Although the neurobiological bases of this recovery pattern require further investigation, the systems screening library supporting episodic memory appear, in clinical practice, to resume functioning relatively normally prior to prefrontal systems – including those serving intrinsic executive functions, executive control of basic cognitive functions, comportment, and emotional regulation.34,81,82 The persistence of these problems despite relative,
though not Inhibitors,research,lifescience,medical necessarily complete, normalization of declarative new learning characterizes post-traumatic dysexecutive syndrome. The clinical and neurobiological impairments that comprise each stage of PTE occur on a continuum and the transitions between these stages during recovery from TBI may not proceed unidirectionally: patients functioning cognitively at the transition point, between stages of PTE may vacillate for days (or longer) between those stages. Nonetheless, identifying the stage of PTE that, best, describes Inhibitors,research,lifescience,medical that patient is useful in that it, Inhibitors,research,lifescience,medical facilitates the development of a treatment plan that is appropriate to the patient’s current clinical status. It also allows clinicians
and the patient’s family members to anticipate the course of continued recovery. By extension, this approach to PTE also helps clinicians to identify deviations from the expected course of recovery after TBI and to recognize the need to evaluate the patient for conditions that explain such deviations. Evaluation of post-traumatïc encephalopathy The evaluation of PTE is predicated on a diagnosis of TBI using the clinical case definitions and initial injury severity descriptions reviewed earlier in this article. As noted above, Inhibitors,research,lifescience,medical consideration of the differential diagnosis for alterations of neuropsychiatric status in the postinjury period is also required, as is characterization Inhibitors,research,lifescience,medical of the neuroanatomy and, where possible, the neuropathophysiology of TBI. Even when the occurrence of TBI is incontrovertible, it, will be necessary to entertain the
possibility that a patient’s encephalopathy reflects not only TBI but also co-occurring noncerebral injuries, Carfilzomib medical conditions, and their interactions with other pre-or postinjury factors. When it is clear that the patient is experiencing PTE, identifying the stage and severity of the encephalopathy is appropriate. The evaluation of PTE is facilitated by the use of MG132 Sigma measures that are designed to assess the key neuropsychiatric feature of each PTE stage. Although consensus is lacking on the optimal assessments of neuropsychiatric status during the post-injury period, expert panels, literature reviews, clinical research reports, and common clinical practice suggest that the measures presented in Table VI may be useful for this purpose.