Chronic Traumatic Encephalopathy - Research Paper Example

CHRONIC TRAUMATIC ENCEPHALOPATHY: A Clinical Case Review PSYC 4080 Somayya Saleemi Dr. Mary E. Desrocher June 30, This researchpaper was completed for PSYC 4080 Section A of Neurospychology of Abnormal Behavior taken with Mary E Desrocher. 1. Introduction Epidemiology Concussion or mild traumatic brain injury (mTBI) is one of the most widespread neurologic disorders that compose around 90% of all brain injuries (Saulle & Greenwald, 2012, p.1). These injuries are common among athletes, in that an estimated of 1.6 to 3.8 million report of sport-related concussion every year in the United States of America alone (Langlois, Rutland-Brown, & Wald, 2006, as cited in Saulle & Greenwald, 2012, p.1). The statistics, nevertheless, is hardly accurate because there could be more, since many athletes do not seek medical attention, or exhibit symptoms, possibly because head trauma is benign and some injuries are not properly diagnosed (Baugh et al., 2012, p.2; Story & Attix, 2010, p.2). DeKosky et al. (2010) stated in their report that, every year, more than 1.5 million Americans have mTBI without being unconscious and without needed hospitalization and that an equal number developed conscious impairing trauma but inadequately severe enough to need long-term hospitalization. At present, the ensuing tauopathy, called chronic traumatic encephalopathy (CTE), has only been observed in individuals with a history of repetitive brain trauma (Stern et al., 2011, p.S461). Dr. Harrison Martland was the first to describe CTE in 1928 when he observed the same symptoms among boxers (Saulle & Greenwald, 2012, p.1). In an article that he wrote for the Journal of the American Medical Association, “Punch Drunk,” he depicted the boxers as “cuckoo,” “goofy,” “cutting paper dolls,” or “slug nutty” (Saulle & Greenwald, 2012, p.1). “Punch drunk” was soon called “dementia pugilistica” where it literally means, “dementia of a fighter” (Saulle & Greenwald, 2012, p.1). The development of active contact sports, nevertheless, showed similar symptoms, and so dementia pugilistica was changed to chronic traumatic encephalopathy in the 1960s (Saulle & Greenwald, 2012, p.1). CTE became popular because of its connection with American sports, such as football, hockey, soccer, boxing, and professional wrestling (Shively et al., 2012, p.3). Affected athletes, many of them retired, struggled later on because of depression, substance abuse, anger, memory and motor problems, and suicide (Saulle & Greenwald, 2012, p.1). Autopsy results that were done on these athletes showed a connection between these emotional, cognitive, and physical symptoms and CTE (Omalu et al., 2011, p. 179; Wortzel, Shura, & Brenner, 2013, p.2). CTE is connected to TBI. Specifically, CTE is a “progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain” (Omalu et al., 2011, p.174). CTE is manifested clinically after a long-standing latent period as a compound syndrome of mood disorders and neuropsychiatric and cognitive injury (Omalu et al., 2011, p.174). Analysis of direct brain tissue shows multifocal or diffuse tauopathy, which may come together with “low-grade and multifocal white matter rarefaction, microglial activation, and parenchymal histiocytes” (Omalu et al., 2011, p.174). Apart from multifocal or diffuse tauopathy, amyloidopathy may also be manifested (Omalu et al., 2011, p.174). CTE commonly shows with prolonged latency duration, although some patients with CTE may not demonstrate this period before clinical symptoms start (Omalu et al., 2011, p.174). Age of Onset It is not clear when CTE begins. Since majority of CTE cases are found in athletes playing in American football, boxing, soccer, and hockey, and since numerous of these athletes start their respective sports at a young age, such as between 11 and 19 years, CTE may begin at any time during this span, after the experience of repetitive blunt forces on the head (Saulle & Greenwald, 2012, p.2). McKee has neuropathologically diagnosed CTE progression in asymptomatic 18-year-old high school football player with a history of concussion (Saulle & Greenwald, 2012, p.2). The incidence of CTE is unknown, but it can differ across groups depending on sport position, duration of career, number of head injuries, age of first head injury, and genetics (Anderson, 2014, p.1; Macciocchi, 2010, p.2). Risk Factors CTE has been linked with athletes who partake in contact sports like American football, boxing, hockey, soccer, and professional wrestling (Saulle & Greenwald, 2012, p.2). A number of other sports that are not