The history of panic disorder in modern medicine demonstrates the difficulty physicians have had for 150 years in separating panic disorder from cardiologic, neurologic, and other medical syndromes. The combination of psychologic and severe physiologic symptoms of panic disorder continues to befuddle physicians’ diagnostic accuracy to this day.
The term panic is derived from Pan, the name of the dwarfish Greek god of nature (D’Aulaire and D’Aulairc 1962). Pan was a lonely and moody god. When he was sad, he went off by himself and hid in a cool cave. If a wanderer happened to come upon him and disturb him, he would let out a scream so terrifying that whoever heard it took to his heels and fled in a fear that was called "panic." Early descriptions of panic attacks were provided in the English literature by Thomas Burton (1924) in his 17th century classic text The Anatomy of Melancholy:
Many lamentable effects this fear causeth in men, as to be red, pale, tremble, sweat, it makes sudden cold and heat to come over all the body, palpitation of the heart, syncope, etc. It amazeth many men that are to speak or show themselves in public assemblies, or before some great personages…
Physicians first began to describe patients with panic disorder in the mid-19th century. Many of these early descriptions were of patients with palpitations and chest pain who were referred to cardiologists. With no modern diagnostic tests (treadmill, angiogram), shorter lifespans of the general population, and four of the main symptoms of panic disorder (chest pain or tightness, tachycardia, dyspnea, and a choking or smothering sensation) being cardio-respiratory symptoms, it was difficult for these early physicians to discriminate patients with organic heart disease from patients with panic disorder. Indeed, Leff (1981), a cross-cultural psychiatrist, pointed out that the words angina, anxiety, and anguish are all derived from the same Greek root, which literally means to press tightly or strangle. Leff suggested that a single term, angh, was used in early Indo-European tests to describe the sensation of tightness or tightness or pressure on the chest, and that differentiation of this term to connote separate emotional and somatic causes of similar sensations only came in the late stage of development of Western society.
One of the earliest descriptions of patients with panic disorder was written by Hope, a British cardiologist. In 1832, he described patients with nervous palpitations in one of the first English textbooks of cardiology:
There are few affectations which excite more alarm and anxiety in the mind of the patient than this. He fancies himself doomed to become a martyr to organic disease of the heart, of the horrors of which he has an exaggerated idea; it is the more difficult to divest him of this impression because the nervous state which gives rise to his complaint imparts a fanciful gloom and desponding tone to his imagination.
A few years later, Williams (1836), another English physician, described patients with nervous and sympathetic palpitations of the heart.
In 1871, Da Costa, a civil war physician, described a syndrome that he labeled "irritable heart disease" that included symptoms of palpitations, tachycardia, dizziness, shortness of breath, chest pain, gastrointestinal distress, and "nervous symptoms" (headache, giddiness, and insomnia). Da Costa, in a description that echoes modern-day theory, noted it was "most likely that the heart became irritable from its over-action and frequent excitement and that a disorder of innervation keeps keeps it so." He theorized that both battle trauma and severe physical illness frequently precipitated the syndrome. After Da Costa's classic description, other wartime physicians described similar conditions in young male soldiers every decade or two.
In 1870, Myers, a surgeon in the Coldstream guards, described a syndrome similar to Da Costa's and labeled it "soldier's heart." During World War I, the subject of soldier's heart became quite popular; 39 papers were published about it in the 1916 British Medical Journal (Skerrit 1983). A new term, "effort syndrome," was introduced in 1917 by Sir Thomas Lewis. He described symptoms of breathlessness, chest pain, giddiness, exhaustion, palpitations, headache, sweatiness, shakiness, flushing, irritability, and cold extremities. With the United States entering World War I, the term "neurocirculatory asthenia" was introduced by Oppenheimer and colleagues in 1918. MacKenzie (1920) later suggested that these heart abnormalities were but a feature of a general condition later suggested to be a "war neurosis."
In 1918, the first provocative research was attempted to study the sympathetic nervous system role in effort syndrome. Fraser and Wilson injected adrenaline and felt they had reproduced these patients' symptoms. However, Wood emphasized in 1941 that injections of epinephrine caused equal symptoms in controls and patients.
Culpin (1920) was one of the first physicians to emphasize the association of effort syndrome with anxiety and phobias and to point out that treatment should be aimed at the underlying nervous problem, not the heart. During World War II, Wood (1941) published an account of 200 cases seen in the first year of the war with major symptoms described as breathlessness, fatigue, nervousness, dizziness, left chest pain, palpitations, headaches, trembling, sighs, and flushes. He concluded that the syndrome was due to an association between effort and fear, and favored psychotherapy as the treatment of choice. Jones and Lewis in 1941 also described the psychiatric conditions associated with effort syndrome, with anxiety the most common condition (31 percent of cases). The use of the term effort syndrome gradually declined during World War II and more specific psychiatric diagnoses came into favor (Skerrit 1983). Finally, Jones and Melleresh (1946), laying the foundation for future studies of lactate's association with panic disorder, found that effort syndrome sufferers would stop exercising at lower blood levels oflactate than controls. This was interpreted as a fear of damaging their hearts or "effort phobia."
