EXCITING NEW DEVELOPMENTS
That separation anxiety is a common antecedent of panic disorder has been noted.
The recent work by Jerome Kagan and associates indicates the frequency of behavioral inhibition in children of patients with anxiety disorders and the possibility that behavioral inhibition may be a precursor of social anxiety disorders. This emphasizes the importance of continuity of adult with childhood anxiety disorders. Investigation of childhood disorders clearly has many technical and ethical problems, but they afford a close look at the early phases of a pathogenic process before it is obscured by multiple secondary reactions and adaptations.
The work of Dan Pine et al. (1998), who demonstrated carbon dioxide sensitivity, paralleling adult panic patients, in anxious children, and more particularly differential CO2 sensitivity between separation anxious and socially anxious children, opens up an entire new field of investigation. Further, the attempt to find a common pathophysiology that underlines both carbon dioxide/lactate hypersensitivity and separation anxiety brings us to the question of endorphinergic regulation since endorphines regulate both of these processes.
That normals have so little effect from lactate and carbon dioxide speaks to the possibility of some protective mechanism that has been impaired in panic patients. A recent pilot study by Smit Sinha et al. (submitted manuscript) showed that the infusion of naloxone prior to lactate infusion led to marked hyperventilation and symptomatic complaint with salient dyspnea, resembling the clinical appearance of the so-called non-fearful panic. It is often not recognized that the definition of panic disorder had changed to include states of acute transient distress that are not accompanied by fearful emotions since such patients commonly exist in medical facilities, where they may undergo negative cardiac catheterizations.
One approach to the phenocopy problem is to subdivide patients with apparently common syndromes by their physiological reactivity. The work of the teams led by Griez in Maastricht and by Bellodi in Milan suggests that the pathophysiology underlying carbon dioxide hypersensitivity is closely tied to a specific genetic causal process. Griez cautiously points out that there may be specific, genetic, cognitive factors, such as anxiety sensitivity, that participate in this process. Studies of CO2 hypersensitivity during sleep, with a view to showing that panic patients are hypersensitive to endogenous carbon dioxide fluctuations, might prove a useful strategy in achieving a homogeneous pathophysiological state.