directly related with CTE, but have well-researched cases of concussion are mixed martial arts, rugby, and horseback riding (Costanza et al., 2011, p.3). Other groups at risk for recurring head trauma and CTE are military veterans, epileptics, and victims of domestic abuse (McKee et al., 2009, p.2). Though every group mentioned have the similarity of head trauma, their differences lie in specific dimensions that impact the severity or chronicity of their injury. See Table 1. Apart from repeated concussive head impacts, some of the risk factors of CTE are the following: length of career and total number of bouts for boxers, age of retirement, increased sparring (for contact sports), Caucasian race, poor performances and slugging type fighters, history of head concussion, epileptics, victims of domestic abuse, genetic variations, such as in ApoE ε3 or ApoE ε4 genotype (Baugh et al., 2012, p.5; Costanza et al., 2011, p.3; Saulle & Greenwald, 2012, p.2; Shively et al., 2012, p.4), and if TDP-43 immunoreactivity is found in the cerebral cortex (McKee et al., 2010, p.3). Table 1: Risk Factors Associated with Chronic Traumatic Encephalopathy Source: Saulle & Greenwald (2012, p.2) 2. Clinical Presentation Current Case Study The patient is John Doe, who first went to his GP in 2006 to complain about initial symptoms of poor concentration and attention, disorientation, dizziness, and headaches. He also expressed extreme irritability, outbursts of violence, aggressive behavior, and confusion. His doctor referred him to a psychiatrist. In 2009, John experienced deficits in memory and judgment and judgment. He also reported worsened cognitive and social functioning that resulted to poor money management, bankruptcy, social phobias, paranoid ideation, and insomnia. He was increasingly quiet and fearful with paranoid tendencies. Sometimes, he acted confident and approachable, but at times, he was socially withdrawn. He was referred to a neuropsychologist for further assessment. In 2011, his new symptoms are motor problems, profound muscle weakness, muscle atrophy, spasticity, poor speech, ocular abnormalities, vertigo, bradykinesia, and deafness. He was referred to a neurologist. In 2013, John was observed as showing Parkinsonism, ataxia, antalgic gait, and dysarthric speech. He also exhibited Parkinsonian symptoms of tremors, masked facieses, poor speech, and dementia. By this time, he was suspected to have CTE and MND. In 2014, John was found on a couch with altered mental status, and he died at a local hospital several hours later. Signs and Symptoms (Early and Late) CTE description describes gait disorders, speech slowing and extrapyramidal signs, neuropsychiatric and behavioral symptoms reportedly predominate early and are prominent throughout the course of the condition. These neuropsychiatric symptoms include mood disorder (mainly depression), paranoia, agitation, social withdrawal, poor judgment and aggression. Cognitive impairment tends to emerge later and typically includes impairment across the domains of orientation, memory, language, attention, information processing speed and executive functioning. Less characteristic of classic CTE, cognitive impairment in CTE reportedly progresses over time. Disease staging and disease phenotypes of CTE have now been proposed based on the level of neuropathological evidence of disease on autopsy rather than clinical presentation. It may be that the description of CTE symptomatology is confounded by the retrospective nature of the datacollection and the heavily biased case selection. Consequently, the reported clinical observations (ie, suicidality, emotional lability, aggression and disinhibition) are likely to be skewed by selection bias. Neurological Effects The neurologic examination is a cornerstone of a dementia workup. CTE is believed to cause signs and symptoms of neurological dysfunction that can affect balance,, gaze, mental status, and movement. McKee et al, discovered in their 51 neuropathically verified CTE cases that evidence of reported movement abnormalities in 21 (41%) of the 51 cases, including Parkinsonism in 18 cases. Neuropsychological and Neuropsychiatric Effects The cognitive and behavioral symptoms associated with CTE are reflective of the regions that have been pathologically determined to be most affected by CTE. As will be explained in further detail in the neuropathology section of this paper, the regions of the brain most severely damaged by CTE include the cerebral cortex and the medial structures of the limbic system (amygdala, mammillary bodies, hippocampus, etc.) (Gavett et al. 2011a; Stern