Since World War II, several cardiologists have published papers supporting the "irritable heart" concept with new terminology such as "hyperkinetic heart syndrome" (Gorlin 1962) or "hyperdynamic beta-adrenergic circulatory state" (Frohlich et al. 1966). In the 1950s and 1960s, the term posttraumatic stress disorder (PTSD) came into favor to describe a psychologic state in young soldiers that resulted from massive trauma. Certainly, PTSD connotes a psychologic condition, but increased central noradrenergic activity has been postulated as a cause, and high levels of peripheral catecholamines have been reported (Kosten et al. 1987). The connection between PTSD and panic disorder is discussed in chapter 6.
Beard in 1880 popularized the term "neurasthenia" for a cluster of illnesses long recognized by medical professionals under such terms as "nervous prostration," "nervous disability," and "nervous asthenia." Among its many symptoms were headache, a variety of kinds of pain, lack of concentration, noises in the ears, pressure and heaviness in the head, morbid fears including specific phobias (fear of disease and work), dizziness, palpitations, insomnia, dyspepsia, sweating, tremors, poor appetite, and exhaustion.
Sigmund Freud (1894) dissected out from neurasthenia a syndrome with a smaller group of symptoms, including free-floating anxiety or anxious expectation as well as anxiety attacks with symptoms of tachycardia, nervous dyspnea, sweating, tremor, diarrhea, dizziness or vertigo, paresthesia, and congestion. Freud also described the anxious expectation and anxiety attacks that often led to common physiologic danger phobias (fears of snakes, thunderstorms, darkness) and to agoraphobia. Although Freud emphasized that some patients would have attacks in which they focused on one symptom such as chest pain, dizziness, or tachycardia, his description did not mention prior accounts of irritable heart syndrome or soldier's heart. Freud initially theorized that sexual deprivation was the main cause of anxiety neurosis, but later progressed to the idea that psychoneuroses were caused by sexual and aggressive impulses going undischarged because they were repressed.
After World War I, Lewis (1940) recognized that the effort syndrome was also "one of the commonest chronic afflictions of sedentary town dwellers." Between the late 1920s and early 1940s, dyspnea associated with sighing respirations was noted by several clinicians as a common manifestation of chronic hyperventilation (Wolf 1947). In 1938, Soley and Schoch reported that all the symptoms of soldier's heart could be accounted for by involuntary hyperventilation and the resulting respiratory alkalosis. Also in the late 1930s, reports of "cardiac neurosis" began to appear in the literature. This was defined by Caughey (1939) as neuroses in which circulatory manifestations are the main subjective and objective features of the clinical problem.
Skerrit (1983) pointed out that medical authors still tend to see anxiety neurosis (or panic disorder) from the viewpoint of symptoms presenting to their own specialty. Thus, cardiologists diagnose patients with mitral valve prolapse (MVP), labile hypertension, hyperdynamic beta-adrenergic state, and atypical chest pain without recognizing a common overlap with panic disorder. Pulmonary physicians similarly write about hyperventilation syndrome; gastroenterologists, irritable bowel syndrome; and neurologists, patients with unexplained dizziness, without recognizing that these symptoms are often part of a larger syndrome — panic disorder.
A historical review would be incomplete without mention of two seminal psychopharmacologic breakthroughs in the treatment of panic disorder in England and the United States. In the early 1960s in England, Roth (1960) described the phobic-anxiety depersonalization syndrome and Sargant (1962) reported the effectiveness of monoamine oxidase inhibitors (MAOI) in patients with atypical depression (a subgroup of depressives who frequently had panic attacks). Meanwhile, in the United States, Donald Klein (1964) described the effectiveness of imipramine in treating chronically ill patients on a psychiatric ward who had symptoms of panic attacks and agoraphobia and had progressively constricted their activities until they were no longer able to travel alone for fear of being rendered suddenly helpless while isolated from family or friends. Klein found that treatment with imipramine decreased acute panic attacks and separation anxiety, and that the patients' agoraphobia gradually decreased as they were pushed to reenter feared social situations and found they were no longer subject to anxiety attacks. The striking aspect of Klein's study was that these patients had been nonresponsive to phenothiazines, sedative-hypnotics, and electroconvulsive therapy. Both Klein's and the English studies led to a biologic revolution in the field of panic disorder or anxiety neurosis, disorders that previously had been thought by many authorities to be primarily environmentally induced and thus treatable only with long-term psychotherapy.