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PSYC 211
Yogita Chudasama

PSYC211 Chapter 16 Notes Schizophrenia • The word means “Split mind” but it does not imply a split or multiple personality • Term invented by Eugen Bleuler (1911/1950), intended it to refer to a break in reality with reality cause by disorganization of the various functions of the mind, such that thoughts and feelings no longer worked together normally • Affects 1% of the world’s population • Very expensive cost to society • There are 3 categories of symptoms → Positive Symptoms (Make themselves known by their presence) o Thought disorders (disorganized irrational thinking) o Hallucinations (Perception of nonexistent object or event) o Delusions (Belief contradictory to reality) → Negative Symptoms (Absent of behaviours that that are normally present) o Flattened emotion response o Poverty of speech o Lack of initiative and persistence o Anhedonia (inability to experience pleasure) o Social withdrawal o Lack of affect o Reduced motivation → Cognitive Symptoms (Closely related to negative symptoms & can be produced by abnormalities in same brain regions) o Difficulty sustaining attention o Low psychomotor speeds (movement of fingers, hands, legs) o Deficits in learning & memory o Poor abstract thinking o Poor problem solving *Negative and cognitive symptoms are not specific to Schizophrenia; they are seen in many neurological disorders that involve brain damage especially to the frontal lobe. Negative symptoms are the first to appear followed by cognitive symptoms. The positive symptoms follow several years later. Heritability • Schizophrenia is a heritable trait. According to both adoption studies (Kety et al., 1968, 1994) and twin studies (Gottesman and Shields, 1982; Tsuang, Gilbertson, & Faraone, 1991). • In children with 2 Schizophrenic parents, less than 50% meaning that several genes are involved or that having a “Schizophrenia gene” imparts a susceptibility to develop Schizophrenia, the disease itself being triggered by other factors. • Carrying a Schizophrenic gene does not mean that a person will necessarily become Schizophrenic. • Another genetic factor is paternal age, children of older fathers are more likely to develop Schizophrenia. (Increased incidence of Schizophrenia caused by mutations in the sperm) • So far, researchers have found no location of a “Schizophrenic gene” • Walsh et al (2008) suggests that a large number of rare mutations play a role in the development of Schizophrenia • Mutations affecting neural differentiation and growth, guidance of axons during brain development, assembly of components of neurotransmitter receptors, and factors that control the formation of synapses could be responsible for susceptibility to Schizophrenia. Pharmacology of Schizophrenia: The Dopamine Hypothesis Dopamine Hypothesis • Positive symptoms of Schizophrenia caused by a biochemical disorder (Over activity of synapses between dopaminergic neurons of the ventral tegmental area and neurons in the nucleus accumbens and amygdala) • Patients with greater amounts of dopamine release showed greater increases in positive symptoms Effects of Dopamine Agonists and Antagonists • Middle 20 century French surgeon Henri Laborit, developed drug to prevent surgical shock but it also seemed to reduce anxiety • Later a French drug company made a related compound called, Chlorpromazine – it had dramatic effects on Schizophrenia • Drug helped keep patients from long hospital visits • Eliminated or helped diminish patients positive symptoms • Hallucinations/delusions went away or became less severe Drugs that produced the positive symptoms of Schizophrenia act as dopamine agonists. (They block the reuptake of dopamine) • amphetamine • cocaine • methylphenidate • symptoms of these drugs can be alleviated with antipsychotic drugs, this further strengthens the argument that the antipsychotic drugs exert their therapeutic effects by blocking dopamine receptors Consequences of Long-Term Antipsychotic Drug Treatment of Schizophrenia • Causes symptoms resembling those of Parkinson’s disease (For most patients this is temporary) o Slowness in movement o Lack of facial expression o General weakness • Much more serious side effect, effects 1/3 of all patients : Tardive Dyskinesia o Means, slow/faulty movement o It is a late developing movement disorder o Opposite of Parkinson’s disease o Patients can’t stop moving o Explained by super sensitivity –increased sensitivity of neurotransmitter receptors; caused by damage to the afferent axons or long-term blockage of neurotransmitter release. *There have been drugs created that do not produce neurological side effects though! They are called Atypical Antipsychotic medications. It reduces both positive and negative symptoms. o Clozapine – Is the first, (it b4ocks D receptors in the nucleus accumbens) following this drug came, risperidone, olanzapine, ziprasidone, & aripiprazole Schizophrenia as a Neurological Disorder • Positive symptoms are unique to Schizophrenia • Negative and cognitive symptoms are similar to those produced by brain damage • Brain