Basic CNS Reactions/Pathology Lecture 7 Flashcards
What happens when axons are cut/what is the axonal reaction?
Proximally = Central Chromatolysis - swelling of cytoplasms and displacement of nissl chrome out of center to periphery (nissl = rough ER and is bluish) due to disruption of neurofilaments/organelles and transport
Distally = Wallerian Degeneration where distal axon degenerates
What is a Louis Body?
can see easily in substantia nigra pigmented nuerons where see rounded eosinophilic core structure with halo around it
proteinacious inclusions of alpha synuclein
What is Lipofuschin?
Prominent non-pathological accumulation that occurs with age
What are astrocytes? what is their role in the CNS? what is Gemistocytic?
Astrocytes are supportive and detoxify and respond to injury
like the fibroblasts of the CNS - get injury and get astrocye activation and proliferation where they start using GFAP (instead of collagen) as an intermediate filament for “scarring” in response to disease process
Gemistocytic = cells stuffed with GFAP
What are 2 Major Accumulations in AStrocytes?
Rosenthal Fiber –> proteinacious accumulation of alpha-Be-Crystalline seen in Astrocytoma or Leukodystrophy or Alexander Disease
Corpora Amylacea = purple things that are age-related starch accumulations
What happens to astrocytes in Liver Failure Cirrhosis? What is that called?
Elevated ammonia results!!
Normally, astrocytes detoxify excitatory NT like Glutamate and transfer ammonias between glutamate and glutamine
With elevated ammonia, astrocytes respond with **enlarging their nucleus and forming more heterochromatin and losing their GFAP **
Results in Big, watery looking atrocytes
*_*Alzheimer’s Type 2 Astrocytosis =_ brain changes with hepatic encephalopathy
What is Alzheimer’s Type 2 astrocytosis?
Brain changes seen with hepatic encephalopathy (NOTHING TO DO WITH ALZHEIMER’S) where you see enlarged nucleus orf astrocytes that are watery-looking and form more heterochromatin and lose their GFAP staining
What are oligodendrocytes? What are some pathologies seen in oligodendrocytes?
Cells that form myelinin CNS and have limited response to injury
JC-Virus with PML - see Viral inclusions in Oligodendrocyte
Multiple System Atrophy - see accumulation of Alpha Synuclein!!!!
See picture
What are Ependymal cells? What happens with they get damaged?
Ependymal cells line ventricles
when get damaged - not too responsive to injury - slough off and don’t come back
Leads to proliferation of Sub-Ependymal Glia –> exposure to CSF stimulates proliferation of glial fragments and can see GLANDULAR EPENDYMITIS
What are microglia? What are some changes that happen with them? What happens when stimulated with antigen?
Brain Macrophages!!!!
get stimulated by antigen and get Rod-Shaped Morphology and migrate towards antigenic stimulus
Then reach stimulus and cluster around it making Microglia Nodule
Then proliferate and phagocytose infected neuron - Neuronophagia
(see picture - example West Nile Virus)
What are the 3 main types of edema? where are they more prominent?
1) Cytotoxic Edema = cell death resulting from incompetence of membrane and water and salt go into the neurons and swells them up –> GRAY MATTER
2) Vasogenic Edema = incompetence of BBB, endothelial TJ breakdown and BV breakdown causing serum components to leak into tissues and cause mass effect –> WHITE MATTER more prominent and extracellular water
3) Interstitial Edema - Forcing water through ependymal lining into deep white matter in setting of **obstructive hydrocephalus **
What are the three types of herniation phenomena and what’s happening with each?
Transtentorial - “Uncal” Herniation - Displacement of medial temporal lobe over the free ege of the tentorium –> *Cerebral Peduncle and 3rd cranial nerve there so see Ipsilateral Fixed Pupil Dilation and Contralateral weakness
Cerebellar Tonsillar Herniation - Displacement of Cerebellar tonsils into Foramen Magnum –> Cerebellar tonsils next to medullary cardiorespiratory centers and life threatening!!!
Subfalcine/Cinglate Herniation – Displacement of Cingulate gyrus under Falx Cerebri –> less life threatening and results in associated weakness in loewr extremities
(SEE PICTURE)
Where is CSF made and what’s it’s flow pathway? Where is it absorbed?
