ICL 10.8: Traumatic Brain Pathology & Herniation Flashcards

1
Q

what causes CNS herniation?

A

anything that increases pressure inside the skull will compress the brain and result in herniation

it’s the only organ totally surrounded by bone so if you increase pressure there’s a problem

  1. hydrocephalus
  2. brain swelling
  3. mass lesion
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2
Q

what are the 3 types of CNS herniation?

A
  1. subfalcine herniation of cingulate gyrus
  2. transtentorial herniation of uncus of the temporal lobe
  3. herniation of cerebellar tonsils through foramen magnum

slide 4

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3
Q

what happens in extreme cases of transtentorial herniation of the uncus?

A
  1. pushing laterally on the brainstem, the midbrain can be pushed against the contralateral tentorium resulting in pressure necrosis of the cerebral peduncle of the midbrain! = Kernohan’s notch

this can be confusing clinically because you’ll start getting symptoms on the contralateral side from where the lesion is – you might think now there’s 2 lesions but it’s not true! = false localizing signs

  1. pushing downward can cause herniation palsy of the 3rd cranial nerve

CN 3 goes right across the tentorium so if you push the midbrain down, CN 3 gets stretched over the edge of the tentorium –> you’ll get loss of pupillary reflex on the side of the lesion

you can also eventually start to push the cerebellar tonsils down into the spinal canal if the patient manages to live that long

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4
Q

what are the vascular consequences of transtentorial herniation?

A

as the midbrain and pons descend, the basilar artery does not follow because it is ‘tethered’ above by the Circle of Willis

this causes the terminal pontine penetrating arterioles to be broken off which causes pontine Duret hemorrhages = ends up being the cause of death

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5
Q

what is hydrocephalus?

A

dilation of ventricular system, usually due to obstruction of CSF flow

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6
Q

what things can cause hydrocephalus?

A
  1. obstruction of CSF flow at the aqueduct of sylvius, arachnoid granulations or from tumors

meningitis or arachnoid scaring can cause problems with the arachnoid granulations!

  1. increased CSF flow (rare)
  2. compensatory to brain atrophy (dementia)
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7
Q

what are the consequences of cranial fractures?

A
  1. damage to vessels = bleeding
  2. damage to dura = infection
  3. damage to brain if fracture is depressed
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8
Q

what are epidural hematomas?

A

bleeding between the dura and the skull and you have to break the bone to do this so it’s always associated with skull fracture

usually results from tearing of middle meningeal artery

there may be a “lucid interval” of several hours following the fracture –> this is because the damage is done by the bleeding and it takes a while for the blood to pool out

epidural hematoma pushes the brain across the midline and could cause subfalcine herniation, transtentorial herniation, and tonsil herniation – these are an emergency!!!

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9
Q

why do epidural hemoatomas always involve skull fractures?

A

the MMA runs between the skull and the dura which are tightly adhered to each other

so the only way to damage this artery is to fracture the skull because the MMA is otherwise very highly protected

also there’s no such thing as an epidural space since the dura is tightly adhered to the skull so the blood has to build up enough pressure to push the dura away from the bone to make room for the blood which takes arterial pressure!

so you have to break the bone and have arterial bleeding from the MMA to get an epidural hematoma

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10
Q

what are subdural hematomas?

A

bleeding between the dura and arachnoid matter

you DON’T have to break the skull; trauma may be mild

usually due to tearing of meningeal bridging veins which go from the arachnoid to the superior sagittal sinus running along the dura –> as your brain shrinks they stretch which can cause bleeding

this can cause a midline shift that would cause subfalcine herniation, transtentorial herniation, and tonsil herniation but not always! sometimes the bleeding stops because it’s venous blood

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11
Q

why are subdural hematomas not as bad as epidural hematomas?

A

subdural hematomas are venous so they’re not under as much pressure and as the bleed pools out, you get some back pressure too which could tamponade the vein

this subdural bleed can then just sit there for a while, like years and the person could be fine…

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12
Q

what is a chronic subdural hematoma?