abnormalities give rise to increased secretion of dopamine in the nucleus accumbens & the accompanying positive symptoms • Many studies found evidence of loss of brain tissue in CT & MRI scans of Schizophrenic patients • Ventricle size of the Schizophrenic patients was more than twice as great as that of normal control subjects. Most likely because of lose of brain tissue • Everyone loses some cerebral grey matter as they age, the rate of tissue loss is greater in Schizophrenia patients Causes for Brain Abnormalities • Inheritance is a defect that renders people susceptible to some environmental factors that adversely affect the brain development • Epidemiology – study of distribution & causes of diseases in population o environmental factors, season of birth, viral epidemics, population density, prenatal malnutrition, & maternal stress o People born in late winter and early spring are more likely to develop Schizophrenia (Seasonality Effect)  Factors responsible for Seasonality Effect : Women more likely to contract viral illness during a critical phase in child’s development In cities, rarely found in country side (more diseases in highly dense populations)   Vitamin D deficiency – plays important role in brain development • Brain damage later in life Obstetric Complications – can lead to Schizophrenia • Diabetes of mother • Rh incompatibility between mother & fetus • Bleeding • Edema • Abnormal fetal development • Complications of labour and delivery >interruption of blood or oxygen supply to the brain Evidence of Abnormal Brain Development • Abnormal prenatal development is associated with Schizophrenia • Schizophrenic children compared to their siblings have a more negative facial expression and abnormal movements • Displayed less sociability and deficient psychomotor functioning • Minor physical anomalies: high-steepled palate or especially wide-set or narrow-set eyes • In Monozygotic twins, one with Schizophrenia usually has a larger lateral & third ventricles, anterior hippocampus was smaller & grey matter in left temporal lobe was reduced • Monozygotic twins : two types, monochromatic (twins share a single placenta) & Dichorionic (each has its own) • Concordance rates of Schizophrenia is higher in monochromatic twins than Dichorionic ones • Rapid loss of brain volume occurs at young adulthood, process of Schizophrenia but lies dormant until puberty when something triggers the neurons Relationship between Positive and Negative Symptoms: Role of the Prefrontal Cortex • Negative symptoms caused by hypofrontality, decreased activity of frontal lobes • Schizophrenic patients do poorly on neuropsychological tests that are sensitive to prefrontal damage • Hypofrontality is caused by the release of dopamine in the prefrontal cortex • Destruction of the dopaminergic input to the prefrontal cortex lowers its metabolic rate & leads to cognitive dysfunctions • Injection of dopamine antagonists into the prefrontal cortex caused behavioural deficits like those produced by prefrontal lesions • Drugs, Ketamine (Special K) & PCP (phencyclidine/angel dust) can cause positive, negative & cognitive symptoms of Schizophrenia • Negative & cognitive symptoms produced by the drugs above are caused by a decrease in metabolic activity of the frontal lobes • Remembering back to chapter 4, PCP is an indirect antagonist of NMDA-receptors (so is ketamine) by inhibiting the activity of NMDA receptors, PCP suppresses the activity of several regions of the brain notably the dorsolateral prefrontal cortex • NMDA & dopamine receptors play an important role in the production of negative/cognitive symptoms: suppression of these receptors cause hypofrontality • Prefrontal hypoactivity causes hyperactivity of mesolimbic dopaminergic neurons • Excitatory glutamatergic neurons of the prefrontal cortex send axons to the ventral tegmental area, where they form synapses with dopaminergic neurons that project back to the prefrontal cortex • Drugs that act as NMDA agonists to reduce symptoms of negative/cognitive symptoms • Direct agonists cannot be used because they increase the risk of seizures • Glycine & D-serine bind to one of these sites and act as indirect agonists • Atypical anti-schizophrenic drugs do the impossible: increase dopaminergic activity in the prefrontal cortex & reduce it in the nucleus accumbens • Aripiprazole is a partial antagonist (drug with very high affinity for a particular receptor but activates that receptor less than the normal ligand does, serves as an agonist in regions of low concentrations of the normal ligand & as an antagonist in the regions of high concentrations.) Major Affective Disorders There are 2 principal types of major affective disorders, first type is characterized by alternating periods of mania and depression- a condition called bipolar disorder. • Affects men & women in equal amounts • Episodes of mania last a few days or several months • Episodes of depression that follow generally last 3 times as long as mania The second type is major depressive disorder (MDD), characterized by depression without mania. • It may be continuous & unremitting or