All your Writing needs covered

Clinical Neuropsychology: Manual Of Mental Disorders

Calculate the price
your order:

275 words
Approximate price
$ 0.00

Clinical Neuropsychology: Manual Of Mental Disorders Question: Describe about the Clinical Neuropsychology for Manual of Mental Disorders.   Answer: 1. The current Diagnostic and Statistical Manual (DSM) system for diagnosing psychiatric illness fail to diagnose disease in a therapeutic manner and the results are suboptimal. Since the past few decades categorical approach to psychiatric disorder has been followed. With this approach, mental disorders are classified according to its typical symptoms and characteristics. The categorical approach utilizes DSM as well as ICD (International Classification of Disease) tool. DSM gives detail on specific terms of disorder and ICD aids in identifying symptoms of disorder (American Psychiatric Association, 2013). The Categorical approach deals with the problem of disease sensitivity and comorbidity by diagnosing mental disorder from typical symptoms during mental health assessment. This process is based on the assumption that different pattern of thoughts and behavior can be organized into different categories of mental disorder. Thus, its sensitivity lies in organizing discrete illness and producing the diagnosis in similar situation. Despite these strengths, this approach has low inter reliability, lots of problem due to overlapping of symptoms. This makes the diagnosis difficult (Ragland & Solomon, 2016). Due to this problem, clinicians have shifted to combining dimensional approach with existing categorical approaches. With this approach, clinicians can quantify a characteristic of disease based on using numerical values in different scales during disease assessment. The benefits of this approach lies in the fact that that it not only helps in identifying the presence of particular disorder but also aids in evaluating the degree of the condition a patient is suffering from (Shedler & Westen, 2014). A clinicians can evaluate this by the question ‘how much?’ to determine the level of severity of the disorder. Thus, in addition to categorical approach, it also takes into account various factors to get access to detailed information on each symptom. Instead of just labeling a disease, dimensional approach facilitates creation of a disease profile for specific patients. However, in relation to disease sensitivity and comorbidity analysis, much more time is consumed in getting each score. Dimensional approach aims to enhance diagnostic precision of psychiatric illness. Dimensional scale measurement will allow better conceptualization and assessment of etiology and psychiatric syndrome. Challenges in user acceptability may occur with this approach because of interpreting underlying mechanism of disease (Cuthbert & Insel, 2013). 2. Autism spectrum disorder is a neurophysiological disorder that impairs social interaction, communication and cognitive development of affected person. Other diagnostic features are poor social development, reduced interest and repetitive behavior. This disease may be caused by genetic or hormonal factors. According to mind blindness theory of autism, children with autism syndrome have delayed development of feelings and thought. Hence, a degree of mind blindness is present in affected person. They find it difficult to interpret others behavior and reduced rate of joint attention. Just et al., (2013) has suggested that this inability to identify mental states of self and other individual occurs because of brain abnormality and it occurs due to weak connection between medial prefrontal region and the posterior superior temporal region. Thus minblindness theory highlighted the social impairment in patients with autistic spectrum but it did not described about non-social characteristics of autism. Another limitation is that this theory is not specific to autism only. Another advanced theory called the emphathising-systemising (E-S) theory explains the combination of both social and non-social characteristics are present in people with autism spectrum disorder. It states that neurological disorder occurs not just because of lower empathy (E), but also because of below-average psychological factor (systemizing-S). Thus, inconsistency between E and S determines whether a person has autism spectrum disorder or not. Sabet et al., (2015) suggest that autistic people have exaggerated form of connectivity in each hemisphere and decreased inter-hemispheric connectivity due to small corpus callosum. Thus, increased interconnectivity disorder is found in specific area of brain in individual with the illness. The E-S theory was further developed by the extreme male brain theory of autism (EMB) which states that females perform better in emphasizing activities and males perform better in systemizing activities. Wen & Wen, (2014) demonstrated that 54% males have systemizing brain while 44% females have brain with empathy activity. People with autism have smaller brain regions like thalamus, prefrontal cortex and superior gyrus compared to normal males. Besides this, normally size of male brain is larger than females, but in people with autism condition have even more larger brain than males. Thus this theory is useful in explaining why increases number of males develops the diseases compared to females.   