 Unique feature sthat influence consequences

o Unique cell types

o Glymphatics allows lymphatics
 Does not recycle
 Cells of the cell type
o Neuroectoderm origin
 Neurons
 Glia
 Astrocytes,
Oligodendroytes
 Epndyomal/chorid
cells
 Stem/progentir
o Mesodermal origin
 Resident microgelial
 Meningeal cells
 Blood vessels and blood cells
 Patterns of response  help to understand
certain conditions
o Acute injury
 Quick onset, initial injury is short live
 Initiated by intial evernt 
1. Intial event: Damage/trauma/infection releases cellular debris
2. Local Inflammatory response by Local resident macrophage
[microglia/astrogliosis, debris clearance]
3. Infiltration of blood immune cells
 Infiltrate inflammation-resolving leukocytes
4. Resolution of neuroinflammation and tissue restoration
 Example  hypoxia from a stroke
o Chronic injury
1. Chronic neural degeneration is usual from an inability to resolve the issue
from insufficient recrutment
 Misfolded Protein aggregates that lead to an increase in damaged tissue
2. Glial cell activation occurs, but is sustained with insufficient recruitment
3. long term neural degeneration and death
 Endothelium more resistant to hypoxia because they’re at the blood brain barrier
 Neurons vary in susceptibility to injury to hypoxia
o Don’t store energy  need continuous O2 and Glucose
 Energy from astrocytes
 Inherit rates of turnover
 Neurons cannot regenerate
 Have mechanism to maintain cell structure
 Protein quality and presence maintained
 Acute damage  o2 depletion, trauma
  Chronic damage  accumulation of abnormal protein aggregates
 Chronic is basically decrease in maintenance ability
 Selective vulnerability
o Differential sensitivity of neuronal population  changes susceptibility to cell injury or
death
 The most sensitive neurons in the brain are:
 Pyramidal cell layer of the hippocampus (especially in area CA1, also
referred to as Sommer sector) which play a role in long-term memory
and spatially-related tasks
 cerebellar Purkinje cells involved in motor learning
 pyramidal neurons in cerebral cortex
 Neurons response to acute injury
o Red neurons with H &E
 Accompany acute hypoxia/ischemia
 Shrinkage of cell body
 Nuclear pyknosis  condensation of the
chromosome
 Disappearance of nucleolus
 Loss of nissle substance  Eosinophilia
 Neuronal response to subacute/chronic injury  degeneration
o First  apoptisis [in situ and trans synaptic]
 Causes apoptosis in downstream neuron
o Regeneration: Axonal reaction
 Loss of connection to motor fibers
 Swelling of the central body
 Pushes the nucleus away from central
location
 Central chromatolysis: dispersion of the
nissl substance from the center to the
periphery of the cell
 Allows for regeneration of axon sprouts

 Neuronal inclusions
o Long term maintenance leads to accumulation of abnormally folded proteins,lipids, or
carbohydrates in cells from chronic insult
 Lewy body  parkinsons
 Neurofibrillary tangle alziehmers
 Astrocytes
o Important role in the function of the CNS
 Maintain ion balance
 Nourish neurons (stored glycogen)
 Form the BBB
 Uptake and recycle neurotransmitters
o GFAP [glial fibuillary acidic protein] is used to stain astrocytes
 o Will proliferate in response to
injury  gliosis [Indicator to
injury]
 Charachterized by
hypertrophy and
hyperplasia
 Most likely to cause an
issue
o Reactive astrocytes form when red
neurons die
 Will take their place and accumulate  Glial scarring
o Gemistocytic astrocytes  swollen astrocytes with prominent nuclei and scant
cytoplasm that becomes bright pink
 Large accumulation of cells
 Space is edema fluid
 Specific injury astrocyte response
o Hepatic encephalopathy
 Changes in the brain from high blood ammonia
 Alziehmer type 2 astrocytes
 Grey matter cells with large nucleus, pale
staining central chromatin, intranuclear glycogen droplets
 High levels of ammonia cross the blood brain and
increases glutamine synthesis
o Chronic gliosis
 Can form inclusion fibers
 Rosenthal fibers
 Accumulations of the astrocytic process,
buildup of ubiquitin
 With long standing gliosis and related to
tumor
 Alexander disease
 Abundant Rosenthal fibers in periventricular, perivascular, and
subpial locations.
 Corpora amylacea
 Lamelated  layered deposition with carbohydrate build up
 Found in the foot processes of astrocytes
 Occur in increasing numbers with age and in neurodegenerative
disease
 Most common in subpial and perivascular areas
 Begin from mitochondria and
 induces Hemo-oxeganse-1 HO1,
 Accumulation of iron
 Oligodendrocytes apoptosis/injury from demyelinating disorders and leukodystrophies
o JC virus  lytic infection with regions of demylenation