may come in episodes • Mania without periods of depression occur but it is rare • Extreme feelings of unworthiness, and strong feelings of guilt • Risk of suicide • Very little energy, move/talk slow • Pace around aimlessly • May cry a lot, may not be able to experience pleasure • Loss of appetite for food and sex • Sleep disturbed • Body functions disturbed: constipation/secretion of saliva decreases Episodes of mania: • characterized by a sense of euphoria • exhibit nonstop speech and motor problems • Talk from topic to topic • Often have delusions • Lack the severe disorganization that is seen in Schizophrenia • Usually defensive when contradicted • Go for long periods of sleep • Work on projects which are often unrealistic Heritability • There is a tendency to develop an affective disorder is a heritable characteristic • close relatives of people who suffer from affective psychoses are ten times more likely to develop these disorders than are people without afflicted relatives • one member of a set of monozygotic twins was afflicted with an affective disorder, the likelihood that the other twin was similarly afflicted is 69% • For dizygotic twins it was only 13% • In studies, that genes on several chromosomes may be implicated in the development of the affective disorders o the strongest candidate is the gene for the serotonin transporter (plays important role in brain development – located on chromosome 17) Biological Treatments • In the 1940’s clinicians noticed that drugs for the treatement of tuberclerosis elevated patients mood. • This led to the creation of a similar drug, Iproniazid, which reduced symptoms of psychotic depression, by inhibiting the activity of MAO, which destroys excess monoamine transmitter substances within terminal buttons o Drug increases the release of dopamine, norepinephrine, & serotonin • Other MAO inhibitors were later discovered but have harmful side effects therefore must be used with caution • Another class of antidepressant drugs were soon discovered without these side effects o Tricyclic antidepressants ▯  inhibit the reuptake of serotonin & norepinephrine by terminal buttons  affects other neurotransmitters  named for the molecular structure o Specific serotonin reuptake inhibitors (SSRI)  i.e. Fluoxetine (Prozac), citalopram (Celexa) & paroxetine (Paxil)  reduce symptoms of OCD (obsessive compulsive disorder)  reduce social phobia  specifically inhibits the reuptake of serotonin without affecting the reuptake of other neurotransmitters o Serotonin & norepinephrine reuptake inhibitors (SNRI)  fewer non specific actions therefore fewer side effects than tricyclic antidepressants ▯  specifically inhibits the reuptake of serotonin without affecting the reuptake of other neurotransmitters  i.e. milnacipran, duloxetine, venlafaxine • Electroconvulsive therapy (ECT) o History, began with physician who found an improvement in psychotic patients who had epileptic seizures o brief electric shock, applied to head, that results in an electrical seizure, used therapeutically to alleviate severe depression o Its usefulness is limited to the treatment of mania and depression o ECT provides faster relief than drugs to patients o Prolonged and excessive use of ECT can cause brain damage, like impairments in memory o ECT decreases brain activity & raises the seizure threshold of the brain, making it less likely for another seizure to occur o Increased seizure threshold appears to be caused by an increased release of GABA & neuropeptide Y Adverse side effects of antidepressants • nausea • anxiety • sexual dysfunction • weight gain • drug failing to relieve depression o between 20 & 40% of patients with major depressive disorder do not show a significant response to initial treatment • treatment resistant depression o A major depressive disorder whose symptoms are not relieved after trials of several different treatments In Chapter 5, we saw, transcranial magnetic stimulation (TMS) • applying a strong localized magnetic field into the brain by passing an electrical current through a coil of wire placed on the scalp • magnetic field induces an electrical current in the brain • TMS applied to the prefrontal cortex reduces symptoms of depression without producing any apparent negative side effects Subgenual anterior cingulate cortex (subgenual ACC) • A region of the medical prefrontal cortex located below the “knee” at the front of the corpus callosum; plays a role in the symptoms of depression • Direct electrical stimulation to the brain may also be useful therapy for treatment resistant depression • Vagus nerve simulation also shows some promises of reducing symptoms of depression • Injections of ketamine or a placebo were given to patients with treatment resistant depression, 71% of the patients showed an improvement of their symptoms Lithium • A chemical element; lithium carbonate is used to treat bipolar disorder • most effective in treating the manic phase of a bipolar affective disorder ; once mania is eliminated, depression usually does not follow • it doesn’t suppress normal feelings of emotions • does not impair intellectual