This article was published in the 2008 Baseball Research Journal
There is no question that, when a hitter takes stock of his prize possessions, the eyes have it. In the early twentieth century, the great ones such as Cobb, Hornsby, and Lajoie refrained from reading newspapers or books. They even stayed away from movie houses, believing they were protecting their vision. One time shortly after his own return to baseball following a two-week hospital stay, Babe Ruth (or more likely his ghostwriter) saluted the comeback of a fellow ballplayer who had suffered from problems with his vision. “I know what it is to be helpless,” he wrote, “but I am thankful there isn’t anything wrong with my eyes.”1
The comeback player Ruth was referring to was George Sisler of the St. Louis Browns. In the fall of 1922, Sisler had just completed another banner year, having hit .420, the second time in three years that the first baseman hit over .400. He and Ruth were by most accounts the best ballplayers in the American League, if not in all of professional baseball. That year Sisler was the top vote getter in a poll of sportswriters delegated to name the junior circuit’s most valuable player. And so the entire sports world was stunned six months later when Sisler was unable to answer the call to spring training because of a sinus infection that followed a bout with influenza. In short order he developed vision problems that rendered him unable to play ball at all in 1923 and arguably reduced his ability to hit a baseball for the remainder of his career.
Contemporary newspaper accounts mentioned that Sisler suffered from a sinus infection, or sinusitis, that affected his vision, but they did not explain how the infection caused the impairment to his vision. Over the years, the exact cause of his vision problems and any relationship to his sinusitis in early 1923 has remained a matter of conjecture. Our purpose in this article is to analyze the available information and use it to offer a reasonable diagnosis that provides a plausible explanation for Sisler’s malady.
As Sisler’s actual medical records are unavailable, the newspaper reports of the day, quoting various treating physicians, take on added significance. They suggest not only what the nature of the problem may have been but also what it was not. We examined the reports to determine whether the vision problems Sisler experienced in 1923 involved the internal structure of the eye itself, the optic nerve (as some have speculated), other nerves of the eye, and/or the muscles of the eye.
In a report by the Associated Press (April 10, 1923), an oculist treating Sisler was quoted as saying that “the star’s vision was normal in each eye.” The report said further that the oculist emphasized the word each, indicating that visual acuity was normal but leaving open the possibility that coordination of the eye movements was impaired.2 Therefore, it appears that the problem was not in the retina of the eye or in the optic nerve. The retina, the structure at the inside of the back of the eye, contains light-sensing cells and the nerve-cell circuitry that leads into the optic nerve. The optic nerve carries the nerve impulses from the eye back to the brain, where it is processed into our sense of vision. If there had been damage to the retina of one eye or to the optic nerve coming from one eye, vision would not have been normal in that eye.
An article in the St. Louis Post-Dispatch (March 27, 1923) mentioned that, in addition to the sinus condition, Sisler had experienced a “muscular disturbance.”3 In typewritten memoirs that Sisler prepared for his family some years later, he wrote that after the 1922 season he “had a case of double vision.”4 The medical term for this is diplopia. “I didn’t quite realize what was happening,” Sisler recalled, “until one day when I was driving I thought I saw two cars in the other lane. There was only one, and I knew something was drastically wrong.”5 In the Post-Dispatch in March 1924, sportswriter J. Roy Stockton noted that Sisler’s “eye was noticeably crossed” in October 1923 and that Sisler had told him that he “couldn’t see one baseball.”6 The condition that could explain all of these reports is a disturbance of one of the muscles that move the eye.
Each eye is attached to six muscles, the extraocular muscles, which move the eye. Each of these muscles is supplied by one of three nerves—the oculomotor, trochlear, and abducens nerves, which are also known as cranial nerves III, IV, and VI, respectively. The most likely cause of double vision in adulthood is diminished function in one of the extraocular muscles, which could result from damage to the muscle itself or from damage to one of the corresponding cranial nerves. Whether the diplopia is caused by muscular damage or nerve damage, the resulting impairment can be variable in duration and followed by either complete or only partial recovery.
A second issue in Sisler’s case is the exact relationship of his diplopia to his sinusitis. It is difficult to accurately determine more than eighty years after the fact, but we can make some reasonable assumptions. In April 1923, Sisler was reported to have been hospitalized for surgery for an “inflamed ethmoid sinus.”7 Exact details of the sinus surgery are lacking. Most likely, the procedure was designed to create an opening in the affected sinus to allow the contents of the sinus to drain. However, Sisler’s diplopia did not resolve until almost a year later, providing clues to what the cause of his diplopia might have been.
If the sinusitis and diplopia are in fact related (as physicians at the time assumed), two possible major mechanisms for Sisler’s diplopia come to the fore. Both are based on the assumption that the sinus infection spread beyond the confines of the infected sinus.
The first major possibility is that sinusitis produced an expansile infected mass within one of the sinuses adjacent to the orbit and that this mass either expanded the sinus or broke through the wall of the sinus to compress either a cranial nerve or an extraocular muscle. in Sisler’s case, the ethmoid sinus (located between the eyes) was reported to be infected, so that the mass would presumably have arisen within that particular sinus. Such a mass arising within the sinus can be uninfected (a mucocele) or infected (a mucopyocele). The report that the ethmoid sinus was infected suggests that it was a mucopyocele. However, successful decompression of such a mass should have produced improvement in Sisler’s diplopia within the course of a few days or weeks. To the contrary, the records indicate that Sisler’s diplopia was not resolved for almost a year, making it unlikely that the mass was a mucopyocele.
