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attention, frontal executive functions (e.g. problem solving, mental
fl exibility, initiation, and inhibition), language, memory and learning
dysfunction. However, the most severely affected cognitive domains
are by far memory and information-processing speed and effi ciency.
The nature of cognitive dysfunction in humans is very impor-
tant to consider when developing and using cognitive assessments
in animal models of brain injury. Although memory dysfunction is
a cardinal feature after TBI, memory impairment is not global and
various domains of memory are affected differentially. In the acute
stages following injury, intervals of retrograde amnesia (RA) and
posttraumatic amnesia (PTA) are often reported, the duration of
which strongly predicts outcome. As time progresses, however,
anterograde memory impairments become predominant and often
persist though life ( 1, 2 ). Memory is often subdivided into: declar-
ative memory (explicit), which includes both episodic memory for
events and semantic memory for general facts, and implicit memory,
which includes procedural learning, priming, and conditioning ( 2 ).
Disruption to episodic memory processes is a hallmark feature of
TBI, whereas implicit, or procedural memory (e.g., motor skills or
puzzle solving), is generally left unimpaired ( 3, 4 ).
Explicit memory is thought to be the result of several levels of
information processing, commonly referred to as encoding, con-
solidation, and retrieval. Encoding refers to the process by which
information is acquired and processed when fi rst encountered. This
includes associating new information with previous knowledge so
that one can integrate knowledge with what one already knows.
Consolidation refers to the processes by which new information is
converted to long-term storage, and is accompanied by changes in
gene and protein expression and subsequent structural changes.
Retrieval refers to the processes that recall the stored information
and bring information from many locations together. The nature
of memory impairments seen in both animals and humans with
brain injury may be the result of memory dysfunction at any of
these levels of information processing.
Another important consideration when assessing cognitive
function following injury is the type of experimental injury model.
It is well known that different injury models (e.g., Weight-drop,
Fluid-Percussion and Controlled Cortical Impact) replicate different
aspects of TBI, and thus cognitive assessments must be viewed in
light of injury model. Several factors, including the type, location,
and severity of injury, histopathological characteristics, and other
factors such as strain and age are important to consider. Changes in
any of these factors may result in varying levels of cognitive impair-
ments. Also, important to this discussion is the evidence that
neural circuitry and neurochemistry of different components of
memory overlap signifi cantly. For example, the hippocampus, long
recognized as a crucial structure in declarative memory processes,
has recently been shown to have extensive connections to areas of
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