processes • Adverse side effects o hand tremors o weight gain o excessive urine production o thirst • Toxic doses produce o nausea o diarrhoea o motor in coordination o confusion o coma • Some patients are unable to tolerate the side effects of lithium • Researchers have not yet discovered the pharmacological effects of lithium that are responsible for its ability to eliminate mania • Founding, 4 weeks of lithium treatment for bipolar disorder increased the volume of cerebral gray matter in the patients brains, a finding that suggests that lithium facilitates neural or glial growth The Monoamine Hypothesis • States that depression is caused by a low level activity of one or more monoaminergic synapses • Monoamine antagonists can produce the symptoms of depression and monoamine agonists can reduce them Tryptophan Depletion Procedure • They studied depressed patients who were receiving antidepressant patients who were receiving antidepressant medication & were currently feeling well. • one day they had patients follow a low-tryptophan diet • next day patients drank an amino acid “cocktail” that contained no tryptophan • very little tryptophan found its way into the brain & the level of tryptophan in the brain fell drastically • tryptophan is the precursor of 5-HT, or serotonin, thus the treatment lowered the level of serotonin in the brain • tryptophan depletion caused most of the patients to relapse into depression • then when they began eating a normal diet again they recovered • tryptophan depletion has little or no effect on the mood of healthy subjects • it does lower the mood of people with personal/family history of affective disorders The Amygdala & the Prefrontal Cortex: Role of the 5-HT Transporter • Functional imaging studied indicate a 50-75% increase in blood flow & metabolism in the amygdale of depressed patients • Activity of the amygdala of depressed patients was correlated with the severity of their depression • The subgenual ACC, shows a lower level of activation in depressed patients • The activity of this region is increased during a manic episode in patients with bipolar disorder • Activity of this region decreases during times of negative mood & increases during time of positive mood • Serotonin transporter in depression, the promoter region- for the 5-HT transporter (5-HTT) comes in 2 forms, short & long • probability of major depression & suicide increased with the number of stressful life events the people had experienced • increase was much greater for people with 1 or 2 copies of the short alleles for the 5-HTT promoter • Depressed people with 2 long alleles for this gene were more likely to respond to treatment with an antidepressant drug than were those one or two short alleles • Presence of short alleles means that fewer 5-HT transporters are produced which in turn means a slower rate of 5-HT reuptake & an increased amount of 5-HT in the brain • We would predict that long alleles not short ones would be associated with an increased risk of depression • Apparent contradiction, serotonin has important roles in prenatal development • Some glutamatergic neurons in the hippocampus & anterior cingulate cortex take up serotonin during a brief period during development , this uptake has effects on the development of these brain regions • Presence of high levels of serotonin in the brain during brain development has a very different effect than it does in adulthood • For example when neonatal mice are treated with a potent SSRI, they show signs of depression in adulthood • Strong positive correlation between the activity of the subgenual ACC & the amygdale in people with 2 long alleles • Found a strong negative correlation between the activity of the dorsal ACC & the amygdale • Both of these correlations were significantly lower in people with 1 or 2 alleles than in those with 2 long alleles • Peoples whose scores indicated the highest risk of depression had the lowest functional connectivity between these brain regions Role of Neurogenesis • Stressful experiences that produce the symptoms of depression suppress hippocampal neurogenesis & the administration of antidepressant treatments, increases neurogeneis Role of Circadian Rhythms • Prominent symptoms of depression is disordered sleep • sleep tends to be o shallow o slow-wave delta sleep (stages 3 & 4) is reduced o stage 1 is increased o sleep is fragmented o awaken frequently, especially towards morning • REM sleep deprivation o Selective deprivation of REM sleep o alleviates depression o therapeutic effect o occurs slowly o some patients show long term improvement even after the deprivation is discontinued o other treatments of depression suppress REM sleep o These facts suggest that REM sleep and mood might be somehow be casually related • Total Sleep Deprivation o Total sleep deprivation also has an antidepressant effect o It is suggested that during sleep, the brain produces a chemical that gas a depressogenic effect in susceptible people o depressed patients whose mood remains stable will probably not benefit from sleep depression whereas those whose mood fluctuates probably will o