- Normal brain, changes in CPP between 60 and 160 mmHg have only minor effects on CBF.
- Following trauma and autoregulatory impairment,
- CBF becomes increasingly dependent on CPP and minor fluctuations can instigate further ischaemic injury.
- As previously mentioned, CPP = MAP− ICP, and CBF = CPP/ CVR, where CVR is cerebrovascular resistance.
- Secondary elevation in ICP may worsen CPP and decrease CBF.
- In patients with traumatic contusion
- Within the contusioned brains
- Reduced
- CBF
- CMRO2
- Normal
- CBV
- Oxygen extraction fraction (OEF)
- In pericontusional regions with no identifiable tissue dysfunction,
- CMRO2 is lower
- Normal
- CBF
- CBV
- OEF
- With reduced CMRO2, OEF increase to compensate.
- Studies using DTI showed that surrounding contusions there is a frequent rim of low diffusion coefficient consistent with cytotoxic oedema
- Which may explain the minimal change in OEF because of widespread microvascular failure and selective neuronal loss.
- Acutely after trauma there is a dissociation between CBF and CBV due to physiological disturbances.
- Because metabolism decreases after severe head injury, determining AVDO2 (Arterio-jugular differences of oxygen) is necessary for accurate interpretation of CBF and diagnosing hypo- or hyperperfusion.
- CBF is generally low during the first 6 hours after injury and increase significantly in the first 24 hours.
- A low CBF
- Not associated with a high AVDO2
- Likely a sign of low oxidative metabolism rather than ischaemia
- In patients without acute hyperaemia, CBF consistently correlates with functional recovery
- i.e. the lowest CBFs exist in patients with the most severe disabilities
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