The Biopsychology of the Neurological Disorders Aspergers Syndrome - Term Paper Example

? The Biopsychology of the Neurological Disorders Asperger's Syndrome Asperger’s syndrome refers to a pervasive developmental condition related to autism, and that manifests highly distinct characteristics. The disorder, which is part of the autistic spectrum, embodies aspects regarding social and communication skills. The term pervasive developmental disorders describe a class of neurological disorders that encompass impaired social and communication proficiency, in addition, to monotonous behaviours. Literature on the disorder remains controversial among researchers, physicians, and the subjects diagnosed with Asperger's syndrome owing to AS multiple effects. The present ASD classification is to some extent a representation of the discovery of autism and may not automatically exemplify the exact character of the spectrum. The paper explores the biopsychology of neurological disorders particularly Asperger’s syndrome. The Biopsychology of the Neurological Disorders Asperger's Syndrome Introduction Asperger syndrome (AS), also referred to as Asperger’s syndrome or Asperger disorder, infers an autism spectrum disorder (ASD) typified by considerable complications in social interaction, as well as obsessive and repetitive models of thought, behaviour and interests. Other categories of ASDs include classic autism, childhood disintegrative disorder, Rett syndrome, and pervasive development disorder. The notion of the spectrum applies because the symptoms of ASD differ from one individual to the other, from mild to severe (Fitzgerald & Corvin, 2001). Asperger syndrome is outlined as a pervasive developmental disorder (PDD) carrying a differentiated pattern of symptoms instead of a single symptom. Asperger syndrome differs from other autism spectrum disorders owing to its relatively normal development of both linguistic and cognitive skills, devoid of delay. Just like other psychological development disorders, ASD begins during childhood and bear a steady course devoid of relapse and may have impairments emanating from maturation-related adjustments in various coordination of the brain (Attwood, 2011). Of the four ASD categories, autism has the utmost similarity to AS in signs and probable causes since its diagnosis details impaired communication and delay in cognitive development. Although not critical for diagnosis, physical clumsiness and nonconforming utilization of language also applies as key characteristics of AS. The precise cause of AS is unknown; research on the disorder suggests a probability of a genetic basis, although with an imprecise genetic etiology. Brain imaging techniques either have not yielded a concise common pathology. There is no single treatment of the disorder, and the effectiveness of the applied interventions is usually informed by limited data. Intervention pursues enhancing of symptoms and function (Klin, Volkmar & Sparrow, 2000). The bedrock of management for the disorder revolves around behavioural therapy centering on certain deficits to address aspects such as poor communication skills, physical clumsiness, and obsessive or repetitive routines. Most children with AS usually improve as they mature, although social and communication difficulties may persist. Characteristics of Asperger’s Syndrome Asperger syndrome, as a pervasive developmental disorder, depicts an outline of symptoms rather than a lone symptom. Asperger’s syndrome correlates with Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) by six main criteria. These include qualitative impairment in social interaction (lack of demonstrated empathy), considerable harm in critical areas of functioning, a general delay in language, but with no considerable clinical delay in cognitive development, and stereotyped and restricted patterns of behaviour, activities, and interests (Fitzgerald & Corvin, 2001). During the first three years of life, there is no considerable delay in cognitive development, especially regarding typical developmental patterns such as the attainment of age appropriate learning skills and adaptive behaviours. Asperger’s Syndrome is also typified by limited interests or extraordinary obsession with definite subjects to the segregation of other activities, as well as peculiarities in speech and language. Although motor deficits are believed to be common in AS, the causes and characteristics of the states deficits are unidentified. Individuals with Asperger’s syndrome also manifest socially and emotionally improper behaviour and the incapacity to interact effectively with peers. Other characteristics include deep preoccupation with a narrow subject, restricted prosody, one-sided verbosity, and physical clumsiness, although the latter remains non-essential for diagnosis. Individuals with Aspeger’s syndrome tend to have normal and above average intelligence, although they possess an enhanced predisposition to comorbid psychiatric conditions such as depression, mood disorders, and obsessive-compulsive disorder (Klin, Volkmar & Sparrow, 2000). Asperger’s children are highly likely to develop mood disorders. Research stipulates that individuals with AS have a predisposition to associated conditions whose symptoms may frequently be diagnosed with clinical depression, antisocial personality disorder, ADHD, bipolar disorder, obsessive compulsive disorder, dyslexia, and general