Patients who are most likely to respond are those who feel depressed in the morning but then gradually feel better as the day progresses • Role of Zeitgebers o Some people become depressed during the winter season when days are short and nights are long o Symptoms to this are called Seasonal Affective Disorder (SAD)  a mood disorder characterized by depression, lethargy, sleep disturbances, & cravings for carbohydrates during the winter season when days are short o Appears to have genetic basis o SAD can be treated by phototherapy : exposing people to bright light for several hours a day o it is caused by a mismatch between cycles of sleep & cycles of melatonin secretion o People with SAD most often show a phase delay between cycles of melatonin & sleep PSYC211 Chapter 17 Notes - Awhile back: • Anxiety disorders, autism, and attention-deficit/hyperactivity disorders were believed to be learned, manly because of poor parenting. • Most mental disorder were believed to be psychogenic in origin (produced by psychological factors) - Now we know: • Yes! Family environment, social class, economic status, and other similar factors can affect the development a mental disorder and may help or stop recovery. ALSO: • Physiological factors: inherited factors and those that adversely affect development or damage the brain • Clinicians developed procedures that damaged the prefrontal cortex or disconnected it from other parts of the brain to treat people with emotional reactions. - Anxiety Disorders: • Characterized by unrealistic, unfounded fear and anxiety. Tension, overactivity of the autonomic nervous system, expectation of a disaster coming, and continuing to look for danger. • Panic disorder, generalized anxiety disorder, and social anxiety disorder have biological causes. 1. Panic Disorder, Generalized Anxiety Disorder, and Social Anxiety Disorder Description - Panic Disorder: • Suffer from episodic attacks of acute anxiety – periods of extreme, unremitting terror at a length of time. • Prevalence: under 2% (women a little more than twice as likely as men to suffer from panic disorder) • Physical symptoms: shortness of breath, clammy sweat, irregularities in heartbeat, dizziness, faintness, and feelings of unreality. • Feels like they are going to die and often seek help from hospitals • Between panic attacks those people suffer anticipatory anxiety (fear of having a panic attack) • Anticipatory anxiety often leads to agoraphobia (fear of being away from home or other protected places) - Generalized anxiety disorder: • Primary characteristics: excessive anxiety and worry, difficulty in controlling these symptoms, and significant signs of distress and disruption to their life • Prevalence: approx. 3% (approx. 2 times greater in women then men) - Social anxiety disorder (social phobia): • Persistent, excessive fear of being exposed to the scrutiny of other people that leads to the avoidance of social situations in which a person has to perform. (speaking or performing in public). If they cannot avoid the situation they experience intense anxiety and distress. • Prevalence: approx. 5% (same for men and women) Possible Causes - Panic disorder, generalized anxiety disorder, and social anxiety disorder all have a hereditary component. - Panic attacks can be triggered in people with a history of panic disorder by a variety of treatments that activate the autonomic nervous system, such as: • Injections of lactic acid (by-product of muscular activity) increases heart rate and rate of respiration • Yohimbine (adrenoreceptor antagonist) – direct pharmacological effects on the nervous system • Doxapram (increases breathing rate) • Breathing air containing an elevated amount of carbon dioxide (increases heart rate and rate of respiration) - The presence of a short allele is associated with higher levels of anxiety. - Functional-imaging studies suggest that the amygdala and the cingulate, prefrontal, and insular cortices are involved in anxiety disorders. - The activation of amygdala was positively correlated with the severity of the person’s symptom. • Evidence: - Adolescents with generalized anxiety disorder showed increase activation of the amygdala and a decrease activation of the ventrolateral prefrontal cortex while looking at angry faces. - College students with a high level of anxiety showed decreased activation of the amygdala and the insular cortex. Treatment - Sometimes treated with benezodinazepins because they target GABAA receptors, which there are a high concentration of in the amygdala. - Serotonin plays a role in anxiety disorders as well. Specific serotonin reuptake inhibitors (SSRIs), preferably with a combination of cognitive behavior therapy are a treatment. - D-cycloserine in conjunction with cognitive behavior therapy. Injections of d-cycloserine facilitated the extinction of a conditioned emotional response in rats only if administered with extinction training. - In anxiety disorders, cognitive behavior therapy often uses procedures that desensitize patients to the objects of situations they fear. 2. Obsessive-Compulsive Disorder Description - Mental disorder