Dissociation of Cerebral Glucose Metabolism and Level of Consciousness During the Period of Metabolic Depression Following Human Traumatic Brain Injury

Abstract

Utilizing [18F]fluorodeoxyglucose positron emission tomography (FDG-PET), we studied the correlation between CMRglc and the level of consciousness within the first month following human traumatic brain injury. Forty-three FDG-PET scans obtained on 42 mild to severely head-injured patients were quantitatively analyzed for the determination of regional cerebral metabolic rate of glucose (CMRglc). Reduction of cerebral glucose utilization, defined as a CMRglc of < or =4.9 mg/100 g/min, was present regionally in 88% of the studies. The prevalence of global cortical CMRglc reduction was higher in severely head-injured patients (86% versus 67% mild-moderate), although the absolute magnitude was similar across the injury severity spectrum (mean CMRglc 3.9 +/- 0.6 mg/100 g/min). The level of consciousness, as measured by the Glasgow Coma Scale, correlated poorly with the global cortical CMRglc value (r = 0.08; p = 0.63). With regards to severity of head injury, this correlation was worst for the severely injured (r = -0.11; p = 0.58) and better for the mildly injured patients (r = 0.50; p = 0.07). In most cases, intraparenchymal hemorrhagic lesions were associated with either focal CMRglc reduction or elevation. It is concluded that the etiologies of CMRglc reduction are likely multifactorial given the complex nature of traumatic brain injury and that the reduction of CMRglc represents a fundamental pathobiologic state following head injury that is not tightly coupled to level of consciousness.

Increased Pentose Phosphate Pathway Flux after Clinical Traumatic Brain Injury: A [1,2-13C2]glucose Labeling Study in Humans

“…Exclusion criteria included the following: (1) terminal illness (e.g., advanced cancer, AIDS); (2) severe previous neurologic disease; and (3) acute complete spinal cord injury. These inclusion and exclusion criteria are consistent with those used for previous publications from the UCLA Brain Injury Research Center (Bergsneider et al, 1997(Bergsneider et al, , 2000Vespa et al, 2003). UCLA's Institutional Review Board approved the protocol, and informed consent was obtained from the patients' legal representatives.…”

“…During this critical postinjury period, there are initially high levels of cerebral glucose consumption, followed by a variable period of normal to mildly depressed glucose metabolism (Bergsneider et al, 1997(Bergsneider et al, , 2000. However, during the same period, many studies have demonstrated a low level of cerebral oxygen consumption relative to the unexpectedly preserved glucose metabolism Jaggi et al, 1990).…”

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

“…Conversely, the damaged tissue needs more energy for its repair than under physiological conditions, resulting in what has been termed a "flow/metabolism mismatch," a factor that aggravates injury in the traumatic penumbra [62,73]. Furthermore, increased glutamatergic release into the extracellular milieu following injury causes marked increases in glucose use and accumulation of extracellular lactate [53,[74][75][76][77][78][79]. This deregulated cerebral metabolism leads to decreased ATP production causing the failure of ATP-dependent ion channels and proteins leading to ionic osmotic alterations that result in cell swelling and culminating in necrosis [80].…”

The Importance of Restriction from Physical Activity in the Metabolic Recovery of Concussed Brain

“…An increasing number of studies on mTBI have focused attention on concussion-induced changes in brain metabolism (Bergsneider et al, 2000;Praticò et al, 2002) including those related to cerebral energy state (Vagnozzi et al, 1999). Hovda and colleagues first suggested the concept of metabolic vulnerability occurring in brain tissue after any concussive episode (Giza & Hovda, 2001;Hovda et al, 1993).…”