Today we're going to go for a ride in our time machine through the 19th century. Grab a cup of coffee, hop into our cozy little machine, lean back, put your feet up, and enjoy.
Debunking ancient theories of asthma:
Our time machine takes us back to 400 B.C and we watch as
Hippocrates and his fellow physicians study respiratory disorders and work on defining asthma as a medical term. Now we fast forward to the year 1816 on a hot and humid day in France and find
Rene Laennec leaning with his ear on one end of rolled up bundle of papers, with the other end on the chest of a large, dusky, perspiring lady who's hunched up on the docotr's bed panting for air.
The object he's using is clearly the first stethoscope, yet on this day he simply called it le cylindre. It would be a few years before he would be pressured by his peers into calling his object the stethoscope. It would turn out to be a revolutionary device responsible for the evolution of a term called asthma throughout the rest of the 19th century. Laennec perhaps had no clue his invention would set off a hunt to redefine asthma, or at least provide the tool for such a task.
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| Laennec's stethoscope |
Over the ensuing years, of which go by fast in the comfy confines of our time machine, we see a growing number of physicians using this tool to help them better diagnose and treat their patients. And it was mainly this tool that sparked a hunt by asthma physicians to redefine asthma so it represents the disease as we know it today. Yet how this evolution occurred is the purpose of our journey through time.
Through our travels thus far we've learned the Ancient Greeks used the term asthma to describe
any condition that causes dyspnea, or shortness of breath. So your dyspnea could be caused by heart failure, kidney failure, or any number of respiratory disorders, and it would still be called asthma. Hence the terms kidney asthma and cardiac asthma.
William Pepper and Louis Star, in their 1885 book "
A System of Practical Medicine" explained that prior to the 19th century all dyspnea and all that wheezes were designated as asthma.
They wrote about the term as covering such an "extensive range of territory, it was found necessary to subdivide the disease into a number of varieties, each author classifying them according to his conception of the cause, seat, and nature of the trouble. Some of these -- e.g.a. dispepticum, still find their place in medical literature, but the vast majority of them, having ceased to be of any practical significance, have been discarded, and are now only interesting as examples of the crude and fanciful notions which prevailed in an age during which science rather retrograde than advanced." (1)
"ALL early historical traces of the affection at present called asthma are lost. Although the disease is said to be mentioned in the Bible, and described by Hippocrates, Areteaus, Galen, and Celsus, there is not the least evidence that those remarks apply to the asthma of to-day. For in the former systems of medicine, all cases presenting the same conspicuous symptoms were, regardless of their anatomical differences, considered as of a kindred nature, and grouped into classes according to imaginary types. (2)
In essence, Laennec's discovery sparked a leap through time. Where 7,000 years of asthma suffering resulted in little progress in the way of asthma wisdom and treatment, the next 81 years would provide for asthmatics more than all those 7,000 years combined.
We learn that between 1816 and 1900 many different theories about what causes asthma were created, and every one of these theories had its followers. Each expert wrote his own definition of asthma based on his beliefs about the disease, and his own remedies based on these beliefs.
This was all done in the process of fine tuning the definition of asthma. Yet in the end, we learn through our time traveling the two theories that won the day were the bronchospasm theory of asthma (often referred to as the spasmotic or convulsive theory of asthma) and the nervous (psychosomatic) theory of asthma.
By the end of the 19th century the ground would be set for an even bigger leap through time as far as asthmatics are concerned. By 1899 adrenaline was isolated, and this set off a wave of wisdom that would greatly improve the lives of asthmatics. Yet for the time being (no pun intended), we find ourselves drifting from cozy doctor's offices in large Victorian homes to laboratories of some of the worlds greatest asthma experts.
First, an attempt to defend ancient asthma theories:
The treatment of asthma is relative to the cause. Before Hippocrates, for example, asthma-like diseases were often believed to be caused due to a spirit, and the remedy would be chants and hymns to expectorate the evil spirit. Occassionally a family member would know of a herbal remedy for you to try, perhaps something mixed in tea, or smoked in a crude pipe.
