Introduction 

We recently advocated for the Liverpool-based physician Richard Caton (1842-1926) as having presented a case of disturbed sleep-related breathing in 1889, despite the title of the publication being “Case of narcolepsy” [1]. Based on his clinical observations, we were of the view that Caton’s “account must rank as one of the earliest documenting many of the typical clinical symptoms and signs of obesity hypoventilation syndrome with associated OSA [obstructive sleep apnoea]” [2]. 

More recently we have become aware of a still earlier description highly suggestive of the clinical characteristics of OSA, dating from 1877, from the London-based physician William Henry Broadbent (1835-1907) [3]. Recent biographical works focused on Broadbent’s neurological contributions [4,5] have neglected any mention of this informative case. 

Broadbent’s report 

The principal subject of Broadbent’s report happens not to be our particular focus of interest. This index case was “A gentleman aged about sixty-four, tall, decidedly but not extremely stout” who had “had two slight and transient attacks of partial hemiplegia, which have left no traces of paralysis”. Examination revealed “all the signs, arterial and cardiac, of very high arterial tension” (i.e. hypertension, although no blood pressure measurements were recorded). Broadbent also noted that his patient was “inclined to sleep”. The patient then suffered an episode in which “it was observed that he looked confused, then his right hand dropped, and a few minutes later speech was completely lost”. Seen an hour later by Broadbent, he was found to have “well-marked right hemiplegia” also affecting face and tongue and “was quite speechless, not from embarrassment of articulation, but distinctly from aphasia”. In addition, “My attention was at once attracted by the breathing, in which the ‘Cheyne-Stokes’ variation was well-marked”. After a few hours, the patient had made a partial recovery of speech and right leg strength, allowing Broadbent more time to observe the periodicity of the breathing. However, no report about this patient’s breathing pattern during sleep was given.

Based on this case, Broadbent was then prompted to mention some other cases in which he had witnessed Cheyne-Stokes’ respiration, one of which is the subject of particular interest in this article. Broadbent’s account of this patient, in its entirety, was as follows: 

Many years ago I observed something very like Cheyne-Stokes’ respiration during sleep in a gentleman now more than eighty years of age. When a person, especially advanced in years, is lying on his back in heavy sleep and snoring loudly, it very commonly happens that every now and then the inspiration fails to overcome the resistance in the pharynx of which stertor or snoring is the audible sign, and there will be perfect silence through two, three, or four respiratory periods, in which there are ineffectual chest movements; finally, air enters with a loud snort, after which there are several compensatory deep inspirations before the breathing settles down to its usual rhythm. In the case to which I allude there was something more than this. The snoring ceased at regular intervals, and the pause was so long as to excite attention, and indeed alarm; and I found, on investigation, that there was not simply obstruction by the falling back of the tongue &c., but actual cessation of all respiratory movements; these then began gradually, but did not at first attain sufficient force to overcome the pharyngeal resistance [3]. 

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Formulation 

Based on the available evidence from Broadbent’s account of the elderly gentleman, who was merely a subsidiary illustrative case in the context of the paper, he exhibited several features which may permit us to hazard a retrospective diagnosis. His sleep, attended with snoring, was clearly fragmented with periodic cessation of respiration, or apnoeic episodes, despite “ineffectual chest movements” indicating respiratory effort against a closed or narrowed airway. No specific timings were given but the periodic nature of the breathing is evident. Hence our retrospective formulation is that Broadbent’s patient most likely suffered from obstructive sleep apnoea.

Discussion 

Whilst some later authors have acknowledged the accounts of William Broadbent [6,7] and of Richard Caton [2,8] as typical of OSA, neither Broadbent nor Caton feature in some dedicated histories of this condition [9]. The clinical observations presented in these cases leave no doubt about the retrospective diagnosis of OSA.  