et al. 2011a). The severity of the clinical manifestation progresses through the course of the disease as the neurodegeneration increases (Stern et al. 2011a). The neuropsychological and neuropsychiatric changes associated with CTE can be classified into the categories of cognition, mood, and behavior. CTE presents with changes in each branch of this symptom triad and the severity of the symptoms appears to progress with the course of the disease. These symptoms generally begin years or decades after repeated brain trauma, when the neurodegeneration is severe enough to manifest clinical symptoms (Stern et al. 2011a). The earliest neuropathological stages of CTE may present without clinical symptoms (Stern et al. 2011a). Early cognitive symptoms primarily include learning and memory impairment as well as executive dysfunction. Mood changes typically include depression, apathy, and irritability, as well as suicidality. The behavioral changes primarily include poor impulse control, with individuals described as having a “short fuse” or being “out of control.” Aggression and increased violence are often experienced. Disinhibition and problems with substance and other forms of abuse also occur. Later in the disease course, these cognitive, mood, and behavioral impairments worsen, with dementia evident in all older cases (i.e., 65 years or greater) with advanced stage CTE. As with most neurodegenerative causes of dementia, the later in the course a patient with CTE is seen, the more difficult it is to differentiate the specific underlying disease based on clinical presentation. That is, once an adequate amount of neural tissue is destroyed, differential diagnosis of most cases of moderate-severe dementia is difficult just based on current presentation. However, the early presentation and course of CTE can distinguish it from most other causes of dementia. The closest symptom profile to CTE is that caused by FTLD, behavioral variant. The symptoms of FTLD typically begin between the ages of 45–65, there is a somewhat rapid symptom progression, and there is a positive family history in approximately 40 % of cases. In contrast, the early symptoms of CTE (Table 1) typically present between the ages of 30 and 50, there is a slow, prolonged course of progression, and there does not appear to be a familial risk. Although not a completely definitive method of distinguishing between CTE and FTLD behavioral variant, all cases of CTE will have had a history of exposure to repetitive brain trauma, whereas FTLD will not typically have such a history Radiological Effects Functional Magnetic Resonance Imaging (fMRI) has been useful in understanding brain-behavior relationships in numerous neurologic diseases (Seeley et al. 2009). Additionally, blood oxygen level dependent (BOLD) fMRI has been able to differentiate between various types of neurodegeneration including AD, FTD, and dementia with Lewy bodies (Galvin et al. 2011; Zhou et al. 2010). Recent studies of high school football players have utilized fMRI and found significant changes (from pre-season to post-season) in fMRI results in those athletes with repetitive subconcussive hits (as determined by helmet accelerometer data) (Talavage et al. 2010). Given its current uses, it is possible that fMRI will be helpful in determining brain-behavior associations in CTE as well as differentiating CTE from other neurodegenerative disorders (Gavett et al. 2011b). 3. Diagnosis The fundamental neuropathologic feature of CTE is the presence of sparse, moderate, or frequent band-shaped, flameshaped, small globose, and large globose NFTs in the brain accompanied by sparse, moderate, or frequent neuritic threads (NTs). For CTE diagnosis, the quantitative classification of NFT and NT topographic sparse, moderate, and frequent distribution are based on the CERAD plaque density scoring system.14 Ghost tangles may accompany NFTs and NTs in different regions of the brain. NFTs and NTs are differentially and topographically distributed in the neocortex, subcortical nuclei/ basal ganglia, hippocampus, brainstem, and cranial nerve nuclei including neurotransmitter synthesizing nuclei: dorsal raphe nucleus, locus ceruleus, basal nucleus of Meynert, substantia nigra. The cerebral cortex revealed a ‘‘skip phenomenon’’ whereby NFTs and NTs were completely absent in many areas in the cortex and were intermittently present in many areas in the cortex, within the same lobe, in a multifocal randomly situated fashion, located in both the gyri and sulci, without any observable consistent pattern. The skipped areas of the cortex were frequently located adjacent to areas with NFTs and NTs. For the multifocal areas of the cortex with NFTs and NTs, the NFTs and NTs were quantitatively distributed from sparsely to frequently. 