Monro-Kellie Hypothesis: The Monro-Kellie Hypothesis is the idea that the head is a closed shell, and that the three major components:

(1) brain,

(2) blood – both arterial and venous, and

(3) CSF, are in a state of dynamic equilibrium.

As the volume of one goes up, the volume of another must go down

Intracranial Hypotension:

If you are leaking CSF, this will decrease the overall fixed volume, the volume of venous blood will increase to maintain the equilibrium. The result is meningeal engorgement (enhancement), distention of the dural venous sinuses, prominence of the intracranial vessels, and engorgement of the pituitary.

The development of subdural hematoma and hygromas is also a classic look (again, compensating for lost volume).

Idiopathic Intracranial Hypertension (Pseudotumor Cerebri):

The classic scenario of a fat middle-aged women with a headache. Etiology is not well understood (making too much CSF, or not absorbing it correctly). It has a lot of associations (hypothyroid, Cushings, vitamin A toxicity). The findings follow the equilibrium idea. With increased CSF the ventricles become slit like, the pituitary shrinks (partially empty sella), and the venous sinuses appear compressed. You can also have the appearance of vertical tortuosity of the optic nerves and flattening of the posterior sclera.

Obstructive Hydrocephalus

Communicating:

This is an obstruction at the level of arachnoid villi/granulation, blocking reabsorption. All the ventricles will be dilated (25% of the time, the fourth ventricle is normal). There are 4 main causes.

(1) Normal Pressure Hydrocephalus: It’s not well understood – and idiopathic. The buzz-phrase is “ventricular size out of proportion to atrophy.” The frontal and temporal horns of the lateral ventricles are the most affected. “Upward bowing of the corpus callosum” is another catchphrase. On MRI you may see transependymal flow and/or a flow void in the aqueduct and 3rd ventricle. The step 1 trivia is “wet, wacky, and wobbly” – describing the clinical triad of urinary incontinence, confusion, and ataxia. This is treated with surgical shunting.

(2) Blood,

(3) Pus, and

(4) Cancer

Anything that plugs up the villi – the three most common causes being SAH, Meningitis, and Carcinomatous Meningitis.

Non- Obstructive:

This is sort of a trick question, with the only answer being something that produces CSF. The only answer you need to know is Choroid Plexus Papilloma (discussed in detail in the tumor section).

Quiz:

ls transcpendymal flow seen more with acute hydrocephalus or chronic hydrocephalus?

 

Answer: Acute

Edema:

Cytotoxic:

This type of Edema can be thought about as intracellular swelling, secondary to a malfunction of the Na/K pump. It tends to favor the gray matter, and looks like loss of the gray-white differentiation. This is classically seen with stroke (or trauma), and is why EARLY signs of stroke involve loss of the GM-WM interface.

Vasogenic:

This type of Edema is extracellular, secondary to the disruption of the blood-brain barrier. It looks like Edema tracking through the white matter (which is less tightly packed than the gray matter). This is classically seen with tumor and infection. You can also see this type of Edema as a LATE stage of cerebral ischemia. Response to steroids is characteristic of vasogenic Edema

Cytotoxic Edema

Vasogenic Edema

  • Failed Na/K Pump (BBB intact)
  • Increased Capillary Permeability (BBB NOT intact)
  • Classic = Ischemia (EARLY)
  • Classic = Tumor, Infection, Ischemia (LATE)
  • White matter + Gray Matter – “blurring”  
  • White Matter (Spares Gray Matter)  

Brain Herniation:

Subfalcine Herniation:

This is just a fancy way of saying midline shift (deviation of ipsilateral ventricle and bowing of the falx). The trivia to know is that the ACA may be compressed, and can result in infarct.

Descending Transtentorial Herniation:

The uncus and hippocampus herniated through the tentorial incisura. Effacement of the ipsilateral suprasellar cistern occurs first:

Things to know:

• Perforating basilar artery branches get compressed, resulting in “Duret Hemorrhages”- classically located in the midline at the pontomesencephalic junction (in reality, they can also affect cerebellar peduncles).

• CN3 gets compressed between the PCA and Superior Cerebellar Artery causing ipsilateral pupil dilation and ptosis

• “Kemohan’s Notch / Phenomenon” -The midbrain on the tentorium is forming an indentation (notch) and the physical exam finding of ipsilateral hemiparesis – which Neurologist’s call a “false localizing sign.” Of course, localization on physical exam is stupid in the age of MRI, but it gives Neurologists a reason to carry a reflex hammer and how one can fault them for that.

Ascending Transtentorial Herniation:

Think about this in the setting of a posterior fossa mass. The vermis will herniate upward through the tentorial incisura, often resulting in severe obstructive hydrocephalus.

Things to know

• The “Smile” of the quadrigeminal cistern will be flattened or reversed

• “Spinning Top” is a buzzword, for the appearance ofthe midbrain from bilateral compression along its posterior aspect

• Severe hydrocephalus (at the level of the aqueduct). Cerebellar Tonsil Herniation: Can be from severe herniation after downward transtentorial herniation). Alternatively, if in isolation you are thinking more along the lines of Chiari (Chiari I= 1 tonsil 5mm, or both tonsils 3mm)