Dr Martland’s clinicopathological conferences served as a valuable vehicle for medical education in the state of New Jersey. Here, he is lecturing on the topic of ‘Punch Drunk’ syndrome. Reproduced with permission from: Harrison Martland Papers, Special Collections in the History of Medicine, George F. Smith Library, Rutgers University Libraries.
Pivotal work on punch drunk syndrome
To understand Martland’s role in the story of punch drunk, we must first look at his scientific predecessors. Dr Wilfred Trotter, an accomplished British surgeon, noted in a talk entitled On Certain Minor Injuries of the Brain delivered in 1924, that concussion is an ‘essentially transient state’ that ‘does not as such comprise any evidence of structural cerebral injury, and is always followed by amnesia for the actual onset of the accident’ (Trotter, 1924). This understanding of concussion would be contested in the years ahead. Dr C. B. Cassasa, one of these contesters, published a report in 1924 that documented perivascular haemorrhages after the incidence of head trauma. He theorized that concussive forces caused turbulent CSF flow within the perivascular lymph space, leading to tears of the fibrils that attached between the vessel walls and surrounding dural walls. These torn fibrils would go on to cause laceration within the vessel walls, resulting in subsequent haemorrhage within the perivascular space (Martland, 1928). In 1927, Dr Michael Osnato and Dr Vincent Gilberti published a case series that provided further evidence of Cassasa’s mechanism. They histologically showed fibrillar attachments and haemorrhages within the perivascular spaces in confirmed clinical cases of concussion. They also proposed that concussions can have more chronic effects, claiming that they were not ‘transient’ entities and could be linked to secondary degenerative changes within the brain (Martland, 1928).
That leads us to Dr Martland’s work. While working with neurologist Dr Christopher Beling, he performed a series of autopsies on 309 traumatic cerebral haemorrhage cases. Martland observed that nine cases of haemorrhage were not associated with any signs of overt cortical injuries or skull fractures (Martland, 1928). The haemorrhages in these cases were microscopic in nature and resembled the perivascular microhaemorrhages described previously by Cassasa, Osnato, and Gilberti (Martland, 1928).
Martland noted these findings and proposed a connection between these cerebral microhaemorrhages and over-punished boxers who experienced neurological symptoms after suffering repetitive head trauma. These boxers were labelled as being ‘punch drunk’. His paper, aptly entitled Punch Drunk, described this phenomenon and provided evidence of its existence. Martland utilized the knowledge of Cassasa’s mechanism with Gilberti and Osnato’s observation of chronic symptoms, to formulate a more complete theory. He believed that patients that survive after the occurrence of head injury—and probable perivascular microhaemorrhages—develop a ‘replacement gliosis’ within the brain, best explaining the ‘post-concussion neuroses and psychoses and the so-called post-traumatic encephalitis’ that resulted (Martland, 1928).
Martland’s paper documented 23 examples of boxers (five of which he examined himself) to piece together the classic clinical presentation of ‘punch drunk’ boxers. He noted that symptoms could present immediately after injury, sometimes during the boxing match itself, as evidenced by minute changes in gait or more obviously when boxers staggered as they walked back to their corners of the ring between rounds. He also highlighted the chronicity of the syndrome in severe cases, noting physical symptoms such as parkinsonian gait, tremulousness, vertigo, and even cognitive symptoms such as ‘mental deterioration’ necessitating asylum institutionalization.
Martland used his skills of observation and practical analysis to form clinical correlates, which were unique aspects of his paper. He was able to stratify boxers into different archetypes to assess their likelihood of developing the syndrome. He noted that the slower ‘slugging type’ boxers were at greater risk of developing these symptoms than those that rely on agility. Boxers that more often took risks to land a knockout punch, as opposed to boxers that relied on points to win, were also more likely to develop ‘Punch Drunk’ syndrome (Martland, 1928; Parker, 1934).
Of course, the skill level of the boxer was also a large factor since second-rate boxers or those that were used for training purposes—in which they were constantly being hit and knocked down several times a day—were at greater risk (Martland, 1928). Similarly, in Martland’s report of a 38-year-old boxer with symptoms of ‘Punch Drunk’ syndrome, he delved into the boxer’s fight history with great detail to thoroughly understand all aspects of the boxer’s history (Martland, 1928). Martland spent enormous effort to understand the nuances of boxing in order to speak knowledgably about the sport.
