Carlson’s chapter on schizophrenia isn’t very clear. I’ve tried to pin down what he thinks on
four questions. (Query: What does Dr. Ramsay think on these points?)
1. WHAT ARE THE SYMPTOMS OF SCHIZOPHRENIA?
1) positive: obsessions, hallucinations, thought disorder #1
2) negative: withdrawal, anhedonia, etc.
3) cognitive: related to and formerly classed with negative
= thought disorder #2
Comment: He really is talking about 2 different sorts of thought disorder:
#1: “Positive”: disorganized irrational thinking: “Schizophrenics have great
difficulty arranging their thoughts logically and sorting out plausible
conclusions from absurd ones. In conversation they jump from one topic to
another as new associations come up. Sometimes they utter meaningless
words or chose words for rhyme rather than meaning.”
o “Probably the most important symptom of schizophrenia”
o This is a pretty good description of “hebephrenic” thought, and it
apparently assorts with positive symptoms. He probably no longer
thinks it’s “the most important”.
#2: “Negative” or “Cognitive”: Poor attention, low motor speed, poor
learning and memory, poor abstract thinking, poor problem solving
o This is different from #1. It pretty well adds up to stupidity, and
Carlson says it isn’t specific to schizophrenia but is also found in
other brain damage syndromes - especially in cases of PFC damage.
Comment: Traditionally, CNS neuron loss was thought to be associated with the
negative symptoms. This was the explanation of why the antipsychotic drugs
couldn’t reverse negative systems.
Carlson now associates both negative and cognitive deficits with
hypofunction in the PFC. The hypofunction is presumably caused by cell
loss – which is worst in the PFC – but it is not identical to cell loss since the
“atypical” antipsychotics can reverse it. Perhaps PFC loss of some cells
causes hypofunction in the cells that remain. 2. WHAT ARE THE CAUSES OF SCHIZOPHRENIA?
1) A genetic tendency – DISC1 gene(sufficient in some cases?)
2) An environmental insult (sufficient in some cases?)
3) Pre- or perinatal cell loss
4) Further cell loss in young adulthood
5) Prefrontal cortex hypofunction plus N.Acc DA over-acitivity
3) WHAT IS THE SEQUENCE OF EVENTS?
1) First the genetic tendency exists - probably a variety of genes - incomplete
penetrance (genetics alone won’t cause the phenotype). In some cases due to
elderly father and mutations in germline (would this be