By Steven P. Roose, Robert A. Glick
The idea of hysteria has lengthy held a vital position in psychoanalytic theories of brain and treatment. but, lately, info from the neurosciences and from pharmacological reports have posed a compelling problem to psychoanalytic versions of anxiety. One significant final result of those stories is the conclusion that nervousness either organizes and disorganizes, that it may be either symptom and signal. In Anxiety as Symptom and Signal, editors Steven Roose and Robert Glick have introduced jointly exotic individuals to deal with those diverse dimensions of anxiety. a piece of unique papers on "Anxiety as Symptom" covers evolutionary, neuroanatomical, genetic, and developmental perspectives. A complementary part on "Anxiety as sign" makes a speciality of the meanings and capabilities of tension within the scientific strategy; contributions deal with anxiousness in its ego-psychological, intersubjective, and relational dimensions.
The illuminating, readable assortment will develop clinicians' know-how of the varied study findings that now tell our realizing of anxiety. No much less importantly, it's going to deepen their appreciation of the richly variegated ways in which nervousness can form, and be formed via, the scientific approach.
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Extra info for Anxiety as Symptom and Signal
However, vocalizing may not have originated as a signal to the mother, but rather in a physiological role. We found that when hypothermic pups were devocalized (by cutting the nerves to the larynx or bypassing the larynx with a small plastic tube), they did not rewarm nearly as fast as vocal pups: they developed fluid in their lungs (pulmonary edema), and some failed to recover if left alone. A physiologic role for ultrasonic vocalization in supporting thermoregulatory response was first proposed in 1990 by Blumberg and Alberts, but has since been shown to be inconsequential at more normal body temperatures (Hofer and Shair, 1993).
A comprehensive theory of panic disorder, therefore, should include careful reference to both. This chapter therefore presents our most current thinking on brain function in panic disorder. THE NEUROANATOMICAL HYPOTHESIS Gorman et al. (1989b) presented a theory to explain the manifold clinical presentations of panic disorder and the curious observation that both medication and psychotherapy treatments effectively block panic attacks. The theory essentially holds that panic attacks themselves originate in hypersensitive loci within the brain stem, that anticipatory anxiety is a kindled effect of limbic lobe origin, and that phobic avoidance is a higher-order cognitive function originating in the prefrontal cortex.
For those most interested in the neurobiological mechanisms of anxiety, studies on drugs and neuropeptide modulators have provided the most compelling evidence that the isolation distress state of young rats provides a useful animal model of anxiety (for a recent review see Miczek, Tornatsky, and Vivian, 1991). In studies during the past 5 or 6 years, it has been found that most major classes of drugs that are useful in human anxiety have powerful and selective inhibitory effects on isolation-induced ultrasonic calls in rat pups, without affecting other behaviors or inducing signs of sedation.
Anxiety as Symptom and Signal by Steven P. Roose, Robert A. Glick