Abstract
Background
Post-traumatic stress disorder (PTSD) is common after subarachnoid haemorrhage (SAH) and causes poor outcome. Knowing which SAH events cause the stress leading to PTSD development could allow for their severity, and so the chances of PTSD, to be reduced. The dramatic nature of SAH onset has meant ictal events have been the presumed cause. Frequent loss of consciousness (LOC) at ictus, and presumed resultant amnesia, however, means this might not be correct. We examined two hypotheses for how SAH patients develop PTSD despite frequent LOC. Firstly, has the frequency of amnesia for ictal events subsequent to LOC been overestimated? Secondly, is it the stress of post-ictal events, rather than ictal events, which causes PTSD?
Method
Sixty SAH patients, 18 months post-ictus, were assessed for PTSD, LOC at ictus, memory for ictal events, as well as which aspects of their SAH, ictal and post-ictal, were psychologically stressful. Patients also underwent neuropsychological examination.
Findings
Of patients, 36.7% had PTSD. Memory overall for ictal events was more common than expected: 50% reported LOC, and only 18% reported no memory. However, memory was not associated with PTSD development. Rather, the key predictor of PTSD was the stress of post-ictal events. The stress of ictal events, cognitive impairment and clinical characteristics were unrelated to PTSD development. Post-ictal events included realizing that their life could have/had changed, that they may have been left with long-term problems, that they could have died and that they had little memory for some SAH events and regaining consciousness.
Conclusions
The traumatic quality of an SAH lies in post-ictal events, rather than ictal events. These events are related to the patients' adjustment to the experience of having had an SAH. Reducing the traumatic severity of these events could potentially reduce the likelihood of PTSD in SAH patients and so improve their outcome.
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Baisch, S.B., Schenk, T. & Noble, A.J. What is the cause of post-traumatic stress disorder following subarachnoid haemorrhage? Post-ictal events are key. Acta Neurochir 153, 913–922 (2011). https://doi.org/10.1007/s00701-010-0843-y
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DOI: https://doi.org/10.1007/s00701-010-0843-y