confounds cognitive neuropsychology’s attempt to determine when, where, and how the disorder develops in the brain. In relation, with ASD and particularly with Asperger’s Disorder, cognitive neuropsychology struggles to understand the higher psychological functions affected. Asperger’s individuals have very capable cognitive reasoning but still lack the ability to perceive other’s thoughts, emotions and facial expressions. “Theory of Mind” (Premack and Woodruff, 1978), proposes an ability to discern emotional and mental states of oneself versus those of another. Understanding that other people have different beliefs and ideas often escapes the individual with Asperger’s. In consequence, this distinct symptom poses a formidable challenge for cognitive neuropsychology. First understanding the source of the concept of one’s mind; and then where in the brain one thinks about or evaluates their personal thoughts or emotions as well as the thoughts and emotions of others. Some research has attributed the complex cognitive problems of autism to levels of the neurochemical transmitter serotonin in the cerebellum, Nunley (2006). The proposed cause includes the, “serotonin system to malfunction in the brains of autistic individuals. . . [it] results in an inability to coordinate the functions of cognition and emotion” (Nunley (Marazziti, D. (2002). Psychiatry, Vol 52(2), 143. 2. Pierce, K & Courchesne, E. (2002). Biological Psychiatry, Vol 52(2), 143). However, this covers only one of the many purposed deficits and abnormalities in several different areas of the autistic individual’s brain. Similarly, the difficulties of higher levels of processing have also been attributed to problems with sensory integration. It appears that the activation levels of sensory mechanisms in the brain remain low, and an additional loss of cognitive appraisal results. As Frith (2003) explains: Another way of identifying the neural basis of autism is to investigate brain systems underlying cognitive functions compromised in this disorder such as face perception and theory of mind. Autistic people fail to activate the fusiform face area during face perception tasks and show weak activation of medial frontal cortex and superior temporal gyrus when performing theory of mind tasks. These problems stem from a lack of integration of sensory processing with cognitive evaluation. (Frith, 2003, p. 149) Identifying the locations of low cerebral and cognitive functioning leads to more puzzling questions revolving around why these areas do not perform correctly. It appears that instead of having active an fusiform face area when observing a particular face, only the inferior temporal cortex strongly reacted to the stimuli. This implies that individuals with ASD process the human face as an object or series of objects (Frith, 2003). Perhaps this identification hindrance has something to do with why individuals with ASD do not perceive varying mental states between themselves and others; rather than the previously mentioned conclusion of the levels of serotonin in the cerebellum. Perceiving a human as an object rather than an actual person would invariably lead to detached or no emotional appraisal at all. In other words, the brain somehow realizes that a perceived object has no emotions, therefore an individual with ASD does not recognize that another person even has thoughts, feelings or state of mind. While it is a hypothetical leap, this theory would futher confound cognitive neuropsychologist’s progress concerning the role of serotonin levels in cognition and emotional evaluation. The next mystery that continues to puzzle cognitive neuropsychologists centers on the simple question: Why? Why do individuals with ASD perceive faces and people as mere objects? No physical detriment to the fusiform face area exists to provide a biological cause for discriminating a person as an object (Frith, 2003). The initial sensory mechanism, the inferior temporal cortex works appropriately. Some where along the path and for some unknown reason connectivity seems to dissipate (Frith, 2003). Tracking the level at which knowledge gets lost or perhaps misinterpreted in the brain leaves cognitive neuropsychologists with an enigma in their midst. No one has specified whether problems center on neurotransmitter levels or maybe a cerebral bypass of the fusiform area entirely. Could the information be being misdirected through various parts of the brain completely? The many possibilities leave cognitive neuropsychologists with plenty of hypothesis but no conclusive answers. Despite all of the numerous possibilities, what brain scans and intensive imaging have provided for cognitive neuropsychologists in the area of autism are these four conclusions, as stated by Nunley (2006) who recounts a study from Columbia University: It [autism] is a heterogeneous disorder with most likely many causes. brain imaging has shown a wide range of anatomical differences all of which reflect problems early in the brains development having to do with neuron growth and pruning.  