Hippocrates believed asthma was caused by an imbalance of the four humors -- yellow bile, black bile, phlegm and blood -- and disease were caused by an imbalance of these humors. This was pretty much the belief of
both western and eastern societies. So one remedy would be bleeding to expectorate excess blood, while another would be concoctions believed to warm the patient.
Galen,
Aurelius Celsus, and other ancient asthma experts may have differed slightly in their descriptions and remedies, yet for the most part they believed in the humoral theory of asthma. Yet
William Cullen in the 18th century swayed from these teachings based on science, and he came up with the more modern nervous and spasmotic theories of asthma.
Robert
Bree, however, was an English physician who believed such modern theories were the subject of quackery. He set out to prove Cullen wrong and ancient asthma experts closer to the truth in his 1797 book "
A Practical Inquiry into Disordered Respiration, distinguishing the Species of Convulsive Asthma, their Causes, and Indications of Cure. (3)
First of all, he wrote that the no science proved the nervouse or spasmotic theory of asthma, especially considering those two conditions cannot even be observed in autopsy. He said you can see phlegm on autopsy, so science supports his theories and those of Galen and Celsus more so than Cullen's.
Now, Bree did not completely reject the spaspotic theory of asthma, he simply considered it as secondary to some other cause. Ernest Schmiegelow explained this in his book "
Asthma, considered specially in relation to nasal disease," (1890 page 4). He wrote that:
"Bree does not actually deny the possibility of bronchial spasms taking some part in the cause of asthma, but it is only secondary; the primary cause is an exudation in the bronchial tubes, by which the lungs (specially the muscles of respiration) are stimulated to contraction, in order to expel the mucus which they contain." (4)
In other words, Bree believed that mucus was the cause of most diseases, including asthma. He believed the contraction of the lungs was a defense mechanism to expel mucus from the lungs. Bree's ideas about asthma are important to our 19th century history because he was considered by many the preeminent asthma expert of the first half of that century.
George Lipscomb was a fellow asthma expert from England who set out to prove Bree wrong. As Mark Jackson described in his 2006 book "Asthma: The Biography," Lipscomb's goal was not to discredit Bree, his goal was to 'elucidate the history of a very prevalent and distressing disease, which has been hitherto but ill explained, and very unsuccessfully treated."
Lipscomb published his own theories in his 1800 book
"Observations on the history and Cause of Asthma." Lipscomb argued that Bree could no more prove Cullen's theories were wrong than Cullen could prove them right because upon death the lungs automatically relax." (5)
So the debate was on. While experts were hard pressed to find evidence to prove either theory, Schmiegelow explained that Bree's theory was disproved as soon as the stethoscope gained favor, as it's easily proven an attack of bronchitis does not precede asthma, and that rales (a lung sound) are heard later during the attack.
Likewise, while Bree was well respected in his day, his ideas about asthma, and even most of his remedies, would slowly give way to to the spasmotic theory of asthma and the nervous theory of asthma
Asthma experts set out to prove their theories of asthma:
The nervous theory of asthma was first described in the 17th century by
Jean Baptiste van Helmont and
Thomas Willis, and in the 18th century by
William Cullen. Most asthma experts in the 19th century believed wholeheartedly that asthma was caused by a nervous response, and the evidence -- so they thought -- was overwhelming.
Ironically, when Cullen's convulsive theory of asthma was proven, this did nothing to disprove the nervous theory. In fact, many experts would go on to prove that beyond a reason of a doubt the convulsive theory of asthma further proved their nervous theory of asthma.
In 1808 Franz Reisseisen performed experiments that proved muscular fibrers wrap around the air tubes of the lungs, according to Jenny Bryan in her book "
Asthma." (6) In our day we know these muscular fibres are smooth muscles we call bronchial muscles.
