Exam 2: CNS Pt1 Flashcards
What is the parenchyma of the CNS?
(functioning part)
- neurons and glial cells
T/F. CNS neurons are incapable of division and injury to theses cells in permanent.
True (but can have Reversibly injured neurons and Irreversibly injured neurons
What is the concept that occurs in the CNS where area/types of neurons that share similar levels of functionality, physical connections, NTs, or similar metabolic requirements are all prone to injury from similar pathological stimuli?
Selective vulnerability
How do Reversibly injured neurons manifest?
- swelling of soma
- “spheroids” (= swelling of axon)
- “central chormatolysis” (= peripheral displacement of Nissl substance)
- axonal sprouting
How does Irreversibly injured neurons manifest?
- shrunken soma
- nuclear pyknosis
- eosinophilia
~all w/in 12-24 hrs - appear as small “red neurons” (‘red is dead’)
- dissolution of nucleolus and Nissl substance
Would Reversibly or Irreversibly injured neurons manifest from times of acute hypoxia or sudden ischemia?
Irreversibly injured axons –> lead to inflammation and cause cerebral edema
Which cells of the CNS when injured manifest by hypertrophy, hyperplasia, and eosinophilia?
Astrocytes (astroglia)
- activation of them = gemistocytic astrocyte
Which cells of the CNS produce myelin and when injured hypertrophy and are usually infected by viruses?
Oligodendrocytes
Which type of CNS cell are the phagocytes of the CNS and after injury hypertrophy and hyperplasia occurs?
Microglia (“neurophagia”)
Which cells of the CNS line ventricles and spinal cord and commonly infected by CMV (cytomegalovirus)?
Ependymal cells
- could be possible choroid plexus dysfunction (recall it produces CSF)
BOARDS: What are the key characteristics on how these manifest?
- Rabies
- CMV (cytomegalovirus)
- Parkinson Disease
- Alzheimer Disease
- Negri body
- owl’s eye appearance
- Lewy bodies
- Neurofibrillary tangles; beta-amyloid plaques (Tau proteins)
What is lipofuscin?
the lipid accumulation occurring with aging
What are 4 things that take up space and therefore may be a cause for injury?
- Blood
- Pus
- Tumor
- Edema
What are the two forms of cerebral edema?
- Vasogenic edema
2. Cytotoxic edema
Which type of cerebral edema develops when the BBB is disrupted and causes EXTRACELLULAR edema?
Vasogenic edema
- can be localized or generalized
What can disrupt the BBB and therefore cause vascogenic edema?
localized– tumor, inf. inflam.
generalized–trauma
Which type of cerebral edema causes INTRACELLULAR edema and develops when membranes of neurons and glial cells are injured?
Cytotoxic edema
What refers to an increase in CSF volume w/in the ventricular system? What are two ways this may occur?
Hydrocephalus
- increase production of CSF (via choroid plexus tumor or altered CSF flow)–rare
- reduced resorption of CSF at arachnoid granulaes
If hyrdocephalus develops proior to closure of cranial sutures around age 2, what occurs? What is it develops after the closure of the cranial sutures?
before–> head enlarges
after–> ventricles enlarge and severe increase in ICP
What percentage of hydrocephalus causes are known?
about 1/2; 50% are idiopathic
congenital (3 in 1,000 live births)
What describes a symmetrical enlargement of ventricular system and is most likely to be results of reduced CSF resorption?
Communicating hydrocephalus
What describes asymmetrical enlargement of the ventricular system (one area enlarged and the other normal)? What could this be due to?
Noncommunicating hydrocephalus
due to obstructed CSF flow –> tumore, gliosis, space-occupying lesion
What describes an increase in CSF volume that is secondary to loss of brain parenchyma from a pathological situation, such as a stroke or from advanced stages of neurodegenerative diseases?
Hydrocephalus ex vacuo
What is the MC cause of overproduction of CSF?
choroid plexus tumor
What involves a displacement of CNS tissues from its normal location in response to increase ICP?
Cerebral herniation
-typically across rigid dural structures or through foramen magnum
What will Cerebral herniations commonly cause?
- sudden reduction of perfusion to herniated CNS tissue–> cause infarction–> which causes inflammation and edema –> increase ICP
(create positive feedback loop)
What are the three common cerebral herniations we are focusing on?
- Subfalcine (cingulate) herniation –MC
- Transtentorial (uncinate) herniation
- Tonsillar herniation
What is the MC type of cerebral herniation?
Subfalcine (cingulate) herniation
What type of herniation occurs when the cingulate gyrus herniates under the falx cerebri and superior to corpus callasum? What does this cause?
Subfalcine (cingulate) herniation
- abnormal posturing –> decorticate rigidity
What type of abnormal rigidity involves brachial flexion, internal rotation of legs? Where does this injury occur b/w?
Decorticate Rigidity (“think cortex is higher and arms flex up”)
injury b/w cortex and red nuclei (midbrain)
What type of abnormal posturing involves all limbs extended and arms are pronated with flexed wrists? Where does this injury occur?
Decerebrate rigidity
brainstem–> b/w red nuclei and vestibular nuclei
What type of herniation occurs when the uncinate fasciculus of the temporal lobe herniates under the tentorium cerebelli?
Transtentorial (uncinate) Herniation