The absence of memory or verbal recall for symptom acquisition, as well as the absence of successful coping for life events, is associated with a number of diagnoses, including traumatic brain injury (TBI), posttraumatic stress disorder (PTSD), pain, and anxiety. Including the "absence of behavior" in the reasoning for assignment of such diagnoses can be important to the description of prior existing conditions, especially if a method of measuring it is outlined. However, while of possible diagnostic importance, the absence of behavior is nonquantifiable and does not address the significant issue of whether absence is because of the disruption or incapacity for behavior. A focus on the absence of behavior potentially introduces a further issue by treating nonobserved and observed behaviors equally.
Confounding any effort is that assessment and treatment planning for highly variable events are not conducted at the time or context of the trauma(s). Therefore, such efforts must be undertaken without the benefit of being able to objectively differentiate the effects of the original and subsequent experiences on the current state [1-2]. Notably, the absence of verbal recall or memory of the initial trauma(s) does not preclude subsequent experiences from being remembered or having an effect on symptom expression. In addition, not having access to the individual's cognitive and emotional capabilities over the same time and context precludes measuring any variation and possible effect. The continuous process of the individual's attempts for adaptation introduces additional timeand context-dependent based efforts that can affect behavior in highly variable ways. Knowing these factors would provide both a historical and contemporary perspective of how the process affects an individual's current functional state .
Further complicating the process of attempting to document the effect of trauma is that the noted absence of behavior is commonly attributed to multiple causative explanations that include genes, "failure to learn," motivation, and neurological damage, all of which can affect prospective considerations for treatment. Genes take on a seemingly irrefutable power, even in the absence of the scientific demonstration of cause and effect. Often overlooked is that possessing the genetic characteristic does not determine the effect, as in the case of the gene associated with alcoholism, which still requires an individual to drink to sufficient excess. Parenthetically, alcoholism can occur without the requisite gene. Additionally, the fact that one monozygotic twin can develop normally and the other be diagnosed as autistic makes an effective case for consideration of additional contributing factors. Similarly, the attribution of failure to learn avoids the question of whether such failure is caused by lack of adequate training. The inferred and assigned construct "lack of motivation" further obscures the failure to improve by blaming the person being treated. Also widely assumed is that neural trauma of a known anatomical structure is sufficient reason not only for the absence but also for the prediction of recovery of behavior . A conceptual model based on known scientific evidence would be beneficial so as to avoid resorting to the use of absence of behavior and potentially engaging in circular logic and self-fulfilling prophecy. The potential for doing no harm can also be improved on.
Existing replicated scientific literature was reviewed for clinical applicability to the aforementioned conditions. The scientific-based relationships for structure and function, the relationship of environmental--and time-based influences on learning, and the presence or absence of declarative memory in fear--and trauma-based symptom acquisition was considered. Two areas of research, fear conditioning and learned nonuse theory, provided substantive findings addressing these criteria. …