Jackson explains that Bree attempted to prove his theories by dissecting the lungs of asthmatics who died of an attack, however this was a problem because asthmatics rarely died. He therefore had to dissect the lungs of people who died of other diseases that were similar to asthma.
Sure, it's true, that many asthma experts throughout the 19th century would note that few asthmatics died from their attacks; that asthma was more of a neusance than something that caused death. (
Henry Hyde Salter noted this, and so did
William Henry Osler -- the father of modern medicine -- near the end of the century.) While this may have been good -- or maybe not -- for most asthmatics, it didn't bode well for science.
Either way, by 1808 Franz Reissesen discovered that the fibres wrap around the air passages of the lungs even to the "minutest bronchi," according to Pepper and Starr. As these fibres contract, the air passages of the lungs become narrower.
Rene Leannec's 1816 invention of the stethoscope allowed physicians to differentiate the unique sounds of asthma from other diseases. Laennec believed in the convulsive (bronchospasm) theory of asthma, and he also believed catarrh (inflammation) to be the most frequent cause of asthma.
Like Bree, he attempted to compare signs and symptoms of disease during life with what he saw on autopsy.
James Thomas Whitaker in his 1893 book, "
The theory and practice of medicine" quotes Leannec as saying "Few terms have been so abused in medicine or made to designate such different diseases (than asthma)." By using his new stethoscope, he aimed to prove asthma was a disease of bronchospasm and nothing more.
Laennec was the first to use such descriptions as rhales and rhonchi to describe lung sounds heard by auscultation, and the sounds heard during an asthma attack he described as rhonchi.
Rhonchi would later be divided into sibilant and sonorous, with sibilant rhonchi (now called a wheeze) being the sound of air traveling through narrowed airways, and sonorous rhonch (now called rhonchi) being the sound of air traveling through secretion filled airways.
The Race to define asthma was on:
The rest of the 19th century consisted of one physician after another coming up with his theory as to the cause of asthma. Each was convinced he was right, and each offered the best proof he could. Historians can argue whether this slowed down search for better asthma wisdom, or actually sped it up.
Franz Daniel Reisseissen was a German physician who studied the lungs, and he concluded that "there is another apparatus appointed for contracting the bronchi, which consists of transverse muscular fibres. As far as the cartilaginous rows extend, these fibres are inserted...." (7)
In other words, according to "
The Cyclopaedia of practical medicine" (edited by John Floyer in 1833, volume 1, page 186), Reissiessen proved muscle fibres wrap around the air passages of the lungs almost all the way to the alveoli. His writings were published in Berlin in 1822.
It wasn't until "the paper by Francis Hopkins Ramadge (1835, you can view his book
here*.) and the prize essays of Bergson and Lefevre (1836) that asthma was really regarded as a neurosis of the respiratory organs," according to Whitaker. (8)
Barry E Brenner described in "Emergency Asthma" (edited by Barry E. Brenner, 1998, page 7) wrote that Ramadge described food as an asthma trigger, recommended moving from the city to country, and of asthma being mostly a nocturnal disease. He discouraged use of opiates because they impede respirations that are already impeded. He mainly recommended strammonium because it "produces a grateful forgetfulness and a balmy oblivion like opiates." (9)
J.B. Berkart in his 1878 book "On Asthma: It's Pathology and Treatment" (volume I, page 23) described that Lefevre observed his own asthma and that of a friend and concluded asthma could only be caused by bronchospasm. Yet he (Lefevre) believed this bronchospasm was caused by the mind. (10)
Berkart wrote that "in essence of the disease he (Lefevre) considered to be an increased irritability of the nerves of the lungs, in consequence of which the slightest irritation applies to the bronchial surface induced spasm of the bronchial tubes." (10)
Whitaker wrote that the view of asthma as a nervous disease was further established by "Romberg (1841) who based his conception of the disease as a spasmus bronchialis, upon the discovery by Reiseissen (1808) of muscular tissue in the finer bronchial tubes, and the contraction of these tubes under galvanization of the lungs by
Charles J.B. Williams (1840), and irritation of the vagus (nerve) by Dr. Francois Achille Longet (1842)."
