Schizophrenia Study Notes PDF

Exam 3 Study Topics Schitzophrenia child onset disorders Breitpsychosis disorder presents with Schitzophrenia Sypmtoms the same symptoms only lasting 1 1 5in aattiinig9 eean...

Exam 3 Study Topics Schitzophrenia child onset disorders Breitpsychosis disorder presents with Schitzophrenia Sypmtoms the same symptoms only lasting 1 1 5in aattiinig9 eean month abnormal motor behaviors negative symptoms Schitzophreniform lasts longer e present continously for six months then one month but less than 6 Other symptoms Mental disorders Labled as psychoses auido hallucinations Severe distortions of reality unrealistic beits disturbances in perception ideas intellectual functions irratic communication affect motivation Social relationships hospitalization impaired motor behaviors is often required symptoms can be  go n e p I of onset ge umptoms most frequently evelop during late teenage If the early onset of early 20 s symptoms the more frequent severe relapes are Women more likely to develop umptoms after age 36 than men sometimes onset later in women Why female estrogen levels decrease with age estrogen may have a neuroprotective effect Schizophrenia is a symptoms vary among thought disorder illogical thinking individuals auditory lack of hallucinations are very reasoning inability to relognize common reality usually insulting commanding communication contused illogical often doesntfollow Iles of semantics  ge rep iliv tones ps 11 Emotions withdrawn preoccupied may be absent extreme apathy nnapropriate udden unpredictable changes iniability to innitate activites motor activity poor hygeine educed 1 3 institutionalized bizzare postures 113 live normally maintain life 3 dont maintain life ridigity Sterotyped movements Ke rocking Pacing Can be agitated violent no two people will have identical symptoms symptoms increase decrease over time Jositive symptoms delusions hallucinations bizzare behavior tend to be older at first onset respond well to antipsychotics that block Dopamine receptors  C negative symptoms decline in normal function reducedspeech flattened affect oss of motivation socially withdrawn anhedonia these symptoms could be mistaken for depression cognitive symptoms impaired working memory executive function attention Negative cognitivesymptoms are the most resistent to antipsychotic drugs patients tend toshow early onset progressive deteroation or time Symptoms not constantly present morbid Phases Pre initial phase detection of non specific problems with or social functioning Cognition motor promodal initial positivesymptoms decliningfunction can be seen  psychotic positive psycoticsymptoms appearent stable phase fewer Sumptoms more ones to be diagnosed 6 months with at least one month of positive symptoms Schitzo typical people develop traits of soniteophrenia Without having the disorder often have family history of schizophrenia very smart people genetic component Tim Crow development of language and genetic changes required for producing understanding speen associated w schiztoprenia development normal languge process is disrupted resulting from incomplete differentiation of th right left hemisphere Of the brain inability to distinguish between thoughts speech  g s d I ane w producing language anatomical differences in control vs patient w schizophrenia Cerebral atrophy reducedvolume due to smaller somas reduced dentritic spine ventricles fluid filled Enlarged density increased cell packing hippocampal cells of patientsw Chitzophrenia more disorganized brain areas show shrinking selected cortical layers atrophied of dentritic spines leads to connectivity failures images show altered networks of neurons inefficency in neuron networks this would impair intergation amongbrain areas needed for sensory cognitive processing leadsto you thinking to an altered reality Diminised Structural connectivity articullary appearant in white matter  ogel the Inn the Conta D a p cal frontal reigons Whihatter 1111 temporal 11 1 If paretial Associated With lower IQ severity of multiple connectivity defects linked to how extreme symptoms are why do these brain changes occur may be due to progressive deteroation rather than the cause of the illness or may be from use of antipsychotics for many years Brain Networks Cannot surpress default network on tupical connetions in default network plays roll in hallucinations delusions Default network not turning off weaker connections between brain areas correlated w attention memory cognitive impairment Reduced function of the Prefrontal cortex hypofrontality reduced bloodflow shows that brain cells less active Wisconsin cardsorting task typo frontality