1879: Berkart describes turning point in asthma history

If I could get my time machine fixed, I would travel through time to the year 1878.  That was the year that Dr. J.B. Berkart published his book "On Asthma: It's Pathology and Treatment." On the day Berkart pulled that first book off the press, he must have admired his work with a smile.  I would have liked to have seen that.

Berkart, as you may have noticed already, is a significant contributor to our history of asthma, particularly as it wends it's way through the 19th century.  In fact, Berkart was among the first to point out that much of what was known about asthma prior to the 19th century should have no bearing on our modern quest to define this disease.

Of this, he wrote the following in his introduction:

The so-called bronchial or spasmodic asthma is, to this day, perhaps the most obscure of all diseases. Not withstanding the attention which asthma, on account of its frequent occurrence and the suffering it entails, has ever received at the hands of physicians, hitherto all their endeavours to elucidate the subject have only led to divergent opinions upon even the most essential points, and to the development of incongruous theories. Indeed, it is not saying too much that, among them there are not any two who fully agree in matters of either observation or inference; but all hold views at variance with one another, while each contends that only his own are consistent with facts, and in harmony with rational pathology. (1, page 1)

Later, as he walks his readers through the history of asthma, he pretty much skipped through 99% of history of asthma, and simply wrote this:   

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.  Thus intense but intense and intermittent dyspnea formed the typical characteristic of the class asthma; and this, with its numerous species and varieties, comprised a promiscuous collecting of diseases having absolutely nothing in common but one symptom.  In that sense, however, the term asthma was employed until the commencement of the present century, so that even, at so late a period, empyema and dilation of the heart were described as asthma paradoxon and asthma nervosum.  Moreover, as before the invention of auscultation and percussion, marked functional disturbances were the sole means of diagnosis, their close similarity in all diseases of the chest must have necessarily rendered an accurate distinction between the several known forms of them impossible. (1, pages 12-13)

By that paragraph, Berkart pretty much sums up our asthma history to this point.  Essentially all that was known about asthma prior to the introduction of percussion and auscultation should simply be ignored. Observations of asthma prior to this time could have been may have been asthma as we think of it today, or it could have been just about any other ailment that causes dyspnea. Or, as noted by Dr. Chevalier Jackson in 1947, "All is not asthma that wheezes." (2, page 128)

Dr. Berkart was a London Physician at the City of London Hospital for Diseases of the Chest, and was one of the foremost experts on asthma at that time.  He must have been, as he accepted the honor of taking over the series of books started by his successor: Dr. Henry Hyde Salter.  

Berkart then describes the events that inspired further investigations into the actual pathological causes of asthma:

It is only after percussion began to be practised that asthma can more clearly be discerned in history. As soon as certain cardiac affections, hitherto imperfectly or not at all known, were by means of it recognised during life, it became at once evident that the dyspnoeal attacks which accompany them were not of nervous origin, as was until then supposed, but were the necessary consequence of the structural lesions. Corvisart,who was the first to perceive this fact, was moreover led to infer that of the prevailing forms of nervous asthma, several, if not all, probably arose in'an analogous way. But his means of diagnosis were as yet too limited to prove that supposition.

The task was thus reserved for Laennec.' His invention of auscultation brought physical diagnosis to such a degree of perfection as to enable him to determine the true value of the numerous forms of the "asthme des praticiens", and to range them in their proper places as mere symptoms of anatomically defined diseases. Yet in that sweeping measure hecould not comprise the intermittent attacks of dyspnoea, of which no adequate cause was discoverable by means of the stethoscope.(1, page 13)

So the climax of our asthma history was when Corvisart and Laennec introduced percussion and auscultation to the medical profession. It was only after this time that a true definition of asthma could be discerned.
While we may have suspected this earlier, Berkert articulated this perfectly.

If I could get this darn time machine fixed, I'd travel back in time to that day when Berkart held that first copy of his book.  I would like to be there and watch as his lips curled upwards as his fingers caressed the warm, crisp hot-off the press book with his name on the cover.

References:

1. Berkart, J.B., "On Asthma: It's Pathology and Treatment," 1878, London, J.& A. Churchill
2. Miller, Hyman, "Physiological basis for the treatment of asthma," California Medical, March, 1947, 66 (3), pages 128-30

1873: Berkart says asthma is merely a symptom

Dr. J.B. Berkart was Asistant-Physician to the Victoria Park Hospital for Diseases of the Chest.  So he was well acquainted with asthma.  Unlike his predecessor, Dr. Henry Hyde Salter, Berkart opposed the nervous and spasmotic theories of asthma.

Berkart understood that, as Dr. C.B. Williams proved in 1840, that the muscles surrounding the air passages could contract or spasm.  However, he believed that Paul Bert, who published the results of his own studies on the contractility of the lungs in 1870, proved that the lungs do not contract during an asthma attack.