According to William Pepper and Louis Star, "It was ascertained by Williams that by irritating the lung he could cause contraction of these fibres, and Longet subsequently proved that the same effect could be produced by galvanizing the pneumogastric nerve." (11)
Berkart wrote that Williams performed experiments that proved without a doubt "that mechanical and electrical stimuli do produce contraction of the air-tubes. Thus the theory of a bronchial spasm obtained the support of experimental physiology. And even those who until then wavered in their opinions as to the possibility of such a spasm saw now no reason for doubting, but readily accepted that doctrine."
Williams must have agreed with Laennec and Berkart that asthma was an abused term. Whitaker noted that in 1768 there were 17 different types of asthma (as described by Savage) and in 1822 this was reduced to 11 (by Richter). This was confusing. Williams wanted to simplify the definition of asthma.
Williams became the first to break asthma into two types: spasmodic and paralytic. Berkart wrote that as of the writing of his (Berhart's) book, the two terms described by Williams were the ones accepted by most experts. However, other doctors would continue to reclassify asthma to their own content and amusement.
Yet while his research led Williams in the correct direction, along came Dr. Francois Achille Longet who, in 1842, did experiments of his own only to prove that, as Berkart wrote (page 27) that "irritation of the pneumogastric nerve always produced spasmodic contraction of the bronchi, whereas section of the nerve led to emphysema, which was described as distention of the air vesicles (what we now call air trapping)." (12)
Longet also believed bronchospasm and emphysema (air trapping) were both parts of asthma. If we could hop into our virtual time machine we could tell him he was right. We could tell him that spasming of the bronchiole muscles (which he referred to as fibres) caused air to become trapped in the alveoli. This we know is air trapping, or what what was grouped back then under the term
emphysema.
If we could do that we could have put an end to the whirlwind of theories that I think delayed progress that may have resulted in beta adrenergic medicine to relax these smooth muscles long before they were finally discovered in 1900. We could have stopped the whirlwind of false steps and experiments that lead to poppycock theories such as the nervous theory of asthma.
So in 1840 Charles Williams -- who was ultimately the same person to come up with the term lub dub to describe the beating of the two chambers of the heart -- became the first to prove that certain irritants cause contraction of the muscular fibres that Reisseissen proved wrap around the air passages in the lungs.
In 1848 histologist Rudolph A. von Killiker confirmed the works of Williams and Reisseissen when he isolated smooth muscles of the lungs, according to John Daintith in his book "
Biographical encyclopedia of scientists." (13)
This essentially proved Cullen wrong, that the muscle was not just a continuation of a nerve. Yet since nerves still connected to muscles, van Killiker's discovery was unable to stop the fallacy of the nervous theory of asthma.
The thing to note about most of these experts is that even while they believed in the bronchospasm theory of asthma, they continued to believe it the nervouse theory of asthma, and their experiments prooved the two co-existed -- or so they thought.
An attempt to disprove the convulsive theory of asthma:
In 1840 William Budd flat out rejected the bronchospasm theory of asthma. Berkart wrote extensively about Budd, and how he aimed to disprove the convulsive theory of asthma
Budd repeated experiments previous authors wrote would produce bronchospasm and he didn't produce the same results. In fact, Berkart wrote that Budd flat out "rejected the theory of a bronchial spasm, and even doubted whether the circular fibres were muscular, as alleged."
Budd, thus, did not believe the fibres discovered to be wrapped around the air passages of the lungs were muscular, let alone that they spasmed and caused narrowing of the air passages that resulted in asthma.
So now we had proof the bronchospasm theory of asthma was fallacious. Or did we?
Budd was proven wrong that same year by Dr. Charles J. B. Williams.
The invention of the spirometer:
1846 was another big year in the history of asthma as this was the year the spirometer was invented. This is a tool that would ultimately help physician measure lung volumes and differentiate between the different causes of dypsnea. I wrote more about the spirometer in
this post.
