Chapter 28 part 2 Flashcards
1
Q
Periventricular leukomalacia
A
- infarcts in supratentorial periventricular white matter
- chalky yellow plaques–white matter necrosis and calcification
2
Q
Multicystic encephalopathy
A
- ischemic damage of white and gray matter
- destructive cystic lesions develop throughout hemispheres
3
Q
ulegyria
A
-thinned out, gliotic gyri that occurs in perinatal ischemic lesions of cerebral cortex
4
Q
status marmoratus
A
- marble like appearance of deep nuclei when irregular myelination occurs
- movement disorders
5
Q
Physical forces associated with head injury may result in:
A
- skull fractures
- parenchymal injuries
- vascular injuries
6
Q
Displaced skull fractures
A
-fracture-bone is displaced into cranial cavity by a greater distance than the thickness of the bone
7
Q
basal skull fracture
A
- symptoms of lower CNS
- orbital or mastoid hematomas
- impact to occiput or sides of head
- CSF discharge from nose or ear
8
Q
diastatic fractures
A
cross sutures
9
Q
concussion- characteristic neurological symptoms
A
- instant onset of transient neurological dysfunction
- loss of consciousness, temporary respiratory arrest, loss of reflexes, amnesia of the event
10
Q
coup injury
A
-point of contact
11
Q
contrecoup injury
A
-impacts with the skull
12
Q
concussion morphology
A
- early stages–edema, hemorrhage
- later- extravasation of blood
- 24 hours–neuronal injury
- old traumatic lesions–plaque jaune (depressed, retracted, yellowish brown patches)
13
Q
Diffuse axonal injury–what indicates it?
A
- surface of brain most affected
- axonal swelling!!!
14
Q
Diffuse axonal injury morphology
A
axonal swelling–hours after injury
15
Q
Hemorrhage can occur in?
A
- Epidural
- Subdural
- Subarachnoid
- Intraparenchymal
16
Q
Epidural hematoma is caused by?
A
- Middle meningeal a
- Temporal skull fractures–trauma!!
- dura separates from inner surface of skull
- rapidly evolving symptoms
17
Q
Subdural hematoma caused by?
A
- bridging veins
- accumulation of blood between dura and arachnoid
- doesn’t have to be trauma!!
- slowly evolving neurologic symptoms
- older patients with brain atrophy–bridging veins are stretched
18
Q
Acute subdural hematoma morphology
A
- Lysis of clot- 1 week
- growth of fibroblasts from dural surface into hematoma- 2 weeks
- development of hyalanized CT (1-3 months)
19
Q
Chronic subdural hematoma morphology
A
-recurrent episodes of bleeding occurs- from thin-walled vessels of granulation tissue
20
Q
posttraumatic hydrocephalus is due to?
A
-obstruction of CSF resorption from hemorrhage into subarachnoid spaces
21
Q
Chronic traumatic encephalopathy (CTE)
A
- dementing illness after repeated head trauma
- atrophic, enlarged ventricles, tau-containing neurofibrillary tangles
- repeated concussions
22
Q
Spinal cord injury morphology
A
- acute phase- hemorrhage, necrosis, axonal swelling
- in time- central areas of neuronal destruction becomes cystic and gliotic
23
Q
hypoxia vs. ischemia
A
- hypoxia: low PO2, impairment of blood’s O2 carrying capacity
- ischemia: interruption of normal circulatory flow
24
Q
biochemical changes in cells from ischemia
A
- depletion of ATP
- Ca levels elevated- act enzymes- cellular injury
- inappropriate release of EAA NTs-binds to NMDA receptors-causes calcium influx
25
penumbra
-at risk tissue- region of transition between necrotic tissue and normal brain
26
Most sensitive neurons to ischemia
- pyramidal cell layer of hippocampus (CA1- sommer sector)
- cerebellar Purkinje cells
- Pyramidal neurons in cerebral cortex
27
Greatest risk for border zone (watershed) infarcts
-between anterior and middle cerebral artery
28
Global cerebral ischemia morphology
- early: eiosinophilia of neuronal cytoplasm, nuclear pyknosis
- subacute: tissue necrosis, macrophage influx, vascular proliferation, reactive gliosis
- repair: removal of necrotic tissue, gliosis
- psudolaminar necrosis: preservation of some layers and destruction of others due to uneven neuronal loss and gliosis
29
embolisms--from where? What is most affected?