anxiety disorder, among others (Attwood, 2008). Mechanism Aspergers syndrome appears to stem from developmental aspects that influence many or all functional brain coordination. Although the precise underlying of Asperger’s syndrome or factors that demarcate it from other ASDs remains unknown, and no concise and generalized pathology for Asperger’s children have emerged, it is probable that AS’s mechanism maybe distinct from other ASDs (Frith, 2001). Neuroanatomical research and associations with teratogens powerfully suggest that the mechanism incorporate alteration of brain development soon after conception. There are several theories that outline the mechanism such as under connectivity theory and mirror neuron system theory, although none can be delimited as possessing a complete explanation. Medical researchers assert that genetic susceptibility plus extra factors contribute to the emergence of either of the ASDs (Frith, 2001). Factors under investigation include drugs, allergies, immune system problems, infections, and environmental pollution. Autopsy studies of persons with pervasive developmental disorders indicate that brain cell structure is distinct, especially in the brain stem area (Attwood, 2008). Diagnosis The standard diagnostic criteria require impairment in social interaction, as well as repetitive and stereotyped patterns of behaviour, interests, and activities, without significant setback in language or cognitive development. The U.S. criteria require considerable impairment in day-to-day functioning, unlike other international standards (Attwood, 2008). Diagnosis is usually carried out between the ages four and eleven. A comprehensive assessment mainly encompasses a multidisciplinary team across diverse settings and includes neurological and genetic assessment, as well as tests centering on cognition, psychomotor function, style of learning, and verbal and non-verbal strengths and weaknesses. The diagnosis of AS (and high functioning autism) are sometimes applied interchangeably; a child may receive diverse diagnoses depending on the screening tool and the person administering the test. Similarly, diagnoses may be swayed by non technical issues such as availability of support (Frith, 2001). Under diagnosis and over diagnosis are some of the challenges that may arise in marginal cases. Treatment Currently, there is no cure for the ASD, and there is no distinct therapy that is effective for all individuals. Nevertheless, a broad range of treatments are available, depending on the severity of the disorder. Intervention encompasses specialized therapy, specialist education, and medication to address certain behavioural challenges (Lyons & Fitzgerald, 2005). The treatment pursues enhancing of the symptoms. The medications may be prescribed to treat certain symptoms inclusive of anti- depressants, anti- spasmodic, anti- seizure medications, anti- anxiety medications, and stimulants. Therapeutic interventions involve applied behaviour analysis, behaviour modification programs, auditory integration training, play therapy, physical and occupational therapy, sensory integration, and speech therapy. Differences from High-functioning Autism The distinction between Asperger’s and other ASDs forms is to some degree an artifact of how autism was discovered. Although persons with Asperger’s syndrome tend to perform better cognitively compared to individuals with autism, the degree of the overlap between AS and high-functioning autism is somewhat imprecise. Largely, relatively few distinctions remain between Asperger’s and autism on factors relating to causation. IQ tests may indicate normal or superior intelligence and an average language development compared with classical autism (Attwood, 2008). Asperger’s syndrome differs from other PDDs and from High Functioning Autism based on the fact that early development is normal, and mostly there is no language delay. In addition, AS children do not possess significant cognitive delays. The standard assumption hinges on the assertion that AS and autism has a shared cause, and both represent variable expressions of an identical disorder. Unlike autism, which is commonly diagnosed during early stages of childhood, Asperger’s syndrome diagnosis occurs until later developmental stages (between the ages of 4 and 9 years of age). This stems from the fact that children with AS bear an inclination towards maintaining normal learning since much of the symptoms may not become noticeable until much later. AS is frequently identified in early childhood, and most individuals fail to receive diagnosis until after puberty. Assistance to central symptoms of AS encompass therapies that apply behaviour management strategies and attend to poor communication skills, obsessive or repetitive routines, and physical clumsiness (Attwood, 2008). Compared to high-functioning autistic individuals, individuals with Asperger’s syndrome tend to possess a high verbal IQ. In addition, Aspergers children have more capability to communicate and interact socially. The Biopsychology of Asperger’s Syndrome Autistic spectrum disorder (ASD) refers to neurodevelopment conditions that may emanate from abnormal connectivity sandwiched between brain regions incorporating neurocognitive networks for certain aspects of social cognition. Evidence from research indicates that functional connectivity of Medial Temporal Lobe structures is abnormal in persons