Proof once again that asthma was spasmotic:
In 1851, Berkart wrote, a man named Romberg (once agin his last name eludes us) as describing asthma as two different affections of the vagus nerve, and he called them bronchospasm and paralysis (which I think is emphysema, yet I'm not 100 percent positive here).
However, that same year Bergson (first name???) denied paralytic asthma existed and he did experiments to prove asthma was only spasmotic (was bronchospasm). Actually, John Reid did experiments earlier, Bergson just appied his experiments and theories to the understanding of asthma.
Still, while Bergson believed asthma was spasmotic in nature, he believed the cause was nervous.
However, in 1864 Alfred Wilhelm Volckman did experiments that once again verified the bronchospasm theory, yet he could find no evidence of the nervous link to asthma. Volkman said he saw no spasms of the muscular fibres surrounding the air passages as a result of stimulation of the vagus.
Berkart also wrote about the theories laid down by Beau Cozart in 1851 that rejected asthma was a disease of bronchospasm and rejected the nervous theory. He (Cosart) insisted asthma was a disease caused by increased sputum in the lungs that was capable of blocking the air passages with mucus plugs. If we could jump into our time machine we could tell him he was right, yet he shouldn't be so quick to reject bronchospasm.
Yet it didn't matter, because the nervous theory of asthma had already won the hearts of so many asthma experts that little attention was paid to this sputum theory of asthma. It didn't help that Beau provided no proof to his theories.
Pepper and Star note that Williams and Longet's bronchospasm of asthma met with "little opposition until 1884, when (M. Alton) Wintrich, after a series of experiments, arrived at conclusions directly opposed to those of Williams and Longet in regard to the contractility of the muscular fibres of the bronchi, and refused to accept the spasm theory on the grounds that it afforded no rational explanation of the phenomena of asthma."
Berkart wrote that Wintrich believed bronchospasm was only a
mild part of asthma, and that tetanus (tonic spasm according to Pepper and Starr) of the diaphragm alone (an idea first proposed by Thomas Wilson in the 17th century) or tetanus of the muscles of respiration with spasm of the glottis or other muscles of respiration were the main causes of asthma. Yet Wintrich may have been thinking of dyspnea more so than asthma.
Wintrich likewise believed bronchospasm was impossible, Berkart wrote (page 34). Instead, he believed dyspnea was primarily a "disturbance of
innervation." In other words, that it caused by a disturbance of nerves to the lungs, according to
dictionary.com.
Wintrich --and again in 1870 Banberger -- believed asthma was caused by spasm of the diaphragm. In 1870 Biermer believed it was a disease of the bronchial tubes, and in 1873 Leber wrote that he believed in both these theories.
In 1873 Leber believed asthma was caused by dilation of the blood vessels in the lungs. In fact, this theory was still believed to be true when epinephrine was later invented in 1900, as the vasoconstricting component of epinephrine was believed to increase blood flow to the lungs and thus made breathing easier that way.
Yet his theory was shunned almost as soon as it was developed.
It's interesting to note that Pepper and Star likewise wrote that Wintrich's experiments were so thoroughly done, and he was so highly regarded as a specialist in respiratory medicine, that his theories gained much support, "and might perhaps have been generally accepted had it not been for the distinguished French physiologist, Paul Bert, who in 1870, with improved methods of scientific research, succeeded in demonstrating that Willis and Longet were after all correct in their statements as to the contractility of the bronchial muscles."
While the bronchospasm theory of asthma was gaining steam, the the debate as to what causes asthma was ongoing.
More back and forth debates as to what causes asthma:
Remember Budd? He's our asthma expert from 1840 who flat out rejected the bronchospasm theory of asthma. In 1855 Guillaume Benjamin Amand Duchenne proved Budd right, or so he thought. As Berkart wrote, Duchenn proved "faradisation of the phrenic nerve caused tetanus of the diaphragm. (You can view Duchen's book
here**)
So who cares what causes the symptoms, Berkart wrote of
Constatt, who believed it doesn't matter the cause of dyspnea because antispasmotics (like belladona found in asthma cigarettes) work equally well for both asthma and emphysema.