3. Attention Deficit Hyperactivity Disorder (ADHD) is a disorder of the brain associated with inattentiveness and hyperactivity that interferes with cognitive development of individuals. Inattention is related to difficulty in sustaining focus, hyperactivity relates to extreme restlessness and impulsivity makes the person socially intrusive without considering the potential harm of the action (DuPaul & Stoner, 2014). Because of the possible symptoms seen in ADHD, many people think ADHD is a societal invention and caused by indiscipline in social life of people. It may be related to presence of distressing family life or environment, struggles in life or watching too much television. However, research suggests that ADHD is caused mainly due to genetic disorder along with interaction of environmental factors. Despite this, the social constructionist theory suggests that there is no clear pathophysiology of the condition. While evidence have suggested difference in brain structure between ADHD and normal patients, the genetic viewpoint is that genetic is responsible for about 75% of ADHD cases in patient. There is great argument regarding the real medical diagnosis of ADHD. There is no set criterion to determine the disease; it is mainly dependent on behaviors like hyperactivity and impulsivity. This behavior depend is context dependent and have no real origin (Roskam et al., 2014). Lead exposure in children might be a factor that affects brain development in children. The social construct theory of ADHD also suggest that it is mainly caused by environmental factors such as living in enclosed spaces, increased stress and burden from family (Bunford et al., 2015). It is also a result of conformity to strict social behavior such as in classroom or due to attachment with video games and computer. This can be found in workplace too due to long sitting hours and too many tasks. Hence, there is a need to make right choices and strategies and just not indulge in following societies rule against one’s own will.   4. Schizophrenia is a mental illness that has impact on how an individual behave, think and feel. Such person may face difficulty in assessing what is real and what is artificial. This chronic disease occurs due to structural changes in the grey and white matter of brain. Changes in the cortical region take place prior to the first manifestation of schizophrenia. Brain structure changes overtime with gradual ventricular enlargement and decrease in hemispheric volume. The superior temporal gyrus region of the brain which is involved in processing language is mainly affected and this lead to the development of symptoms of the disease. A study on people with schizophrenia has showed that mostly changes take place in the temporal and frontal lobe of brain and people with these changes later develop schizophrenia. Anomalies in brain structure are seen both in grey matter and white matter. The connection related to processing of language is disrupted and myelination in this region takes place (Kong et al., 2012). Psychological changes take place prior to onset of symptoms of schizophrenia. This occurs due to changes in brain structure particularly prefrontal lobes of the brain. Prefrontal lobe is extremely responsive to environmental stress. This leads to the manifestation of psychological changes such as memory impairment, hallucinations, delusions, inattentiveness and many others (Kahn & Keefe, 2013). After the manifestation of schizophrenia, neurological changes take place due to abnormal brain chemistry. Brain structure impairs in patients with schizophrenia and it is mainly associated with enlarged brain ventricle leading to decrease in brain tissue volume. The frontal lobe is the region which is associated with decision making and reasoning property in people, but in people with the condition, low function is seen in the frontal lobe (Hirjak et al., 2014). Psychological changes are associated with loss of emotional function reduced ability to express and plan things in life. People struggle in sustaining to activities (Frith, 2014). 5. Endophenotypes are the term used to classify behavioral symptoms on the basis of clear phenotypes and identification of possible genetic connection. It helps to different between symptoms for diseases like ADHD, Alzheimer’s and many others. In case of people with schizophrenia, the most visible symptoms is psychosis which is associated with personality changes, abnormal behavior and low level of social interaction. However the distinct phenotype of the illness is overload of stimuli and impaired memory. As these phenotypes have clear genetic connections too, that is why they have been identified as endophenotypes of schizophrenia. These phenotypes reflect the neurobiological mechanism of the disease that represents the most overt symptoms of schizophrenia. The genes involved in endophenotypic traits in schizophrenia include RELN, FABP7 and CHRNA7. They are linked to schizophrenia phenotype of prepulse inhibition. It is a phenomenon which weak prestimulus inhibits the reaction of individual to stronger stimulus. The criteria involve in assessment of endophenotypes of psychiatric disorder is that the endophenotype should be associated with specific illness; it should be heritable and present in individuals despites their clinical status. Other criterion is it should be separated from other symptoms of illness (Ross, & Freedman, 2015). As psychiatric illness is mostly associated with multiple risk factors, one endophenotypes related to the mechanism of illness most frequently develops. In schizophrenia brain changes occurs throughout the life span. One endophenotype that is useful to detect the risk of schizophrenia is sensory gating which is a process of filtering out unnecessary stimuli from other environmental stimuli (Ripke et al., 2013).     