In this context, it may be of note that both Broadbent and Caton were physicians whose interests included neurology [4,5,10]. Broadbent formulated a hypothesis to explain the clinical observation that axial muscles were relatively spared in cases of hemiplegia [1], a hypothesis which was approved of and cited by John Hughlings Jackson (1835-1911). Broadbent and Jackson were respectively the proposer and seconder of a motion to establish the Neurological Society of London in 1885, the first organisation dedicated to neurology in the United Kingdom [12]. In 1875, Caton had been the first to record the electric currents of the brain in animals [13], experimental observations which proved foundational to the development of electroencephalography in the 1920s and 1930s. 

It is also noteworthy that Broadbent’s principal, index case concerned a patient with recurrent transient hemiplegic episodes followed by a major stroke in whom he documented Cheyne-Stokes respiration, whilst the subsidiary case provided one of the earliest descriptions of OSA. Although Broadbent did not unify these observations into a single pathophysiological concept, they anticipated an association that was not firmly established until more than a century later. It was only in the twenty-first century that large observational studies and meta-analyses demonstrated the high prevalence of sleep-disordered breathing following stroke and transient ischaemic attack, its persistence over time, and that OSA is an independent risk factor for stroke and all-cause mortality even after adjustment for conventional vascular risk factors [14,15].

References

  1. Caton R. Case of narcolepsy. Transactions of the Clinical Society of London 1889; 22: 133-137.
  2. Elhadd K, Larner AJ. Richard Caton’s “Case of narcolepsy”: obesity hypoventilation syndrome in the 1880s? Sleep & Breathing 2025; 29: 143. https://doi.org/10.1007/s11325-025-03299-y
  3. Broadbent WH. On Cheyne-Stokes’ respiration in cerebral haemorrhage. Lancet 1877; 1 (2792): 307-309. https://doi.org/10.1016/S0140-6736(02)21857-7
  4. Eadie M. William Henry Broadbent (1835-1907) as a neurologist. J Hist Neurosci 2015; 24: 137-147. https://doi.org/10.1080/0964704X.2014.928751
  5. Larner AJ. William Henry Broadbent (1835-1907). Journal of Neurology  2025; 272: 376. https://doi.org/10.1007/s00415-025-13119-8
  6. McNicholas WT, Luo Y, Zhong N. Sleep apnoea: a major and under-recognised public health concern. J Thorac Dis 2015; 7: 1269-1272. https://doi.org/10.3978/j.issn.2072-1439.2015.07.29
  7. Pham LV, Schwartz AR, Polotsky VY. Integrating loop gain into the understanding of obstructive sleep apnoea mechanisms. J Physiol 2018; 596: 3819-3820. https://doi.org/10.1113/JP276590
  8. Lavie P. Nothing new under the moon. Historical accounts of sleep apnea syndrome. Arch Intern Med 1984; 144: 2025-2028. https://doi.org/10.1001/archinte.144.10.2025
  9. Peters BR, Guilleminault C. A short history of obstructive sleep apnea syndrome. In: Chokroverty S, Billiard M (eds). Sleep Medicine. New York: Springer, 2015: 357-363.
  10. Larner AJ. Richard Caton (1842-1926). Journal of Neurology 2025; 272: 221. https://doi.org/10.1007/s00415-025-12935-2 
  11. Broadbent WH. An attempt to remove the difficulties attending the application of Dr. Carpenter’s theory of the function of the sensori-motor ganglia to the common form of hemiplegia. Br Foreign Med Chir Rev 1866; 37: 468-481.
  12. Larner AJ. The Neurological Society: 1885-1907. Amazon, 2025: 9-10.
  13. Caton R. The electric currents of the brain. BMJ 1875; ii: 278. https://doi.org/10.1136/bmj.2.765.257
  14. Seiler A, Camilo M, Korostovtseva L et al.Prevalence of sleep-disordered breathing after stroke and TIA: a meta-analysis. Neurology 2019; 92: e648-e654. https://doi.org/10.1212/WNL.0000000000006904
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