Pretty much Constatt was correct, yet with greater wisdom comes greater treatments as we would learn in 1900.
Another neat theory that came along in 1855 was by a Dr. Ludwig Traube who denied nervous asthma but believed asthma was rare and the dyspnea that resulted was caused by "fluxionary hyperaemia of the bronchial mucous membrane." What he is referring to here is "swelling of the bronchial mucus membrane," wrote Berkart. This is what we now refer to as inflammation.
Traube also believed asthma was caused by sputum in the air passages of the lungs, according to Jackson.
Ah, if we could only jump into our time machine we could tell Traube he was on the right track. It would take another 130 years for asthma experts to realize Traube was on the right track, that asthma is a disease of chronic inflammation.
Likewise, Traube wrote that this inflammation cannot be diagnosed during a person's lifetime, and can only be diagnosed by the symptoms it presents with, such as dyspnea and wheezing.
Then in 1859
Bervenisti, as Berkart continued, brought attention once again to the differentiation of the different causes of lung diseases that he believed were probably unrelated to asthma. He (Bervenisti) believed that a doctor could not possibly diagnose bronchospasm by listening to lung sounds alone. That sonorouis and sibilant rhonchi are also present with a pulmonary embolism, which also causes dyspnea.
Once again, if we could jump into our time machine we could tell him he was right, that lung sounds can help with a differential diagnosis. For example, heart failure would result in coarse crackles throughout the lungs or half way up, pneumonia often results in crackles in one lobe of the lungs, a wheeze indicative of air traveling through narrowed air passages (asthma), and rhonchi indicative of air traveling through sputum (bronchitis).
In a way I'd like Mr. Bervenisti to come talk to the doctors that exist today who still believe all dyspnea is bronchospasm. I'd like Mr. Bervenisti to set them straight.
Convulsive and nervous theories both win the day:
Jean Antoine Villemin became famous as the person to prove that tuberculosis was contagious after rabbits he injected with tuberculosis from humans contracted the disease.
In 1860 Jean Antoine Villemin tried to disprove the nervous theory with his own scientific experiments, yet once again the nervous theories were so popular Villemin's common sense approach was ignored.
Villemin actually came up with a theory in a circuitous way describing what we now call air trapping.
Deprived of "nutrition," Berkman wrote in describing Villemin's theory, "the air vesicles (alveoli) became impaired, they were unable to efficiently perform expiration. At the same time respiratory surface was reduced, and the blood accumulated in the bronchi (inflammation) to such an extent as to convert their mucous membrane into a kind of erectile tissue.
"This condition gave rise to no symptoms," Berkart continued, "either subjective or objective." The only time symptoms occurred
Villeman's theory here might be a little off, yet our time traveler would benefit history if he could somehow convince Villemin not to give up trying to convince other experts that they were wrong and he was sort of on the right track. Your time traveler's attempts might prevent the 130 year delay.
So this is how it went throughout most of the 19th century. Is asthma caused by the vagus? Is it spasmotic? Is it a result of spasms of the diaphragm? Is it a result of paralysis of the air passages? Is asthma both spasmotic and emphysema?
The debate was pretty much ended when Henry Hyde Salter entered the picture. Salter would become the pre-eminent asthma expert of the second half of the 19th century. In fact, he was so famous he was even consulted to be the asthma doctor for a boy who would one day become President of the United States (
I'll write about that in the coming weeks).
Salter published the original version of "On Asthma: It's Pathology and Treatment," in 1864 (Salter's book was published prior to Berkarts). Based on his own experience with asthma, and observations of his own patients, he accurately described the asthma patient during an asthma attack.
He wrote that he saw enough evidence to believe in the spasmotic theory of asthma, yet he also believed that bronchospasms were caused by nervous stimulation. He also believed asthma was an inflammatory disease and wrote about asthma as a hereditary disorder.