6. Down syndrome and Alzheimer’s disease are inter-related as the both the disease have common genetic condition. Down syndrome is a genetic chromosome 21 disoredr which leads to physical disability, developmental problem, delay in intellectual development and other diseases. On the other hand, Alzheimer’s is a neurophysiologic disorder that leads to memory loss and serious intellectual disorder affecting daily life activities. There is a connection between the two disease and children with Down syndrome at more risk of Alzheimer’s disease when they grow up.  People who suffer from Alzheimer’s are also more likely to develop dementia which is related to impairment of cognitive function such as reasoning and thinking ability. The link between the two diseases is the extra copy of chromosome 21. Chromosome 21 carries the APP genes which codes for APP (Amyloid precursor protein). In people with Down syndrome, excess amount of APP protein leads to development of beta-amyeloid plaques in brain. This interferes with normal functioning of brain and creates risk of Alzhemier’s disease and dementia. About 50% of patients with Down’s syndrome develop the brain plaques and eventually develop dementia due to Alzheimer’s disease by the time they reach the age of 70 years (Hartley et al., 2015). People with Down syndrome above 40 years develop numerous plaques and neurofibrillary tangles and there is maximum chance of pathophysiology of Alzheimers disease. These plaques contain beta-amyloid peptide from APP genes. In Down syndrome, over expression of APP takes place and amyloid-beta is major factor in the pathogenesis of Alzheimer’s disease. Amyloid-beta is neuronal in origin and localized in endosomes. People with Down syndrome also have increased oxidative stress compared to normal people (Elizabeth Head, 2012). 7. Neural development is the process that provides insight into the cellular and molecular mechanism involved in nervous system development. Neurotrophins are group of protein that facilitates the development and function of neurons. These protein molecules regulate cell division and overgrowth of neurite. The neurotrophins binds to particular tyrosine kinases receptor that induces dimerization and auto-phophorylation of receptors. It leads to the formation of a complex of receptor and neurotrophin which is endocytosed. This complex is then transported to the soma (Neural migration). In between the process, it initiates signal transduction cascade that inhibits the apoptosis of genes and thus neural cell survives eventually. Other examples of neurotrophin factors that promote survival of neuron include nerve growth factor (NGF), neurtrophin-3, fibroblast growth factor and many others (Park & Poo, 2013). Another type of neurotrophin is the brain-derived neurotrophic factors that play an important role in synapse plasticity and development of brain. A recent study demonstrated its role in synapse formation and plasticity. Synapse formation is promoted by regulating the axon morphology and increasing the number of excitable synapse and inhibitory synapse. It also enhances the number of functional synapses by the facilitating the maturation of those cellular components that triggers the release of neurotransmitter. This long term modification will be crucial in providing synaptic plasticity to an individual (Harrington & Ginty, 2013). Neurulation is the process of development of neural tube (embryo’s central nervous system) from the embryo. The human brain development initiates from the third week of gestation period and it progressed to differentiation of neural progenitor cells. Neurotrophic factors play a role in this development by acting against the apoptosis cascade. It target distinct neurons at synaptic connection and makes connection with target cells. These factors are present in embryo during gastrulation and neurulation process. Neurotrophin-3 is expressed in the neural tube and tyrosine kinase C (TrkC) is present in the neural plate. A neural tube differentiates TrkC gets localized in specific region of the tube. Thus neurotrophic factors and TrkC plays a role in early neural development (Davis, 2014).             8. Meiosis is a type of cell division that divides the chromosome number by half and enables sexual recombination in organisms. It produces four gamete cells and the number of orginal chromosome is restored back in the offspring. The diploid parent cell consists of two chromosome copies. It divides to form four haploid cells which have half the number of original chromosome. The first meiotic division is called meiosis I. The first stage in this case is the prophase I where the chromatin fibre condenses to form sister chromatids. It is then followed by condensation of chromosome into tetrad structure in the prophase I. This pair of chromosome exchanges their DNA by recombination process. During Metaphase I the chromosome pair aligns at the centre of the cell and the centriole moves towards the poles. The spindle fibre is formed which attaches to the chromosome. In the next stage which is the anaphase I, the spindle fibres pull each chromosome towards the poles. During Teleophase I the chromosomes are arranged in nuclei and cytokinesis takes place which leads to formation of two separate daughter cells. This phase is followed by meiotic division of haploid cells called Meiosis II. In prophase II new set of spindle fibres are formed and they align the equatorial plate in Metaphase II.  