There are other mental and behavioral abnormalities of a more subtle type that remain as sequelae to serious cerebral injury. As the stage of posttraumatic dementia recedes, the patient may find it impossible to work or to adjust to his family situation. Such patients are often abnormally abrupt, argumentative, and suspicious. Unlike the postconcussion syndrome described above, in which there is a certain uniformity, these traits vary with the patient’s age, past experience, and environmental stresses. Extremes of age have been particularly important in our experience. The most prominent behavioral abnormality in children, described by Bowman and colleagues, is a change in personality. They become impulsive, impatient, unable to sit still, or may become heedless of the consequences of their actions and lacking in appreciation of social norms—much like those who in the past had recovered from encephalitis lethargica. Some adolescents or young adults show the general lack of inhibition and impulsivity that one associates with frontal lobe disease. In the older person, it is the impairment of intellectual functions that assumes greater prominence. In most instances, these more serious behavioral changes can be traced to contusions in the frontal and temporal lobes. In cases without obvious structural brain damage, cognitive deficiency after trauma has been widely attributed to diffuse axonal injury. Attempts to validate this by modern techniques such as diffusion tensor imaging have met with some success, such as the series described by Kraus and colleagues.
The tendency is for many such symptoms to subside slowly although not always completely, even in those in whom an accident has provoked a frank outburst of psychosis (as may happen to a person who is bipolar or a paranoid schizophrenic). These forms of what had colorfully in the past been called “traumatic insanity” were analyzed for the first time a century ago by the noted neuropsychiatrist, Adolf Meyer.
Chronic traumatic encephalopathy The cumulative effects of repeated or even single cerebral injuries, constitute a type of head injury that until recently was difficult to classify. The subject of a delayed neurodegenerative cerebral disease that follows mild traumatic brain injury after many years is best introduced by an exposition of the long-appreciated condition in boxers who had engaged in many bouts over a long period of time. This historically important syndrome serves to introduce the more recently emphasized and seemingly ubiquitous chronic encephalopathy in other professional athletes. It refers to the development after years in the ring of dysarthric speech and a state of forgetfulness, slowness in thinking, and other signs of dementia. Movements are slow, stiff, and uncertain, especially those involving the legs, and there is a shuffling, wide-based gait. In other words, a parkinsonian and dementing syndrome emerges and sometimes a moderately disabling ataxia, but there is no mistaking these for idiopathic Parkinson or Alzheimer disease. The plantar reflexes may be extensor on one or both sides. The clinical syndrome was reanalyzed by Roberts and colleagues, who found it present to some degree in 37 of the 224 professional boxers they examined. More recent studies show that in about one-half of all professional boxers, both active and retired, the CT scan discloses ventricular dilatation and sulcal widening and a cavum septi pellucidi (why the latter, which is ostensibly a developmental anomaly, would be overrepresented in boxers is unclear). These anatomic abnormalities had been demonstrated many years before by pneumoencephalography and were found to be related to the number of bouts (Ross et al;
Casson et al).