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Chapter 16

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McGill University
PSYC 211
Yogita Chudasama

Chapter 16: Schizophrenia and the Affective Disorders Notes taken by: Ashley Brown Contact for mistakes: [email protected] Mental disorders include deficient or inappropriate social behaviours, illogical/incoherent/obsessional thoughts, inappropriate emotional responses (incl. depression, mania, or anxiety), delusions, and hallucinations. - caused by abnormalities in the brain both structural and biochemical Schizophrenia Description Has been around for thousands of years. The major symptoms are universal. Literally means “split mind” but does not imply a split or multiple personality. Schizophrenia: a serious mental disorder characterized by disordered thoughts, delusions, hallucinations, and often bizarre behaviours; has three categories of symptoms: (1) positive, (2) negative, and (3) cognitive - positive symptoms: a symptom evident by its presence, such as delusions, hallucinations, or thought disorders o appear to involve excessive activity in some neural circuits that include dopamine as a NT o thought disorder: disorganized, irrational thinking; probably most important symptom  can’t differentiate between plausible conclusions and absurd ones  loose associations  incoherence  neologism o delusion: a belief that is clearly in contradiction to reality  persecution: false beliefs that others are plotting and conspiring against oneself  grandeur: false belief’s in one’s power and importance, like they think they have godlike powers or special knowledge no one else possesses  control: the person believes that he or she is being controlled by others through such means as radar or a tiny radio receiver implanted in his or her brain o hallucination: perception of a nonexistent object or event  with schizophrenia are most commonly auditory, typically voices talking to the person  olfactory hallucinations are also seen often making them think someone is trying to kill them with poison gas - Negative symptom: a symptom characterized by the absence of behaviours that are normally present: social withdrawal, poverty of speech, flattened emotional response, lack of affect, and reduced motivation o Anhedonia: inability to experience pleasure o Not specific to schizophrenia o Both these and cognitive symptoms appear to be caused by developmental or degenerative processes that impair the normal functions of some of regions of the brain - Cognitive symptom: a symptom that involves cognitive deficits, such as difficulty in sustaining attention, deficits in learning and memory, poor abstract thinking, and poor problem solving o Low psychomotor speed or the ability to rapidly and fluently perform movements of fingers, hands, and legs o Both these and negative symptoms are not specific to schizophrenia (both involved in many neurological disorders esp. those involving damages to frontal lobes) Symptoms appear gradually and insidiously over a period of 3 to 5 years - negative symptoms first to emerge - then cognitive - positive symptoms follow several years later Heritability Appears to be heritable  strong evidence given by adoption and twin studies Not one gene  either several genes or having a “schizophrenia gene” that imparts a susceptibility to develop schizophrenia, the disease being triggered by other factors - strong evidence for the latter Another genetic factor is paternal age - children of older fathers are more likely to develop schizophrenia - mutations in the spermatocytes has been linked as a cause for the increased incidence of schizophrenia Epigenetic (on top of the genes) mechanisms may contribute to the development of schizophrenia in addition to mutations - epigenetic changes might be responsible for a decreased expression of reelin, a protein involved in neuronal migration Abnormalities in non-coding RNA (ncRNA) may be responsible for excessive or inadequate amounts of normal proteins during critical stages of development, which could produce effects as deleterious as those caused by mutant proteins Pharmacology of Schizophrenia: The Dopamine Hypothesis Evidence suggest that the positive symptoms of schizophrenia are caused by a biochemical disorder. - the dopamine hypothesis suggest that the positive symptoms are caused by over activity of synapses between dopaminergic neurons of the VTA and neurons in the nucleus accumbens and amygdala Effects of Dopamine Agonist and Antagonist Chlorpromazine: a dopamine receptor blocker; a commonly prescribed antischizophrenic drug - not effective in treating neuroses or affective psychoses - eliminates, or at least diminishes, positive symptoms (but not negative symptoms A lot of drugs made that relieve the positive symptoms  all have in common the fact that they block D 2nd D do3amine