After a routine operation, such as orthopedic surgery, many patients experience perioperative neurocognitive disorders (PND), including acute cognitive deficits (delirium) and longer-lasting cognitive impairments also known as postoperative cognitive dysfunction (POCD), which in some cases may lead to permanent dementia.
Delirium is a severe neuropsychiatric syndrome characterized by acute cognitive deficits and inattention arising as a consequence of generalized illness.
Thus, irrespective of roles in acute cognitive deficits, it seems that inflammation significantly contributes to subsequent neuronal death, denervation and cognitive impairment.
Microglia primed by primary pathology to produce exaggerated IL-1β responses to subsequent inflammatory stimulation [ 30] were implicated in the acute cognitive deficits in both of these studies.
Animal model studies using LPS to mimic acute inflammation are consistent with this, showing causative roles for IL-1β and cyclooxygenase-1-mediated prostaglandins in acute cognitive deficits [ 50].
The first explicit attempt to model delirium in rodents administered the muscarinic receptor antagonist atropine intraperitoneally and demonstrated acute cognitive deficits in a blind alley maze and EEG slowing reminiscent of delirium [ 21].
In parallel, we tested the hypothesis that severity of underlying neurodegenerative pathology would predispose to acute cognitive deficits using mice with none, intermediate, or severe neurodegenerative pathology upon challenging them with systemic inflammation or vehicle control (Table 1).
Recent studies in currently euthymic patients with BD suggest that such deficits can persist even after apparent clinical recovery, and so cannot be entirely ascribed to acute, state-related cognitive deficits that are well known to occur in acute episodes of emotional disease [ 6].
We demonstrated an effect of severity of neuropathology on risk of acute and fluctuating cognitive deficits.
This was initially attributed to neurotoxic effects of anaesthetics/sedatives but there is an emerging consensus that the primary insult is the inflammatory trauma of surgery in the older patient inducing acute or lasting cognitive deficits.
Our findings suggest that subjective memory complaint determined via the memory question in the acute hospital setting is an unreliable indicator of objective cognitive deficit.