In the Anaphase II, sister chromatids are pulled apart and chromosomes are enclosed in nuclear membrane in telophase II. This is followed by cytokinesis and results in formation of four haploid daughter cells that develop into a sperm or egg cells (Wang et al., 2015). There are key steps in meiosis where there is chance of spontaneous mistakes. The genetic constitution is altered and the and unexpected crossing over leads to increased genetic variability in a population. The crossing over of sister chromatids occurs during metaphase I and random alignment of chromosomes gives rise different gene combination in the offspring. In rare cases, failure to separate homologous chromosomes lead over accumulation of chromosome in one cell and lack of chromosome in another cell. This process of non-disjunction of chromosomes leads to production of gametes with odd number of chromosomes. It may give rise to variety of syndromes like Kleinfelter’s syndrome, Turner’s syndrome, and other syndrome (Marchett et al., 2015). Mitosis is a multi-step process during which chromosome is divided into two daughter cells. The first phase is called karyokinesis where nuclear division takes place. It consist of five phases mainly prophase, metaphase, anaphase and telophase. The second phase is called cytokinesis wherein cytoplasmic components separate into two daughter cells. Due to error in mitosis, two types of errors occur and it has benign or deadly consequences. Silent mutation can occur where no change in DNA sequence is found or missense mutation may occur when DNA sequence are changed. This type of mutations may lead massive disruption in cell cycle and formation of tumours. Chromsomal abnormalities may also take place when chromosomes fail to attach to spindle fibres and the daughter cell either has one extra or one missing copy of chromosome after division. It leads to disorders like Down syndrome, Alzheimer disease and may other condition (Yoshida et al., 2013).   9. Rett syndrome is a rare neurological disorder of the brain that mainly affects girls. Its clinical manifestation includes small hand and foot, decreases size of head called microcephaly, repetitive hand movements and many others. It occurs due to mutation in the X chromosome; however its clear pathophsyiology is not clear. Autisms spectrum disorder is group of developmental disorders that affects normal life activities. Due to the wide range of symptoms associated with autism, the common concept of autism spectrum disorder came up. It impairs social interaction, verbal and non-verbal communication skills, behavior and specific interest of a child. Great debate exists regarding whether Rett syndrome should be classified as autism spectrum disorder or not. I feel that it can be classified as autism spectrum disorder because there is overlap of symptoms between the two diseases. In order to better understand the two disease and the type of neuropathological development in both case, a study was done that measures the symptoms using autism behavior checklist (ABC) in group girls with Rett syndrome. This data was then compared with girls with severe mental retardation. In relation to motor ability and development level, Rett syndrome scored higher than sever autism due to sensory scales. The Rett syndrome originally came in the 4th edition of Diagnostic and Statistical manual of mental disorder (DSM-4). Other diseases in this group included Asperger syndrome and childhood disintegrative disorder. Rett syndrome can be classified as autism spectrum disorder because certain medical characteristic of the disease is same as symptoms for autism. DSM-5 is related to new disorder which is completely different from autism and called as social communication disorder. Acccording to this Rett syndrome may not come under DSM or autism spectrum disorder at all. This is because if symptoms of mental disorders like anxiety and depression is not present in Rett syndrome, then it will not be diagnosed under DSM diagnosis of mental illness. This change is related to new guidelines for mental disorder classification (Huguet et al., 2013).     10. On the other hand, dyscalculia is associated with difficulty in comprehension of numbers and facts in mathematics. It can occur in all age group of people. This mathematical disability may be caused by injury in the brain. It is caused by a difference in the function and structure of the region of brain involved with mathematics. Butterworth & Kovas, (2013) suggest this inefficiency may occur due to lesser grey matter in brain cells or reduced brain activity in the region of the brain that processes mathematics such as the intra parietal sulcus region. A brain imaging study showed that in children with dyscaclculia, there is decreased activity in parietal and frontal lobe of the brain involved with mathematical cognition. Damge or injury to parietal lobe also leads to this condition. The similarity in the two diseases lies in the fact both are learning disability and associated with structural and functional changes in brain. Due to the symptoms, dyslexia is often confused with dyscalculia. While dyslexia is the most common type of learning disorder, dyscalculia impairs writing, reading and number interpretation in children too (Lander et al., 2013). Thus these all categoreiies of ADHD that is related to behavioral disorder that occurs due to overactivity and impulsivity.   