Autism Spectrum Disorders and Schizophrenia - Research Paper Example

AUTISM SPECTRUM DISORDERS AND SCHIZOPHRENIA: CO-MORBIDITY, NEUROPSYCHOLOGICAL, GENETIC, AND ENVIRONMENTAL FACTORS, AND IMPLICATIONS FOR TREATMENT Course Professor Date Introduction Since their earliest descriptions, autism and schizophrenia have been connected in a number of ways. Both schizophrenia and Autism Spectrum Disorders (ASDs) are considered to be psychiatric disorders which impair various domains like communication, social interaction, stereotyped behaviors, interests, or activities (Tordjman, et al., 2006). Communication impairments are found in ASDs along with early onset schizophrenia. Verbal communication impairments includes a delay in speech, poor or disorganized speech; nonverbal communication impairments include poor eye contact, reduced facial expression, and abnormal emotional expression (flat, bizarre or inappropriate affect) (Tordjman, et al., 2006). Cognitive dysfunctions include attention, verbal and nonverbal communication deficits, poor social interactions and withdrawal or social isolation (Sasson, et al., 2011). Theory of Mind (ToM) is defined as the natural ability to attribute mental states to explain and predict behavior in others (Gavilán-Ibáñez & García-Albea Ristol, 2013). Research has shown evidence of deficits with ToM in ASD and Schizophrenia. Common ToM deficits include empathizing with other people, recognizing other people’s emotions, facial affect recognition and social cue perception (Fitzgerald, 2012). These difficulties often lead to misinterpretations of social cues and paranoid ideation amongst individuals with Asperger’s Syndrome and schizophrenia. Furthermore, negative symptoms also overlap between the disorders. Various signs like flat affect, avolition, alogia, apathy, anhedonia, and asociality may also be observed in ASDs and schizophrenia. The common features may be explained by similarities in neuropathology, genetic, and environmental factors. There are also distinct differences between the two disorders. Patients with schizophrenia have been shown to have more specific impairments with cognitive abilities rather than the general cognitive impairments that are typically seen with patients with ASD (Gavilán-Ibáñez & García-Albea Ristol, 2013). Patients with schizophrenia have failed abilities in how they understand figurative language like proverbs, metaphors as well as ironies (Gandal, Nesbitt, McCurdy, & Alter, 2012). One main factor that differentiates the disorders is their average age of onset. Patients with schizophrenia typically have normal development that is not disturbed until their twenties, whereas children are typically diagnosed with ASDs early on, due to disruption in normal development. Positive symptoms such as hallucinations, delusions, and disorganized speech are differentiating features of schizophrenia. From a phenomenological perspective, ASD may be viewed as a disturbance of inter-subjectivity, including sensory-motor integration, imitation, affect attunement, and holistic perception (Gallagher & Schmicking, 2009). These individuals are often more disturbed by motor functions and sensory stimuli, which may be observed though difficulties with sitting, crawling, walking, or abnormal motor patterns (Gallagher & Schmicking, 2009). These individuals may misunderstand what is appropriate, particularly within the social context (Gallagher & Schmicking, 2009). Phenomenological experiences of schizophrenia may occur due to defective meta-representations, such as difficulties with basic awareness, abilities to infer about the mental states of others, and shared representations, which causes self-other confusion (Gallagher & Schmicking, 2009). Both schizophrenia and autism are disorders of cerebral specialization. In most instances, this occurs at the embryonic period in the life of a human being. In addition, the two diseases share a history of diagnostic. This had not yet been resolved until the 1980’s during the DSM-III publication. Presently, it is believed that the diseases are heterogeneous. However, in the past, there was much confusion that arose as a result of specific areas of social dysfunction (Sasson et al., 2011). There are a number of literatures that have arisen to illustrate how abnormalities that may arise from social cognition may be result in social deficit. The main focus in the research of the two diseases is how the underlying neuropsychological as well as neural features may result in social dysfunction. Social cognition is one of the areas where schizophrenia and autism intersect. It refers to the cognitive aspects of social experience like processing, perception and the interpretation of social information. The various abilities of social cognitive may range from detection of biological motions to mentalizing skills like the formation of attributes and the theory of the mind. The attention of research in both diseases came about as a result of restricted use in explaining as well as improving dysfunction socially (Sasson et al., 2011). This social impairment discovered in schizophrenia has been seen to be resistant to treatment. The resistance continues even after the psychotic