Of Bert, Berkart wrote:

"In many of his experiments he failed to demonstrate the contractility of the lungs, but at last he succeeded in doing so; and he found, as the reason of his failure, that he "insufflated the lungs too much", which circumstance impedes their contraction.  But if Paul Bert has thus proven the contractility of the bronchial muscles, he has at the same time conclusively shown the impossibility that asthma can be due to a spasmodic stricture of the bronchial tubes in those cases in which it forms an integral part of the disease, namely, in emphysema. For that same cause which hinders the success of the physiological experiments fully exists under those pathological conditions. (1, page 537)

Berkart believed that Henry Hyde's theory that asthma is nervous simply because asthma leaves behind no physical signs was poppycock. (2, page 49-50) Of this, Berkart said:

For the absence of physical signs is no safe indicator of the absence also of pathological conditions, and all the positive evidence derived from experimental physiology only goes to show that the "bronchial muscles may contract"; but as to "how" and as to "when" nothing is known. (1, page 537)

Berkart likewise explained:

I  am prepared to show that, were even the entire nervous system bent upon producing a spasmotic contraction of the bronchial muscles, it would fail in its attempts, because they are in cases of asthma in such a state of nutrition as to be utterly incapable of contracting at all." (1, page 537)

Instead, asthma being the result of a neurosis that causes spasms of the air passages, Berkart postulated that asthma was merely a symptom that accompanies other diseases: (1, page 537)(2, page 110)

1. Emphysema
2. Bronchitis
3. Other pulmonary affections 
4. Cardiac affections (1, page 537)(2, page 110

Furthermore, he said asthma is most often secondary to emphysema and bronchitis, and "the rare cases in which these are supposed to be absent could only constitute an exception to the rule.  The exception, however, does by no means invalidate the rule." (1, page 438)

The proof that the exception "does by no means invalidate the rule," was proved, according to Berkart, by the experiments of Walshe.  Of this, Berkart wrote: 

So well has this fact been recognised by all clinical observers, that they more or less explicitly mention "an acute relaxation" (Walshe*, Diseases of the Lungs, 1871, page 209) of the bronchial walls in cases of acute bronchitis.  Therefore, what holds good in the acute, still more forcibly applies to the chronic affection.  Here indeed, are the bronchial muscles so completely soaked with serum, that, were this the sole change they undergo, it alone would surfice to render contraction of the muscles a matter of impossibility.  But very often the first outbreak  of an asthmatic attack is preceded by pathological changes of greater moment than bronchitis -- namely, by catarrhal pneumonia, the anatomical basis of whooping-cough, measles, etc; and that disease inflicts such injuries upon the bronchial walls, that their contraction is irrevocably lost." (1, page 538)

He therefore argued that there was no point in debating what causes the attack, as such debates were frivolous.  He said:

Gentlemen, we shall never arrive at the true nature of bronchial asthma if we continue to confine our attention to an attack itself, to its immediate causes, and to its peculiar type of respiration. In asthma, as well as in any other disease, the history of the case and its sequele will have to be carefully considered ; and then we shall find that, indeed, asthma is no independent disease, no dynamic affection of a nerve, but that it really forms a link in a chain of diseases, which commence with affections of the bronchi and terminate with emphysema, whilst asthma itself represents the stage intermediate between these two. (1, page 538)

As Salter was ultimately proved correct in his assertion that asthma was indeed a disease of bronchospasm, he was eventually proved wrong that asthma was a neurosis.  To the contrary, Berkart was ultimately proved wrong in his assertion that asthma was not a disease of bronchospasm, and was eventually proved correct that asthma was not a neurosis.

Berkart believed that asthma starts as a chronic catarrh, often in childhood, and over time develops into emphysema.  Since emphysema is rarely found in children, it usually gradually develops unnoticed into adulthood.

He said that even as the lungs become increasingly diseased, breathing is generally easy. "But when an obstacle arises," he said, "which for its removal requires a greater force than that of ordinary respiration, then the inability to effect the removal shows the deficient nutrition of the organ. It is this stage of developing emphysema-this stage of deficient elasticity of the lungs-which constitutes the anatomical basis of bronchial asthma." (1, page 538)

He thus explains asthma this way:

In typical bronchial asthma, the lungs are greatly distended, the thorax is in a position of extreme inspiration, and all the respiratory muscles are firmly contracted. Inspiration is short and abrupt, and the effort of the respiratory muscles, although prolonged and greatly increased, remains ineffectual. If an obstacle arise to the entrance and exit of air from the lungs, say the impaction of a tough pellet of mucus in a bronchus, a supplementary force is necessary in order to displace the obstacle and to effectually carry on the respiratory function. Such additional aid to expiration is obtained by deep inspiration; and this is easily effected, because it proceeds from the action of the inspiratory muscles, to which the lungs deficient in elasticity cannot offer any great resistance. Hence the easy and rapid overdistension of the lungs. (1, page 538)

As far as what triggers an asthma attack, Berkart noted both internal and extarnal "exciting causes," all of which "produce an obstacle to the interchange of gases, against which the deficient expiratory forces will for a long time labour in vain." (1, page 538-539)

These exciting causes were: (1, page 538-539)

1. Tough and fibrinous sputa: The thicker it is, the harder the lungs have to work to expectorate it
2. Inhalation of foreign bodies: Epecacuanha, pollen, etc. 
3. Heat from ambient air:  It causes sputum to become crusty, forcing lungs to work extra hard
4. Excitement, laughter: Sputum is displaced from one part of lung into another, diminishing the surface of respiration
5. Edema (fluid) in lungs:  Occurs when kidney's become diseased
6. Thrombosis and embolism (blood clot): Causes asthma symptoms (1, page 538-539)

In conclusion, Berkart wrote:

