A neuroanatomical hypothesis for panic disorder

Abstract

Anxiety disorders, the most common psychiatric conditions in the United States, have generated a great deal of research and scientific debate. Panic disorder, the best-studied anxiety disorder, is often believed to be either a biological disease or a psychological disease. The authors present a neuroanatomical model of panic disorder that attempts to reconcile these views. The model locates the three components of the disease--the acute panic attack, anticipatory anxiety, and phobic avoidance--in three specific sites of the CNS: the brainstem, limbic system, and prefrontal cortex, respectively. The authors suggest experiments to test their model.

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

“…Attempting to explain clinical observations that both pharmacological intervention and cognitive behavioral therapy are successful in treating PD, Gorman and colleagues (1989b) posited a neuroanatomical hypothesis of panic consisting of a network of cortical, limbic and brainstem structures implicated in mediating the phobic avoidance, anticipatory anxiety and panic attacks observed in PD patients; the neuroanatomical hypothesis of PD was revised based on preclinical rodent models identifying the neural structures mediating fear-conditioning and avoidance behavior (Gorman et al, 2000). As Klein has repeatedly indicated (Klein, 1993;Klein, 2002;Preter and Klein, 2008), although panic and fear share many characteristics they have important physiological distinctions such as the lack of HPA-axis activation in panic (Hollander et al, 1989;Kellner and Wiedemann, 1998;Levin et al, 1987;Woods et al, 1988), which is a common neuroendocrine response to fear-related stimuli like exposure to a predator (Blanchard et al, 1998), predator odor (Masini et al, 2005;Masini et al, 2006), or conditioned fear (Cordero et al, 1998), and the presence of dyspnea in panic, which rarely occurs in natural fear responses (Klein, 1993;Preter and Klein, 2008).…”

Olfactory Hallucinations without Clinical Motor Activity: A Comparison of Unirhinal with Birhinal Phantosmia

“…Indeed, confusion can also occur with respect to what has been called chronic hyperventilation syndrome [330], panic disorder [331,332], hyperventilation induced seizures [333], phobic anxiety depersonalization syndrome [293] and Rett’s syndrome [334]. Hyperventilation induced seizures, albeit rarely tonic-clonic or partial [333], has been the subject of many case reports [300,329,335].…”

Functional neuroanatomy in panic disorder: Status quo of the research

“…Gorman et al[10] introduced a neuroanatomical model that was aimed at integrating the different views of PD as either a biological or a psychological disease. The authors suggested experiments to test their theories.…”

“…According to Gorman et al[10] three components of PD: (1) acute panic attacks, (2) anticipatory anxiety; and (3) phobic avoidance are located in three specific sites of the CNS: The brainstem, limbic system, and prefrontal cortex. These three neural systems were suggested to be structurally and functionally closely connected, reflecting manifold interactions of the three mentioned clinical features.…”

“…These three neural systems were suggested to be structurally and functionally closely connected, reflecting manifold interactions of the three mentioned clinical features. Hence, according to Gorman et al[10] different treatments for PD and agoraphobia not only affect different symptoms of the illness but also different parts of the brain. Thus, according to the authors, antipanic drugs like tricyclic antidepressants (TCAs) or monoamine oxidase inhibitors (MAOIs) block brainstem-provoked panic attacks; benzodiazepines and relaxation training reduce anticipatory anxiety via the limbic system, and desensitization and cognitive therapies relieve phobic avoidance by influencing functions of the prefrontal cortex.…”