signs have been managed effectively. This research paper seeks to look into how social cognitive ability directly leads to social functioning in both schizophrenia and autism. Literature Review Currently, the focus of social cognition has been authenticated by a number of studies that show how social cognitive ability contributes directly to social functioning in autism and schizophrenia. Hence, social cognition may act as a basis for understanding the core of social dysfunction and look into the various areas that would require remediation. As a viable research target, social cognition has resulted in the rise of many literatures that seek to address social dysfunction. By looking into common grounds of both diseases, processes that are deficit specific instead of disorder specific may be analyzed (Sasson et al., 2011). Social recognition may be defined as the cognitive-emotional processes that happen in an individual and other people. It may comprise of various processes like action observation, theory of mind, emotional processing, judgment, attribution style as well as action observation. Hence, social cognition depends on the how successful integration of emotional, social, cognitive as well as self-referent information. Deficits in this domain contribute uniquely to social skill deficits and mediate the correlation between neurocognition and social skills (Meyer & Kurtz, 2009). There are various differences that exist between autism and schizophrenia. Children with Asperger’s do not have language delays and often have Average or High Average IQs. There are also alterations in the phenomenology of these two disorders; individuals with Asperger’s are often more aware of their limitations which may create additional anxiety or depression. Those diagnosed with Asperger’s tend to be more anxious, antisocial, and have more difficulties with socialization than those with high-functioning autism (World Psychiatric Association, 2002). Individuals with Asperger’s also have increased paranoid ideations and delusions (Gallagher & Schmicking, 2009). Other differences include differences in executive functioning, lateralization and motor ability (World Psychiatric Association, 2002). Individuals with Asperger’s tend to perform better with set-shifting and inhibition tasks and have increased difficulties with coordination that is often viewed as clumsiness. Functional magnetic resonance imaging data has revealed that individuals with autism have decreased activation in the primary motor cortex and supplementary motor area than individuals with Asperger’s, however those with Asperger’s had extended activation after movement (Sasson et al., 2011). The DSM-5 Task Force recognizes these differences but also highlights commonalities, including social dysfunction, difficulties with attention, visual-perceptual difficulties, and communication (APA, 2013). Since these two disorders are now considered variations of the same disorder, they are reviewed as the same disorder and compared with schizophrenia. History of ASDs The Diagnostic and Statistical Manual of Mental Disorders (DSM) Task Force has altered the diagnostic criteria for ASD with every new edition of the DSM. Research is vitally important to make conclusions on appropriate medication and behavioral treatment programs and the results of these studies are important to the mental health field for proper treatment of clients with these disorders (Sasson et al., 2011). The overlap between these two conditions dates back to 1968, when the DSM-II included children with autism under the diagnosis of schizophrenia, childhood type. The DSM-III separated the disorders in 1980; introducing infantile autism. The separation occurred after Isreal Kolvin noticed differences such as age of onset, familial histories, symptomatic differences, and different treatment responses (Meyer, Feldon, & Dammann, 2011). His work influenced the conceptualization of psychotic disorders and developmental disorders as separate categories. Autism comes from the Greek word autos, meaning self. It was first introduced by a Swiss psychiatrist Eugen Bleuler. He used the term in 1911, to describe social withdrawal in adults with schizophrenia (Tordjman, et al., 2006). In 1943, Leo Kanner and Hans Asperger borrowed the term to describe a syndrome observed in eleven children, which at the time meet the criteria for childhood schizophrenia (Tordjman, et al., 2006). He witnessed these children had no obvious signs of focal cerebral disease and they were presenting with symptoms of impaired social interaction, bizarre and restricted range of interests, impaired language and poor communication skills (Kolb & Whishaw, 2003). He observed some children were able to preserve intellectual functioning, while others were not. In some cases, children with ASDs may excel in specific abilities, such as music, mathematics, and art. In 1994, Asperger’s syndrome was included in the DSM-IV. These individuals tend to be viewed as higher functioning individuals with symptoms of autism, and exhibit early speech and good grammar (Kolb & Whishaw, 2003). They also may excel in some capacities such as calculations, music, art, and reading. Hyperlexia, an unusual