The second major possibility is that the infection could have spread from within the sinus into the adjacent orbit. Two possible mechanisms for such spread would be osteomyelitis (infection spreading to involve the bony wall of the orbit) or spread of infection through small openings in the wall without infection of the wall itself. Because the cranial nerves that control the extraocular muscles have a course that comes close to the walls of the ethmoid sinuses, infection extending beyond the orbital wall could produce inflammation of those nerves and impair their ability to control the extraocular muscles. Alternatively, osteomyelitis of the sinus wall may have directly caused inflammation of the extraocular muscles, which could become scarred as a result, their motion thereby becoming limited for a prolonged period. Again, the duration of Sisler’s diplopia is helpful in trying to deduce its cause. A yearlong delay in recovery from a cranial neuropathy (if the infection had been adequately treated by surgery) would be unusually long. Therefore, excluding other causes as unlikely, we arrive at the conclusion that the most likely cause of Sisler’s diplopia was not damage to one of the cranial nerves but rather prolonged inflammation of one of the extraocular muscles.
Whatever its cause, Sisler’s diplopia appears to have produced a subtle but long-term effect on his ability to hit a baseball. By March 1924 he did note substantial improvement. “Neither eye has lost efficiency and gradually they are working together better,” he said, adding that “the angle at which I do not see accurately is very small.” Nonetheless, in his opinion he could not play “great baseball.”8 This suggests that some element of diplopia remained, perhaps brought on solely by the eye fatigue of focusing on the pitcher while at bat. This residual difficulty, and its effect on his hitting, was apparent to Bob Shawkey, a 16-game winner with the Yankees in 1924. “When he came back, we soon learned something,” Shawkey said. “When he was up at the plate, he could watch you for only so long, and then he’d have to look down to get his eyes focused again. So we’d keep him waiting up there until he’d have to look down, and then pitch. He was never the same hitter again after that.”9 This suggests that Sisler at bat experienced short, intermittent periods of diplopia, which were likely brought on by the exertion placed on his weakened extraocular muscles during just a few seconds of gazing at the pitcher while awaiting a thrown ball.
If Shawkey noticed this new quirk in George Sisler’s batting style, presumably so did other pitchers. In 1923 Sisler was 30 years old. His composite batting average over the previous three seasons was .400. In 1924, when he returned to baseball, he hit .305. In 1926 his average fell below .300 (.290) for the first time since his rookie season in 1915. And his strikeouts increased from 60 in the period 1920—22 to 83 in 1924—26. More dramatically, his slugging percentages—.632, .560, and .594 in 1920— 22—fell to .421, .479, and .398 in 1924—26.
In the spring of 1925, Sisler became the first major-leaguer to appear on the cover of Time. There the question was put succinctly: “Will he, fans wonder, regain his former prowess?”10 He responded that year by batting .345, clubbing 12 home runs, and driving in 105 runs. Each figure was a post-illness high that few of his contemporaries would cry over. Yet years later, when asked about that performance, Sisler said he was aware of the numbers that he put up in 1925 but that they “never gave me much satisfaction. That isn’t what I call real good hitting.”11
Certainly Sisler’s comments about his 1925 season were not flippant. The Browns’ star was grateful for a recovery that permitted him to return to baseball. But the limited extent of that recovery would always leave him and other followers of his game wondering what might have been, and where an additional eight sea- sons of unimpeded vision would have landed him among the giants of the game.
RICK HUHN is the author of The Sizzler: George Sisler, Baseball’s Forgotten Great (University of Missouri Press, 2004) and Eddie Collins: A Baseball Biography (McFarland, 2008).
JIM PROVENZALE, a neurologist and neuroradiologist at Duke University Medical Center, is interested in the relationship between baseball and medicine.
DAVID A. GOSS is professor of optometry at Indiana University and has been a member of SABR since 1993.
The authors wish to thank Peter Drochelman, the grandson of George Sisler, for his assistance in attempting to locate his grandfather’s medical records.
- Babe Ruth, quoted in his syndicated column, St. Louis Post-Dispatch, 10 May 1925.
- Unidentified oculist, quoted in Associated Press report, 10 April The quote appears in The Scrapbook of Baseball History, by J. A. Deutsch,
- M. Cohen, R. T. Johnson, and D. S. Neft (Indianapolis: Bobbs-Merrill, 1975), 115.
- Unidentified “local specialist,” quoted in St. Louis Post-Dispatch, 27 March 1923.
- George Sisler, typewritten memoirs to his family, date unknown, 12.
- George Sisler, quoted in In the Shadows of the Diamond, by Michael Santa Maria and James Costello (Dubuque, Iowa: Elysian Fields Press, 1992),
- St. Louis Post-Dispatch, 4 March 1924.
- St. Louis Post-Dispatch, 12 April 1923.
- St. Louis Post-Dispatch, 24 March 1924.
- Donald Honig, The Greatest First Basemen of All Time (New York: Crown, 1988),
- Time, 30 March 1925, 28.
- George Sisler, quoted in Baseball’s Greatest Hitters, by Thomas Meany (New York: A. S. Barnes), 187.