I may, therefore, in conclusion, state that asthma is a symptom which accompanies diseases of the lungs in which deficient elasticity is the prominent feature, and in consequences in which the existing expiratory forces are only able to overcome an obstacle to respiration after prolonged and increased efforts." (1, page 539)

Berkart, therefore, believed that asthma was not a disease entity of it's own, but rather was a symptom of, in most cases, bronchitis and emphysema. Therefore, despite physicians not being able to find physical signs that asthma exists, these signs do exist.  Berkart said:

A patient may daily expectorate several spittoonfuls of mucus, and yet the most practised and most careful observer may fail to detect, by means of percussion and auscultation, the least trace of disease. The reason is that the mucus forms and stagnates in a bronchus or bronchi, situated at some distance from the surface of the chest, in which position the adventitious sounds are, as the bronchial respiration is normally, obscured by the intervening healthy tissue of the lungs  (2, page 51-52)

Salter originally published his ideas in various articles throughout the 1950s, and later in the 1969 book: "On Asthma: It's Pathology and Treatment."  Berkart also published his ideas in various articles, and in 1978 published the book: "On Asthma: Its Pathology and Treatment."  While both authors used the same title for their respective books, the theories postulated were opposites.

Both Salter and Berkart are important to our asthma history in that they were both responsible for garnishing attention to our disease.  However, while their opinions were well established regarding the cause of asthma, the debate was ongoing.

*Walter Hayle Walshe (1812-1892)

References:

1. Berkart, J.B., "On the Nature of the so-called bronchial asthma," British Medical Journal, November 8, 1873, 2 (671), pages 537-539
2. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London

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1865: Dr. See supports diaphragmatic theory of asthma

Germain See (1818-1896) was a German physician wrote several articles on asthma and other lungs diseases in the various medical publications of his era, and he is referenced more than once in this asthma history.  It is obvious, that through his writings, he was well acquainted with respiratory disease, including our asthma.

In 1865 he gave his support to the ideas of Alton Wintrich and Heinrich Bamberger that asthma was not caused by spasms of the muscular fibres in the lungs, and instead was caused by spasms of the diaphragm. (1, page 5) (2, page 2) 

In his 1890 book, Ernest Shmiegelow said See reviewed all the theories of the day.  He quotes See:

"Asthma is a neurosis in the medulla oblongata, that is to say in the centre of respiration, caused by an acquired or native elevated reflex irritability in this organ. The cause of the attacks must be sought for in irritations, which originate in pneumogastric nerves or other peripheral nerves. The effect of the reflex exhibits itself in the motory nerves of the inspiratory muscles, specially those of the diaphragm. We have, therefore, before us a permanent neurosis, whose attacks are caused by an irritation especially of the pneumogastric nerves, and which is always concluded by a tetaniform contraction of diaphragm, this theory only (in contrast to the bronchial spasm) can explain the dilatation of the lungs... The principal factor in the asthmatic attacks is therefore not (as in the bronchial spasm) a direct motor effect of the pneumogastric nerve, only the sensitive pneumogastric fibres take a part in this respect as they lead the irritation up to the noeud vital of the spine, whence the irritation spreads through the nervi phrenici to the diaphragm. " (1, page 9-10)

Joseph Berkart, in his 1878 book, said See divided asthma into three elements: (2,page 2)

1. Dyspnoea
2. Bronchial exudation
3. Emphysema of the lungs (2, page 2)

See believed asthma was always accompanied by organic lesions, and diseases such as chronic bronchitis and emphysema, but never caused by them. (2, page 37)

While others, such as George Kidd, believed asthma was a symptom of emphysema or chronic bronchitis, See believed it was, according to Berkart: (2, page 37)

...always a substantive disease, accompanied, but never produced by organic lesions. He recognised, however, only one form of it. In his opinion, asthma was essentially a neurosis of the vagus and its branches, and manifested itself by a tetanus of all the respiratory muscles, and by a bronchial exudation. The presence of these two "elements" combined was alone characteristic of the affection, whereas emphysema of the lungs was only their constant attendant. Emphysema, he maintained, was not an essential, but merely the consequence of the inspiratory traction during, and the bronchial exudation after, the attack.

Berkart said a goal of German experts, such as See, was, to...

"...maintain that, to warrant a diagnosis of pure bronchial asthma, the bronchial mucous membrane should appear healthy, nor should any other cause for the dyspnoea be discoverable. Still, not all supporters of this definition adhere to it throughout. They admit that asthma may be complicated 'with' or 'grafted on' other cardiac and pulmonary affections. But, as these affections are themselves capable of producing asthmatic seizures, the distinction in a given case between this symptom and the supposed complication would be purely arbitrary." (2, page 3)

In other words, according to Berkart, pure bronchial asthma was only diagnosed when there were no other scars found upon the lungs or the heart, at least according to the Germans. (2, page 3)

References:

1. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis
2. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, J. & A. Churchill
3. Brown, Orville Harry, "Asthma, presenting an exposition of nonpassive expiration theory," 1917, St. Louis, C.V. Mosby Company; reference used: ee, Germain: Nouv. Diet, de Med. et de Chir. Practiques, 1865, iii, p. 585, pages 36, 89
4. Gee, Samuel, A lecture on permanent asthma, delivered at the Hotel Dieuj, by Prof. Germain See, translated from the Union Medicale, by H. McS. Gamble, "Gailard's Medical Journal," volume 37, edited by Edward Samuel Galliard, 1884, New York

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1860: Villemin's asthma theories ignored

Jean Antoine Villemin (1827-1892)

Most people of the civilized world were aware of a killer by the name of consumption, although no one knew where it came from nor what to do about it.  If you caught it you probably going to die. Fear of this killer created a feeling of doom and gloom that spread across Europe and the United States.