reading ability found in individuals with normally impaired cognition, is a condition sometimes found in individuals with Asperger’s syndrome. These individuals will often teach themselves to read around three to five. Reading fluency may be impaired due to articulation and prosodic defects, and rate of speech (Kolb & Whishaw, 2003).They may have an unusual ability to remember categories such as words, street names, and television shows. History of Schizophrenia There has also been a change to the diagnosis of schizophrenia. The DSM-5 Task Force has excluded the subtypes of schizophrenia and now a more broad definition is included (Sasson et al., 2011). Implications of the removal of schizophrenia subtypes may include more general treatment options, which may be tailored depending on the specific needs of the patient instead of typical experiences of the subtype. Schizophrenia comes from the Greek word schizo meaning split, and phrene meaning mind. During the middle 19th century, the French physician, Bénédict Morel used the term démence précoce to describe cases of the young that often lead to chronic deterioration (Jablensky, 2010). Thomas Clouston, a Scottish psychiatrist coined the term “adolescent insanity,” to describe the same symptomatology. Emil Kraepelin conducted longitudinal studies with a large number of clinical cases that exhibited a pattern of cognitive and behavioral deficits. These individuals had primary difficulties with cognition (“general decay of mental efficiency”) and executive functioning (“loss of mastery over volitional action”), and he referred to them as suffering from dementia praecox (Jablensky, 2010). In 1908, Bleuler coined the term schizophrenia; he provided a fundamental distinction between basic (essential) and accessory (additional) symptoms of the disorder (Sasson et al., 2011). Accessory symptoms included delusions and hallucinations that are now identified as “positive” symptoms; basic symptoms included thought and speech deficits, ambivalence, affective incongruence, and withdrawal from reality (“autism”) (Jablensky, 2010). ASD Definition Currently there is a lot of debate on the classification of autistic disorder and Asperger’s syndrome. While there has been an abundance of research regarding the etiologies of both disorders, the exact neuropsychological, genetic, and environmental factors remain elusive (Sasson et al., 2011). The DSM-5 Task Force recently eliminated the distinction between autistic disorder and Asperger’s syndrome, and combined them as two variants on the same spectrum (APA, 2013). Currently the disorders are labeled as Autism Spectrum Disorders (ASDs) under the Pervasive Developmental Disorder (PDD) category. Research conducted by the DSM-5 task force provided evidence of inconsistencies with the application of the separate disorders. The rationale of DSM-5 Task Force’s rationale is to combine the disorders in attempts to reduce misdiagnoses (APA, 2013). For instance, in 2012, McPartland, Reichow and Volkmar re-evaluated 657 individuals who participated in DSM-IV clinical trials. They found 39.4% of the individuals no longer met criteria for ASD after applying the new DSM-5 criteria (McPartland, Reichow, & Volkmar, 2012). Sensitivity varied based on diagnostic subgroup; individuals previously diagnosed with autism disorder continued to meet new criteria with 78%, those previously diagnosed with Asperger’s disorder met new criteria by 25%, and those previously diagnosed with PDD NOS met new criteria by 28% (McPartland, Reichow, & Volkmar, 2012). Another factor which was included was cognitive ability. Those who obtained IQ’s over 70 met new criteria by 70% and those with IQ’s at or less than 70 met new criteria by 76% (McPartland, Reichow, & Volkmar, 2012). The DSM –IV-TR defines autistic disorder as a pervasive developmental disorder with an onset prior to age three, with impairments in three domains: (1) social interaction, (2) communication, (3) restrictive repetitive and stereotyped behaviors, interest or activities (Tordjman, et al., 2006). Commonly, there is no period of normal development, although 20% of children may begin to develop normal language for one to two years and then loses the few words acquired or stagnates developmentally (APA, 2000). A complete list of DSM-IV-TR criteria for autistic disorder is presented in Table 1. The DSM-IV-TR also defines Asperger’s syndrome as a pervasive developmental disorder. The criteria include impairments with social interaction and restrictive repetitive and stereotyped behaviors, interest, or activities (Sasson et al., 2011). There is no significant language delay or other cognitive delays outside of social interactions. A complete list of DSM-IV-TR criteria for Asperger’s syndrome is presented in Table 2. Asperger’s syndrome appears to occur as early as age two, but does not require a set age of onset as autistic disorder did. It is important to note, the DSM-5 criteria for ASD includes (1) deficits in social-emotional reciprocity, (2) deficits in non-verbal communication, (3) and deficits in developing and maintaining relationships. It also includes as least two of the following: (1) Stereotyped or repetitive speech, motor