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Panic attacks are an enormously intriguing clinical puzzle that has widespread ramifications in medicine and neurology. For instance, almost half of all panic patients are initially seen in medical emergency rooms, with complaints of chest pain and difficulty breathing which resemble an acute heart attack. Another widespread somatic disorder, migraine headache, is often co-morbid with panic anxiety. Further, asthma, emphysema and smoking predispose to panic disorder. To account for such observations, including the striking air hunger which is not a feature of common danger-incited fear, we came to hypothesize that a dysfunction in endogenous opioid activity - which modulates a phylogenetically old system that modulates breathing and pain perception, as well as social-affiliative behavior and separation anxiety - might explain these otherwise obscurely related clinical states. The original suffocation false alarm theory of panic disorder hypothesizes a dysfunction in a specific adaptive emergency mechanism which evolved to detect and deal with imminent suffocation (Klein 1993). The spontaneous panic is viewed as a false alarm emanating from an episodically hypersensitive suffocation sensor, overreacting to physiological fluctuations (e.g., increasing CO2) or perceptions (e.g., still air in complete enclosures). The expanded suffocation false alarm theory is an attempt to subsume its diverse aspects - the phenomenology of clinical panic, its intriguing antecedents of traumatic loss and separation anxiety, and its respiratory dysregulation - under a single dysfunction, that of regulatory opioid systems.
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