4. Pathophysiology Overall Autopsy Gross Neuropathology The gross changes of CTE are typically observed in late-stage disease. Advanced cases of CTE demonstrate generalized atrophy, most prominent in the frontal and medial temporal lobes; enlargement of the lateral and third ventricles; cavum septum pellucidum; and septal fenestrations. There also may be thinning of the hypothalamic floor, shrinkage of the mammillary bodies, and atrophy of the hippocampus, entorhinal cortex, and amygdale (Stern et al., 2011). Microscopic Neuropathology CTE is characterized by a unique pattern of microscopic changes. There are extensive tau-immunoreactive neurofibrillary tangles (NFT), neuropil neurites (NT), and glial tangles (GT) in the frontal and temporal cortices. Unlike Alzheimer disease (AD) or many other tauopathies, the tau immunoreactive abnormalities tend to cluster at the depths of sulci, around small blood vessels, and in superficial cortical layers. In advanced cases, there are tau-immunoreactive inclusions in the limbic and paralimbic regions, diencephalon, brainstem, and subcortical white matter. The specific soluble and insoluble tau isoforms found in CTE are indistinguishable from those found in AD, and the ratio of tau isoforms with 4 versus 3 microtubule binding repeats is approximately 1 in both diseases. Importantly, these changes seen in CTE usually occur in the relative absence of beta-amyloid (A!) deposits. In addition to the widespread tau immunoreactivity, the majority of CTE cases also are marked by TDP-43 proteinopathy. The TDP-43 inclusions can be widespread and are typically found in the brainstem; basal ganglia; diencephalon; medial temporal lobe; frontal, temporal, and insular cortices; and subcortical white matter. In a subset of individuals with CTE, abundant TDP-43 immunoreactive inclusions and neurites are found in the anterior horns of the spinal cord and motor cortex, combined with corticospinal-tract degeneration, loss of anterior horn cells of the spinal cord, and ventral root atrophy. These individuals develop a progressive motor neuron disease that appears very similar to amyotrophic lateral sclerosis (ALS) and is characterized by profound weakness, muscular atrophy, spasticity, and fasciculations. The fact that an ALS-like condition is found in some individuals with CTE suggests that some forms of clinical ALS may be associated with TBI. 5. Histopathological Classification (4 distinct stages) 6. Clinicopathological Correlations The distribution of the tau abnormalities in CTE suggests distinctive core pathology within the amygdalo-hippocampal-septo-hypothalamic-mesencephalic continuum, i.e. the Papez circuit. The early involvement of these anatomical regions, sometimes referred to as “emotional” or “visceral” brain, may underlie many of the early behavioral symptoms, including the tendency toward emotional lability, aggression and violent outbursts. The early involvement of the hippocampus, entorhinal cortex and medial thalamus may explain episodic memory disturbance as a frequent presenting symptom. Neurofibrillary degeneration of the frontal cortex and underlying white matter most likely contributes to the dysexecutive symptoms. Although less common and generally less severe, neurofibrillary degeneration in the dorsolateral parietal, posterior temporal, and occipital cortices likely accounts for the visuospatial difficulties. The parkinsonian features found in 42% of cases are likely due to degeneration of the substantia nigra pars compacta. The gait disorder, variously described as staggered, slowed, shuffled, or frankly ataxic, may result from a combination of cortical and subcortical frontal damage, degeneration of cerebellar tracts in the brainstem, direct cerebellar injury, as well as Parkinsonism from substantia nigra pathology. Similarly, speech abnormalities, most often described as slowed and slurred, likely reflect multiregional degeneration. Symptoms of dysarthria, dysphagia, and ocular abnormalities probably result from degeneration of brainstem nuclei, e.g. the hypoglossal and oculomotor nuclei (McKee et al., 2009, p.9). 