Loren A. McLendon BS, Stephen F. Kralik MD, Patricia A. Grayson NP and Meredith R. Golomb MD, MSc. The Controversial Second Impact Syndrome: A Review of the Literature. Pediatric Neurology. In press.
Second impact syndrome is a devastating injury that primarily affects athletic children and young adults. It occurs when a second concussion occurs before symptoms from the first concussion have resolved. Diffuse and often catastrophic cerebral edema results. Reports of second impact syndrome are few, and some argue that second impact syndrome is simply diffuse cerebral swelling unrelated to the first concussion.
Ovid and PubMed were searched from years 1946 to 2015 using the terms “second impact syndrome,” “repeat concussion,” and “catastrophic brain injury.” In addition, review articles were found using a combination of the terms, “concussion,” “second impact syndrome,” and “repetitive head trauma.”
Seventeen patients in seven publications met the criteria of having two witnessed hits and persistent symptoms from the first to the second concussion. Ten of the 17 (59%) included individuals were football players. All were male. Ages ranged from 13 to 23 years. All children with poor outcomes (death or permanent disability) were younger than 20 years, while four of the five players with good outcomes were older than 19 years. The lag time from first to second concussion ranged from one hour to four weeks, and in many cases, at least one of the two hits appeared minor.
American football, male gender, and young age appear to be associated with second impact syndrome. Controversies surrounding this syndrome are discussed. There is a need for prospective studies to clarify risk factors and outcomes of second impact syndrome to guide return-to-play recommendations for young athletes.
From the article:
There is disagreement about how far apart the two hits can be when considering second impact syndrome. Bey and Ostick reported that second impact syndrome only occurs when the second hit occurs within a maximum of ten days from the first hit because of the cascade that is disrupted during the first traumatic brain injury. However, it is possible that children may be at risk for second impact syndrome as long as postconcussive symptoms persist after the first hit. Some animal work suggests increased susceptibility to neuronal injury when multiple concussions are closely spaced, which might help explain the pathology behind second impact syndrome. An animal study in juvenile rats showed that young rats that received a second concussion one day after the first had more difficulties with recognition tasks and a decreased cerebral metabolic rate of glucose when compared with rats that suffered a second concussion five days later. This suggests that severity of symptoms and cerebral pathology increased when concussions occurred close together. A longer window between the first and second hits might decrease risk, but further research on this issue is needed...
Most examples of second impact syndrome have been reported in the United States, leading some to question its existence. In 2001, McCrory suggested that second impact syndrome should have been reported in each country if it truly existed. He noted that no examples of second impact syndrome had been diagnosed among Australian football players in spite of less protective equipment, although some did have diffuse cerebral edema on postmortem examination. However, this may be a result of different rules, fewer players, and lighter weight players. When compared with Australian-rules football, American-rules football allows harder hits and tackles. In the past few years, there have been about 240,000 adult and child regular Australian rules players a year, compared with 3.5 million U.S. American rules youth football players. In general, Australian-rule football players have had an average body mass index (BMI) around 24.5 while in American football, linemen are often in the obese range with a BMI greater than 30. Australia is now catching up with American obesity rates, and this may increase their risk of second impact syndrome. Rugby, another game that is popular in many countries, lacks the protective equipment of American football but also tends to have lower force hits and tackles due to a combination of rules and lower BMI players. ..
Another consideration is that athletes tend to underreport head injury. One survey of American college football players found that, for every one head injury the players reported, there were 27 unreported head injuries. Athletes tend to “play through” the discomfort rather than be removed from the game. For offensive linemen, there are 32 unreported head injuries for every one reported. Now that recognition of second impact syndrome as a possible entity has increased, there are increasing media reports of it outside the United States, including a male teenage rugby player in Ireland and a female teenage rugby player in Canada. We did not incorporate these individuals into the analysis because they appeared in the news media, not the medical literature, and the news reports contained few details. The continued overall rarity of well-documented second impact syndrome in the medical literature despite the high number of student athletes and increasing recognition suggests that there must be additional, possibly genetic, risk factors that play a role in this condition.
Several mechanisms for second impact syndrome have been suggested. Bey and Ostick proposed that diffuse edema after the second hit leads to compression of the parenchyma and vasculature, causing global brain injury. A more widely accepted mechanism is that the brain's vasculature loses its ability to autoregulate after the first traumatic brain injury. This disruption of autoregulation leads to cerebral edema and engorgement of the vasculature after the second hit because the brain cannot compensate for the edema by decreasing blood flow. Another suggested mechanism is that shearing forces from the concussion lead to axonal injury, which is then further amplified by multiple mild head blows. Multiple concussions may cause metabolic disturbances in the brain that make it vulnerable to further injury. These disturbances include increased metabolism leading to free-radical formation and damage to the neuronal cells. One marker of high metabolism, N-acetylaspartate, appears to be a possible marker for assessing resolution of concussion. Metabolic abnormalities after a concussion may leave the brain more susceptible to further injury.