symptoms neg cog symptom esemble deficts seen after a prefrontal lobotomy poor social functioning no motivation attention deficts Schizophrenia the immune system emotionally blunting pro inflamity cytokines are elevated inability to shift strategies anti intramitory cytokinesreduced While problemsolving levels return to normal after treatment w anti psychotics unclear whether cytokines cause the symptoms or are a result of the symptoms Elevated maternal cytokines predict higher Sk of schizophrenia in offspring influenza Link individuals w immune disorders are an increased genetic risk schitzoprenic individuals experience more nfections tistory described as early as 0006C causeis unknown still strong genetic factor but not 100 t genetic 48 i of monozygotic twins will both develop Canidate suspected to be involved genes genes corolates of characteristics typical of Sanitzophrenia genetic such as eye tracking disfunction alleles involved in neurotransmitters receptors gene mutations that affect brain development Gwas data Showed that involved in Schitophrenia genes are a disruption of communication between onotrophic meta trophic families of receptors failure of information processing basedon abnormal Synaptic regulation most likely not a single connectivity disorder gene develop disorder f multiple bad genes mutildleBad genes contribute to the development of Schitzophrenia Epigenetics a schitzophrenia Reelin glycoprotein secreted by neurons neurons into correct guides positioning during fetal development reelin acts like a candy trail to prenatal stress in early life lead neurons to correct roduces epigenetic spots when reelin is ffects that  p gn evelopment in the wrong spot ZELN has higher gene methylation neurons cannot be to produce reelin to guide read gene Reduction of reelin could explain the cell disorganization that is seen with Sahitzophrenia these affects are highly linked to stress viral infection prenatal Discl gene mutations in the DISC1 gene may contribute to the risk of Schitzophrenia Disct codes for proteins essential for neural development Can be disrupted by a chromosome translocation contributes to cognitive effects vulnerability prenatal insult genetic vulnerability increases the Likelihood genetic  p n g to un p i oxygen depervation during delivery drug use infection endocrine disorders prenatal infection severe malnutrition elevated risk of exposure to viral infection schitzophrenia are particulary in 2nd trimester Most commonly seen in people who have family history with Dyschotic disorders early infancy symptoms passivity apathy Worse symptoms reduced response to verbal commands develop more more difficult temporment during adolescence Poor somatosensory performance excessive synaptic pruning takes more symptoms place in early childhood so emerge Two hit modle 1st Genetic vulnerability enviormental insults Neurodevelopmental abnormalities neuron formation synaptogeneisis migration pruning apoptosis nd Excessive pruning leading later enviormenta to abnormal neuronal insults such as connectivity function stress substance abuse HPA axis disfuntion both of these can lead to development of schizophrenia Neurochemical basis of schizophrenia Dopamine most prominate chemical The dopamine hypothesis Excessive dopamine function results in positive symptoms Why was this theorized amphetamines can produce psychotic reaction in healthy individuals that can be eversed by blocking dopamine Strong correlation between D2 receptor blockade α the reduction of positive symptoms found more recently to be a DA imbalance reduced DA in mesocortical Neurons sympt excess DA in mesolimbic Neurons sympt gagging E.fi i ien IIi ÉEiÉÉi.ir nothingtoturn off DA in mesolimbic system failure toturnon DA in  mesocortical Early mesocortical cell loss due to genetics environmental stress that alter brain development will cause loss of inhibitory control of mesolimbic cells start of positive symptoms Hypoglutamate hypothesis hypoglutamatric activity in pateints with schitzophrenia blocking NMDA receptors w pop ketamine w L will cause hypoglutamate produces a psychotic syndrome seen in schit patients in healthy individuals worsens symptoms in Schitzophrenic patients descending glutamate neurons excite mesocortical DA neurons hypoglutamate would cause low DA release in PFC exacerbating  g 1 g i su no Other glutamate neurons excite inhibitory that inhibit the mesolimbic gaba neurons DA patmay low glutamate would lead to exess DA release in NA causes positive symptoms Childhood onset disorders 3 main categories Trauma and stressor related disorders disorders of attachment Neurodevelopmental disorders Autism ADHD tics tourettes