A 37 yo woman has extensive thrombosis (sinus sagittalis superior, rectus, transversus right), some lesions and bleeding, being somnolent and very hard to take a history. Suddenly she becomes agitated, complains about horrible headache, is restless, fidgety and simultaneously less vigilant, develops an abducens palsy.
We hypothesize that she has a plateau wave of increased intracranial pressure – so called A waves and thus discuss the theory behind these.
Here is the short version:
- Raised ICP is (per se) pretty harmless – the brain works less, but is not really destroyed by raised pressure, UNLESS it’s perfusion decreases.
- The symptoms of raised ICP (without reduced perfusion) are: headache, symptoms of papilledema (visual disturbance, field defects, …), somnolence, abducens palsies, the Cushing response.
- It is not really clear where you should measure the ICP. The most reliable place is the ventricles (because the CSF equalizes the various pressures around the ventricles), yet it does not mirror the point of maximum pressure. The primary lesion (e.g., in traumatic brain injury) is not really helpful, because it is destroyed already. So we often chose the perilesional parenchyma, where pressure might counteract perfusion and thus damage tissue through ischemia. Finally, you can measure in the lumbar thecal sac – this can be equivalent to intraventricular pressure if no communication disturbance exists.
- Plateau waves can arise from anywhere in the vicious circle decreased CPP -> vasodilation -> ICP increase -> decreased CPP. Often, a decrease in arterial pressure causes them. They can lead to tissue ischemia.
- You can treat plateau waves (or avoid them) by keeping the blood pressure up, reduce vasodilation (e.g. hyperventilation) or ICP (e.g. mannitol) or CSF (e.g. by carbonic anhydrase inhibitors or lumbar drainage). I am surprised as to how few people think of increasing blood pressure to break through them.
References. This is mostly folklore and can be found in many textbooks on neurointensive care.