movements, or manipulation of objects, (2) Extreme propensity to follow routines, ritualized patterns of verbal or nonverbal behavior, or excessive resistance to change, (3) Highly restricted, fixated interests that are abnormal in intensity or focus, (4) Hyper-or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment. The symptoms must be present in early childhood and they must impair daily functioning (APA, 2013). Schizophrenia Definition The DSM-IV-TR defines schizophrenia, as a multidimensional disorder involving abnormalities in thinking, perception, communication/language, and/or behavior. Positive symptoms include hallucinations, delusions, and disorganized speech. Negative symptoms include flat affect, asociality, avolition (lack of motivation), anhedonia (lack of pleasure in normally pleasurable acts), and alogia (lack of unprompted speech) (APA, 2000). Full criteria for schizophrenia is listed in Table3. The DSM-IV-TR lists four subtypes of schizophrenia; paranoid type, disorganized type, catatonic type, undifferentiated type, and residual type. These subtypes are no longer included in the DSM-5, and therefore are irrelevant in this doctoral project. Table 1 DSM-IV criteria for Autistic disorder­­­­­­­­­­­­­­­­­­­­_________________________________________ A. A total of six (or more) items from (1), (2), and (3), with at least two from (1) and one each from (2) and (3): 1. qualitative impairment in social interaction, as manifested by at least two of the following: a. marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction b. failure to develop peer relationships appropriate to developmental level c. a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest) d. lack of social or emotional reciprocity 2. qualitative impairments in communication as manifested by at least one of the following: a. delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime) b. in individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others c. stereotyped and repetitive use of language or idiosyncratic language d. lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level 3. restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following: a. encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus b. apparently inflexible adherence to specific, nonfunctional routines or rituals c. stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or complex whole body movements) d. persistent preoccupation with parts of objects B. Delays or abnormal functioning in at least one of the following area, with onset prior to age 3 years: (1) social interaction, (2) language as used in social communication, or (3) symbolic or imaginative play. C. The Disturbance is not better accounted for by Rett’s Disorder or Childhood Disintegration Disorder. Table 2 DSM-IV criteria for Asperger’s Syndrome­­_____________________________________ A. qualitative impairment in social interaction, as manifested by at least two of the following: (1) marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction (2) failure to develop peer relationships appropriate to developmental level (3) a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest) (4) lack of social or emotional reciprocity B. restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following: (1) encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus (2) apparently inflexible adherence to specific, nonfunctional routines or rituals (3) stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or complex whole body movements) (4) persistent preoccupation with parts of objects C. The disturbance causes clinically significant impairment in social, occupational, or other important areas of functioning. D. There is no clinically significant general delay in language (e.g., single words used by age 2 years, communicative phrases by age 3 years). E. There is no clinically significant delay in cognitive development or in the development of age-appropriate self-help skills, adaptive behavior (other than in social interaction), and curiosity about the environment in childhood. F. Criteria are not met for another specific Pervasive Developmental Disorder or Schizophrenia. Table 3 DSM-IV criteria for Schizophrenia_____________________________________­­­­______ A. Characteristic symptoms: Two (or more) of the following, each present for a significant portion of time during a one month period (or less if successfully treated): (1) Delusions (2) Hallucinations (3) Disorganized speech (e.g., frequent derailment or incoherence) (4) Grossly disorganized or catatonic behavior (5) Negative symptoms, i.e., affective flattening, alogia, or avolition. Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts, or two or more voices conversing with each other. B. Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care are markedly below the level achieved prior tp the onset (or when the onset is in childhood or adolescence, failure to achieve expected level of interpersonal, academic, or occupational achievement). C. Duration: Continuous signs of the disturbance persist for at least six months. This six month period must include at least one month of symptoms (or less if successfully treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or two or more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences). D. Schizoaffective and Mood Disorder exclusion: Schizoaffective Disorder and Mood Disorder with Psychotic Features have been ruled out because either (1) no Major Depressive, Manic, or Mixed Episodes have Occurred concurrently with the active-phase symptoms; or (2) if mood episodes have occurred during active-phase symptoms, their total duration has been brief relative to the duration of the active and residual periods. E. Substance/general medical condition exclusion: The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition. F. Relationship to a Pervasive Developmental Disorder: If there is a history of Autistic Disorder or another Pervasive Developmental Disorder, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least a month (or less if successfully treated). Social cognition in schizophrenia Social dysfunction in schizophrenia has led to various researches being carried out to look into the factors that may lead in the impairments. Social cognition has been regarded as the main domain of cognitive functioning mainly in schizophrenia. This construct came from the late 1960s and early 1970s and focuses mainly on how different individuals process various information within various social context (Harvey & Penn, 2010). The ability to recognize affect in faces of others is an important component of social cognition. Most researchers have discovered that adults who are schizophrenic are impaired in various social cognitive domains like becoming aware of biological motions, the scanning of faces visually (Loughland et al., 2012), emotional perception (Kohler et al., 2010; Harvey and Penn, 2010) and the perception of social cues (Van’t Wout et al., 2009) Conceptualization of ASD Many cognitive explanations are used to conceptualize ASD. One of the most researched and widely used is ToM, which proposes individuals with ASD suffer from “Mindblindness”. The theory states individuals with ASD has difficulties with their abilities to infer about the mental states of others. These deficits or delays causes’ problems with understanding how other’s think, feel, and act. The Executive Dysfunction theory postulates deficiencies in executive functioning causes ASD deficits in attention, need for sameness, perseveration, and impulsivity (Crespi & Thiselton, 2011). Executive functions involve planning, inhibition, initiation, judgment, problem solving, self-perception, impulse control, organized search, and flexibility of thought and action. It is believed these functions are controlled within the prefrontal cortex, which is also the location believed to control ToM. Weak Central Coherence Theory suggests ASD is caused by the inability to see things holistically. It states the core issue of ASD is the tendency to only view things segmentally or in fragmented parts. This would account for the deficits in ASD but also the strengths such as “savant” skills. This theory explains social deficits as well as cognitive difficulties such as selective attention, and focus to detail. Alterations in the limbic system have been theorized to cause the emotional and cognitive disturbances in ASD (Palmen, Engeland, Hof, & Schmitz, 2004). These variations include increased cell packing density, reduced cell size in hippocampus, modifications in the subiculum, amygdala, entorhinal cortex, mammillary bodies, and septal nuclei (Palmen, Engeland, Hof, & Schmitz, 2004). These adjustments are believed to hinder brain development and symptoms are viewed as products of an immature brain. Other Neuropathological theories include cerebral developmental abnormalities, such as abnormally large brains “megaencephaly,” white matter abnormalities, apoptosis (programmed cell death) dysfunction, and abnormal Purkinje cell levels (Palmen, Engeland, Hof, & Schmitz, 2004). Alterations in the cholinergic system, such as the basal forebrain and the GABAergic system are believed to cause the brain abnormalities based on early neuronal development flaws (Palmen, Engeland, Hof, & Schmitz, 2004). Genetic theories hypothesize abnormalities in ASD functioning occurs from chromosomal mutations and copy variants. The gluten-free/casein-free (GFCF) diet evolved out of the GFCF theory that symptoms of ASD are produced (or exacerbated) due to allergic reactions to peptides and proteins in foods containing gluten and casein. It is believed the brain processes these chemicals as opioids and creates difficulties with social skills, cognition, behavior, and speech. Conceptualization of schizophrenia From a psychodynamic perspective, schizophrenia can be conceptualized as a result of the disintegration of the ego. These individuals were believed to have difficult childhoods and rejecting mother figures, which resulted in weak egos, inability to recognize reality and incapability of appropriately mediating between the id and superego. Fixation and regression are defense mechanisms commonly used by individuals with schizophrenia. The social cognitive theory can be employed to explain both disorders. The theory suggests that people acquire knowledge by directly looking at others during social interactions, media influences