A

so subdural hematomas can pool out a lot of blood and then the bleeding can sometimes just stop and blood will just sit there in the skull between the dura and the arachnoid….so what can happen is it will become a chronic subdural hematoma

there’s an immune response to this giant pool of blood – in the brain you don’t get fibroblasts and granulations but in the dura you do!! so fibroblasts will grow on the underside of the dura to make another layer of collagen so in the end it looks like you’ve got 2 layers of dura and in-between is all the blood!

so the evolution is lysis of the clot –> granulation tissue envelops the lesion –> a fibrous capsule forms over 1-3 months

if all goes well, the macrophages will then remove all the old blood and the patient will be fine other than the weird 2 layers of dura OR the granulation tissue has lots of thin vasculature in it which can also bleed and if there’s repeat trauma and they can bleed again and cause a larger subdural hematoma – the hemorrhage can wax and wane depending on what happens

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13
Q

what is a cerebral contusion?

A

a small area where there is death of brain tissue

so there’s focal necrosis usually in the gyral crests which makes sense because trauma is coming from the outside so you won’t find damage in the sulci!

old lesions are depressed and yellow from hemosiderin

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14
Q

what are the 2 types of contusions?

A
  1. small acute contusion = involves the crest of the gyrus
  2. small acute infarct = spares the crest of the gyrus

microscopically you can’t tell these apart though! you can only tell them apart on gross anatomy

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15
Q

what are chronic contusions?

A
  1. depressed lesions –> look like parts of the brain were just carved out
  2. brown-yellow from hemosiderin

this pattern of inferior frontal and anterior temporal damage is common with angular momentum injuries such as motor vehicle accidents –> your brain sloshes inside the skull and it hits the crista galli so you end up scraping the frontal lobe and banging the temporal bone on the sphenoid bone so that’s why they’re both damaged in MVAs

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16
Q

what are coup contusions?

A

a contusion at the site of the trauma

17
Q

what are contrecoup contusions?

A

contusions on the opposite side of the brain from the site of trauma

so if you hit your windshield, you damage the frontal lobe (coup contusion) and then when your head whips back it also causes damage to the occipital lobe (contrecoup)

these usually result from falls from a standing position or from sudden deceleration

18
Q

what causes diffuse axonal injury?

A

it results from angular acceleration within skull like shaking or oblique impacts –> if your brain is sloshing around you’re going to be stretching some axons to the point that they break = diffuse axonal injury

can be from MVA or shaken baby syndrome

involves long axon tracts of deep white matter, corpus callosum, cerebral peduncles, brain stem

microscopically there are axonal swellings but on an MRI maybe you don’t see anything at all and it’s because you’re doing damage to the axons

diffuse axonal injury is present in 50% of patients who develop coma after trauma so it may explain persistent vegetative state in the absence of gross lesions

19
Q

what do you see histologically with diffuse axonal damage?

A

swollen axons!

this is due to continued transport of proteins after the axon is damaged and once they get to the break point they just pile up and cause axonal swelling

the person has to die exactly at the right time to actually see this because the body will fix it pretty quickly

slide 36

20
Q

what is shaken baby syndrome?

A

if you shake a baby you can get a subdural hemorrhage and you can get widespread damage to white matter = diffuse axonal injury

both of these cause encephalopathy!! = brain isn’t working properly

  1. head movement leads to stretching of and injury to brainstem axons
  2. brainstem damage leads to apnea resulting in global brain ischemia
  3. brain ischemia leads to brain swelling
  4. brain swelling leads to increased intracranial pressure
21
Q

what is a cerebral concussion?

A

a transient functional impairment that leads to amnesia for the moment of injury

there is no demonstrable anatomic abnormality! so it’s different from a contusion or hemorrhage and it’s kind of hard to know what the problem is

22
Q

what happens in the brain when there’s a cerebral concussion?

A

a cellular and metabolic crisis! neurons aren’t killed they’re just damaged so what happens is:

  1. potassium and glutamate efflux lead to increased energy demands
  2. calcium influx leads to mitochondrial dysfunction and protease activation

this results in impaired axonal transport and microglial reaction

if it’s bad enough the neurons will die and then this would be classified as a contusion

but if it’s just a concussion it will take a few days for the mitochondria to work and make ATP to start working and pump the sodium out, the potassium in etc.

if you have a second concussion during the recovery phase this produces much more severe injury which is why the QB has to sit out till the next game to give this subcellular crisis a chance to resolve

23
Q

which conditions are post-traumatic syndromes?

A
  1. post-traumatic epilepsy
  2. post-traumatic hydrocephalus
  3. post-traumatic dementia if there’s repeated trauma that causes a slow deterioration of the cortex = “punch drunk syndrome” like with boxers –> looks like Alzheimer’s microscopically with AB and tau plaques and tangles but there’s a difference in the location so it got it’s own name: chronic traumatic encephalopathy
  4. post -traumatic psychiatric disorders