CSF is made by the choiroid plexus in lateral, 3rd, and 4th ventricles and exits the foramen of Lushke/Megendie to circulate in subarachnoid spaces and is resorbed in the arachnoid granulations in the Parasagital Regions
What’s the difference between communicating and non-communicating hydrocephalus?
Communicating is where the ventricular system is patent and can communicate with subarachnoid space –> Typically arachnoid granulation obstruction
Non-Communicating is where the ventricular system is obstructed –> implies obstruction in the ventricular outflow tracts like the brainstem and can see interstitial edema and water being pushed along the outside surfaces/ependymal surfaces
Describe contusions? What kinds are there?
Contusion is parenchymal brain injury - like brain bruising
Coup Contusion = blow to stationary head making contusion at point of impact
Contrecoup Contusion = fall on back of head while rotating making contusion on Opposite point of impact
Remote Contusion = reselmbles an old infarct and can see a lot in orbitofrontal area where blood disrupts tissues and they become necrotic and fall away, can see hemosiderin there, can get post-traumatic epliepsy from these
What happens in diffuse traumatic axonal injury? ?How does that present?
Shearing forces deep in brain cause by low strain rate injury like MVA
Acutely, swollen axons
Presentation= prolonged traumatic unconsciousness
Example - MVA and instantly comatose at impact but no hemorrhage
What is chronic traumatic encephalopathy? What parts of the brain do you see it in?
Progressive Taupathy occurs as a consequence of repetitive mild TBI and clinically is associated with symptoms of irritability, impulsivity, aggression, depression, short term memory loss, and heightened suicidality 8-10 years after injury
Seen in Deep sulci and perivascular areas
Random tau in cortical areas
What is an Epidural hematome? How does it present and what causes it?
ARTERIEAL BLEEDS
Due to damaged meningeal artery (often middle meningeal)
Unilateral
Associated with skull fracture
What is a subdural Hematoma? What do you see with a subdural hematoma? How does it heal?
Rupture of Bridging Veins that drain the cortical surface into sinuses
can be unilateral or bilateral
often due to Trauma in elderly people and can be very large bc more space available from age-related atrophy
Heals by forming “neomembrane” to wall off the hemorrhage and at risk for repeat bleeds and chronic neurologic dysfunction (see picture)
Compare and contrast epidural and subdural hematomas?
Epidural - often from skull fracture puncturing an ARTERY and mostly unilateral causing Dura to press down into brain
Subdural - often in old people and comes from bridging VEINS rupturing into subdural space and can form neomembranes between dura and brain from arachnoid proliferation
BOTH have mass effect and can be life threatening
See Picture
What do you see in brain after ischemia?
Liquefactive Necrosis
Edema and mass effect
What areas are most vulnerable in global ischemia? (ie cardiac arrest) What kind of necrosis do you see?
Arterioborder zone ischemia - area between vascular teritorries with most remote blood supply
Laminar necrosis - selective damage to cerebral neocortex in global ischemic events (layers 3, 5, 6 more vulnerable)
What is the temporal pathology of ischemia?
Acute - cytotoxic edema, red dead neurons
Subsacute - Foamy macrophages and vascular proliferation
Remote - cavitation
What kind of lesions do you see in HTN cerebrovascular disease?
Lacunar Infarcts - occur when you KO small penetrating vessels coming off the circule of willis
***Indicative of Chronic HTN and see Small punched out lakes **
What happens in Subarachnoid hemorrhage?
is a Ruptured Saccular aneurysm until proven otherwise
Occur at branch points in circle of willis
get rupture and massive hemorrhage
Clinical Presentation = HA –> Prostrate –> bleed –> die
What’s probably causing intra-parenchymal bleeding in deep areas?
HTN!!!!
spontaneous deep intracerebral hematoma from longstanding cerebroascular disease
associated with HTN
What are you more likely to think if lobar intra-parenchymal hemorrhage? like in a lobe of cortex?
Older patient with sudden lobar hemorrhage in lobe of cortex –> AMYLOID DEPOSITS IN BV WALL!!!!
_Lobar Intracerebral Hematoma!!!! _
spontaneous in otherwise healthy person but in old person think _Amyloid Angiopathy _
What is Amyloid Angiopathy?
Stain with Congo-red to see vascular deposits of **Amyloid Beta Protein **
more common in elderly
(VS Amyloid Beta Precursor protein used to ID damaged axons in diffuse axonal injury)