After obtaining his medical degree from Stassburg in 1853, Jean Antoine Villemin was sent to Val de Grace, the military school at Paris, for further study.  While a professor at Val de Grace he made the observation that men living in close quarters in barracks were most likely to catch the disease. So he set out to perform an experiment.  (1)(2, page 664)

Villemin obtained some tissue from a man who died of tuberculosis, and he inoculated it into rabbits.  He knew the rabbits were probably going to die, although he knew that he could save the lives of millions of people around the world if his experiment succeeded.  

Every day he checked on his rabbits, and by the third month his diligence paid dividends, as he observed tuberculosis lesions.  He published the results of his study, and they were ignored by the medical community.  By respecting his experiments physicians could have limited the spread of one of the most dreadful diseases ever to inflict mankind, yet their ignorance prevented them from doing so.

Villemin's work would ultimately be proven true by other scientists.  Yet until that time, Villemin worked overtime trying to convince the medical community that he was correct.  He would ultimately become a hero, although that time wouldn't arrive for several more years.  

By his investigations into the lungs, he was able to learn about other diseases as well, including asthma.  In 1860, he tried to disprove the nervous theory of asthma with his own scientific experiments, which were described by Dr. J. B. Berkart in 1878: 

Villemin professed to have demonstrated the pathological changes that deprived the pulmonary tissue of its elasticity, and predisposed the bronchial mucous membrane to hypersemia. He stated that emphysema originated in a proliferation of the inter-capillary nuclei, whose advancing growth tended to compress the alveolar vessels. As the nutrition of the air-vesicles became impaired, they were unable to efficiently perform expiration. At the same time, the respiratory surface was reduced, and the blood accumulated in the bronchi to such extent as to convert their mucous membrane into a kind of erectile tissue. This condition gave rise to no symptoms, either subjective or objective. Its existence became manifest only by the readiness with which trifling incidents produced their effect. Hyperaemia (inflammation?) rapidly ensued, and led to the dyspnoeal attacks that other writers consider as nervous asthma. The chronic inflammation of the alveoli, described by Villemin, is, however, not recognised by other observersIronically, 130 years later, asthma was found to be a disease of chronic inflammation. Should we go back now and give Villemin cretic in retrospect? (3, pages 33-34)

Like his tuberculosis theory, his asthma theory was ignored by the medical community. This was because the nervous theory was so popular at this time that there was no room for any other theory.  Villemin was yet another victim of how hard it is to change the minds of people who are already set in their ways. 

However, in the decades that followed Villemin's publication of his work on tuberculosis, the works of Louis Pasteur and Robert Koch would force the medical community to look at Villimin's work and accept it as fact.

Further reading:

• 1855:  Traube doubts nervous theory of asthma

References:

1. "Jean Antoine Villemin," britannica.com, http://www.britannica.com/EBchecked/topic/629218/Jean-Antoine-Villemin, accessed 3/3/14
2. Garrison, Fielding Hudson, "An introduction to the history of medicine," 3rd edition, 1821, Philadelphia and London, W.B. Saunders Company
3. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, J. & A. Churchill
4. "Obituary: Jean Antoine Villemin," The British Medical Journal, Nov. 13, 1892, 1860:  Villemin's asthma theories ignored, accessed 3/3/14

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1841: Romberg verifies nervous theory of asthma

Moritz Heinrich Romberg (1795-1873)

By 1841 there seemed to be quite a bit of evidence in support of the nervous theory of asthma.  It was in this year that Dr. Moritz Heinrich Romberg verified this evidence, hence proving once and for all that asthma was definitely nervous, or so many supporters of the theory believed.

In the 17th century Jean Baptiste van Helmont and Thomas Willis came up with the idea that asthma was nervous.  In the 18th century William Cullen further supported this theory. Then, in the 19th century, the experiments of various physicians seemed to provide the evidence in support of the nervous theory of asthma.  (1, page 506)

In 1835 Francis Ramadge wrote papers, in 1836 Joseph Bergson and Amedee Lefevre wrote prize essays, all of which seemed to provide support for the nervous theory of asthma.  Based on this evidence, Romberg also supported this theory, and he did experiments to put an end to any arguments once and for all. (1, page 506)

J.B. Berkart, in his 1878 book "On Asthma," said Romberg described "two affections of the vagus... of which are productive of dysponeal attacks:

• Bronchial spasm:  He generally referred to this as "bronchial cramp" or spasmus bronchialis.  (2, page 28)(3, page 4) 
• Paralysis: This was essentially paralysis of the muscles of respiration, or emphysema (2, page 28)

There were also later studies that likewise verified the works of Romberg.  Alfred Wilhelm Volkman (1801-1877) and M. M. Valentin proved that irritation of the pneumogastric, or vagus, nerve causes contraction of the air tubes, or bronchioles. (4, pages 5-6

Orville Brown, in his 1917 book, described Volkman's experiment:

Volkmann tied a tube into the trachea of an animal and set a candle before the opening and then stimulated the vagus and the flame showed that air was thereby caused to come from the lungs. (2, page 33)

These results were verified again by Ludwig Traube, Paul Bert, and others.