Disruptive control  disorders ODD CD externalizing Normal child development Gestation period prenatally when the brain is establishing its ortical connections this time skills to process sensory uving information language cognitive skills there is some research that autism These skills will develop in a specific order may be related to a Brain connections mistiming of developme remain to atypical leading table till about 1 2 of brain connections years ge Adolescence Critical period when the brain re wires itself in a different manner external internal events can occur which may lead to physical mental disorders Early life stress death of loved one eat child is unable to cope  e si s y dhood case different patterns of White Grey matter Smaller hippocampus which could impair memory learning also influences amygdala emotional processing Harlows monkey experiment Nature of attachment monkies who were fed with a wire cage mother ended to want the Cloth mother who did not Her any food as they grew Showed that contact comfort was pertered over food John Bowlbly Suggested that children deprived of their mothers where at risk for physical mental Iness could lead to extreme anxiety r sycopathic personality Strange situation experiment  I n p im d o the attachment types Strange situation Secure attachment style the infant will and explore this is Normal engage request the infant will upset when mother get Shows positive emotions when the mother eturns II Avoidant attachment style infant is more focused on toys than mom infant is less distressed when the mother leaves less positive emotion upon mothers return I Anxious ambivellent infant does not engage in exploration infant shows extreme protest when mother leaves When mother returns the infant shows anger ambivalence towards her Mad at her for leaving some infants may also show inconsistent attachment Avoidant attachment style is associated with agression in middle Childhood Anxious ambivilent pattern associated ith passive Withdrawl mood disorders suchas anxiety mitationlearning turning a vision brain system response to observing an action into a motor plan hat leads to a motorrepresentation of the bserved action Mirror Neurons Mirror neurons play a Neurons in your brain fire as it you role in understanding rformed the actionthat your anothers empathy observing known in multiple areas for example if you see someone crying mirror Neurons fire You will feel the sameway Theory of mind bility to understand anothers mental state tting yourself in someone else shoes  utism spectrum disorder theory ofmind delayed development of theory of mind mirror neurons not as strong cereal box task Adolescense interests desires awakening of new hormones increased risk taking anxiety disorders mood disorders substance bude psychosis someof thesedisorders such as nxiety may not follow into adulthood but some isorders such as schizophrenia do uring adolescense individual starts to becomemore peer orientated meeting new people Sexual a romantic interests develop Vulnerable to mood disorders more sensitive to positive Negative rewards  I Sk taking canlead to psychopathologies based children tend to show increased risk King morelikely to take risks if peersare around Why is risk taking evolutionarily beneficial exploremore motivated to form romantic connections Attachment conduct oppositional disorder attachment disorders Reactive attachment disorder children do notseek comfort support from an tachment figure when distressed direct result from inadequate rule out other caregiving disorders first 2 Disinhibited social engagmentdisorder Like RAD but children are okay with Strangers disorder CD  C dolescents impact on children agressive violent behaviors Often lack in personal relatio ctivly violate the Safley of others Often perform poorly at school bullying threatening others often comefrom a not great cruel behaviors start fights enviorment Neurobiology Smaller and underactive amygdala ink between severity of CD symptoms insulavolume in limbicreigon Awarness forones self deciphersyour feelings deficits in empathy Oppositional defiant disorder ODD Children adolescents show excessive presistent anger defience of authority loses temper easy frequently argues w adults purpostuly annoy others Vindictiveness Three categories of behaviors angry irritable mood loosingtemper being annoyed  g resentful angry I argumentitive defiant to authority figures I being vindictive CD ODD are disorders externilizing Often co morbid with ADHD influence genetic Neurobiology of ODD impaired fear conditioning reduced cortisolreactivity to stress Altered Serotonin noradrenaline amygdala hyporeactivity to negative