The neurochemical differences occur early and are pervasive rather than localized to any one area.    …enough research [is not] yet [available] to say exactly in what way the autistic brain functions differently than the non autistic brain, but there is a huge number of current research projects going on in this area. (Eigsti & Shapiro 2003).  The journey of cognitive neuropsychology towards finding a concrete location in the brain that directly contributes to the symptoms of ASD appears a long and complicated one. Autism, with all its complexities may never quite have one tried and true explanation. With so many combinations of deficits, and so many commonly co-morbid disorders, just one conclusion for the basis of all the various problems does not seem probable. In terms of the progress that cognitive neuropsychology has made in understanding higher psychological functions, it appears that with all the different data and hypothesis proposed more confusion than answers arise. However, like pieces of a puzzle, once researchers discover how all the tiny elements fit together, hopefully the bigger picture will appear with clarity. Until then their progress with understanding higher levels of psychological processing seems at a standstill. Likewise, this obstacle of neuropsychologist’s understanding does not only apply to individual’s with ASD. The examples provided show one population of individuals in which cognitive neuropsychologist’s lack answers to questions of higher order psychological functions. Comparing the processes of a normal functioning brain to an irregular one still does not explain how each element therein works within the organ itself. Many clues of the brain still await discovery; and many correspondences need verification before in depth understanding of high order psychological function occurs. Some of the primary roles of neurotransmitters and brain areas still need to sorting out as well. Neuroscience, like most scientific disciplines needs time and hard work to bring forth valuable revelations. References Baron-Cohen, S., Frith, U., & Leslie, A. M., (1985). Does the autistic child have a “theory of mind”? Cognition, 21, 37-46. Baron-Cohen, S., Jolliffe, T., & Wheelwright, S. (1997). Is there a “language of the eyes”? Evidence from normal adults, and adults with autism or asperger syndrome. Visual Cognition, 4 (3), 311-331. Bauman, M. L., & Kemper*, T. L. (2003). The Neuropathology of the Autism Spectrum Disorders: What Have We Learned?. In Autism: Neural Basis and Treatment Possibilities, Bock, G. & Goode, J. (Eds.) (pp. 112-121). Hoboken, NJ: Wiley. Retrieved June 20, 2006, from Questia database: http://www.questia.com/PM.qst?a=o&d=107376862 Bock, G. & Goode, J. (Eds.). (2003). Autism: Neural Basis and Treatment Possibilities. Hoboken, NJ: Wiley. Retrieved June 20, 2006, from Questia database: http://www.questia.com/PM.qst?a=o&d=107376738 Caramazza, A. (Ed.). (1990). Cognitive Neuropsychology and Neurolinguistics: Advances in Models of Cognitive Function and Impairment. Hillsdale, NJ: Lawrence Erlbaum Associates. Retrieved June 20, 2006, from Questia database: http://www.questia.com/PM.qst?a=o&d=10089490 Frith, C. (2003). What Do Imaging Studies Tell Us About the Neural Basis of Autism?. In Autism: Neural Basis and Treatment Possibilities, Bock, G. & Goode, J. (Eds.) (pp. 149- 163). Hoboken, NJ: Wiley. Retrieved June 20, 2006, from Questia database: http://www.questia.com/PM.qst?a=o&d=107376894 Lord, C. & Volkmar, F. (2002, September). Genetics of childhood disorders: XLII. Autism part I: diagnosis and assessment in autistic spectrum disorders. Journal of the American Academy of Child and Adolescence Psychiatry. 41(9), 1134-1136. Nunley, K. (2006). Hot topics from psychology and neuroscience. Retrieved online June 19th, 2006, from http://helpforteachers.com/hottopics.htm#autism Premack, D., & Woodruff, G. (1978) Does the chimpanzee have a ‘theory of mind’? Behavioral and Brain Sciences, 4, 515-526 Read More