characterized by obsessions and compulsions. - Obsession: unwanted thought that will not leave them which preoccupies them - Compulsion: feeling obliged to performing a behavior even if you don’t want to - Obsessions include concern or disgust with bodily secretion, dirt, germs, etc., fear that something terrible might happen and a need for order, symmetry, or exactness. - Compulsions usually falls into 4 categories: counting, checking, cleaning and avoidance. - Unlike Schizophrenia people with obsessive-compulsive disorder recognize that their thoughts and behaviors are senseless and desperately that they would go away. - Compulsions often become more demanding until they interfere with people’s careers and daily lives. - Chances is having Obsessive-compulsive disorder is 1-2%. Females slightly more then males - OCD commonly begins in young adulthood. - Some investigators believe that the compulsive behaviors seen in OCD are forms of species-typical behaviors (ex. Grooming, cleaning) released from normal control mechanisms by brain dysfunctions. Others say that it is pathological examples of a natural behavioral tendency to develop and practice social rituals. Possible Causes - OCD is partly caused by hereditary factors. A greater concordance for obsessions and compulsions in monozygotic twins then in dizygotic twins was found. Also found that OCD is associated with Tourette’s Syndrome. - Tourette’s syndrome: neurological disorder that appears during childhood, characterized by muscular and vocal tics and sometimes by compulsive uttering of obscenities and repeating. - Believed that OCD and tic disorders are produced by the same underlying genotype. - OCD can also be caused by birth trauma, encephalitis, and head trauma. Symptoms seem to appear with damage to or dysfunction of the basal ganglia, cingulated gyrus, and prefrontal cortex. - Tic disorders can be caused by group A β-hemolytic streptococcal infection (can trigger autoimmune diseases where immune system attacks and damages certain tissues of the body, in this case parts of the brain. - Symptoms of OCD appear to be produced by damage to the basal ganglia. - Several functional-imagining studies have found evidence of increased activity in the frontal lobes and caudate nucleus in patients with OCD. -Cognitive behavior therapy and drug therapy produced similar results to treatment Treatment - Severe OCD has been treated with cingulotomy -surgical destruction of specific fiber bundles in the subcortical frontal lobe, including cingulum bundle and a region that contains fibers that connect the basal ganglia with the prefrontal cortex. As well as capsulotomy -destroys a region of a fiber bundle the intercapsule that connects the caudate nucleus with the medial prefrontal cortex, this is a last resort procedure because it can’t be undone and there were some adverse side effects. Deep Brain Stimulation (DBS) of the basal ganglia or fiber tracts connected with them to treat OCD –appears to reduce the symptoms of OCD. - It was thought that obsessive-compulsive behavior may be the result of overactivity of the direct pathway and an imbalance between the direct and indirect pathways. - 3 drugs are regularly used to treat the symptoms of OCD: clomipramine, fluxetine, and fluvoxamine. they are specific blockers of 5-HT reuptake, serotonergic agonists. Serotonin has an inhibitory effect on species-typical behaviors. Brain regions that have been implicated in OCD receive input from serotonergic terminals. Serotonergic activity in inhibiting compulsive behaviors is underscored by three compulsions: Trichotillomania (compulsive hair pulling), Onychophagia (compulsive nail biting), and Acral lick dermatitis (disease of dogs, some dogs will continuously lick a part of the body. - NMDA receptor agonist, D-cycloserine helps the treatment of OCD, the drug facilitates the extinction of conditioned emotional responses. 3. Autistic Disorder Description - Chronic disorder that includes symptoms like failing to develop normal social relations with other people, impaired development of communicative ability, and the presence of repetitive, stereotyped behavior. Most of the time displaying cognitive impairments. - Incidence approx. 13 in 10 000. It is 4 times more common in males than females. - Social impairments are much more common in males but the cognitive and communicative impairments are more evenly shared by males and females. - Before it was believed that autism was more prevalent in families with higher socioeconomic status, but more recent studies show that the frequency of autism is the same in all social classes. - Autistic disorder is one of several pervasive developmental disorders that have similar symptoms: Asperger’s disorder, Rett’s disorder, and childhood disintegrative disorder. - A diagnosis of autistic disorder requires the presence of 3 categories of symptoms: 1. Impairments of social interactions: Social impairments are the 1 symptoms to emerge. Infants with autistic disorder do not seem to care whether they are help. When they get older they do not enter into social relationships with other children. In severe cases they do not seem to recognize the existence of other people. - It is suggested that some of the symptoms of autism stem from an abnormality in the brain that prevent from forming theory of the mind. They are unable to predict and explain the behavior of the other people in terms of mental states. They can not depict the thoughts, feelings, and intentions of other people from their emotional expressions, tone of voice, and behavior. 