Although ‘Punch Drunk’ was a colloquialism that was well known within the boxing world, there was little said of it within the medical literature. Prior to Martland’s landmark paper, post-concussive syndrome was not recognized as a clinical syndrome at all. Martland noted that when boxers visited ‘eminent physicians,’ they were often turned away after being told that there is essentially no such syndromic association between boxing and the patients’ symptoms.
Martland put much more faith in the trainers, promoters, and boxers themselves, citing the value of the observations made by the numerous individuals that make a living in the sport (Martland, 1928).
Legacy of Martland’s work
Dr Harry Parker built on Martland’s thesis and presented more evidence of its existence, noting ‘punch drunkenness’ can present as a ‘medley’ of symptoms through different symptomatic time courses (Parker, 1934). J. A. Millspaugh, a naval lieutenant, published an article in 1937 that presented more examples of cognitive dysfunction in naval boxers who suffered from dementia and disorientation (Millspaugh, 1937). Millspaugh also introduced new nomenclature to the literature, re-terming ‘punch drunk syndrome’ as dementia pugilistica, which is still used today. Lastly, he analysed the landscape of regulations, rules, and precautions taken by boxing committees to ensure the safety of its boxers. Just as Martland had done, he further proposed that the medical attendant must be responsible enough to stop the fight if the attendant feels that the ‘mental hygiene’ of a defeated boxer is in danger (Millspaugh, 1937).
As diagnostic technology advanced, it demystified the histopathological consequences of repetitive head trauma, showing that Martland’s theory describing a relationship between microhaemorrhages and punch drunk symptoms was inaccurate. Corsellis et al. (1973) published the first robust neuropathological study, which looked at patient histories and autopsy specimens of 15 different retired boxers—the largest case series of the time. They confirmed that many of these boxers had a multitude of symptoms, ranging from physical symptoms such as parkinsonism, to changes in affect and cognition. The authors went beyond the scope of the patient’s post-fight days and deliberately looked at the subjects’ personalities and intelligence prior to the development of their symptoms. Importantly, Corsellis et al. (1973) and studies that followed, found that the boxers’ symptoms arose most likely due to cerebral degeneration along with histopathological changes found in the brain secondary to protein deposition. Today, this proteinopathy theory is considered to be the most comprehensive explanation for the development of CTE (McKee et al., 2009). Neuroimaging and some pathological studies have shown the presence of haemosiderin after concussion; however, the pathophysiological role of microhaemorrhages in CTE, if one exists, is not yet confirmed or denied. It is worth mentioning that Martland made a small but often overlooked point in his 1928 piece. He states: ‘It is conceivable that the milder forms of concussion may be attributed to distension of the perineuronal spaces causing hydraulic shock to the neurons without the occurrence of actual hemorrhages’ (Martland, 1928). Although this does not fit with Martland’s primary hypothesis, this statement may ironically provide more insight into the pathophysiology of concussions given today’s understanding of concussive head trauma and the questionable role of perivascular haemorrhages.
Martland’s opposition of boxing’s barbarism was prominently evident in his writing. He also shared the same sentiments regarding football (Ginley, 1969). In 2005, the most popular and monetarily prosperous sport of the time: American football, was now under the microscope when Omalu et al. published a paper describing CTE in a retired National Football League (NFL) player (Omalu et al., 2005). This study, along with subsequent works performed by others (McKee et al., 2009), brought the issue of CTE back into the forefront of neurotrauma, sports, and journalism where it continues to remain today. Similar to Martland’s writings on boxing, criticisms of the NFL from today’s medical community have served as impetus for continued evolution of football safety as insightful regulations and player health monitors are annually fine-tuned for optimal player safety. Other sports, such as soccer, have also been implicated in a similar fashion. Currently, research within the field is booming and collaborators in medicine, sports, and legislation are all working towards safer environments to prevent the development of CTE.
Martland’s seminal work on ‘Punch Drunk’ syndrome came well before the development of proper diagnostic techniques needed to evaluate his hypothesis. However, his work in introducing the paradigm to medical literature—based solely on observation and trust in ‘laymen’—laid the foundation for those confirmatory studies that built upon his thesis.
His warnings on repetitive head trauma in the realm of sports continue to resonate almost a full century later. His work is worth remembrance as present-day studies continue to elucidate the occurrence of brain injury in sports.
Source: https://academic.oup.com/brain/article/141/1/318/4774567?utm_source=TrendMD&utm_medium=cpc&utm_content=Brain_1&utm_campaign=Brain_TrendMD_1&login=false
