I am not going to get into debates with people, many of whom appear know much more about the case than me, despite not having read any of the evidence, expert reports etc nor having sat through about seven or so weeks of that evidence being given in court. However, I am going to provide some information about the evidence. AH never claimed that he knew that he suffered from cognitive impairment. He remembers nothing about the accident and the fact that he suffered amnesia was never challenged by the prosecution. It would not be surprising bearing in mind the nature of the accident, injuries he sustained and his treatment (given Ketamine at the scene a known side effect of which is amnesia). In researching potential causes of the accident (and the 'cascade' of errors as descibed by a Human Performance Factors expert) issues of cognitive impairment were looked into (as indeed they were by the AAIB). The case was never about A-LOC or G-LOC, although that was all that was considered by the AAIB; neither defence nor prosecution experts said such had or may have occurred. However, there is a potential area of impairment below this. It is not widely known but involves relatively low levels of Gz that do not prevent blood circulation to the brain but do involve a reduction of oxygenation to the blood. The physiology is interesting. Gz straining involves muscles consuming more oxygen thus depleting the normal amount in the blood. G suits restrict the diaphragm reducing lung expansion. Low levels of Gz have a pooling effect in the lungs which, coupled with the diaphragm issue, results in less oxygenation of the blood in the lungs. This in turn results in a de-saturation of oxygen in the blood that continues circulating. The subject can continue to function, particularly with regard to learnt motor skills, but has reduces judgement and the ability to deal with abnormal situations. This was the evidence presented from eminently qualified experts by the defence and was the issue in the case.