Abstract
In recent years, an avalanche of data, comprising more than 95 percent of all the brain findings ever linked to behavior, has inundated psychiatry.1 New investigative tools have uncovered a vast storehouse of measurable brain oddities that correlate seductively with classical psychiatric syndromes. In particular, state-of-the-art computerized scanners2–4 now provide increasingly fine resolution of brain images that have led to a bonanza of apparent empirical support for the neuropsychiatric school of thought.
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Notes
Yudofsky and Hales, “The Reemergence of Neuropsychiatry,” p. 4.
Andreasen, The Broken Brain, pp. 108, 172–173, 176.
Nancy Andreasen, Gregg Cohen, Greg Harris, Ted Cizaldo, Jussi Parkkinen, Karim Rezai, and Victor Swayze, “Image Processing for the Study of Brain Structure and Function: Problems and Programs,” Journal of Neuropsychiatry 4:2 (Spring, 1992), pp. 125–133.
Robert Hendren and Janet Hodde-Vargas, “Neuroimaging in Schizophrenia,” Psychiatric Times (September 1992), pp. 17–18.
Jeffrey Coffman, “Computed Tomography in Psychiatry,” in Brain Imaging: Applications in Psychiatry, ed. Nancy Andreasen (Washington D.C.: American Psychiatric Press, 1989), pp. 1–3.
Nancy Andreasen, “Nuclear Magnetic Resonance Imaging,” in Andreasen, ed., Brain Imaging, p. 67.
Edward Edelson, “Scanning the Body Magnetic,” Science 83 (July-August 1983), pp. 60–65.
Michael Devous, “Imaging Brain Function by Single-Photon Emission Computer Tomograph,” in Andreasen, ed., Brain Imaging, pp. 148–150.
Henry Holcomb, Jonathan Links, Caroline Smith, and Dean Wong, “Positron Emission Tomography: Measuring the Metabolic and Neurochemical Characteristics of the Living Human Nervous System,” in Andreasen, ed., Brain Imaging, pp. 235–236.
Sandra Blakeslee, “Scanner Pinpoints Site of Thought as Brain Sees or Speaks,” New York Times (1 June 1993), pp. Cl, C3.
Gina Kolata, “Improved Scanner Watches the Brain As It Thinks,” New York Times (14 July 1992), pp. Cl, C6.
Nora D. Volkow and Laurence R. Tancredi, “Biological Correlates of Mental Activity Studied With PET,” American Journal of Psychiatry USA (April 1991), pp. 439–440, 442.
Andreasen, The Broken Brain, pp. 166–171, 226.
Hendren and Hodde-Vargas, pp. 19–20.
Tomb, Psychiatry for the House Officer, p. 25.
Andreasen, The Broken Brain, p. 178.
Andreasen et al., “Image Processing,” pp. 125–133.
Ruben Gur, Roland Erwin, and Raquel Gur, “Neurobehavioral Probes, for Physiologic Neuroimaging Studies,” Archives of General Psychiatry 49 (May 1992), pp. 409–414.
Hendren and Hodde-Vargas, pp. 18–20.
Robert Innis, “Neuroreceptor Imaging with SPECT,” Journal of Clinical Psychiatry 53:11 (November 1992 supplement), pp. 29–34.
John Lauerman, “Windows on the Brain: Functional Brain Imaging Techniques Add Objective Scale to Psychiatric Evaluation and Treatment,” Psychiatric Times (February 1993), pp. 16–17.
Donald Mender, notes for lecture on CT, MRI and PET scanning in psychiatry given in 1988 at St. John’s Episcopal Hospital, Smithtown, New York.
Marc Schuckit, “An Introduction and Overview to Clinical Applications of Neuro SPECT in Psychiatry,” Journal of Clinical Psychiatry 53:11 (November 1992 supplement), pp. 3–6.
Ronald Van Heertum, “Brain SPECT Imaging and Psychiatry,” Journal of Clinical Psychiatry 53:11 (November 1992 supplement), pp. 7–12.
Nora Volkow and Laurence Tancredi, “Current and Future Applications of SPECT in Clinical Psychiatry,” Journal of Clinical Psychiatry 53:11 (November 1992 supplement), pp. 26–28.