neurotransmission Suggest stimuli low punishment Sensitivity not botheredbygetting in trouble may Comprimise the ability of children to make associations Sympathetic nervous system between innapropriate behaviors hyporeactivity to incentives and forth coming punishments Lowbasalheartratewhen sensationseeking not making link between orbitofrontal cortex hyposensitivity to rewards action consequence Because dopamine function  not correct hyposensitivity to rewards impaired functions of insula cortex impaired over emotional cognitive control behavior not able to look at behavior and less to themselves if its appropriate not Autism Spectrum disorder euro developmental disorder difficulties in three areas Specialized in one of threetypes of thinking socialinteractions 1 Visual theworld words as communication thinking viewing images behavioral processes 2 pattern Like in music math can recognize thinking Patternsvery easy 3 fact thinking largenumber of facts on atopic Autism onset  developmentally symptoms of utism are not typically seen till 8months 0 a can be 2 6 months year toddler preschool age Social impairment imitation responses to emotions facial processing impairment can also experience Language delays sometimes nonverbal repetitive behaviors tead Size Autism Link at birth head will be small to normal size accelerating growth starting at 4 months Larger head size apparent around lyear MRI studies show that Children 2 4 ys Who have Utism have cerebral larger Olume when compared to  Ipica or enviormental genetic initially Autism was thought to be influenced by nviormental factors we now know Autism is strongly genetic 69 95 1 concordiance rate between MZ twins 0 241 for dz twins Autism is believed to share common enetic processes w schizophrenia Autism is also commonly CO morbid w ADHD 441 Concordinance rate arents age onset of Autism young parentshave the lowest risk fathers over so have 4 the chance of having a child Older parents have risk highest w Autism if mother is unable to absorb antioxidants more likely to develop autism Gut bacteria Autism Current research shows that individuals w utism have a different microbiome than gut hose without this means it may be possible to reduce symptoms of autism w bioactive food modify bacteria reduce the severity gut Mirror Neurons responsible for our ability to understand quickly instinctivly what others feel experience help us differentiate facial expressions which elps us develop empathy less activity in Mirror Neurons while viewing motional expressions link between cortical activity severity of negative umptoms  severity of 54m less activity more sumptoms Brain contributes individuals w autism show fewer whole brain connections particularly in visual processing default network reduced activity those w Autism showed more connetions between primary sensory areas subcortical areas thalmus basal ganglia more connected Zesult better pattern recognition visual strength Empathy Autism more systemizing to objects events could cause  1 I emp facial focus those w Autism typically avoid eye contact Will focus on mouth 6 12ms Amygdala mirror neurons Frontal lobe temporal lobe high order frontal lobe function doesnt fully develop cerebral volume 3 101 larger more in frontal lobe temporal lobe involvedinstocial language processing as well as facial but reduction of activit overgrowth Savant Sundrom special abiites w memory  more men than Women emphasis on detail lack of emotional social processing ADHD inattention inattention letting mind wander difficulty paying attention hyperactivity impulsivity to details difficulty focusing appear disorganized hyperactivity Unable to engage in activities difficulty waiting turn that require mental effort keeping still easily distracted remaining in seat conduct issues problems learning Hyperactivity typically lessens w age attentional problems may worsen thebrain ADHD 1 decrease in cerebral volu 81 decrease in total cortical volume overactive Saliance a default Networks Executive function reigons frontal Striatal Cerebellar involved all related to executive function these areas recive dopaminegeric NE innervation but DOP NE are reduced in ADHD PFC sumptoms may be a result rom underactivity of Dop in PFC ou need just the right amount of dopamine to dotasks and focus increase dop NE when time to focus When NE binds to prymidal cells in PFC makes into you want to hear more clear When DOP binds it weakens irrelevant Nto  dp hip C appen as efficiently focused organ stracted fatigue alert stress get f y impulsive very strong genetic factor 75 91 1 medication Stimulants methylphenidate ritalin anphetiimines aderall dexedrine Blocks re uptake