All of the following are true about changes in brain metabolism after traumatic brain injury, except:
Ans. d. Increased CSF lactate is associated with good prognosisAfter damage to the brain parenchyma, pyruvate dehydrogenase activity decreases (specifically E-1 subunit) and pyruvate carboxylase activity increases leading to accumulation of lactate in the brain and CSF, as well as increased uptake from the circulation. During the course of the illness, earlier the fall in CSF lactate, better is the prognosis.''Dysregulated brain glucose metabolism and lactate accumulation are seen folio wing traumatic brain injury (T131). The underlying molecular mechanism is poorly understood. Pyruvate dehydrogenase (PDH), the rate-limiting enzyme coupling cytosolic glycolysis to mitochondria[ citric acid cycle, plays a critical role in maintaining homeostasis of brain glucose metabolism.' Traumatic brain injury-induced phosphorylation of pyruvate dehydrogenase: a mechanism of dysregulated'Study demonstrates that TBI causes a significant reduction in PDH enzyme, disrupt-acid-base balance and increase oxidative stress in blood Also, lower PDH enzyme in blood is related to the increased gliosis and loss of its PDH El-infinity subunit PDH in brain tissue, and these effects of TBI were prevented by pyruvate treatment. '-Role of pyruvate dehydrogenase complex in traumatic brain injury. J Emerg Trauma Shock ( class="Style1">'Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an impoant role in the clinical course of severe head injury. Patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing orable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Aerial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation. '- Prognostic signcance of ventricular CSF lactic acidosis in severe head injury. J. Neurosurg (
Shut down of pyruvate dehydrogenase activity
Accumulation of lactate in brain
Increased lactate uptake from circulation
Increased CSF lactate is associated with good prognosis