reading questions for

Nancy Andreasen's The Broken Brain

Chapters 1-3

• How has our understanding of mental illness changed since the last century? How should we now view the mentally ill?
• Why is "The Broken Brain" a good name for this book?
• What is the difference in Freud's and Kraepelin's approaches to mental illness?
• How did Kraepelin's classification of disorders help the diagnosis of mental illness?
• How would behavioral therapy differ from the Freudian approach? From the biological approach?
• Which of the three methods would you say is based on the "medical model"?
• How close did your answer to the third question in chapter 2 come to Andreasen's description of the different therapies?
• Why is "reciprocal inhibition" (also known as "systematic desensitization") a behavioral therapy?
• How does the example of breakthroughs in the treatment of Parkinson's disease show the relatedness of the various neurological disciplines?
• Why are the "somatic" therapies (i.e. drugs and surgery) called "medical"?

Chapter 4

• What is "affect" and how does it help define the nature of "affective disorders"?
• "Dysphoria" is a major symptom of depression. What are others?
• "Euphoria" is a major symptom of mania. What are others?
• What is the relationship between depression and mania in bipolar affective disorder?
• When Andreasen says that schizophrenia is a chronic illness while affective disorders are episodic, how does that effect our judgment of the severity of the illness?
• "Schizophrenia" means "splitting of the mind", but is it the same as "split, or multiple, personalities"?
• What is the difference between a delusion (such as paranoia) and hallucinations? What are other symptoms of schizophrenia? Why are some symptoms called "florid", or "positive", while others are called "defect", or "negative"?
• What are the physical symptoms of anxiety disorders, and how do they tie in with the "autonomic nervous system"? Psychological symptoms?
• What was Freud's role in the definition of anxiety disorders?
• How do phobic disorders, anxiety states, and post-traumatic stress disorders differ from one another? What are the differences between panic, generalized anxiety, and obsessive-compulsive disorder?
• How do symptoms of dementia compare and contrast with symptoms of other disorders?

Chapter 5

• How did "natural experiments" lead to the "localization hypothesis"?
• Distinguish between "cerebral specialization" and "cerebral dominance". How do "Broca's area" and "Wernicke's area" exemplify these two concepts?
• Both Andreasen and Isaacson (in The Undaunted Psychologist) say that there are no accurate metaphors to describe the functions of the brain. How do some of the models in this book and in Isaacson's chapter fall short?
• Where is the cerebral cortex?
• Look at Fig.2 on page 93, then read pages 94-95. What different senses do the occipital and temporal lobes moderate? What else does the temporal lobe control (remember Isaacson)?
• Why would the parietal lobe, which is home to the "somatosensory area", be thought to control "spatial orientation"?
• How would the "motor control area" in the frontal lobe differ from the "somatosensory area"? What else does the frontal lobe control?
• Again going back to Isaacson, which parts of the brain described by Andreasen may be part of the neocortex? The limbic system? The R-complex?
• The thalamus ("marriage bed") comes up often in later chapters. What is its function? What do the basal ganglia do?
• How do the cerebral hemispheres (left and right) effect motor control and language functions?
• What does H.M., who had his hippocampus removed and then suffered anterograde amnesia, show us about how memory works in the brain? How does anterograde amnesia highlight the difference between short-term and long-term memory?
• How does the neuroendrocine system ("hormones") connect the brain with the rest of the body?
• What is an "action potential" and what is its course through a neuron? Which comes first in an action potential, the axon or dendrites?
• What is the role of neurotransmitters, and what is their connection to the action potential?
• How, according to Andreasen, can knowledge of the brain change our views of mental illness?

Chapter 6 & 7

• What is diagnosis, and why is it so important to treating mental illness?
• What is DSM-III? How does it reflect the medical model (over psychodynamic or behavioral models) of mental illness?
• How does DSM-III help diagnosis and treatment (think especially in terms of "reliability" and "validity")?
• In terms of "history", "differential diagnosis", and laboratory confirmation, how has psychiatric diagnosis changed with the return of the medical model?
• How do brain imaging (like CT, NMR, and PET scans), neurochemical tests (such as MHPG measures), and mapping electrical activity (or "EEG") each differ from one another? What role does each type of laboratory test play in diagnosis?

Chapter 8 & 9

• Why are psychoactive drugs considered "treatments" for mental illness, as opposed to both restraints and psychotherapy?
• What is the difference between side and target effects? For example, list both types of effects for chlorpromazine.
• How did the effect of chlorpromazine (a neuroleptic) change when it was chemically altered into imipramine (an antidepressant)?
• How do antianxiety agents differ from antipsychotics, even though both are called "tranquilizers"?
• Which different disorders do MAOIs and lithium treat? How is lithium different from antianxiety agents?
• What is the "placebo effect", and why does it force researchers to use double-blind trials when testing new drugs?
• Why is speaking of the "cause" of a particular illness likely to lead to confusion?
• Now that you have read about brain functions (e.g. the roles of brain structures and neurotransmitters) and the diagnosis of mental illness (e.g. the classification of schizophrenia and affective disorders), you can understand the sections on the causes of different disorders. What are the types of ways the brain can "break down" (e.g. through abnormalities in brain structure)?
• How can we trace these different types of causes? For example, what do twins studies tell us about genetic factors for schizophrenia or affective disorders?

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