These men confirmed that asthma was nervous, and this influenced the remedies used to treat it, often resulting in physicians prescribing such medicines that calmed the nerves and relaxed the mind in order to prevent and treat asthma. (4, pages 5-6)

The experiments of these men helped enshrine the image of asthma as nervous for greater than the next hundred years. 

References:

1. Whitaker, James Thomas, "The theory and practice of medicine," 1893, New York, William Wood and Company
2. Berkart, J.B., "On Asthma: It's Pathology and Treatment," 1878, London, J. & A. Churchill
3. Schmiegelow, Ernest, "Asthma, considered specially in relation to nasal disease," 1890, London, H. K. Lewis; he references the following source; Bergson, Das krampf. Asthma der Erwaohsenen, Nordhausen, 1850.
4. Thorowgood, John Charles, "Notes on Asthma: It's Nature, Forms, and Treatment," 1878, London, J. & A. Churchill

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1842: Longet's proves nervous theory of asthma

William Longett (1811-1871)

In 1808 Dr. Franz Reisseissen discovered muscular fibers wrap around the air passages in the lungs, and in 1840 Dr. Charles Williams proved these fibers spasm in the presence of certain stimuli.  Yet there remained one missing link necessary to prove the spasmotic and nervous theories of asthma.  The man up to the task was Dr. Francois Achille Longet of France. 

Longet did a variety of experiments on the anotomic nervous system, which is a system of nervous system that controls involuntary action, such as the beating of your heart, your rate of breathing, digestion, sexual arousal, dilation and contraction of the pupils, salivation, etc. In other words, it controls all the actions of the body that a person does not control (the brain controls them). 

In 1840 he must have heard of the experiments of Williams, so it was only a few years later, in 1842, that he aimed to see if he could find the missing link between the brain and the lungs to prove that the brain, or the nervous system, was responsible for asthma.  

Dr. J.B. Berkart, in his 1878 book "On Asthma," explains: 

Yet one link was wanted to complete the chain of evidence in favour of a bronchial spasm. As yet nothing was known of the innervation of the bronchi. Irritation (galvanization) of the vagus (pneumogastric) had produced no effect upon their calibres, and Dr. Williams was therefore led to conclude that "the muscular fibres seem not to be excitable through the nerves of the lungs".

Soon, however, Longet not only confirmed in the main the results obtained by Williams, but added that in his experiments irritation of the pneumogastric nerve always produced spasmodic contraction of the bronchi, whereas section of the nerve led to emphysema. Of the bronchial stricture he could satisfy himself by watching with a magnifying glass, but as to the occurrence of a similar process in the pulmonary tissue he had no means of judging. Still, he believed that such took place, although the presence of muscular fibres in the air-vesicles was then as doubtful as it is to-day. For, since section of the vagus causes emphysema, i.e., distension of the air vesicles, there must be muscular fibres which, if liable to paralysis, are liable also to spasm. (1, pages 26-27)

Now, just for the record here, the vagus nerve is a main nerve that runs down from the brain and supplies the heart, lungs and the various organs of the body. Longet proved irritation of this nerve would cause bronchospasm.

However, Berkart said that some of Longet's experiments, along with those of others, often led to incorrect speculations.  He said:

It cannot fail to be observed that those hasty applications of the results of the experiment to the pathology of asthma led here, as they always do, to unwarrantable conclusions. If, indeed, Longet were correct in this, that bronchial stricture and emphysema are due the one to a plus, the other to a minus state of irritability of the vagus, it would necessarily follow that, as asthma and emphysema are almost always associated, spasm and paralysis of the self-same muscles could co-exist at the same time, each independently of the other, manifesting itself in its own peculiar way. Such deduction necessarily follows from the premisses. (1, pages 28-29)

Regardless, while Williams proved irritation of the muscular fibers in the lungs may cause bronchospasm, Longet proved irritation of the vagus could cause bronchospasm. Thus, for the rest of the century various authors referred to the experiments of Williams and Longet as proving both the spasmotic and nervous theories of asthma.

The experiments of Williams and Longet were later verified by other physicians, including Moritz Heinrich Romberg, Alfred Wilhelm Volkman, Traube, Bernard, and Bert.  They all proved that irritation of the vagus caused "contractions of the air tubes."  (3, pages 5-6)

Based on this evidence, most authors on the subject of asthma believed in the nervous and spasmotic theories of asthma, citing Reisseissen, Williams, Longet and Volkman as promulgators of the evidence.

References:

1. Berkart, J.B., "On Asthma: It's Pathology and Treatment," 1878, London, J. & A. Churchill
2. Brown, Orville Harry, "Asthma, presenting an exposition of nonpassive expiration theory," 1917, St. Louis, C.V. Mosby Company
3. Thorowgood, John Charles, "Notes on Asthma: It's Nature, Forms, and Treatment," 1878, London, J. & A. Churchill

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1840: Dr. Williams proves spasmotic theory of asthma

Charles J. B. Williams (1805-1889)

Healthcare workers may recognize the name Dr. Charles James Blasius Williams because he was the first person to use the terms "lub-dub" to describe the sounds emitted by the two chambers of the beating heart.  This is what history best remembers him for.