receptors There are drugs that produce the positive symptoms of schizophrenia - amphetamine, cocaine, methylphenidate, and L-DOPA - all are dopamine agonist Mesolimbic pathway (which begins in the VTA and ends in the nucleus accumbens and amygdala) is more likely to be involved with the positive symptoms of schizophrenia - if reinforcement mechanisms were activated at inappropriate times then inappropriate behaviours such as delusions might be reinforced - amygdala is involved in conditioned emotional responses and it received a strong projection for the mesolimbic dopaminergic system The Search for Abnormalities in Dopamine Transmission in the Brains of Schizophrenic Patients Studies found that dopaminergic neurons in schizophrenic patients release more dopamine - amphetamines caused the release of more dopamine in the striatum of schizophrenic patients than in normal subjects - patients with greater amounts of dopamine release showed greater increases in positive symptoms Also a possibly the schizophrenic’s brains contain a greater number of dopamine receptors - post mortem studies found that their might be a modest increase in the number of D 2eceptors in the brains of schizophrenics - unlikely that these increases are the primary cause of the disorder Consequences of Long-Term Drug Treatment of Schizophrenia Until recently the drugs that were commonly used to treat the disorder caused symptoms resembling those of Parkinson’s disease (slowness in movement, lack of facial expression, and general weakness) One-third of patients who took the classic antischizophrenic drugs for an extended period showed a serious side effect  developed tardive dyskinesia - a movement disorder characterized by involuntary movements of the face and neck - appears to be the opposite of Parkinson’s disease - caused by supersensitivity  the increased sensitivity of neurotransmitter receptors o caused by damage to the afferent axons or long0term blockage of NT release o in this case, it is the D2dopamine receptors in the caudate nucleus and putamen that overcompensates The new atypical antipsychotic medications not only don’t cause tardive dyskinesia but they reduce the positive and negative symptoms - Clozapine: the first of this type of medication; blocks D re4eptors in the nucleus accumbens Schizophrenia as a Neurological Disorder Positive symptoms - can easily be related to one of the known functions of dopaminergic neurons, reinforcement - unique to schizophrenia (and amphetamine/cocaine psychosis) Negative and cognitive symptoms are similar to those produced by brain damage caused by several different means - brain abnormalities in schizophrenics cause these symptoms - these abnormalities give rise to increased secretion of dopamine in the nucleus accumbens and the accompanying positive symptoms Evidence for Brain Abnormalities in Schizophrenia The presence of negative and cognitive symptoms suggest that schizophrenia may be associated with brain damage (or abnormal brain development) of some kind Evidence of loss of brain tissue - lateral ventricle is significantly larger (more than twice the size) in the brains of schizophrenics than the brains of normal people - rate of cerebral gray matter loss with age is greater in schizophrenics Possible Causes of Brain Abnormalities Heritable disease but not all children of schizophrenic patients show schizophrenia - disorder caused by an interaction between genetic and environmental factors - the absence of the “schizophrenic genes” does not guarantee that a person will not develop schizophrenia Epidemiological Studies Epidemiology: the study of the distribution and causes of diseases in populations Evidence from these studies indicates that the incidence of schizophrenia is related to several environmental factors: season of birth, viral epidemics, population density, prenatal malnutrition, and maternal stress Seasonality effect: the increased incidence of schizophrenia in people born during late winter and early spring - pregnant women may be more likely to contract viral illness during a critical phase of their infant’s development - occurs mainly in cities but rarely in the countryside  more evidence suggesting that it is a result of the viral infection of the mother since disease spreads more in cities than in the country - cold weather and crowding contribute to this effect Vitamin D deficiency is a risk factor for schizophrenia An urban environment may also affect people’s susceptibility to schizophrenia postnatally as well as prenatally Research has found that maternal infection with at least two other infectious diseases (rubella and toxoplasmosis) are associated with an increased incidence of schizophrenia During the Hunger Winter a severe food shortage that occurred in the Netherlands, there was a large increase in the amount of offspring with