2. Absent or deficient communicative abilities: language development is abnormal or even nonexistent. Often echo what is said to them and may refer to themselves like others do, 2 nd or 3 person. May learn words and phrases by rote but fail to use them productively and creatively. Those who acquire reasonably good language skills talk about they’re own preoccupations without regard to the other persons interests. Interpret speech literally. 3. Presence of stereotyped behaviors: Show abnormal interests and behaviors. May show stereotyped movements like flapping their hands back and forth or rocking back and forth. May become obsessed with investigating objects, sniffing them, feeling their texture, etc. Often insist on routine and may become violently upset they are hindered from doing so. No make-believe play and are not interested in fantasy. If not mentally retarded they may be physically adept and graceful. Some have isolated skills. 4. Possible Causes - At first it was believed to be biological origins, afterwards it’s argued that it is learned/taught by bad parents. Now it is believed that autism is caused by biological factors and that parents should be given help and sympathy, not blame. Heritability - Some forms of autism seem to be heritable. Concordance rate for autism in monozygotic twins is approx. 70%, dizygotic twins approx. 5%. The concordance rte for autistic spectrum disorders is 90% for monozygotic twins and 10% dizygotic twins. - Can be cause my mutations, especially those that interfere with neural development and communication. Brain Pathology - Because it is heritable it can be evidence that the disorder is a result of structural or biochemical abnormalities in the brain. - A variety of medical disorders, especially those that occur during prenatal development can produce symptoms of autism. Approx. 10% of all cases of autism have biological causes. - Evidence in recent years show significant abnormalities in the development of the brain of autistic children. - Autistic brain is n average slightly smaller at birth it begins to grow abnormally quickly and by 2 to 3 years of age it is 10% larger then a normal brain. Then the growth of an autistic brain slows down and by adolescence is only 1-2% larger then normal. - Not all parts of the autistic brain show same pattern of growth. - The regions that appear to be most involved in the functions that are impaired in autism show the greatest growth early in life and the slowest growth between early childhood and adolescence. - The growth pattern of “lower-order” regions of the cerebral cortex (such as primary visual cortex and extrastriate cortex) are respectively normal in the autistic brain. - The amygdala show an abnormal pattern of growth during development. By 4 years of age it is larger in autistic children. By the time of early adulthood it is the same size as the amygdala of nonautistic people but contain fewer neurons. - Autistic brains also show abnormalities in white matter. The volume of white matter containing short-range axons was increased but the volume of white matter containing long-range axons that connect distant regions of the brain was not. It is suggested that the production of excessive numbers of neurons early in development may cause the development of such a large number of short- range axons that the development of long-range axons is inhibited. - The hyperconnectivity of local regions of the cerebral cortex might possibly account for the exceptional isolate talents and skills. - Found that little or no activity in the fusiform face area of autistic adults looking at pictures of human faces. - Poor at recognizing facial expressions of emotion or the direction of another person’s gaze and low rates of eye contact with other people. - Suggested that social deficits may be the result of abnormal development of the mirror neuron system (helps us understand what the person we are looking at feels or is trying to accomplish), it is thinner in autistic children. - Little is known about the nature of the brain abnormalities responsible for communicative deficits but it is suggested that it has to do with regions of temporal lobe involved in language abilities. It was found that the auditory cortex of autistic adults responded to sounds but did not show different activation with speech. - Behavioral symptoms can be the cause of increased activity of caudate nucleus. 5. Attention-Deficit/Hyperactivity Disorder (ADHD) Description st - Most common behavior disorder that shows itself in childhood. Usually 1 discovered in classroom. They have difficulty withholding a response, ac
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