7. Neurological Sequelae Historically amyotrophic lateral sclerosis (ALS) has been thought to be a sporadic disease with no single causative factor (Saulle). Literature has reported risk factors to include trauma to the brain or spinal cord, strenuous physical activity, exposure to heavy metals, cigarette smoking, radiation, electrical shocks, and pesticides. Given these risk factors, the literature strongly correlates a history of head trauma with increased incidence of ALS. In a case control study, Chen et al. reported that having repeated head trauma within the 10 years prior to diagnosis had a 3-fold higher risk of ALS. The same group also did a meta-analysis of 8 ALS studies and estimated a pooled odds ratio of 1.7 (95% CI: 1.3, 2.2) for at least one previous head injury. Another study reported increased ALS incidence and mortality in professional Italian soccer players when compared to the general population. Additionally, an incidence study of 7,325 Italian professional soccer players showed an ALS incidence 6.5 times higher than expected. 8. Treatments and Prevention Clearly, the easiest way to decrease the incidence of CTE is to decrease the number of concussions or mild traumatic brain injuries (McKee et al., 2009, p.12). In athletes this is accomplished by limiting exposure to trauma, for example, by penalizing intentional hits to the head (as is happening in football and hockey) and adhering to strict “return to play” guidelines. Proper care and management of mild traumatic brain injury in general and particularly in sports will also reduce CTE. No reliable or specific measures of neurological dysfunction after concussion currently exist, and most recommendations are centered on the resolution of acute symptoms such as headache, confusion, sensitivity to light, etc. Asymptomatic individuals have been shown, however, to have persistent decreases in P300 amplitudes in response to an auditory stimulus at least 5 weeks after a concussion, thereby casting doubt on the validity of the absence of symptoms as a guidepost. Neuropsychological tests have also helped provide estimates of the appropriate time for athletes to return to practice and play. Studies using event-related potentials, transcranial magnetic stimulation, balance testing, multitask effects on gait stability, PET, and DTI MRI have all shown abnormalities in concussed athletes or nonathletes with TBI lasting for 2 to 4 weeks. These studies indicate that safe return to play guidelines might require at least 4 to 6 weeks to facilitate more complete recovery and to protect from reinjury, as a second concussion occurs much more frequently in the immediate period after a concussion. In addition, experimental evidence in animals suggests that there is expansion of brain injury and inhibition of functional recovery if the animal is subjected to overactivity within the first week. 9. Ruling Out Other Diseases and Disorders Clinical Comparisons Pathological Signs CTE, AD, and FTD: pathogenetic issues Differential diagnosis between CTE, AD, and FTD: the places Neuropathology 10. Conclusion Summary Current Research Future Direction and Consideration 11. References Anderson, P. (2013, August 22). Chronic traumatic encephalopathy: 2 distinct presentations? Medscape.com, 1-4. Baugh, C.M., Stamm, J.M., Riley, D.O., Gavett, B.E., Shenton, M.E., Lin, A.,...Stern, R.A. (2012). Chronic traumatic encephalopathy: Neurodegeneration following repetitive concussive and subconcussive brain trauma. Brain Imaging and Behavior, 1-11. Costanza, A., Weber, K., Gandy, S., Bouras, C., Hof, P.R., Giannakopoulos, P., & Canuto, A. (2011). Contact sport-related chronic traumatic encephalopathy in the elderly: Clinical expression and structural substrates. Neuropathology and Applied Neurobiology, 37(6), 570–584. DeKosky, S.T., Ikonomovic, M.D., & Gandy, S. (2010). Traumatic brain injury—football, warfare, and long-term effects. New England Journal of Medicine, 363(14), 1293–1296. Gardner, A., Iverson, G.L., & McCrory, P. (2014). Chronic traumatic encephalopathy in sport: A systematic review. British Journal of Sports Medicine, 48, 84-90. Gavetta, B.E., Cantua, R.C., Shenton, M., Lin, A.P., Nowinski, C.J., McKee, A.C., & Stern, R.A. (2011). Clinical appraisal of chronic traumatic encephalopathy: Current perspectives and future directions. Current Opinion in Neurology, 24, 525–531. Lin, A.P., Ramadan, S., Stern, R.A.H., Box, N., Stanwell, P., McKee, A.C.R., Cantu, R., Nowinski, C., & Mountford, C.E. (2011). In vivo L-COSY identifies neurochemical changes in professional athletes with repetitive head injuries. Proceedings of International Society for Magnetic Resonance in Medicine, 19, 2212. Macciocchi, S. (2010). Risk and harm associated with sports concussion. National Academy of Neuropsychology, 25(2), 2-4. McKee, A.C., Cantu, R.C., Nowinski, C.J., Hedley-Whyte, T., Gavett, B.E., Budson, A.E.,… Stern, R.A. (2009). Chronic traumatic encephalopathy