Granulation of
ependymal cells

 Ependymal cells may be injured or lost, can be from tumors

o Damage to ependymal cells can lead to
 Proliferation  forms tubules and nodules
[granulation]
 Can be from
 Chronic hydrocephalus
 Chronic intravenous infection
 Formation of a rosettes
 Acellular region from
damage/overgrowth

 Microglia  resident macrophages of the NCS

o Sense injury and migrate and become rod cells
o Nucleus becomes elongated and all align in the same orientation
o Maintain contact with the axons as they migrate
o Sense the damage through the pathogen recognition receptors
o Resident cells that can become in the ameboid phenotype
 Kinds of microglia
o Rod microglia
 Sense injury  migrate  and line in the same direction to the injury
o Micrgolia in cortex
 Sense damage and change phenotype
 M1  associated with proinflammitory state
 M2 resolving state, phagocytic
 Result of infiltrating microglia
o Form
 Microgliod nodule that surround the neuron
  Neuronophagia  engulfing the dying neuron
 Increased intracranial pressure and consiquences
o 3 compnentes coexist
 Brain
 CSF
 Blood
o Monro-Kellie
 Dynamic equilibrium under a certain volume
 Constant volume from all three
 Change in one/addition of the other must displace one of the other
components
 Tumor or something is addition of the 4th component 
 Decrease of CSF/CBV
 At stage 3 cannont change or compensate for increases
in Brain

 Vasogenic edema  loss of tight junctions

o Oxidative stress
o Glial activation decrease astrocyte regulation
o Will allow extra fluid to rush into through BBB
o Effects
 white matter mostly[Inflammation/tumor]
 Can be
 focal [Inflammation/tumor]
o Vessels of tumor is highly leaky
 or generalized [ischemic]
 Cytotoxic edema
o Injury to astrocyte  infection/toxic insult,
o Leads to deregulation of sodium/potassium pumps
o Begins to import accumulating sodium and begins to sodium
 Secondary increase in h20
o Basically a transfer of fluid from intracellular sources due to astrocyte swelling
o Endothelium tries to rebalance the fluid but exasterabete the problem
o BBB remains intact
 Basogenic edem affects white matter
o Movement of proteins
o Vessles of the tumor are extremely leaky and don’t allow for tight junctions
o Hypoechoic region
o Primarily effecting white matter
 Cytotoxic edema
o BBB remains intact
o Swelling of the endothelium leads to blurring
 Abnormal accumulations and mass
o Centerline of this brain has been shifted
 Accumulation of fluid
 Hydrocephelus
o Excessive accumulation of CSF from widening of the ventricles
 Increases in pressure
o Common causes  aquaductal stenosis
 Communictin vs noncommunicating hydrocephelsis
o Communicating  widing of the all the ventricles
 Blockage occurs after exting the ventricles
 Impaired CSF reabsorbtion
 Obstruction of flow through the subarachnoid space or at the level of
the arachnoid granulations,
 From overproduction, loss of reabsorbtion of CSF
o Noncommunicating CSF
 Blocked ventricular system [aquaduct]
 Lateral/3rd ventricle will be enlarged  abstructed/noncommunicating
with eachother
o 4th ventrical will be normal
 Not communicating with the subarrachnaiod or eachother
 Hydrocephalus ex vauo
o Brain atrophy leads to enlarging
 Seen in dementia, alziehmers
o Ventricles enlarge to compensate
 Hernation of the brain possible displacement areas
o Subfalcine (cingulate)
 Midline shift of singulate gyrus is to hurnate
 Compression of the ACA
o Transtentorial (uncal)
 Medial aspect of temporal lobe pressing the tentorium
 Compression of the 3rd nerve
o Transtentorial (central)
 Progressive compression of brainstem, with initial damage to the brainstem
o Downward Tonsillar
o Upward Tonsillar
 Increased Intracranial pressure spinal tap leads to herniation
 Infants skulls can expand to hydrocephalus
o Sunsetting sign
Nonncommunicating
hydrocephalus
Communicating
hydrocephalus
Hydrocephalus ex vacuo