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Flashcards in CNS Trauma - Cochran Deck (25):
1

Describe the tissues traversed as one travels from the skull into the brain parenchyma. Include the spaces in between these tissues!

Skull (and periosteum)

Epidural space

Dura Mater

Subdural space

Arachnoid mater

Subarachnoid space

Pia mater

Brain parenchyma

2

What does "leptomeninges" refer to?

What is the name given to the potential space surrounding arachnoid and pial vessels?

The arachnoid and pia mater. From the greek "leptos", meaning fine or thin.

Virchow-Robin spaces.

3

What venous sinuses are housed within the falx cerebri?

The tentorium cerebelli?

Superior and inferior sagittal sinuses, straight sinus.

Transverse sinuses, straight sinus (*intersection of falx)

4

Trace the path followed by CSF secreted in a lateral ventricle through its reabsorption into a venous sinus.

From the lateral ventricle, travels into the third by way of the Interventricular foramen of Monro. Reaches the fourth ventricle by the central aqueduct (of Sylvius). Leaves the ventricular system via the Foramina of Luschke (2x, lateral) or Magendie (1x, midline). Reabsorbed from the basal cisterna via arachnoid granulations.

5

Describe the components of the blood-brain barrier.

How are substances transported across it?

Comprised of vascular endothelium (with abundant tight junctions, pericytes) as well as astrocyte processes and basement membrane.

Small and lipophilic substances can freely diffuse across; large or charged must be actively transported.

6

In which compartment is fluid found in vasogenic edema?

What tissue does it usually affect?

Describe its pathogenesis.

The extracellular compartment.

The white matter.

Increased permeability of the BBB due to tumors, VEGF, and inflammatory states.

7

In which compartment is fluid found in toxigenic edema?

What tissue does it usually affect?

Describe its pathogenesis.

Intracellular compartment.

Gray matter.

Cellular energy failure causes decreased pumping. Sodium enters the cell, and water follows. (may also be due to excess glutamate, extracellular potassium, cytokines, etc)

8

What occurs in a subfalcine herniation?

What causes it?

Complications?

The cingulate gyrus herniates under the falx.

Asymmetric expansion (eg mass effect)

May compress the anterior cerebral artery.

9

What occurs in a transtentorial herniation?

What causes it?

Complications?

Inferior displacement of the uncus around the tentorium cerebelli.

Asymmetric expansion.

Ipsilateral CN III compression, contralateral brainstem compression, PCA compression, and duret hemorrhage.

10

Why is mydriasis seen in tentorial herniation?

What is Kernohan's notch?

What is the prognosis for a duret hemorrhage?

Again, what do all of these stem from?

Compression of the ipsilateral third cranial nerve, in which the pupillary constrictor fibers travel along the exterior.

Creasing of the contralateral cerebral peduncle against the tentorium. Causes ipsilateral weakness & babinski signs.

Duret hemorrhages are fatal (brainstem!)

These all arise from Transtentorial herniation.

11

What occurs in a tonsillar herniation?

What causes it?

Complications?

Escape of the cerebellar tonsils inferiorly through the foramen magnum.

Symmetric expansion in the posterior fossa.

Compression of the medulla can cause cardiopulmonary arrest (fatal)

12

Distinguish a communicating hydrocephalus from a non-communicating one.

Give some causes for each.

Communicating hydrocephalus has ventricular patency; non-communicating has an obstruction.

Communicating: Overproduction of CSF or decreased absorption (meningitis, subarachnoid hemorrhage, thrombosis)

Non-communicating: Tumor, malformation (eg ventricular atresia), meningeal thickening (eg Meningitis)

13

In the context of head trauma:

What is the difference between open and closed?

Primary vs secondary?

Open vs closed refers to the overlying skull and skin.

Primary vs secondary refers to injury being caused directly or indirectly by the trauma (eg hemorrhage and subsequent ischemia).

14

Blunt trauma can feature distinctive patterns of bony, parenchymal, and vascular injury depending on how it occurs.

Describe three patterns of bony fracture.

Linear: Single full-thickness fracture.

Comminuted: Multiple radiating fractures.

Depressed: Bony fragments displacing inward.

15

What is a concussion?

What are its clinical features?

Pathophysiologic change resulting from CNS trauma without evident structural abnormalities.

Patients present with immediate and generally transient neurologic impairment (physical, cognitive, emotional. +/- consciousness).

16

What is a contusion?

Where are they most likely to occur?

Bruising of the brain due to trauma; involves small blood vessels, neurons, and glia.

In crests of gyri overlying rough areas of skull (notably anterior and middle cranial fossae).

17

Describe the morphology (gross and microscopic) of an acute contusion.

How do they appear months to years later?

Wedge-shaped, with the apex away from the trauma. Superficial hemorrhaging of the cortex & meninges with perivascular blood accumulation, edema.

Indentation/cavitation of the gyri with discoloration. Histology yields hemosiderin-laden macrophages and fibrillary astrocytes.

18

Does contrecoup tend to occur with stationary trauma or moving trauma?

How does this happen?

Usually with a fall.

The brain may "bounce" from the initial impact. Alternately, the parenchymal opposite the impact may experience a "stretch", producing damage.

19

What is diffuse axonal injury, and how does it occur?

How does it present?

Rapid accelerations can widely disrupt axons.

These patients tend to experience immediate unconsciousness. Often deadly, though lesser degrees may just feature milder neurologic defects.

20

What regions of the brain are most susceptible to DAI?

Describe its morphology, acutely and chronically.

The corpus callosum, paraventricular white matter, cerebellar peduncles, and superior colliculi.

Initially display clusters of hemorrhage. Later show thinning, gray discoloration of WM, and hydrocephalus.

21

Describe the appearance of DAI on histology.

What markers will be present?

How does this change with time?

Axonal swelling at the site of damage due to accumulation of axonally transported stuff. Microglia may be present.

Beta-amyloid positive.

The relevant fiber tracts may degenerate.

22

Name the hemorrhage described by each criterion

1. Lucid interval between incident and worsening of symptoms.

2. Can be caused by escape of blood from the ventricular system.

3. Prone to re-bleeds.

4. Results from MMA tear.

5. More common in the elderly (why?)

1. Epidural hematoma.

2. Subarachnoid hemorrhage.

3. Subdural hematoma.

4. Epidural hematoma.

5. Subdural hematoma; brain atrophy stretches the subarachnoid veins which tear.

23

Name 3 sequelae of traumatic brain injury.

Hydrocephalus (especially if subarachnoid hemorrhage)

Post-traumatic epilepsy

Chronic traumatic encephalopathy.

24

Full contact athletes are presumably at a higher risk of long-term neurological deficits (encephalopathy) resulting from trauma.

What symptoms might they demonstrate?

What might be found on histology?

Behavioral changes (impulsivity, aggression, depression, memory loss), eventually dementia, altered gait, speech abnormality, and parkinsonism.

Tau in NFTs and glial tangles, plus TDP-43 inclusions (???)

25

Recap! Name the pathology:

1. Presents with a crescent-shaped lesion on CT.

2. Infarcts the ACA.

3. May result from increased VEGF expression.

4. Results from bilateral posterior fossa expansion.

5. Classically results from a temporal bone fracture.

6. Especially affects the corpus callosum or cerebellar peduncles.

1. Subdural hematoma

2. Subfalcine herniation

3. Extracellular (vasogenic) edema

4. Tonsillar herniation

5. Epidural hematoma

6. Diffuse axonal injury (DAI)