in athletes: Progressive tauopathy following repetitive head injury. Journal of Neuropathology & Experimental Neurology, 68(7), 709–735. McKee, A.C., Gavett, B.E., Stern, R.A., Nowinski, C.J., Cantu, R.C., Kowall, N.W., Perl, D.P., Hedley-Whyte, E.T., Price, B., Sullivan, C., Morin, P., Lee, H., Kubilus, C.A., Daneshvar, D.H., Wulff, M., & Budson, A.E. (2010). TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy. Journal of Neuropathology & Experimental Neurology, 69(9), 918–929. McKee, A.C., Stein, T.D., Nowinski, C.J., Stern, R.A., Daneshvar, D.H., Alvarez, V.E., … Cantu, R.C. (2012). The spectrum of disease in chronic traumatic encephalopathy. Brain: A Journal of Neurology, 1-22. Omalu, B.I., Bailes, J., Hamilton, R.L., Kamboh, M.I., Hammers, J., Case, M., & Fitzsimmons, R. (2011). Emerging histomorphologic phenotypes of chronic traumatic encephalopathy in American athletes. Neurosurgery, 69(1), 173-183. Omalu, B.I., DeKosky, S.T., Hamilton, R.L., Minster, R.L., Kamboh, M.I., Shakir, A.M., & Wecht, C.H. (2006). Chronic traumatic encephalopathy (CTE) in a national football league player: Case report and emerging medicolegal practice questions. Neurosurgery, 59(5), 1086-1093. Saulle, M., & Greenwald, B.D. (2012). Chronic traumatic encephalopathy: A review. Rehabilitation Research and Practice, 1-9. Shively, S., Scher, A.I., Perl, D.P., & Diaz-Arrastia, R. (2012). Dementia resulting from traumatic brain injury: What is the pathology? Archives of Neurology, 69(10), 1245–1251. Stern, R.A., Riley, D.O., Daneshvar, D.H., Nowinski, C.J., Cantu, R.C., & McKee, A.C. (2011). Long-term consequences of repetitive brain trauma: Chronic traumatic encephalopathy. PM&R, 3(10S2), S460-S467. Tartaglia, M.C., Hazrati, L.N., Davis, K.D., Green, R.E.A., Wennberg, R., Mikulis, D.,…Tator, C. (2014). Chronic traumatic encephalopathy and other neurodegenerative proteinopathies. Frontiers in Human Neuroscience, 8(30), 1-6. Wortzel, H.S., Shura,R.D., & Brenner, L.A. (2013). Chronic traumatic encephalopathy and suicide: A systematic review. BioMed Research International, 1-6. 12. List of Abbreviations DTI- Diffusion Tensor Imaging Presentation and Paper Requirements The paper will be at least 10 pages in length, and no more than 20. You will use APA format, and we will discuss this format in class when we talk about the paper in more detail. I would like papers in 12-point font, double-spaced. I will present you with a template for the paper, with sections that you can adapt for your particular case. Grading of Presentation and Papers v On clarity of content. v Rationale for choices must be clear and scientifically justified. v An expansion of the presentation. v Use paragraph format. Lists of questions are fine for the interview section, with numbers or bullets. v Use the same headings, but expand on what specific sources and research studies have found on the best assessment and treatment tools. v Use APA format for citations (Publication Manual, 6th edition – online www.apa.org) Headings for the paper. 1) Case Background: Demographic information and presenting symptoms (why they are coming to see you). About 1-2 pages of information here. Given what you know about the disorder, create a hypothetical case that will outline your decision making about the disorder. Come up with some basic demographic characteristics (imagine you had a phone call in which you received the following information about a potential patient/client): v Current Age v General Symptoms (people usually mention 2-3 problems that bring them in) v Age of Onset of Symptoms v Duration of Disorder v Severity (is the person coping or functioning?) 2) Questions that will be asked in the interview (as many as you think are needed, but no longer than a page of numbered or bulleted questions). Initial interview – What general types of information will you collect? – What symptoms will you ask about? – Will you use a standardized interview that is specific to the disorder? – Will the interview be structured or unstructured? – Will others be interviewed at the same time, or outside of the interview session with that patient/client? 1 reference at minimum will help you to guide your questions – e.g. DSM manual, research on interviews for the disorder. 