Commonly detected brain metabolites at intermediate (TE = 144 ms) to long (TE = 288 ms) echo time include N-acetylaspartate for neuronal integrity, creatine for cellular energy, choline for membrane turnover, and lactate for anaerobic metabolism. MRS at short (TE = 35 ms) echo time can further detect glutamate/glutamine for excitatory brain injury and myo-inositol for astroglial proliferation. The most commonly reported finding in the setting of head trauma is a reduction in N-acetylaspartate or N-acetylaspartate/creatine, sometimes accompanied by an elevation in choline and sometimes in otherwise normal-appearing brain, which may reflect microscopic DAI and/or Wallerian degeneration [32,45,46]. A study in concussed athletes found that decreased N-acetylaspartate/creatine took a longer time to resolve than the symptoms, suggesting that metabolic recovery is slower than clinical recovery [18]. Despite the interesting findings in MRS research, there is insufficient evidence to support the routine clinical use of MRS at the individual patient level [45]. MRA Head and Neck There is no relevant literature to support the use of MRA in the initial imaging evaluation of subacute or chronic head trauma with unexplained cognitive or neurologic deficit(s). Head Trauma MRI Head Brain MRI is the most useful initial imaging for the evaluation of subacute or chronic head trauma with unexplained cognitive or neurologic deficit(s). Conventional MRI will include a combination of T1-weighted, T2-weighted, T2*-weighted (gradient-echo), and diffusion-weighted imaging. It is more sensitive than CT for subtle findings adjacent to the calvarium or skull base (eg, focal encephalomalacia at the inferior frontal or anterior temporal lobes as chronic sequelae of previous contusions). It is also more sensitive for small white matter lesions (microbleeds) as chronic sequelae of previous traumatic axonal injury or DAI, although it is still far less sensitive than neuropathological investigation (microscopic analysis) [32].
Head Trauma PCAs. Commonly detected brain metabolites at intermediate (TE = 144 ms) to long (TE = 288 ms) echo time include N-acetylaspartate for neuronal integrity, creatine for cellular energy, choline for membrane turnover, and lactate for anaerobic metabolism. MRS at short (TE = 35 ms) echo time can further detect glutamate/glutamine for excitatory brain injury and myo-inositol for astroglial proliferation. The most commonly reported finding in the setting of head trauma is a reduction in N-acetylaspartate or N-acetylaspartate/creatine, sometimes accompanied by an elevation in choline and sometimes in otherwise normal-appearing brain, which may reflect microscopic DAI and/or Wallerian degeneration [32,45,46]. A study in concussed athletes found that decreased N-acetylaspartate/creatine took a longer time to resolve than the symptoms, suggesting that metabolic recovery is slower than clinical recovery [18]. Despite the interesting findings in MRS research, there is insufficient evidence to support the routine clinical use of MRS at the individual patient level [45]. MRA Head and Neck There is no relevant literature to support the use of MRA in the initial imaging evaluation of subacute or chronic head trauma with unexplained cognitive or neurologic deficit(s). Head Trauma MRI Head Brain MRI is the most useful initial imaging for the evaluation of subacute or chronic head trauma with unexplained cognitive or neurologic deficit(s). Conventional MRI will include a combination of T1-weighted, T2-weighted, T2*-weighted (gradient-echo), and diffusion-weighted imaging. It is more sensitive than CT for subtle findings adjacent to the calvarium or skull base (eg, focal encephalomalacia at the inferior frontal or anterior temporal lobes as chronic sequelae of previous contusions). It is also more sensitive for small white matter lesions (microbleeds) as chronic sequelae of previous traumatic axonal injury or DAI, although it is still far less sensitive than neuropathological investigation (microscopic analysis) [32].