Scott Woods, “Regional Cerebral Blood Flow Imaging with SPECT in Psychiatric Disease: Focus on Schizophrenia, Anxiety Disorders, and Substance Abuse,” Journal of Clinical Psychiatry 53:11 (November 1992 supplement), pp. 20–25.
Blakeslee, “Scanner,” pp. C-1, C-3.
Kolata, pp. C1, C6.
Volkow and Tancredi, “Biological Correlates,” pp. 439–440, 442.
Andreasen, The Broken Brain, pp. 28, 120–121, 194, 225, 238.
Juan M. De Lecuona, K. Sunny Joseph, Naveed Iqbal, and Gregory Asis, “Dopamine Hypothesis of Schizophrenia Revisited,” Psychiatric Annals 23:4 (April 1993), pp. 179–185.
Tomb, pp. 25–26.
Winson, p. 238.
Andreasen, The Broken Brain, pp. 233–234.
Tomb, pp. 42–43, 45–46.
Andreasen, The Broken Brain, pp. 181–182, 234.
Burr Eichelman, “Aggressive Behavior: From Laboratory to Clinic,” Archives of General Psychiatry 49 (June 1992), pp. 489–490.
Markku Linnoila and Matti Virkkunen, “Aggression, Suicidally, and Serotonin,” Journal of Clinical Psychiatry 53:10 (October 1992 supplement), pp. 46–51.
Andreasen, The Broken Brain, p. 230.
“Genes, Viruses, Hormones and Schizophrenia Etiology,” Clinical Psychiatry News, August 1992, p. 22.
Andreasen, The Broken Brain, pp. 185–188.
Morton Low, “Evaluation of Psychiatric Disorders and the Effects of Psychotherapeutic and Psychotomimetic Agents,” in Current Practice of Clinical Electroencephalography, ed. Donald Klass and David Daly (New York: Raven, 1979), pp. 395–410.
John Horgan, “Eugenics Revisited,” Scientific American 268 (June 1993), pp. 122–131.
Kaplan and Sadock, Synopsis of Psychiatry, p. 79.
Larry J. Siever and Kenneth L. Davis, “A Psychobiological Perspective on the Personality Disorders,” American Journal of Psychiatry 148:12 (December 1991), p. 1648.
Tomb, pp. 41–43, 153–155.
Eichelman, p. 489.
Lishman, pp. 168–171.
Arnold Merriam, Alice A. Medalia, and Bernard Wyszynski, “Schizophrenia as a Neurobehavioral Disorder,” Psychiatric Annals 23:4 (April 1993), pp. 171–174.
Richard Restak, “See No Evil,” The Sciences (July-August 1992), p. 18.
Tardiff, p. 495.
Tomb, pp. 123–124.
Since the 1970s, a syndrome first labeled “episodic dyscontrol” and now known as “intermittent explosive disorder” began to draw particular psychiatric interest in the quest to explain human violence as a limbic disturbance. Patients with this diagnosis are prone to sudden assaultive episodes; between paroxysms their behavior remains nonviolent, and they may experience remorse or amnesia for their destructive acts. Affected patients are more likely than the general population to have undergone traumatic births, exhibited behavioral difficulties as children, caused motor vehicle accidents, and shown constitutional sensitivities to alcohol. On laboratory testing, many demonstrate electrical disturbances and other evidence of limbic brain damage. Sparser data from different patients implicate damage within nonlimbic regions, such as frontal structures that regulate social inhibitions, in the genesis of aggressive behavior. Evidence includes a generally increased but still rough association of violence with seizures, head injuries, abuse during childhood, malnutrition, learning disabilities, diminished IQ, subtle defects on neuropsychological testing, and assorted electroencephalographic abnormalities.
Andreasen, The Broken Brain, pp. 120–121.
Eichelman, p. 489.
Merriam et ah, pp. 174–177.
Restak, “See No Evil,” pp. 18, 19.
Tardiff, pp. 494–495.
Tomb, pp. 122–123.
Martin Drooker and Robert Byck, “Physical Disorders Presenting as Psychiatric Illness: A New View,” Psychiatric Times (July 1992), pp. 19–23.