While this fact is definitely important to our history, what we are mostly interested in is the fact that Dr. Williams was the first person to effectively prove the spasmotic theory of asthma by discovering that the muscular fibers that wrap around the air passages may spasm under certain conditions.

According to his own memoirs, Williams was the youngest of nine siblings. His mother was the eldest daughter of a respected surgeon, whose name was also Williams. She died shortly before her son Charles started college at Edinburgh University in 1820.

Despite Williams proof that the certain stimuli may cause the air
passages of the lungs to spasm, some physicians continued to
argue this in no way proved this had anything to do with asthma.
Other physicians, however, believed this proved nervous asthma
caused spasms of the air passages.  The above picture shows
how far science expounded upon the experiments of Williams
in the years between the publication of his work in 1840 and
the publication of Dr. Henry Hyde Salter's 1860 book,
Asthma: It's Pathology and Treatment." The caption under
the picture read: "Diagram showing the four ways in which the bronchial tubes may be narrowed.
1. Bronchial catarrh. 2. Recent bronchitis. 3. Old bronchitis 4. Asthma.  (6, page 39)

His father was Rev. David Williams, who came from an eminent family of many teachers and scholars. Along with being a Reverend, his father was also a successful tutor, having "prepared several gentle men for the university, who have since attained distinction as scholars." He educated his son at home until he was accepted at Edinburgh University in 1820, where he began his pursuit to become a physician. (1, page 1, 6, 9)

Williams credited his father with exposing him to subjects he wouldn't have been exposed to had he attended the public schools, subjects which would help him in his later endeavors, such as "Geography, History, Biography, Natural History, and above all, Natural Science." (1, pages 2-3)

Williams would have learned about Franz Reisseissen, who discovered in 1808 that muscular fibers wrap around the air passages of the lungs.  He would have learned about Rene Laennec, who believed Reisseissen's evidence was proof enough of both the spasmotic and nervous theories of asthma.

J.B. Berkart, in his 1878 book "On Asthma: It's Pathology and Treatment," said: (2, page 17)

Laennec assumed that they, being muscles, were endowed with contractility, and therefore liable to spasm. Such a spasm, he thought, might probably have been the cause of that fatal dyspnoea; but whether this supposition were correct or not, the case itself seemed to indicate the existence of a nervous asthma. Yet, notwithstanding the negative results of physical diagnosis and post mortem examination, he had doubts on the subject. Hesitatingly he admitted spasmodic asthma, with this limitation, however, that it generally consisted of nervous and organic affections combined.(2 page 17-18)

He would have been well aware of the evidence in support of the nervous theory of asthma, that asthma is a neurosis of the respiratory organs, that came from the papers of Francis Ramadge in 1835, the essays of Joseph Bergson and Amedee Lefevre in in 1836, and the verification of this evidence by the experiments of Moritz Romberg in 1841.   (4, page 506)

Williams must have been aware of these studies, and believed this evidence was too overwhelming not to support the nervous theory of asthma.

Yet other physicians did not believe this was enough evidence to support any theory, especially Dr. William Budd, who performed experiments in 1840 that he believed disproved the spasmotic theory AND the nervous theory of asthma.

Yet our doctor Williams would have something to say about Dr. Budd's experiments.  Dr. Williams would prove them wrong, and he did it that same year: in 1840.

Dr. Berkart explained:

As the bronchial contractility was denied as often as asserted, Dr. C. J. B. Williams again took the question in order to settle the matter in dispute. He, indeed, succeeded in showing, by experiments conducted with all necessary precautions, that mechanical, as well as chemical 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.  (2, page 26)

Still, while Reisseissen discovered that muscular fibers wrap around the air passages, and while Williams proved that they may spasm under certain circumstances, this did not prove that they spasmed during an asthma attack. (3, pages 193-194)

Berkart said:

Yet one link was wanted to complete the chain of evidence in favour of a bronchial spasm. As yet nothing was known of the innervation of the bronchi. Irritation of the vagus had produced no effect upon their calibres, and Dr. Williams was therefore led to conclude that "the muscular fibres seem not to be excitable through the nerves of the lungs."(2, page 26)

This evidence would also come in 1840 by the experiments of Dr. Francois Achille Longet.  

Williams was among the physicians of his era to support that idea that the definition of asthma was too vague, including too many ailments that cause symptoms similar to asthma yet have nothing to do with the lungs.  He therefore wanted to simplify the definition. 

Berkart said:

Dr. Williams himself, assuming a plus and minus state of contractility, described two forms of asthma—the one spasmodic, the other paralytic. The former was supposed to be represented by the isolated attacks of dyspnoea which generally accompany emphysema; the latter by those which appear in connection with chronic pituitous catarrh. (2, page 26)

Wolff Freudenthal, in his 1917 article in A Weekly Review of Medicine titled "Bronchial Asthma, said:

In 1841, Doctor (J. B.) Williams, in Tweedie’s Dissertations of Diseases of the Organs of Respiration, describes two forms of asthma—a spasmodic and an atonic or paralytic form. He found “that defect of these properties (excessive contractibility of the bronchial tubes) would disorder the process of breathing, and is led to believe that there may perhaps be a nervous asthmaor dyspnea “from weakness or paralysis of the circular fibres, or of the. nerves which regulate their contractions.” (5, page 2)

Williams was correct that asthma needed to be redefined, yet his most impressive contribution to the history of asthma was his experiment proving that the muscular fibers that wrap around the lungs may contract when irritated by certain stimuli.

