Recovery of injured cingulum in a patient with traumatic brain injury

The cingulum is the neural fiber bundle that connects the basal forebrain and medial temporal lobe. The cingulum contains the medial cholinergic pathway, which originates from the basalis nucleus of Meynert in the basal forebrain. Therefore, it is important for memory function （Malykhin et al., 2008; Hong and Jang, 2010）. In the past, identification of the cingulum on conventional brain MRI has been impossible because it cannot discern the cingulum from other adjacent structures. Diffusion tensor tractography （DTT）, derived from diffusion tensor imaging （DTI）, allows three-dimensional visualization and estimation of the cingulum （Malykhin et al., 2008）.

Co-culture of astrocytes with neurons from injured brain A time-dependent dichotomy

As supportive cells for neuronal growth and development, much effort has been devoted to the role of astrocytes in the normal state. However, the effect of the astrocytes after injury remains elusive. In the present study, neurons isolated from the subventricular zone of injured neonatal rat brains were co-cultured with astrocytes. After 6 days, these astrocytes showed a mature neuron-like appearance and the number of surviving neurons, primary dendrites and total branches was significantly higher than those at 3 days. The neurons began to shrink at 9 days after co-culture with shorter and thinner processes and the number of primary dendrites and total branches was significantly reduced. These experimental findings indicate that astrocytes in the injured brain promote the development of neurons in the early stages of co-culture while these cells reversely inhibit neuronal growth and development at the later states.

Recovery of injured fornical crura following neurosurgical operation of a brain tumor: a case report

The fornix, which is involved in transfer of episodic memory, is an important structure of the Papez circuit between the medial diencephalon and the medial temporal lobe. Many studies using DTI have reported on injury of the fornix in patients with brain injury （Nakayama et al., 2006; Sugiyama et al., 2007; Wang et al., 2008; Chang et al., 2010）. However, only a few studies on recov- ery of an injured fornix in patients with brain injury, including traumatic brain injury and stroke, have been reported （Yeo et al., 2011; Yeo and Jang, 2013a, b）. In this study, using follow up DTT images, we reported on a patient who showed recovery of injured fornical crura following a neurosurgical operation for a brain tumor.

Cognitive disorder and changes in cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury

BACKGROUND： Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated that cognitive disorder is closely related to nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor. OBJECTIVE： To summarize the cognitive disorder and changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury. RETRIEVAL STRATEGY： A computer-based online search was conducted in PUBMED for English language publications containing the key words ＂brain injured, cognitive handicap, acetylcholine, N-methyl-D aspartate receptors, neural cell adhesion molecule, brain-derived neurotrophic factor＂ from January 2000 to December 2007. There were 44 papers in total. Inclusion criteria： ① articles about changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury; ② articles in the same researching circle published in authoritative journals or recently published. Exclusion criteria： duplicated articles. LITERATURE EVALUATION： References were mainly derived from research on changes in these four factors following brain injury. The 20 included papers were clinical or basic experimental studies. DATA SYNTHESIS： After craniocerebral injury, changes in these four factors in brain were similar to those during recovery from cognitive disorder, to a certain degree. Some data have indicated that activation of nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor could greatly improve cognitive disorder following brain injury. However, there are still a lot of questions remaining; for example, how do these factors change at different time points after brain injury, and what is the relationship between associated factors and cognitive disorder. CONCLUSION： It is necessary to comprehensively study some associated factors, to analyze their changes and their relationship with cognitive disorder following brain injury, and to investigate their effects at different time points after brain injury.