Tag: Mild traumatic brain injury

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The New Neurometabolic Cascade of Concussion

The New Neurometabolic Cascade of Concussion

Neurosurgery 75:S24–S33, 2014

Since the original descriptions of postconcussive pathophysiology, there has been a significant increase in interest and ongoing research to study the biological underpinnings of concussion.

The initial ionic flux and glutamate release result in significant energy demands and a period of metabolic crisis for the injured brain.

These physiological perturbations can now be linked to clinical characteristics of concussion, including migrainous symptoms, vulnerability to repeat injury, and cognitive impairment.

Furthermore, advanced neuroimaging now allows a research window to monitor postconcussion pathophysiology in humans noninvasively. There is also increasing concern about the risk for chronic or even progressive neurobehavioral impairment after concussion/mild traumatic brain injury. Critical studies are underway to better link the acute pathobiology of concussion with potential mechanisms of chronic cell death, dysfunction, and neurodegeneration.

This “new and improved” article summarizes in a translational fashion and updates what is known about the acute neurometabolic changes after concussive brain injury. Furthermore, new connections are proposed between this neurobiology and early clinical symptoms as well as to cellular processes that may underlie long-term impairment.

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Delayed Neurological Deterioration After Mild Head Injury: Cause, Temporal Course, and Outcomes

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Neurosurgery 73:753–760, 2013

Mild head injury (MHI) complicated by an intracranial hemorrhage (ICH) is a common cause of hospital admission after head trauma. Most patients are treated nonoperatively, remain neurologically stable, and are discharged uneventfully. However, a small percentage of patients suffer delayed neurological deterioration (DND). Little is known about the characteristics of DND after an MHI complicated by ICH.

OBJECTIVE: To identify the cause, temporal course, and outcomes of patients who deteriorated neurologically after presenting with MHI and ICH. METHODS: A retrospective review was performed of all adult patients presenting over 54 consecutive months with MHI and ICH. Patients who were treated nonoperatively after initial head computed tomography and had a subsequent DND (Glasgow Coma Scale score decrease $2) were identified. Demographics, neurological status, clinical course, radiographic findings, and outcome data were collected.

RESULTS: Over 54 months, 757 patients with MHI plus ICH were admitted for observation; of these, 31 (4.1%) experienced DND. Eighty-seven percent of patients deteriorated within 24 hours after admission. Twenty-one patients (68%) deteriorated as a result of progressive intracranial hemorrhage, and 10 patients (32%) deteriorated as a result of medical causes. Seven patients (23%) died. Variables significantly associated with mortality included age . 60 years, coagulopathy, and change in Marshall computed tomography classification.

CONCLUSION: The incidence of delayed neurological deterioration after MHI with ICH is low and usually occurs within 24 hours after admission. It results in significant morbidity and mortality if it is the result of progressive intracranial hemorrhage. Further research is needed to identify risk factors that can allow early detection and improve outcomes in these patients.

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