Tomb, pp. 118–120.
Frank Ayd, “Novel Antipsychotics, Antidepressants Surveyed in S. E,” Psychiatric Times (August 1993), pp. 7–8.
Miriam Tucker, “Clozapine-like Antipsychotics Seen as Wave of the Future,” Clinical Psychiatric News (January 1993), pp. 1,13.
Freedman, p. 862.
Jonathan Pincus and Gary Tucker, Behavioral Neurology (Oxford: Oxford University Press, 1985), pp. 131, 137–138.
Andreasen, The Broken Brain, pp. 222, 230.
Winson, p. 238.
Andreasen, The Broken Brain, pp. 136–137.
Linda Barr, “Serotonin in Obsessive-Compulsive Disorder,” Psychiatric Times (July 1993), pp. 24–25.
Jeffrey Cummings, “Neurobiological Basis of Obsessive-Compulsive Disorder,” Psychiatric Times (January 1993), p. 16.
Roberto Dominguez, “Serotonergic Antidepressants and Their Efficacy in Obsessive-Compulsive Disorder,” Journal of Clinical Psychiatry 53:10 (October 1992 supplement), pp. 56–59.
Tomb, pp. 75, 79.
Siever and Davis, pp. 1648–1650, 1653.
Schizotypal personality disorders and frank schizophrenia in particular share common genetic determinants, atten-tional deficits, eye movement abnormalities, and, during crises, increased dopamine metabolism. Among impulsive personality disorders, certain varieties tend to occur in the same families, suggesting a genetic element common to such subtypes. Impulsively antisocial traits correlate with biological indices of an impaired ability to suppress negatively reinforced behaviors; the indices include a reduced sedation threshold, disinhibited motor function, accelerated habituation of skin conductance, and decreased sympathetic response. Patients whose personality disturbances involve mood lability exhibit sleep patterns similar to those seen in depression, exaggerated behavioral reactions to drugs that enhance the action of norepinephrine, and improvement after treatment with several other chemicals that affect neurotransmitter function. Personality disorders dominated by anxiety show chronically reduced thresholds for sedation, weak habituation, and sympathetic overactivity (Siever and Davis, pp. 1648–1655).
Siever and Davis, pp. 1651–1653.
De Lecuona et al, pp. 182, 184.
Kaplan and Sadock, pp. 72–74.
Ross Baldessarini, Chemotherapy in Psychiatry (Cambridge: Harvard University Press, 1985), p. 40.
Tomb, pp. 25–26.
Paul Genova, “Is American Psychiatry Terminally Ill?” Psychiatric Times (June 1993), p. 19.
Tomb, pp. 26–27.
Horgan, p. 127.
Capra, p. 120.
Unfortunately, the molecular paradigm, applied successfully to the structure of the gene in the 1940s, 1950s, and 1960s, has today become overgeneralized in its application to other areas, including neuropsychiatric research (Capra, pp. 103–104, 113–114, 119–120).
Andreasen, The Broken Brain, p. 182–183.
Kaplan and Sadock, p. 74.
Tomb, pp. 42–43, 45–46.
It is a gross oversimplification to seek only single causes for any illness. The “single lesion” myth of disease causality arose originally in the germ theories of the nineteenth century, expanded into molecular biology and genetics, and has now been misapplied to the treatment of many multifactorial disease processes. A more balanced view must also account for the fact that the response of a host organism contributes at least as much to pathological states as does the virulence of a noxious agent (Capra, pp. 111, 150, 153–154).
Perceptual distortions only indirectly related to brain processes seem to figure strongly in the genesis of aggression. Schizophrenia, mania, cocaine-induced paranoia, and other delusional states number among the most potent identified antecedents of violence. Beyond frank psychosis, simple mismatch between perception and behavioral abilities— producing, for example, frustration in the mentally retarded— can lead to assaultive outbursts. Animal models support these observations in humans: External interference in rats’ ability to smell alters aggressive behavior in experimental contexts. Social factors correlate with violent behavior. Animal studies suggest that some brain disease processes produce violence only indirectly by changing territorial behavior. The politics of social dominance and even parental input contribute to violence in societies of rodents and primates. Among human psychiatric patients, such factors as institutional settings, interpersonal space, childhood neglect, inappropriate physical restraint, domestic trigger situations, and the psychotherapist’s behavior may all play inflammatory roles. The most powerful predictors of violence in clinical psychiatric practice turn out to be such quasi-tautological factors as previous assaultive history, violent plans, availability of a weapon, and past record of other impulsive behaviors like suicide, sexual promiscuity, profligate spending, property destruction, and reckless driving.
