Chapter 28 Part 1 Flashcards
1
Q
Acute neuronal injury
A
- accompanies acute CNS hypoxia/ischemia insult
- red neurons-12-24 hours after insult–shrinkage of cell body, pyknosis of nucleus, disappearance of nucleolus, loss of Nissl substance (chromatolysis), intense eosinophilia of cytoplasm
2
Q
Chronic Neuronal injury
A
- Characteristic feature-cell loss (selectively involving functionally related groups of neuron
- reactive glial changes-best indicator at early stages
3
Q
Axonal reaction
A
- Change in cell body during regeneration of the axon-best seen in anterior horn cells
- increased protein synthesis associated with axonal sprouting
- enlargement of cell body, peripheral displacement of nucleus, dispersion of nissl substance from center to periphery of cell
4
Q
Neuronal inclusions
A
- Manifestation of aging
- genetic disorders of metabolism
- viral infection
- degnerative diseases
5
Q
Viral infections–neuronal inclusions
A
- Herpes-Cowdry bodies
- Rabies-Negri bodies
- CMV-in nucleus and cytoplasm
6
Q
most important histopathologic indicator of CNS injury
A
gliosis
7
Q
Gliosis
A
- hypertrophy and hyperplasia of astrocytes
- nuclei of astrocytes enlarge, become vesicular, develop prominent nucleoli
- gemistocytic astrocytes-eccentric nucleus, swollen cytoplasm
8
Q
Alzheimer type II astrocyte
A
- in longstanding hyperammonemia–chronic liver disease, wilson disease, metabolic disorders of urea cycle
- large nucleus, intranuclear glycogen, chromatin
9
Q
Rosenthal fibers
A
- thick, elongated, brightly eosinophiic, irregular structures that occur within astrocytic processes
- in regions of long-standing gliosis
- characteristic of pilocytic astrocytoma
- Alexander disease (leukodystrophy)
10
Q
Corpora Amylacea
A
- polyglucosan bodies
- round, faintly basophilic, PAS-positive
- located where there are astroctyic end processes
- occur in old age
11
Q
Lafora bodies
A
-in cytoplasm of neurons in myoclonic epilepsy
12
Q
What are microglia?
A
-resident macrophages of CNS
13
Q
Microglia respond to injury by doing what 4 things?
A
- proliferating
- developing elongate nuclei (rod cells)
- forming aggregates around small foci of tissue necrosis (microglial nodules)
- congregating around cell bodies of dying neurons (neuronophagia)
14
Q
Glial cytoplasmic inclusions
A
- primarily alpha-synuclein
- found in multiple system atrophy
15
Q
What are ependymal cells?
A
-ciliated columnar epithelial cells lining the ventricles
16
Q
Ependymal granulations
A
- small irregularities on ventricular surfaces due to disruption of ependymal lining and proliferation of subependymal astrocytes
- due to infiltration or dilation of ventricular system
17
Q
Pressure within cranial cavity rises in 3 clinincal settings:
A
- generalized brain edema
- increased CSF volume (hydrocephalus)
- focally expanding mass lesion
18
Q
2 main pathways of edema formation in brain
A
- vasogenic edema (increased vascular permeability)
- cytotoxic edema (increase in intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury
19
Q
Gneralized edema-brain structure
A
-gyri flattened, sucli narrowed, ventricular cavities compressed
20
Q
Interstitial edema (hydrocephalic edema)
A
-increase in intravascular pressure causes an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter
21
Q
Non-communicating/obstructive hydrocephalus
A
-if ventricular system is obstructed and doesn’t communicate with subarachnoid space
22
Q
Communicating hydrocephalus
A
- ventricular system is in communication with subarachnoid space
- enlargement of the entire ventricular system
23
Q
Hydrocephalus ex vacuo
A
compensatory increase in ventricular volume secondary to brain atrophy
24
Q
What is a subfalcine (cingulate) herniation? what does it compress?
A
- cingulate gyrus under falx
- anterior cerebral a
25
What is a transtentorial herniation? What does it compress?
