NBME 24 Answers ↦
Exactly. To add to this, communicating hydrocephalus can be subdivided as follows:
Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet
High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure
not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question
If anyone like me also got "decreased absorption in choroid plexus", as their wrong answer it's because the choroid plexus doesn't "absorb" it produces.
If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510.
Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus.
So this patient has a leaking berry aneurysm which undergone to surgery and repaired but in two days she developed widening of the SA space which could be explained by increased CSF production but a decreased in absorption, which is due to blockage of the arachinoid granulations by the leaked red and white cells therefore there is a decreased movement of the CSF via the arachinoid villi
this would cause a non-communicating hydrocephalus with enlarging of the lateral and 3rd ventricles but normal 4th ventricle and subarachnoid space