Abstract
Evaluation of the chronic effects of spinal cord injury (SCI) has long focused on sensorimotor deficits, neuropathic pain, bladder/bowel dysfunction, loss of sexual function, and emotional distress. Although not well appreciated clinically, SCI can cause cognitive impairment including deficits in learning and memory, executive function, attention, and processing speed; it also commonly leads to depression. Recent large-scale longitudinal population-based studies indicate that patients with isolated SCI (without concurrent brain injury) are at a high risk of dementia associated with substantial cognitive impairments. Yet, little basic research has addressed potential mechanisms for cognitive impairment and depression after injury. In addition to contributing to disability in their own right, these changes can adversely affect rehabilitation and recovery and reduce quality of life. Here, we review clinical and experimental work on the complex and varied responses in the brain following SCI. We also discuss potential mechanisms responsible for these less well-examined, important SCI consequences. In addition, we outline the existing and developing therapeutic options aimed at reducing SCI-induced brain neuroinflammation and post-injury cognitive and emotional impairments.
Highlights
As the primary relay center of neural transmission between the brain and the rest of the body, damage to the spinal cord can be a devastating event
We and others [37,38,39,40,49,51,73,74,75] show that cognitive impairments and depression are detected weeks to months after isolated thoracic experimental spinal cord injury (SCI) and that progressive neuronal loss and microglial activation occur in brain regions involved in memory and learning
We and others have reported [39,40,55,57] that SCI triggers up-regulation of cysteine chemokine ligand 21 (CCL21) in a number of brain regions including thalamus, hippocampus, and cerebral cortex; increased thalamic CCL21 levels are associated with microglial activation and hyperpathia
Summary
As the primary relay center of neural transmission between the brain and the rest of the body, damage to the spinal cord can be a devastating event. Additional examination is needed as reports from subsequent studies have been mixed, with some showing no observable neuronal loss in the cortex following SCI [53,54] Reasons for these disparate results are not fully understood; injury severity, time after injury, and differences in experimental modeling can all affect pathological outcomes. Combined widely did not [73] Toafter this end, ourthe laboratory has shown that These discretefindings, regions of the brain with exhibitthe significant explored theory impaired neurogenesis being one of the underlying mechanisms of cognitive signs of cell cycleof arrest and decreased numbers of immature neurons in the male murine hippocampus decline, provide an explanation as to findings, why SCIcombined patients have significantly highertheory risk of after SCImay to the [38,40]. Adult neurogenesis is clear in rodents, whether and to what extent adult neurogenesis occurs in humans remains controversial [86,87]
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