Eichelman, pp. 489–490.
Restak, “See No Evil,” pp. 18–19.
Tardiff, pp. 494–498.
Freedman, pp. 858–859.
Theodore Lidz, “Images in Psychiatry: Adolf Meyer,” American Journal of Psychiatry 150:7 (July 1993), p. 1098.
Owen Flanagan, The Science of Mind (Cambridge: M.I.T. Press, 1991), p. 95.
Steven Cooper, “Neuroscience in the Future of Psychiatry,” American Journal of Psychiatry 145:2 (February 1988), p. 272.
W. W. Meissner, “The Psychotherapies: Individual, Family, and Group,” in Nicholi, ed., The New Harvard Guide, p. 463.
Tomb, pp. 154–155.
Eric Marcus, Psychosis and Near Psychosis (New York: Springer-Verlag, 1992), pp. 217–249.
Glen Gabbard, Susan Lazar, and Elizabeth Hersh, “Cost-Offset Studies Show Value of Psychotherapy,” Psychiatric Times (August 1993), p. 21.
Yudofsky and Hales, “The Reemergence,” p. 4.
“Don’t Replace Psychotherapy With a Pill, Experts Remind Public-Sector Psychiatrists,” Psychiatric News (3 July 1992), p. 13.
Elio Frattaroli, “The Mind-Body Problem and the Choice of Intervention,” The Psychiatric Times (November 1991), pp. 75–76.
Gabbard et al., p. 21.
Restak, “See No Evil,” p. 20.
American Psychiatric Association, Biographical Directory (Washington: American Psychiatric Association, 1989), p. 1573.
Thomas Szasz, The Myth of Mental Illness (New York: Harper & Row, 1974), p. 262.
Frattaroli, p. 73.
Genova, p. 20.
An extreme example of neuropsychiatric control of patients by doctors occurred in Russia. This was not simply a result of Communist totalitarianism. Balinksy first imported the neuropsychiatric tradition from Greisinger’s Germany to St. Petersburg, home of the Russian Tsar, in the nineteenth century. Korsakov, Bekhterev, Sechenov, and Pavlov then promoted neuropsychiatry in pre-Revolutionary Russia. Its hold hardened into stone when the first Russian institute of psychology opened at the University of Moscow in 1911; the institute purposely imported German staff and materialist ideas to use as its own. Though the chaos of the Soviet Revolution in 1917 brought a brief respite of ferment and eclectism, the grip of materialistic dogma soon afterward grew tighter than ever and finally became a stranglehold around psychiatric practice. From then on, classification of psychiatric illnesses in Russia embraced an almost exclusively somatic bias. Its criteria for psychiatric diagnoses included electroencephalographic findings, odd body shapes, and even heart abnormalities. Punitive neuropsychiatric treatments like sulfazine, atropine, and insulin coma were employed (Mender, notes for a seminar on Soviet psychiatric diagnosis).
Capra, pp. 134, 148–149.
The early success of chemicals in preventing and curing infectious diseases inspires modern enthusiasm for drug treatment techniques in general; however, confusion abounds regarding the real cause of this success. The decrease in infectious diseases over the last 150 years has stemmed more from general improvement in nutrition and sanitary conditions than from any other factor (Capra, pp. 131–142).
Richard Restak, “Brain by Design,” The Sciences (September-October, 1993), pp. 32–33.
Capra, pp. 155, 249.
Restak, “Brain by Design,” pp. 32–33.
Herbert Marcuse, One-Dimensional Man (Boston: Beacon Press, 1964), p. 158.
Hearnshaw, p. 122.
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© 1994 Donald Mender
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Mender, D. (1994). Neuropsychiatry’s Current State. In: The Myth of Neuropsychiatry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-6010-8_2
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