3) Assessment tools that will be chosen (most likely 3+ - maximum depends on topic but should be selected to assess expected problems in the population). Justify your choices with references that show these are effective tools. What has been found in previous studies? How were the studies conducted? Here you will provide your list of tools, describe each one, and justify your choices (about 4 pages minimum). Assessment Tools – These may assess symptoms (through use of questionnaires, scales that will tell you whether someone meets a diagnosis), – Might also assess some aspect of cognitive function. At minimum, Mental Status exam and IQ tests. You can also add tests to assess for cognitive dysfunction that might be expected to be affected in the disorder (see subheadings in Assessment notes). You might test all cognitive domains or just a few depending on what is found in the literature. – Possibly medical and neuroimaging tests (Are they necessary in the case you are seeing ? – this is a critical question and whether or not you include them is based on your review of the literature and what we know about the neurobiology of the disorders). Choose at least 2 general references here to inform the choice of tools, and you can include empirical references that support your choices if there are any available (this will depend on the topic). Some research studies exist for particular disorders and the best means of assessment; it will depend on your topic. Some suggestions for assessment tools include the following (although you can ask me about things that aren’t on the list): Magnetic Resonance Imaging (MRI), Magnetic Resonance Spectroscopy (MRS), Positron Emission Tomography, Electroencephalograms, Psychological Tests (e.g. standardized intelligence tests, memory tests), psychiatric questionnaires, and qualitative interview techniques. 4) Treatments that will be chosen and justification for your choice. Review the research on the efficacy of the treatments you have chosen. Don’t discuss treatments you have rejected in detail, but you can include a paragraph on this if you like (optional and will not necessarily add to your grade). Long term plans would be great if you can find literature to support the efficacy of long-term treatment. Treatment Plan – Explore the literature on treatment (use general sources to begin with to find out what the options are). The lecture notes on Treatment can give you some options to explore. – The point is to justify your selection with literature on the efficacy of treatments for the disorder you choose. – Alternative treatments are fine, but make sure there is scientific research to back it up (i.e., clearly tested hypotheses, use of scientific method to explore the question). – Combinations of treatments are fine, so long as you justify your decision. Combining more than two treatments can be problematic, but check the literature to inform your choices with empirical research. – Educational interventions would be fine and probably done for all children with behavioural or academic problems. – Your treatment goal is to propose a plan that will deal with the person’s immediate problem. However, you may wish you add some information on long term treatments (depends on the disorder). At minimum you will have 2 sources that will help you, more can be used. For treatment, some suggestions include: pharmacotherapy, electroshock treatment, hypnosis, cognitive therapy, psychodynamic therapy, humanistic therapy, art therapy, and family therapy. Multiple treatments are typically used in ideal situations. If you are not sure about your selection, please come to see me. References v At least 6 (1 on symptoms, 1 on interviews/diagnosis, 2 on assessment, 2 on treatment). You will most likely find more, but limit to no more than 15-20 at the top end (it will depend on the topic). v Recent articles are best (within past 10 years). v Can use older articles to inform your sections on symptoms and diagnosis, basics of assessment and treatment. v Use PsycInfo or PubMed to do your searches. v Don’t give us details on the research studies in the presentation – just citations. You should have at least 6 empirical articles that form the body of your paper. That is, use journal articles (not web-based articles) that test how effective your chosen methodology is in the assessment or treatment of the disorder you are studying. I am not requiring a date limit (i.e., you can use articles from the 1980s or 90s if they are classic articles); however, recent research will be of greater interest to the class. You can also use book chapters and review articles for sections of the paper that include background information on the technique you are presenting. Web-based information is fine to write about; however, it should come from a reputable source (a university, hospital, registered private practitioners), as there is a lot of information on the web that is not necessarily based on scientific principles. Read More