Trauma And Hydrocephalus Pathology Flashcards
Hydrocephalus
Increased amount of CSF in the CNS for whatever pathological reason.
The skull and CNS is a finite space and doesnt expand, so increases in CSF volume is bad.
Usually caused by with impaired flow or decreases resorption from the arachnoid granules.
What is the normal CSF circulation pathway?
1st and 2nd ventricles -> 3rd ventricle -> 4th ventricle -> foramina of luschka and magendie-> subarachnoid space
absorbed in the subarachnoid space via the subarachnoid granules
Non-communicating hydrocephalus
Most commonly caused by a mass obstructing foramen of monro or cerebral aqueduct
Caused by a localized obstruction to CSF flow with the ventricle system
- causes only a portion of the ventricles to enlarge, not the whole thing.
Communicating hydrocephalus
The entire ventricular system is enlarged and is caused by a reduction of CSF resorption
The entire ventricle system enlarges not just a portion
Hydrocephalus ex vacuo
Compensatory hydrocephalus
Hydrocephalus that occurs secondarily due to a loss of brain volume due to neurodegenerative defects
Causes increases in CSF due to open space being present
What are the three main types of brain herniations?
Subfalcine (cingulate)
- herniated of the cingulate gyrus through the falx cerebri due to asymmetrical expansion
- compresses the anterior cerebral artery
Transtentorial (uncinate)
- herniated of the medial temporal lobe through the tentorium
- displaces the CN 3 which shows blown pupils
- compresses the posterior cerebral artery
- can cause hemiparesis ipsilaterally via the kenohan’s notch formation
- can cause depressed consciousness
- can cause duret hemorrhages which are flamed-shaped hemorrhages in the midbrain/pons
Tonsillar
- cerebellar tonsil herniation into brain stem
- almost always fatal due to impingement of the respiratory/cardiac centers in the medulla
Coup vs contrecoup injury
Coup = CNS/brain damage seen at the site of impact
Contrecoup = CNS/brain damage seen opposite the site of impact.
both result in contusions
How can you determine the site of a contusion injury?
They are wedge-shaped and the widest aspect of the contusion is the site of impact
What is the apperance of old traumatic brain lesions
They appear depressed, retracted yellowish/brown patches
* the coloring is due to residual hemosiderin-laden macrophages*
Chronic traumatic encephalopathy (CTE)
Profound neurologic defects caused by Repeated concussions
Results in accumulation of tau protein tangles in the cerebral cortex/CNS which causes neurodegeneration of white matter
Epidural hematomas
Traumatic injury affecting the dural vessels
the middle meningeal artery is most susceptible
Almost always stems from skull fractures in children and adults
- common in infants also but is usually shaking
Blood accumulates under arterial pressure (not venous)
- this dissects the dura away from the inner skull surface
Clinical signs of epidural hematoma
Patients are lucid for several hours before neurologic signs appear
- at this point, brain tissue loss is occurring
Requires rapid neurosurgical emergency
Subdural hematoma
Rapid movement of the brain during trauma which treats bridging veins in the subarachnoid/Subdural spaces in the dural sinuses
Results in venous bleeding into the Subdural space
Higher rates in older adults and infants
Most commonly occurs in the lateral aspects of the cerebrum but can be bilateral and anywhere
Subdural hematoma clincial signs
Typically manifests within 48hrs (slower than epidural)
Neurologic signs are attributed to which part of the brain is experiencing pressure increases
Symptoms are non-localizing and slowly progress into neurologic deterioration
Natural healing steps of a Subdural hematoma
1) lysis of the clot (1 week after injury)
2) growth of granulation tissue (2 weeks after injury)
3) fibrosis growth (1-3 months after injury)