Salter believed some exciting factor (like dust or sterss) was recognized by the abdulla oblongotta, and a signal was sent via the pneumogastric nerve to the bronchiole fibres that wrap around the lungs signalling them to constrict. In this way asthma was a nervous condition.
Salter offered the following examples as proof asthma was started in the brain:
- Many patients feel fine as soon as they enter the doctor's office
- Mental emotion can bring on a paroxysm of asthma
- Mental emotion can resolve a paroxysm of asthma
- Remedies that relax the nervous system resolve asthma, such as tobacco, antispasmodics, and sedatives, nervous depressants. Examples include tobacco, alcohol, morphine, and especially chloroform.
Berkart noted that in 1843 George Hirsh said he (Hirsh) didn't understand how asthma could affect so many boys if it were a nervous disorder. Salter better described this in his book, stating that asthma is a disease that causes the boy to yearn for his mother. It's this yearning that results in an asthma attack.
Thus, it's for this reason Salter justifies using remedies to calm the mind such as smoking cigarettes, alcoholic drinks, formaldehyde, and sedatives. (to see more Salter remedies
click here). Salter didn't deny the convulsive theory of asthma, yet his main focus was on the nervous theory because he believed the mind caused the convulsions or spasms in the lungs.
Pepper and Star explained that by the time the third edition of their book "A System of Practical Medicine" was published in 1885, Williams and Longet's bronchospasm theory of asthma was readily accepted. They wrote that "most modern pathologists have arrived at the conclusion that bronchial asthma is a spasmotic contraction of the middle and finer bronchi dependent on some derangement in the function of the pneumogastric nerve."
Likewise, Whitaker added that "whatever doubt still hung about the contraction of the bronchial tubes themselves would seem to have finally been dissipated by Lazarus (1891), who devised an ingenious apparatus wherewith he could, with the aid of curare and tracheotomy, experiment on animals in life, and whereby he produced the characteristic dyspnea of the disease by irritation of the vagus nerve."
Brenner (page 9) noted that sometime around 1900 Willem Einthoven (the inventor of the EKG) evaluated the bronchospasm theory of asthma and spasming diaphragm theory of asthma and proved the bronchospasm theory.
So based on experiments and personal observation, and with the appraisal of highly rated doctor's like Henry Hyde Salter, the bronchospasm and nervous theory of asthma won the day. The nervous theory remained popular until it was disproved in the 1950s. However, it really wasn't until the 1980s that the theory was laid to rest.
The bronchospasm theory of asthma lives on.
Click here for more asthma history.
References:
- Pepper, William, Louis Star, "A System of Practical Medicine," Volume 3, page 184
- Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, Chapter II, "History of Asthma," page 12
- Bree, Robert, "A Practical Inquiry into Disordered Respiration, distinguishing the Species of Convulsive Asthma, their Causes, and Indications of Cure, London, 1810. I could not find the 1790 edition online, yet this one serves our purpose.
- Schmiegelow, Ernest, "Asthma, considered specially in relation to nasal disease," 1890, London, page 4
- Jackson, Mark, "Asthma: The biography," 2009, London, pages 86-88 (If you're interested in a good asthma history book, this is it.)
- Bryan, Jenny, "Asthma," 2008, page 8
- Floyer, John, ed., "The Cyclopaedia of practical medicine," 1833, volume 1, page 186
- Whitaker, James Thomas, "The theory and practice of medicine," 1893
- Brenner, Barry E, ed, "Emergency Asthma" 1998, page 7 (chapter one is a history of asthma written by Brenner)
- Berkart, J.B.,"On Asthma: It's Pathology and Treatment, 18xx, volume I, page 23 (Berkart started his book with a good history of asthma up to his time. I base much of this post on his thorough asthma history.)
- Pepper, op cit, page 194
- Berkart, op cit, page 27
- Daintith, John, "Biographical encyclopedia of scientists."
Other readings:
