Drs Minns and Brown provide a broad review of inflicted head injuries (IHIs) from medical, epidemiological, legal, and social viewpoints. The most extensively treated topics, clinical (neurological) manifestations and biomechanics of infant and toddler head injury, consume the first third of the text. The text expands on the 2005 article by Dr Minns1 on the same topic. In both, he postulates 4 different clinical presentations for IHI. Six percent of IHIs are attributed to a “hyperacute encephalopathic or cervico-medullary syndrome,” in which acute cervicomedullary injury results in immediate apnea, leading to death or severe hypoxic-ischemic injury. Here the pathologic studies of Geddes et al2 are referenced. They observed children with IHI to have microscopic or gross evidence of injury at the cervicomedullary junction but little evidence of traumatic axonal injury. These observations were very helpful in redirecting our thinking to the role of such injuries and apnea as a cause of morbidity. Unfortunately, they jumped from there to totally unsupported conclusions that these injuries might result from minor traumatic events. Additionally, they postulated that the apnea with accompanying hypoxia might be the cause of the subdural and retinal hemorrhages seen in these children, instead of a direct result of the original trauma. They have subsequently recanted their “unified hypothesis,” but not until after it had severely damaged child protection.3 The second pattern is an “acute encephalopathic” one, with extensive symptoms of intracranial and retinal bleeding and cerebral dysfunction. Dr Minns placed 53% of the cases in this category and attributed it to shaking or repetitive whiplash injury, with or without accompanying impact. A third group of 21% of the victims had a “subacute nonencephalopathic” presentation, with intracranial bleeding and extracranial evidence of abuse but without the severe neurological symptoms. Finally, 20% had a “chronic extracerebral presentation” of enlarging head size from chronic subdurals and variable symptoms of increased intracranial pressure, but they lack other signs of abuse. The earlier mentioned figures are from a Scottish database, extensively reported in the text. Although these clinical formulations are presented as discrete scenarios, I feel they are more likely extremes, while most children have some blend of these patterns. For example, we often see children with chronic subdurals, picked up by increasing head sizes, who in retrospect have a postnatal jump in head size, simultaneous with a period of irritability and vomiting. Many, on skeletal survey, are also found to have healing rib or other fractures. It is naive to assume these children did not sustain severe head injuries with immediate concussion simply because no one is admitting it or no one recognized the cause of the symptoms at the time.