Surely his experiment didn't prove the spasmotic thoery of asthma, yet it made this theory look highly probable.  His experiment met with little opposition for the next 14 years (Wintrich, 1854), and would be noted by nearly every physician writing on the subject of asthma for the rest of the century.   

References:

1. Williams, Charles J. B., "Memoirs of Life and Work," 1884, London, Smith, Elder, & Co. 
2. Berkart, J.B., "On Asthma: It's Pathology and Treatment," 1878, London, J. & A. Churchill
3. Geddings, W.H., author of the chapter on "Bronchial Asthma," in the book  "A System of Practical Medicine," edited by William Pepper and Louis Star,Volume 3, 1885, Philadelphia, Lea Brothers and Co.
4. Whitaker, James Thomas, "The theory and practice of medicine," 1893, New York, William Wood and Company
5. Freudenthal, Wolff, "Bronchial Asthma," New York Medical Journal: A Weekly Review of Medicine, edited by Edward Swift Dunster, James Bradbridge Hunter, Frank Pierce Foster, Charles Euchariste de Medicis Sajous, Gregory Stragnell, Henry J. Klaunberg, Félix Martí-Ibáñez, volume CV, January-June, 1917 (Saturday, January 6, 1917), New York, A.R. Elliot Publishing, Co., pages 1-5
6. Salter, Henry Hyde, "Asthma: It's Pathology and Treatment," 1864, Philadelphia, Blanchard and Lea

Further reading:

1. Geddings, W.H., author of the chapter on "Bronchial Asthma," in the book  "A System of Practical Medicine," edited by William Pepper and Louis Star,Volume 3, 1885, Philadelphia, Lea Brothers and Co.
2. Biermer, Anton., "On Bronchial Asthma," in the book, " Clinical Lectures on Subjects Connected with Medicine Connected with Medicine, Surgery, and Obstetrics," by various German authors, 1866, London, New Sydenham Society,  pages 171-194
3. Williams, Charles James Blasius, Alexander Tweedie, William Wood Gerhard, "Tweedies dissertations of diseases of the organs of respiration," 1841, London, Lea and Blanchard

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1835: Lefevre questions nervous theory of asthma

Amedee Lefevre (1798-1869) was yet another physician who believed in the spasmotic and nervous theories of asthma.  Yet while he believed asthma was nervous, he was not prepared to deny there weren't organic lesions as yet discovered in asthmatic lungs. (1, page 505)(2, page 23-24)

Orville Brown, in his 1917 book," said Lefevre was an asthmatic who observed by studying his own asthma that he expectorated large amounts of sputum. (3, page 31)

Of this, J.B. Berkart, in his 1878 book, said: 

Lefevre (in 1835)... reverted to the opinion of Laennec. Himself an asthmatic, he had watched his own case and that of a friend, and arrived at the conclusion that the dyspnoea could be produced only by a bronchial spasm. In looking thus upon asthma as a nervous affection, he still was not prepared to deny the possible existence of organic lesions; adding, however, that if such were present, they were of so fleeting a nature as to elude detection. The essence of the disease he considered to be an increased irritability of the nerves of the lungs, in consequence of which the slightest irritation applied to the bronchial surface induced spasm of the bronchial tubes. (2, page 23-24)

However, Berkart suspected that the patient's he was studying were not asthmatics, and therefore his experiments (of which he performed with  Joseph Bergson) did not support his theory that asthmatic lungs might possibly have organic lesions.  He said: (2, page 24) 

The cases, however, which he himself reported, do not confirm his views. It is difficult to recognise a nervous affection, much less a bronchial spasm, in the dyspnoeal attacks, which terminated always with the expectoration of thick masses of mucus. The expectoration was of a grey colour, very viscid, in consistency like boiled maccaroni, filamentous in shape, and, when disentangled, appeared as if moulded to the bronchi. Sputa of that kind sufficiently distinguish the preceding dyspnoea as the symptom of a fibrinous (croupous) bronchitis, and there can be no doubt that Lefevre and his friend were subject to that disease. (2, page 24)

So while he thought he was on to something with his theories, he probably added little evidence to advance either the spasmotic nor the nervous theories of asthma. The reason was mainly due to the inability to differentiate bronchitis with asthma.

Of interest is he also observed spirals in asthmatic sputum.  This would be an observation that would inspire investigations by later physicians that would ultimately lead to a new theory about asthma.  (1, page 505)

He also wrote a book called De 'lasthme , of which you can read if you can read French.  

