Summary of Brain herniation
PATHOLOGY & CAUSES
Brain tissue displacement: through skull opening or dural fold
Damages associated with herniated section
- Gyrus forced under falx cerebri → cerebral artery compression → cerebral ischemia then edema → ↑ ICP
- Temporal lobes squeezed through notch in tentorium cerebelli → basilar artery stretched → tearing, bleeding (Duret hemorrhage)
- Brain herniates through fracture/surgical site (craniectomy) → decortication of herniated gyrus
- Cerebellar tonsils herniate in foramen magnum → brainstem, spinal cord compression
- ↑ ICP
SIGNS & SYMPTOMS
↓ level of consciousness, coma
Glasgow Coma Scale (GCS) 3–5
Mydriasis (dilated pupils)
Loss of brainstem reflexes (blinking, gagging, pupillary reflex)
Head CT scan/MRI
- Depending on the cause, results show mass lesions (e.g. tumor, aneurysm, infarction, hemorrhage etc.) and subsequent displacement of the brain away from the mass, depending on localization
Paracetamol (manage fever)
↓ metabolism → ↓ O2 consumption + ↓ CO2 production → no systemic vasodilation → ↓ cerebral blood volume → ↓ ICP
- Decompressive craniectomy
HTS boluses → support circulation
- HTS → ↑ serum osmolarity → draw excess water from brain tissue → ↓ ICP
- Helps avoid ↑ PaCO2 or hypoxemia → systemic vasodilation → ↑ ↑ cerebral blood volume → ↑ ICP
Transcript for Brain herniation
Brain herniation is what it’s called when some brain tissue moves outside of the skull, or moves across or into a structure with the skull.
Brain herniation typically happens in response to increased intracranial pressure, which refers to a high pressure within the skull.
An intracranial pressure above 15 mmHg is considered high.
OK - let’s start with some basic brain anatomy. The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which has a cortex - an outer region - divided into four lobes including the frontal lobe, parietal lobe, temporal lobe, and the occipital lobe.
There are also a number of additional structures - including the cerebellum, which is down below, as well as the brainstem which connects to the spinal cord.
Now zooming in, the brain and spinal cord is covered by the meninges, which are three protective layers of the brain.
The inner layer of the meninges is the pia mater, the middle layer is the arachnoid mater, and the outer layer is the dura mater.
These first two, the pia and arachnoid maters, form the subarachnoid space, which houses the cerebrospinal fluid, or CSF.
CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients.
The outer membrane is the dura mater, which forms the meningeal folds, such as falx cerebri and tentorium.
The falx cerebri is a meningeal fold that goes down into the longitudinal fissure that separates the hemispheres of the brain.
The free edge of the falx cerebri is in close contact with the central part of the brain called corpus callosum, which connects the left and right hemisphere.
There’s also the tentorium which is a meningeal fold located in the back of our skull, that separates the cerebrum from the cerebellum.
The free edge of the tentorium is in close contact with the brainstem, which is the region that connects the brain and the spinal cord.
The skull has a set volume and the pressure inside of the skull is kept relatively constant.
In other words, the sum of the volumes of the brain, cerebrospinal fluid, and intracranial venous and arterial blood is always about the same. So, if there’s an increase in the volume of any one of these three, there’s a compensatory decrease in the other two.
For example, when a high-speed golf ball hits you in the head, an artery could rupture within the skull.
As the artery bleeds, the blood starts to pool, it leads to what’s called a mass effect within the skull, and that mass effect increases the intracranial pressure.
To help reduce the volume and pressure back to normal, there’s less CSF production and more CSF reabsorption.
Over time, if the arterial bleed continues, then it might overwhelm the bodies ability to compensate, and the intracranial pressure starts to get quite high, and that can lead to brain herniation.
So brain herniation can be caused by either a focal mass effect, like the arterial bleed, or a diffuse mass effect - depending on whether the problem is in one area or involves the entire brain.
In addition to intracranial bleeds, other causes of focal mass effects are tumors and abscesses.
All of these focal masses also create surrounding inflammation which causes local edema, and that makes the focal mass even larger.
Diffuse mass effects are caused by generalized cerebral edema, which is an excessive buildup of fluid throughout the brain tissue.
There’s cytogenic edema which is when there’s fluid build up within the cells of the brain, due to a retention of sodium and water, and there’s also vasogenic edema, which is when fluid builds up right outside of the cells, in the interstitial space.
Depending on the size and location of the mass effect, there’s a possibility of brain herniations - and it can either be supratentorial and infratentorial herniation.
Supratentorial herniation refers to displacement of the cerebrum which is above the tentorium, and infratentorial herniation refers to herniation of the cerebellum which is below the tentorium.
Alright, so supratentorial herniations include four types of displacement and these differ by the exact part of the cerebrum that is affected.
The first type of supratentorial herniation is uncal herniation, also referred to as transtentorial herniation.
In this herniation, the innermost part of the temporal lobe, called uncus, slips down towards the tentorium and puts pressure on the brainstem.
The uncus can squeeze the oculomotor nerve resulting in an oculomotor nerve palsy.
In oculomotor nerve palsy the eyeball is in a “down and out” position due to a loss of innervation of muscles controlled by the nerve.
Also, the affected pupil becomes dilated and fails to constrict in response to light.
The posterior cerebral artery can also be compressed, which results in ischemic stroke of the occipital part of the brain, which is responsible for processing of visual information. This leads to homonymous hemianopia, which is a loss of vision in either the left or right halves of the visual fields of both eyes.
The vision is lost in halves that are contralateral to the posterior cerebral artery that is affected.
Although there is a partial loss of vision, macular function is spared, meaning that central vision is still sharp and detailed.
This is because the part of the occipital lobe in charge of the macula is gets blood from both the posterior cerebral artery as well as the medial cerebral artery.
Uncal herniation stretches and sometimes breaks branches of the paramedian basilar artery which nourish the brain stem. That causes small linear or flame-shaped hemorrhages called Duret hemorrhages which can be seen on autopsy.
So, let’s say there’s a focal mass effect on the right side of the skull, which increases intracranial pressure and squeezes the uncus down onto the brainstem.
Now the uncus isn’t only directly compressing the right side of the brainstem, but indirectly, it’s also pushing the left side of the brainstem against the free edge of the tentorium forming what’s called a kernohan’s notch.