Asperger’s syndrome during face processing. The biological condition coupled with the compositions and functions of the brain of persons with AS differ significantly across the population and may not always compare to the severity of the disorder. Early autopsy research indicated a broad variety of neurological dissimilarities and/or damage in the individual brains of persons with autism. Contemporary autopsy results indicate that persons with AS may belong to diverse subgroups with uncommon development in brain structures that translate into similar behavioural symptoms and developmental limitations. This makes Asperger’s syndrome a spectrum disorder owing to its biological conditions, behavioural features, and developmental outcomes. The broad array of the causes and the presentation of the disorder complicate research and treatment for persons with Asperger’s syndrome as a sole population. Recent microscopic forensic studies reveal a number of features dominant in a large number of persons with autism, although not in all people with autism. Some of the heterogeneous findings (functional and structural features) prominent in persons with autism that can be related to AS include alterations in size and thickness of the Cerebral Cortex; alterations within the functional activity of the Frontal Lobe; changes in the neural fibres of the Corpus Callosum; alterations within the make-up and functionality of the Limbic system; alterations within the functional activity of the Temporal Lobes, and alterations in the structures and functional activity of the Thalamus. Current research suggests that the potential cause of AS hinges on brain abnormalities, even though a biological cause has not yet been established. It is believed that unusual migration of cells during the embryo development results to improper formation of neural circuits in the brain. However, the how and why of the occurrences is yet to be determined. Twin and family research indicate that there is a genetic vulnerability to AS and the other ASDs, although a distinct gene for AS has not been identified. It is probable that multiple genes cause Asperger's syndrome as the severity of symptoms differs across persons. The current research on the disorder points out to structural abnormalities in the brain as the core causes of AS. The abnormalities affect neural circuits that regulate thought and behaviour (Attwood, 2011). In addition, researchers assert that gene (environment) interactions make some genes turn on or off or disproportionately, which hinders the customary formation of embryonic brain cell during early development. Through the application of brain imaging techniques, scientists have been able to reveal structural and functional dissimilarities in certain brain regions between the brains of normal versus Asperger’s syndrome children. One of the studies revealed a lack of activity within the Frontal Lobe of AS children when requested to respond to activities that demand them to use judgement. Another significant difference in brain activity arose when the children were asked to respond to facial expressions (Lyons & Fitzgerald, 2005). Other investigations on brain functions have revealed unusual levels of certain proteins in the brains of adults with AS associated with obsessive and repetitive behaviours. The Frontal Lobe is essential to the majority of functions linked to AS, such as language and executive functions. Current research stipulates that dysfunction in the Frontal Lobe may contribute to some of the deficits apparent in individuals with ASD, inclusive of social cognition, language, working memory, problem solving, imitation, and facial expressions. Asperger’s children have also manifested decreased activation in the medial prefrontal cortex compared to a control group. The functions of the Temporal Lobe relate to most of the deficits examined in persons with ASDs such as social cognition, receptive language, empathy, joint attention, and action observation (Lyons & Fitzgerald, 2005). One of the propositions advanced by scientists details that dysfunction in the Superior Temporal Sulcus, which may mediate facial processing, underpin the social deficits that characterize AS. Conclusion The extent of the overlap between Asperger’s syndrome and high-functioning autism is blurred. A number of factors obscure the effective diagnosis of Asperger’s Syndrome. The diagnosis of AS is constrained by the absence of a standardized diagnostic screen. The diagnosis applies diverse screening instruments and a variety of diagnostic criteria. Challenges in diagnosis emanate from disagreement on diagnostic criteria, disagreement regarding the distinction between AS and other ASD forms, and whether AS exists as a distinct syndrome. References Attwood, T. (2008). The complete guide to Asperger’s Syndrome. London, UK: Jessica Kingsley. Attwood, T. (2011). What is Aspergers? Retrieved from http://www.tonyattwood.com.au/index.php?option=com_content&view=article&id=62&Itemid=719 Fitzgerald, M. & Corvin, A. (2001). Diagnosis and differential diagnosis of Asperger syndrome. Advances in Psychiatric Treatment 7 (1): 310-318. Frith, U. (2001). Autism and Asperger Syndrome. New York, NY: Cambridge University Press. Klin, A., Volkmar, F. & Sparrow, S. (2000). Asperger syndrome. New York, NY: Guilford Press. Lyons, V., & Fitzgerald, M. (2005). Asperger Syndrome: A gift or a curse? New York, NY: Nova Science. Read More