Tag: metabolism

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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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Spinal cord traction, vascular compromise, hypoxia, and metabolic derangements in the pathophysiology of tethered cord syndrome

Neurosurg Focus 29 (1):E9, 2010. (10.3171/2010.3.FOCUS1085)

The definition of tethered cord syndrome (TCS) relies mainly on radiological criteria and clinical picture. The presence of a thickened filum terminale and a low-lying conus medullaris in symptomatic patients is indicative of TCS. The radiological definition of TCS does not take into account cases that involve a normal-lying conus medullaris exhibiting symptoms of the disease.

Methods. The authors performed a MEDLINE search using the terms “tethered cord” and “pathophysiology.” The search returned a total of 134 studies. The studies were further filtered to identify mostly basic research studies in animal models or studies related to the biomechanics of the filum terminale and spinal cord.

Results. Spinal cord traction and the loss of filum terminale elasticity are the triggers that start a cascade of events occurring at the metabolic and vascular levels leading to symptoms of the disease. Traction on the caudal cord results in decreased blood flow causing metabolic derangements that culminate in motor, sensory, and urinary neurological deficits. The untethering operation restores blood flow and reverses the clinical picture in most symptomatic cases.

Conclusions. Although classically defined as a disease of a low-lying conus medullaris, the pathophysiology of TCS is much more complex and is dependent on a structural abnormality, with concomitant altered metabolic and vascular sequelae. Given the complex mechanisms underlying TCS, it is not surprising that the radiological criteria do not adequately address all presentations of the disease.

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