Schizophrenia

Schizophrenia

Greek for "split mind", split between the emotional and intellectual aspects of experience. there are NO DEPENDABLE LAB TESTS, only rely on observation for diagnosis
1. DIAGNOSED based on deteriorating functioning for at least 6 months.
SYMPTOMS
1. DELUSIONS - unjustifiable beliefs. HALLUCINATIONS - false sensory experiences. DISORGANISED SPEECH. DISORGANISED BEHAVIOUR and WEAK OR ABSENT SIGNS OF EMOTION
2. symptoms vary so much that two people diagnosed with schizophrenia could be nothing alike. POSITIVE SYMPTOMS are symptoms that are PRESENT WHEN SHOULD BE ABSENT (hallucinations, delusions). NEGATIVE SYMPTOMS are ones that are ABSENT WHEN SHOULD BE PRESENT such as emotions
3. COGNITIVE SYMPTOMS include limitations of thought and reasoning. IQ is a few points below the rest of the population. DIFFICULTY understanding ABSTRACT concepts. MAIN PROBLEM IS disordered thought from ABNORMAL INTERACTIONS BETWEEN THE CORTEX, THALAMUS AND CEREBELLUM.
4. SOME CONDITIONS RESEMBLE SCHIZOPHRENIA in their symptoms, such as mood disorder patients have trouble with delusions. people with substance abuse have trouble with hallucinations and people with huntington's disease have trouble with hallucinations, delusions AND disordered thinking.
STATS - since the mid 1900s, schizophrenia has been declining in many countries, it appears to be less severe than it used to. occurs in ALL ETHNIC GROUPS. MORE COMMON IN CITIES than rural areas. 10 TO 100 TIMES MORE COMMON IN US AND EUROPE.
1. more common in men than women. more severe in men. people with schizo DIE YOUNGER on average. can get ACUTE - sudden onset or CHRONIC - gradual onset
  1. usually diagnosed after 20. people who are diagnosed later in life showed problems in childhood such as attention and memory deficits.
2. SCHIZOPHRENIA MYSTERIES - more common in people with type 2 (adult onset) diabetes. women with schizophrenia before birth usually give birth to daughters, breakdown after birth, usually have sons.
GENETICS IN SCHIZOPHRENIA
1. DOESN'T DEPEND ON A SINGLE GENE. TWIN STUDIES do show a genetic basis however and the more closely biologically related people are, the greater risk of schizophrenia. e.g. MONOZYGOTIC TWINS have a higher CONCORDANCE RATE than DZ twins. HOWEVER MZ twins only have 50% concordance, not 100%. DZ TWINS AND SIBLINGS have the same genetic resemblance but DZ twins have a higher similarity (due to environment)
2. ADOPTION - children with a mother with schizophrenia have a high probability of schizophrenia too even if adopted by mentally healthy parents. therefore suggests a GENETIC BASIS. HOWEVER, we cannot be sure that the schizophrenia isn't due to PRENATAL ENVIRONMENT, for example, people with S will smoke, drink, use drugs, eat unhealthily.
3. MORE THAN 12 GENES ASSOCIATED with schizophrenia. such as DISC1, which controls the generation of new neurons in the HIPPOCAMPUS. HOWEVER, no statistically significant relationship between schizo and any of the genes previous studies identified.. (SANDERS et al. 2008)
4. A PROMINENT hypothesis is that cases of schizophrenia arise from new mutations. however schizophrenia is present in 1% of the population so is there really a mutation that is THAT common. could the mutation be in any of several hundred genes. MORE LIKELY that it is a DELETION of a gene, a common error in reproduction. Schizophrenia is more common in children of older fathers.
NEURODEVELOPMENTAL HYPOTHESIS - schizophrenia develops due to abnormalities in the prenatal or neonatal (new born) development of the nervous system. the developing brain is vulnerable to other disturbances. brain development could be affected by poor nutrition, low birth weight, premature birth, complications during delivery. Schizophrenia has been linked to HEAD INJURIES IN EARLY CHILDHOOD. however could be that early symptoms of schizophrenia increased the risk of head injuries.
1. SEASON OF BIRTH EFFECT IN S. 5-8% greater probability of developing schizophrenia if born in winter. could be due to CONDUCTING VIRAL INFECTIONS in autumn of being pregnant, the virus will impair the child's crucial stage of brain development.
BRAIN ABNORMALITIES IN SCHIZOPHRENIA
1. people with schizophrenia have less than average grey and white matter and larger than average ventricles (fluid-filled spaces in the brain). the strongest deficits were in the left temporal and frontal areas. the THALAMUS IS SMALLER THAN AVERAGE. also weaker than average connections from dorsolateral prefrontal cortex to other brain areas.
  1. people with schizophrenia show deficits of memory and attention, the same as someone with damage to temporal or prefrontal cortex would. cell bodies are also smaller than normal. people with schizophrenia have LESS THAN NORMAL ACTIVITY IN THE LEFT HEMISPHERE.
    1. PROBLEMS WITH STUDYING BRAIN ABNORMALITIES - people with schizophrenia are more likely to take drugs / alcohol etc so the brain abnormalities might result from this. not sure if brain damage in schizophrenia is progressive (gets worse over time) or gets worse as the person ages. studies have shown that in young people, no difference in severity compared to older people. NEURONS might be SHRINKING but not dying.
TREATMENTS
1. chlorpromazine relieves the positive symptoms of schizo. antipsychotic drugs also alleviate symptoms. these drugs all BLOCK DOPAMINE SYNAPSES. the drugs that are most effective are the most effective at blocking dopamine receptors.
  1. DOPAMINE HYPOTHESIS - schizophrenia results from excess activity at dopamine synapses in certain brain areas. e.g. neurons release dopamine at a faster than average rate and synthesise more to replace the molecules they do not absorb. higher dopamine release. FOR THE DOPAMINE HYPO - drugs such as cocaine induces SUBSTANCE-INDUCED PSYCHOTIC DISORDER with the positive synptoms of schizophrenia.
2. GLUTAMATE HYPOTHESIS - states that there is DEFICIENT ACTIVITY AT GLUTAMATE SYNAPSES, especially in the prefrontal cortex. DOPAMINE INHIBITS GLUTAMATE RELEASE OR GLUTAMATE INHIBITS DOPAMINE RELEASE.
  1. schizophrenia is associated with lower than normal release of glutamate and fewer than normal receptors in the prefrontal cortex and hippocampus. SUPPORT FOR THE GLUTAMATE HYPOTHESIS - Phencyclidine (PCP) 'angel dust' inhibits the NMDA glutamate receptors, shows intoxication and slurred speech and in larger doses it produces positive and negative symptoms of schizophrenia.
    1. EVIDENCE found when PCP and KETAMINE are given to preadolescents, therefore schizophrenia and the effects of PCP develop well after puberty.

Next up

Description

Resource summary

Similar

	Created by becky.waine about 11 years ago