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To the Editor:
We read with interest the article by Franz et al.1 on Aβ-42 and tau in CSF after severe traumatic brain injury (TBI). The authors report decreased CSF Aβ-42 in TBI cases compared with patients with dementia and controls. Low CSF Aβ-42 also correlated with poor outcome after TBI. The authors conclude that their findings indicate a possible pathophysiologic role of Aβ in TBI.
Of the 29 CSF samples in their TBI group, 14 were ventricular CSF (V-CSF) samples obtained through a intraventricular catheter placed for intracranial pressure, whereas 15 were lumbar CSF (L-CSF) samples collected by lumbar puncture at different time points (up to 284 days) after trauma. In both control groups, L-CSF was analyzed. In their statistical comparisons, all TBI cases were treated as one group, regardless of whether V-CSF or L-CSF was analyzed.
It is well known that the concentration of different compounds varies markedly between different CSF spaces. For example, the levels of the monoamine metabolites HVA …
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