as well as experiences. Hence, evaluating the changes in behavior of individuals will mainly rely on people, their actions as well as the environment that they are placed in. Environment may refer to the various factors that may influence the behavior of people (Miller, 2005). The social environment may include friends, family members as well as workmates. In the learning process, the individual’s internal mental condition is significant. This is because it is responsible for processing the entire learning procedure that will result in the change of behavior. There are several cognitive perspectives that conceptualize symptoms cognitive impairments play a major role in the maintenance of schizophrenia. Schizophrenia has been conceptualized based on deficiencies in selective attention, and symptoms has been associated with the inabilities to concentrate. Others propose lack of self-monitoring is the main cause of symptoms. Hallucinations and delusions are thought to occur due to inability to recognize they are self-generated. Poor memory and defective perceptions are believed to create schizophrenic symptoms due to attending to unimportant or irrelevant aspects of the environment and poor concentration, which leads to disorganized thinking and behavior. The diathesis–stress model postulates there is genetic predisposition to developing schizophrenia. However, the occurrence of the disorder is dependent upon environmental factors. This theory weighs both nature and nurture and takes into consideration the impact of psychological events and stress. This may explain why twins that share genetic factors are not guaranteed to both develop schizophrenia due to different life experiences. Dopamine is theorized to play an important role in the development of schizophrenia. Hyperactivity of the dopamine system is theorized to be responsible for positive symptoms. Glutamate is hypothesized to play a role in the development, suggesting, increased glutamate uptake in the frontal cortex and reduced cortical glutamate release are involved in positive symptoms. Serotonin 5-HT is hypothesized to play a role in schizophrenia, particularly negative symptoms. Abnormalities in the Limbic system, dorsolateral prefrontal cortex, temporal lobe and temporal horn are also associated with the development of schizophrenia. Limbic system abnormalities may account for inappropriate fear and other emotions, poor memory, behavior, and olfactory hallucinations (Gillig, 2009). The prefrontal cortex is responsible for facial recognitions and deficits in this area may be responsible for social difficulties. Abnormalities in gray matter, abnormal cortical volume, and enlarges ventricles are suspected to have an impact on schizophrenic symptomatology. Hypofrontality refers to lower cerebral blood flow in the anterior region of schizophrenic’s brains. Decreased activity in the frontal cortex has been shown based on brain imaging technology. Imaging has also shown left inferior frontal CBF to Broca’s area and in the striatum, thalamus, and medial temporal cortex, which may account for the auditory hallucinations. Gene expression abnormalities and genetic linkage are theorized to be primary causes of schizophrenia. Maternal malnutrition generates alterations in the brain that result in learning, attention and adaptation deficits, which is theorized to create the cognitive and social inflexibility associated with schizophrenia. Epidemiology ASDs occur more commonly in males than females. Males are diagnosed with ASDs four to five times higher than females; and females with the disorder more commonly meet criteria for intellectual disability (APA, 2013). Males have a slightly greater incidence of schizophrenia than women do. The median rate of autistic disorder prevalence is 5 out of 10,000; there were no significant changes to the prevalence of ASDs as compared to the findings in the DSM- IV (APA, 2013). According to the Centers for Disease Control and Prevention, the estimated prevalence rate of ASD is 1 in 88 births (Centers for Disease Control and Prevention, 2012), is found worldwide and equally in diverse ethnicities (APA, 2013). Schizophrenia is recognized worldwide and adult prevalence is reported to be 0.5% to 1.5% (APA, 2013). There appears to be a hereditary link for both ASDs and schizophrenia. ASDs have a hereditability of more than 90% (Palmen, Engeland, Hof, & Schmitz, 2004). Individuals with ASDs tend to have a 5% chance of siblings exhibiting the same symptoms. Individuals with first-degree relatives with schizophrenia are ten times more likely to develop the disorder (APA, 2013). Both disorders have higher incidences in monozygotic twins than in dizygotic twins, indicating there is a genetic link. Results of comorbidity between the disorders are variable; however, recent studies have shown childhood onset schizophrenia is preceded by and comorbid with PDD in 30-50% of cases. Various studies examining a 20-40 year follow up on the course of illness with individuals with schizophrenia are consistent in reporting a chronic, persistent course of illness for 50% to 70% of the patients (Harvey & Davidson, 2002). Current Treatment Individuals with schizophrenia are