Astrocytes, reactive astrogliosis, and glial scar formation in traumatic brain injury

Traumatic brain injury is a global health crisis,causing significant death and disability worldwide.Neuroinflammation that follows traumatic brain injury has serious consequences for neuronal survival and cognitive impairments,with astrocytes involved in this response.Following traumatic brain injury,astrocytes rapidly become reactive,and astrogliosis propagates from the injury core to distant brain regions.Homeostatic astroglial proteins are downregulated near the traumatic brain injury core,while pro-inflammatory astroglial genes are overexpressed.This altered gene expression is considered a pathological remodeling of astrocytes that produces serious consequences for neuronal survival and cognitive recovery.In addition,glial scar formed by reactive astrocytes is initially necessary to limit immune cell infiltration,but in the long term impedes axonal reconnection and functional recovery.Current therapeutic strategies for traumatic brain injury are focused on preventing acute complications.Statins,cannabinoids,progesterone,beta-blockers,and cerebrolysin demonstrate neuroprotective benefits but most of them have not been studied in the context of astrocytes.In this review,we discuss the cell signaling pathways activated in reactive astrocytes following traumatic brain injury and we discuss some of the potential new strategies aimed to modulate astroglial responses in traumatic brain injury,especially using cell-targeted strategies with miRNAs or lncRNA,viral vectors,and repurposed drugs.

Microsurgical repair of severed thoracic spinal cord and clinical outcome:technical case report

Background:This report describes a case of successful repair of severed thoracic spine in a young man who presented with a penetrating stab injury to spine resulting in Brown-Séquard syndrome.Surgical technique and postoperative management is discussed.Case presentation:A 34-year-old fit and well healthy man was admitted with a history of stab injury to the thoracic spine at thoracic T2/3 level with ASIA impairment score(AIS)score D with an incomplete spinal cord affecting his left lower limb with complete paralysis and right lower limb paresis with impaired sensation below T6 level to L5.Neuroimaging confirmed a penetrating knife injury traversing the T2/3 level causing hemi-section of the spinal cord confirmed intraoperatively.He underwent an urgent exploratory surgery of his spine and a T2/3 laminectomy was performed to aid removal of the knife.The dura was noted to be contused and severed spinal cord was noted to be severed with associated cord oedema.A microsurgical repair of the severed cord was performed with duroplasty followed by intense neuro-rehabilitation.On a 3 month follow up his AIS score is E with lower limb power is 5/5 bilaterally and he is able to mobilise independently up to 8-10 steps without any supportive aid and with crutches he is independently functional and mobile.Conclusion:This is the first documented case of microsurgical repair of severed thoracic spinal cord secondary to traumatic knife injury.In the management of such scenario,apart from the removal of foreign body,repair of the cord with duroplasty should be carefully considered.The role of spinal neuroplasticity in healing following timely repair of the spinal cord along with intense rehabilitation remains the key.This had resulted in a good clinical and functional outcome with in a 18-month follow up.