schizophrenia - specific cause: thiamine deficiency – or more precisely an abrupt build-up of toxins in the brains of the developing fetuses when their mothers suddenly began eating a normal diet - underweight women are more likely to give birth to babies who later develop schizophrenia - low birth-weight babies have a higher incidence of schizophrenia Obstetric Complications Good evidence indicates that obstetric complications can also cause schizophrenia Most important factors are: - complications of pregnancy: incl. diabetes of the mother, Rh incompatibility between mother and fetus, bleeding, and preeclampsia (also called toxaemia, a condition characterized by high blood pressure, edema, and protein in urine) - abnormal fetal development: low birth weight, congenital malformations, and reduced head circumference - complications of labour and delivery: emergency Caesarean section, atonic uterus, and fetal oxygen deprivation o most important characteristic is interruption of the blood flow or oxygen supply to the brain Evidence for Abnormal Brain Development The children who subsequently became a schizophrenic displayed more negative affect in their facial expression and were more likely to show abnormal movements In watching kids eating lunch the ones who later developed schizophrenia displayed less sociability and deficient psychomotor functioning A few physical anomalies, like a high-steepled palate or especially wide-set or narrow-set eyes have also been shown to be associated with the incidence of schizophrenia - the factors that produce minor physical anomalies are at least partly independent of the genetic factors associated with schizophrenia In discordant monozygotic twins (one has the disorder, the other doesn’t) the one with schizophrenia has larger lateral and third ventricles - also the anterior hippocampus was smaller in schizophrenic twin - total volume of the gray matter in the left temporal lobe was reduced Two types of monozygotic twins: - monochorionic: share a placenta - dichorionic: each develop with its own placenta The placenta plays an extremely important in prenatal development - transports nutrients to the developing organism from the mother’s circulation and transports waste products to her - also serves as barrier through which toxins or infectious agents - monochorionic twins show much higher concordance rate for schizophrenia Not a degenerative process, rather there is a sudden, rapid loss of brain volume typically during young adulthood - disease process begins prenatally and then lies dormant until puberty when some unknown mechanism triggers degeneration of some population of neurons Dramatic evidence for loss of cortical gray matter during adolescence in patients with early-onset schizophrenia - degeneration starts in the parietal lobes, waves of destruction continue rostrally to the temporal lobes, somatosensory and motor cortex, and dorsolateral prefrontal cortex - symptoms shown by the patients were associated with the cortical regions that were undergoing tissue loss Dorsolateral prefrontal cortex was the region of the brain most strongly affected by genetic influences Relationship Between Positive and Negative Symptoms: Role of the Prefrontal Cortex There is evidence that there is a relationship between the over activity of dopaminergic neurons that causes positive symptoms and the brain abnormalities that cause the negative and cognitive symptoms Abnormalities in the prefrontal cortex is associated with schizophrenia - hypofrontality: decreased activity of the prefrontal cortex; believed to be responsible for the negative symptoms of schizophrenia - schizophrenics do poorly on neuropsychological test that are sensitive to prefrontal damage - might be caused by a decrease in the release of dopamine in the prefrontal cortex PCP and ketamine can caused positive, negative, and cognitive symptoms of schizophrenia - negative and cognitive symptoms produced by these drugs are apparently caused in a decrease in the metabolic activity of the frontal lobes - PCP (and ketamine) is an indirect antagonist of the NMDA-receptor, suppressing the activity of several regions of the brain, especially the dorsolateral prefrontal cortex o Also decrease the level of dopamine utilization in that region Evidence suggest that prefrontal hypoactivity causes hyperactivity of mesolimbic dopaminergic neurons - excitatory glutamatergic neurons in the prefrontal cortex sends axons to the VTA where they synapse with dopaminergic neurons that project back to the prefrontal cortex - also these form synapses with GABA-secreting neurons in the ventral tegmental that inhibit another set of dopaminergic neurons that project to the nucleus accumbens - thus decreased activation of the prefrontal cortex causes an increase in the rele
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