Reference American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub. Bunford, N., Brandt, N. E., Golden, C., Dykstra, J. B., Suhr, J. A., & Owens, J. S. (2015). Attention-deficit/hyperactivity disorder symptoms mediate the association between deficits in executive functioning and social impairment in children. Journal of abnormal child psychology, 43(1), 133-147. Butterworth, B., & Kovas, Y. (2013). Understanding neurocognitive developmental disorders can improve education for all. Science, 340(6130), 300-305. Cuthbert, B. N., & Insel, T. R. (2013). Toward the future of psychiatric diagnosis: the seven pillars of RDoC. BMC medicine, 11(1), 1. Davis, M. I. (2014). Neurotrophic Factors and Ethanol Neurotoxicity. InHandbook of Neurotoxicity (pp. 1671-1732). Springer New York. DuPaul, G. J., & Stoner, G. (2014). ADHD in the schools: Assessment and intervention strategies. Guilford Publications. Elizabeth Head, F. (2012). Alzheimer’s Disease in Down Syndrome. European Journal Of Neurodegenerative Disease, 1(3), 353. Retrieved from Frith, C. D. (2014). The cognitive neuropsychology of schizophrenia. Psychology Press. Harrington, A. W., & Ginty, D. D. (2013). Long-distance retrograde neurotrophic factor signalling in neurons. Nature reviews Neuroscience,14(3), 177-187. Hartley, D., Blumenthal, T., Carrillo, M., DiPaolo, G., Esralew, L., Gardiner, K., … & Lott, I. (2015). Down syndrome and Alzheimer’s disease: Common pathways, common goals. Alzheimer’s & Dementia, 11(6), 700-709. Hirjak, D., Wolf, R. C., Stieltjes, B., Hauser, T., Seidl, U., Schröder, J., & Thomann, P. A. (2014). Cortical signature of neurological soft signs in recent onset schizophrenia. Brain topography, 27(2), 296-306. Huguet, G., Ey, E., & Bourgeron, T. (2013). The genetic landscapes of autism spectrum disorders. Annual review of genomics and human genetics,14, 191-213. Just, M. A., Keller, T. A., & Kana, R. K. (2013). A theory of autism based on frontal-posterior underconnectivity. Development and brain systems in autism, 35-63. Kahn, R. S., & Keefe, R. S. (2013). Schizophrenia is a cognitive illness: time for a change in focus. JAMA psychiatry, 70(10), 1107-1112. Kong, L., Bachmann, S., Thomann, P. A., Essig, M., & Schröder, J. (2012). Neurological soft signs and gray matter changes: a longitudinal analysis in first-episode schizophrenia. Schizophrenia research, 134(1), 27-32. Landerl, K., Göbel, S. M., & Moll, K. (2013). Core deficit and individual manifestations of developmental dyscalculia (DD): the role of comorbidity.Trends in neuroscience and education, 2(2), 38-42. Marchetti, F., Bishop, J., Gingerich, J., & Wyrobek, A. J. (2015). Meiotic interstrand DNA damage escapes paternal repair and causes chromosomal aberrations in the zygote by maternal misrepair. Scientific reports, 5. Park, H., & Poo, M. M. (2013). Neurotrophin regulation of neural circuit development and function. Nature Reviews Neuroscience, 14(1), 7-23. Ragland, J. D., & Solomon, M. (2016). Categorical Dimensions of Social Impairment and Disrupted Functional Connectivity in Autism Spectrum Disorders: When Does Continuous Become Discrete?. Biological Psychiatry,80(2), 90-91. Ripke, S., O’Dushlaine, C., Chambert, K., Moran, J. L., Kähler, A. K., Akterin, S., … & Kim, Y. (2013). Genome-wide association analysis identifies 13 new risk loci for schizophrenia. Nature genetics, 45(10), 1150-1159. Roskam, I., Stievenart, M., Tessier, R., Muntean, A., Escobar, M. J., Santelices, M. P., … & Pierrehumbert, B. (2014). Another way of thinking about ADHD: the predictive role of early attachment deprivation in adolescents’ level of symptoms. Social psychiatry and psychiatric epidemiology, 49(1), 133-144. Ross, R. G., & Freedman, R. (2015). Endophenotypes in schizophrenia for the perinatal period: criteria for validation. Schizophrenia bulletin, 41(4), 824-834. Sabet, J., Underwood, L., Chaplin, E., Hayward, H., & McCarthy, J. (2015). Autism spectrum disorder, attention-deficit hyperactivity disorder and offending. Advances in Autism, 1(2), 98-107. Shedler, J., & Westen, D. (2014). Dimensions of personality pathology: an alternative to the five-factor model. American Journal of Psychiatry. Wang, S., Zickler, D., Kleckner, N., & Zhang, L. (2015). Meiotic crossover patterns: obligatory crossover, interference and homeostasis in a single process. Cell Cycle, 14(3), 305-314. Wen, W., & Wen, S. W. (2014). Expanding upon the ‘extreme male brain’theory of autism as a common link between other major risk factors: A hypothesis. Medical hypotheses, 82(5), 615-618. Yoshida, K., Toki, T., Okuno, Y., Kanezaki, R., Shiraishi, Y., Sato-Otsubo, A., … & Kon, A. (2013). The landscape of somatic mutations in Down syndrome-related myeloid disorders. Nature genetics, 45(11), 1293-1299.