- medial aspect of temporal lobe is compressed against tentorium
- CN3
- PCA
26
Kernohan notch
- when the herniation is large enough, the contralateral cerebral peduncle may be pressed
- results in hemiparesis ipsilateral to side of herniation (in trantentorial herniation)
27
duret hemorrhage
secondary hemorrhagic lesions in midbrain and pons that accompany progression of transtentorial herniation
28
Tonsillar herniation
- cerebellar tonsils through foramen magnum
| - brain stem compression--life threatening
29
Spina bifida (spinal dysraphism)
- asymptomatic--spina bifida oculta
| - neural tube does not close all the way
30
myelomeningocele
- extension of CNS tissue through defect in vertebral column
- usually lumbosacral region
- motor and sensory deficits in lower extremity
- superimposed infection that extends into the cord
31
meningocele
-only meningeal extrusion through defect in vertebral column
32
encephalocele--what is it? Risk factor?
- malformed brain tissue extending through a defect in the cranium
- most common in posterior fossa
- risk factor- folate deficiency during 1st week of gestation
- neural tube closure--complete by day 28
33
Anencephaly
- malformation of anterior end of neural tube
- absense of brain and calvarium
- disrupted at 28 days
34
area cerebrovasculosa
remains in forebrain place (in anencephaly)
| -flattened remnant of disorganized brain tissue
35
neurons from germinal matrix zone to cerebral cortex--2 paths
- radial migration (become excitatory neurons)
| - tangential migration (become inhibitory neurons)
36
lissencephaly
reduction in number of gyri
37
agyri
no gyrial pattern-extreme case
38
lissencephaly- 2 general patterns
- type 1: smooth surfaced form-mutations that disrupt the signaling for migration and cytoskeletal motor proteins that drive migration of neuroblasts
- type 2-rough/cobblestoned surfaced from--disrupt the stop signal for migration--mutations in enzymes that place sugars onto proteins
39
polymicrogyria
- small, numerous, irregularly formed cerebral convolutions
- gray matter with 4 layers with entrapment of meningeal tissue at point of fuse that would otherwise be by the cortical surface
40
neuronal heterotopias
- group of migrational disorders that are associated with epilepsy
- presence of collections in neurons in inappropriate locations along the pathway of migration
41
periventricular heterotopias--mutation?
- gene encoding filamin A--actin binding protein--responsible for assembly of complex meshwork of filaments
- DCX (dbl cortin)- on X chromosome-results in lissencephaly in males and subcortical band heterotopias in females
42
Holoprosencephaly-severe and less severe cases? associated with?
- incomplete separation of cerebral hemispheres across midline
- severe- midline facial abnormalities
- less severe- arhinencephaly- absence of olfactory CNs
- associated with trisomy 21
- mutations in SHH signaling pathway
43
Agenesis of corpus callosum
- absense of white matter bundles that carry cortical projections from 1 hemisphere to the other
- Bat wing deformity- misshapen lateral ventricles
44
Arnold-Chiari malformation (type II)
- misshapen midline cerebellum with downward extension of vermis through foramen magnum
- hydrocephalus, lumbar myelomeningocele
45
Chiari-type 1 malformation
- less severe
- low-lying cerebellar tonsils extend down into vertebral canal
- can be symptomatic because of impaired CSF flow and medullary compression
46
Dandy- walker malformation
- enlarged posterior fossa
- cerebellar vermis absent or present in rudimentary form
- large midline cyst in its place
- expanded, roofless 4th ventricle
47
Joubert syndrome
- hypoplasia of cerebellar vermis with elongation of superior cerebellar peduncles and altered shape of brainstem
- "molar tooth sign" on imaging
48
hydromyelia
-expansion of ependyma- lined central canal of cord
49
syringomyelia--what is it and when does it manifest?
- fluid filled cavity in inner portion of cord
- may extend into brainstem--syringobulbia
- can be associated with chiari malformations, intraspinal tumors, traumatic injury
- destruction of adjacent gray and white matter; gliosis
- manifests in 2-3 decade of life--loss of pain and temp in UE