References:

1. Sakula, Alex, "Charcot-Leyden crystals and Curschmann spirals in asthmatic sputum," Thorax, 1986, 41, pages 503-507
2. Berkart, J.B., "On Asthma: It's Pathology and Treatment," 1878, London, J. & A. Churchill; The reference used by Berkart is as followed:  "Recherches sur l'Asthme, M&noire couronne' par la Society de MfSdecine de Toulouse."—JournalHebdomad., 1835.
3. Brown, Orville Harry, "Asthma, presenting an exposition of nonpassive expiration theory," 1917, St. Louis, C.V. Mosby Company.  The above mentioned theory of vessel turgescence comes from this reference also on page 25; he refers to the same source as Berkart

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1808: Reisseissen discovers smooth muscles along air passages

Samuel Thomas von Sommering (1755-1830)
was a German physician and anatomist who,
confirmed Reisseissen's discovery. (6, page 4)

Dr. Franz Daniel Reisseissen (1773-1828) was a German physician who studied the lungs, and proved that smooth muscles line the air passages. This was a significant discovery, and set the stage for later physicians to prove the spasmotic theory of asthma.

He performed experiments in 1808, and the results were published as essays in Berlin in 1822.  (1, pages 196-197)

W.H. Geddings, in the 1885 edition of A System of Practical Medicine, said Reisseissen discovered...

...smooth muscle fibres of the bronchial tubes. These fibres are found not only in the large and medium-sized bronchi, but even in those of the smallest calibre."(2, page 185, 193)

Emanuel Aufrecht (1844-1903)
attended school in Berlin
and was a student of Ludwig Traub
and Rudolf Virchow.
He graduated from medical school in 1866.
He became a physician at
 Magdeburg-Alstadt City Hospital in 1868,
and physician in chief of Internal Medicine
at Magdeburg in 1879.
He worked out the arrangement
of the bronchial muscle fibres. (7, page 163)
While chief of clinical medicine at Magdeburg,
he published a book with his colleagues in 1902
called "Diseases of the Bronchi, Lungs and Pleura."
(8, title page)

Gedding said the discovery was "The first step toward a truly scientific theory of the pathology of asthma."

Without his discovery, none of the discoveries that readily proved asthma was spasmotic would have been possible, including those of Charles J.B. William and Francois Longett.

Rene Laennec, in his 1819 book "Mediate Auscultation" said there were various theories as to the structure of the lungs prior to Reisseissen's discovery.  For instance, Laennec said: (3, page 154)

(Marcello) Malpighi conceived that the air cells (later to become known as alveoli) were formed by the inner membrane of the bronchi being divided, previously to their termination, into cells like those of a sponge. Helvetius fancied that he had ascertained by direct experiment, that the air cells were formed by a simple cellular tissue, disposed without any regular order, and derived from the cellular envelopes of the various vessels by which the lungs are traversed. (Albrecht von) Haller entertained almost the same opinion, which is, indeed, that of the greater number of anatomists. (3, page 154)

M. Varnier confirmed Reisseissen's experiments
that the bronchi may constrict when stimulated.
He believed "irritating fluids or fumes forced
into the lungs caused contraction therof."
There were also various other physicians
who confirmed Reisseissen's experiment,
including: Prochaska, Gotfried, Reinhold,
Treviranus, and Wedemeyer
(6, page 4)(7, page 27)

The speculation ended when, according to Laennec, Reisseissen...

...by means of a great many microscopical observations and mercurial injections, has ascertained that the bronchi, at their extremities, are subdivided into a multitude of small canals, terminated by cul-de-sac of globular form, grouped somewhat in the manner of terminal branchlets of cauliflower. (3, page 154)

John Forbes quoted Reisseissen as saying...

... that, although it appears difficult to follow the muscular fibres further, analogy leads us to admit their existence in the smaller branches, and perhaps even in the aircells. (4, page 186)

Dr. J.B. Berkart, in the 1878 edition of his book "On Asthma: It's Pathology and Treatment, said that while Reisseissen was aware of muscular fibres surrounding the large and small air passages, their function remained a mystery to him. (5, page 17)

The significance of these muscular fibres has still not been determined as of this writing, as I explained in my post "Asthma: The Appendix of the Lungs.

However, the significance of their impact on asthma lead to a massive search that would last for the duration of the 19th century. The hunt was on to learn more about them and what they did. This task was begun by Charles J.B. Williams and Francois Longett.  Yet the debate would continue on for the duration of the century.

References:

1. Addison, Thomas, J.M. Bourgery, and George Rainey, "On the air cells of the lungs," The Edinburgh Medical and Surgical Journal, volume 69, 1848, pages 192-214
2. Geddings, W.H., author of the chapter on "Bronchial Asthma," in the book  "A System of Practical Medicine," edited by William Pepper and Louis Star,Volume 3, 1885, Philadelphia, Lea Brothers and Co.
3. Laennec, Rene Theophile Hyacinthe, "A treaties on the diseases of the chest, and on mediate auscultation," translated by John Forbes, 1838, New York, Philadelphia, Samuel S. and William Wood, Thomas Cowperthwaite and Company
4. Forbes, John, ed., "The Cyclopaedia of practical medicine," 1833, volume 1, page 186
5. Berkart, J.B., "On Asthma: It's pathology and treatment," 1878, London, J. & A. Churchill
6. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis
7. Brown, Orville Harry, "Asthma, presenting an exposition of nonpassive expiration theory," 1917, St. Louis, C.V. Mosby Company
8. Hoffman, Friedrich Albin, Ottomar Rosenbach, Emanuel Aufrecht, writers, John H. Musser, editor, Alfred Stengel, translator, "Diseases of the Bronchi, Lungs and Pleura," 1902, Philadelphia, New York and London,asthma history, COPD history, inhalation therapy history, medical history W.B. Saunders and Company. 

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