commonly treated with antipsychotics. The original or “typical” antipsychotics have been available since the 1950s. These include Thorazine, Haldol, Trilafon, and Prolixin (National Institute of Mental Health, 2009). Typical antipsychotics were produced to target negative and positive symptoms. They work by blocking the effects of dopamine; they are most effective with treating positive symptoms (hallucinations and delusions) (Meltzer & Massey, 2011). In the 1990s “atypical” antipsychotics were introduced; these included Risperdal, Zyprexa, Seroquel, Geodon, Abilify, and Invega (National Institute of Mental Health, 2009). Atypical antipsychotics work by blocking many dopamine receptors and blocking serotonin; they target negative and positive symptoms and appear to decrease extra-pyramidal side effects (EPS), which involve uncontrollable movements (Meltzer & Massey, 2011). Empirically supported treatments for schizophrenia include a variety of psychosocial interventions such as social skills training, vocational rehabilitation, and psychotherapy (Twamley, Veste, & Bellack, 2003). Common issues that may arise due to symptoms associated with schizophrenia include difficulties with communication, maintaining relationships, and self-care (National Institute of Mental Health, 2009). Cognitive Behavioral Therapy (CBT) can help individuals learn to manage their symptoms by targeting neurocognitive impairment that may cause vulnerabilities to aversive experiences (Gillig, 2009). CBT focuses on dysfunctional cognitive appraisals and maladaptive behaviors (such as social withdrawal) (Gillig, 2009).Treatment can help patients make connections about how their perceptions of events alter their beliefs and behaviors. Reality testing can help refute delusions. Methods such as progressive muscle relation and breathing techniques may help to lower anxiety and increase social interaction. Individuals with ASDs are commonly treated with behavior and communication methodologies, dietary changes, psychotropic medication, and alternative medicine. Applied Behavior Analysis (ABA) is a common behavioral therapy that encourages positive behaviors and discourages negative behaviors (Centers for Disease Control and Prevention, 2012). Developmental, Individual Differences, Relationship-Based Approach (DIR) focuses on emotions and relationships, as well as perceptions such as sight, smell and sound (Centers for Disease Control and Prevention, 2012). Treatment and Education of Autistic and related Communication-handicapped Children (TEACCH) use visual cues to break down each step to specific skills (i.e., getting dressed) (Centers for Disease Control and Prevention, 2012). Relationship Development Intervention (RDI) is a parent centered program that focuses on social skills and interaction. Occupational and speech therapy are often recommended. Sensory Integration Therapy helps with sensitive sensory perceptions. The Picture Exchange Communication System (PECS) uses pictures to teach communication skills (Centers for Disease Control and Prevention, 2012). Dietary changes include the elimination of gluten and casein intake and addition of specific vitamins and minerals. Two antipsychotic drugs (Risperidone and Aripripazole) are used to treat individuals with ASDs that experience aggressive tendencies, tantrums, and self-injurious behaviors. Alternative treatment is more controversial, and includes chelation (treatment to remove heavy metals like lead from the body), injections of the hormone secretin, and deep pressure (Centers for Disease Control and Prevention, 2012). Reference American Psychiatry Association.(2000). The Diagnostic and statistical manual of mental disorders-fifth edition. Arlington: American psychiatric association. Centers for Disease control and prevention.(2012, May 240. Autism Spectrum disorders (ASDs). Atlanta, GA, Fulton. Crespi,B.,& Thiselton,D.(2011). Comparative Immunogenetics of Autism and Schizophrenia. Genes, Brain and Behavior, 689-701. Derntl,B & Herbel, U.(2011). Deficits in social cognition: A marker of psychiatric disorders. Europena Archives of psychiatry and clinical neuroscience, 145-149 Gillig, P.(2009). Cognitive behavior therapy for people with schizophrenia. Psychiatry, 32-39 Kolb,B.,& Whishaw,I.(2003). Fundamentals of Human neuropsychology-fifth edition. New York: Worth Publishers Meyer, U., Feldon, J.,& Dammann,O.(2011). Schizophrenia and autism: Both shared disorder-specific pathogenesis via perinatal inflammation? Neuropsychiatric disorders and pediatric psychiatry, 26-23 Miller, K. (2005). Communication Theories: Perspectives, Processes, and Contexts (2nd ed.). New York, New York: McGraw-Hill. National Institute of Mental health.(2009, September 08). Schizophrenia. Bethesda MD Palmen, S.,Engeland,H.,Hof,P.,& Schimitz,C.(2004). Neuropathological findings of autism brain, 2572-2583 Penn D, Addington J, Pinkham AE. Social cognitive impairments. In: Lieberman J, Stroup TS, Perkins DO, editors. The American psychiatric publishing textbook of schizophrenia. Washington, DC: American Psychiatric Publishing; 2006. p. 261–74. Sasson, N.J., Pinkham, A.E.,Carpenter, K.L.H &Belger, A. 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