Basic features

  • Free title page and bibliography
  • Unlimited revisions
  • Plagiarism-free guarantee
  • Money-back guarantee
  • 24/7 support

On-demand options

  • Writer's samples
  • Part-by-part delivery
  • Overnight delivery
  • Copies of used sources
  • Expert Proofreading

Paper format

  • 275 words per page
  • 12pt Arial/Times New Roman
  • Double line spacing
  • Any citation style (APA, MLA, CHicago/Turabian, Havard)

Guaranteed originality

We guarantee 0% plagiarism! Our orders are custom made from scratch. Our team is dedicated to providing you academic papers with zero traces of plagiarism.

Affordable prices

We know how hard it is to pay the bills while being in college, which is why our rates are extremely affordable and within your budget. You will not find any other company that provides the same quality of work for such affordable prices.

Best experts

Our writer are the crème de la crème of the essay writing industry. They are highly qualified in their field of expertise and have extensive experience when it comes to research papers, term essays or any other academic assignment that you may be given!

Calculate the price of your order

You will get a personal manager and a discount.
We'll send you the first draft for approval by at
Total price:

Expert paper writers are just a few clicks away

Place an order in 3 easy steps. Takes less than 5 mins.

error: Content is protected !!
Open chat
Need Homework Help? Let's Chat
Need Help With Your Assignment? Lets Talk