- cardiac mural thrombi--most common
- thromboemboli arising in arteries- atheromatous plaques in carotid arteries
- paradoxical emboli, cardiac surgery, emboli of other material
- MCA and ICA most affected!!
30
Infarcts-- 2 groups based on presence of hemorrhage
- begin with loss of blood supply and nonhemorrhagic
| - secondary hemorrhage--occurs from ischemia-reperfusion injury- petechial
31
non-hemorrhagic infarct-microscopic morphology
- 12 hrs: ischemic neuronal change, vasogenic edema, glial cells swell
- 48 hours-phagocytic cells
- 1 week- reactive astrocytes
- months: meshwork of glial fibers with new capillaries and perivascular CT
32
4 most important effects of hypertension of brain
- lacunar infarcts
- slit hemorrhages
- hypertensive encephalopathy
- hypertensive intracerebral hemorrhage
33
Lacunar infarcts
- small cavitary infarcts
- lakelike spaces, less than 15 mm wide
- tissue loss surrounded by gliosis
34
slit hemorrhages
- rupture of small penetrating vessels and development of hemorrhages
- hemorrhages resorb in time--leave a slitlike cavity surrounded by brownish discoloration
35
hypertensive encephalopathy--what is it? caused by?
- diffuse cerebral dysfunction--headaches, confusion, vomiting, convulsions, sometimes coma
- malignant hypertension- over years suffer multiple infarcts
36
intraparenchymal hemorrhage
- rupture of small intraparenchymal vessel
- sudden onset of neurologic symptoms
- middle to late adult life
37
risk factor most commonly associated with deep brain parenchymal hemorrhages
- hypertension-->vessel wall abnormalities--atherosclerosis in large arteries, hyaline arteriosclerosis in smaller arteries, necrosis in severe cases
- hyaline change in arteriolar walls- weaker, vulnerable to rupture
38
carcot-bouchard microaneurysms
- minute aneurysms- in vessels less than 300 um in diameter
| - most commonly within basal ganglia
39
hypertensive intraparenchymal hemorrhage--acute? old hemorrhage?
- extravasation of blood with compression of adjacent parenchyma
- central core of clotted blood--surrounded by a anoxic neuronal and glial changes and edema
- macrophages
- reactive astrocytes
- old hemorrhage- cavitary destruction with rim of brownish discoloration
40
risk factor most commonly associated with lobar hemorrhages? gene?
- CAA (cerebral amyloid angiopathy)
- amyloid peptides are deposited in walls of meningeal and cortical vessels- weakens the vessel wall-hemorrhage
- polymorphism in gene that encodes ApoE
41
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)- genes? characterized by?
- autosomal dominant disorder
- mutations in NOTCH3 gene- misfolding of NOTCH3- expression in vascular smooth muscle
- recurrent strokes and dementia
42
Most frequent cause of clinically significant subarachnoid hemorrhage?
- rupture of a saccular (berry) aneurysm in a cerebral a
| - 90% in anterior circulation
43
rupture of aneurysm- subarachnoid hemorrhage clinical features
- rupture of aneurysm- 5th decade of life
- greater than 10mm- 50% risk of bleeding per year
- occurs with acute increases in intracranial Pressure=straining at stool/ sexual orgasm
- healing-meningeal fibrosis and scarring- can cause obstruction of CSF flow or resorption
44
4 vascular malformations of the brain
- arteriovenous malformations
- cavernous malformations
- capillary telangiectasias
- venous angiomas
45
arteriovenous malformations (AVM)
-tangled network of vascular channels-arteriovenous shunting!!!
46
cavernous malformations
-dilated BVs that are characterized by multiple distended caverns of blood filled vasculature through which the blood flows very slowly
47
capillary telangiectasias
- dilated, thin walled vascular channels
| - most common in pons!!
48
venous angiomas (varices)
-characterized by an enlarged collection of veins which, other than their size, are microscopically normal
49
Foix-Alajouanine disease
-arteriovenous malformation of spinal cord and meninges-associated with ischemic injury to spinal cord
50
AVM (arteriovenous malformation)- clinical features
- males=2X frequent
- 10-30 years age- present as seizure disorder, intracerebral hemorrhage or subarachnoid hemorrhage
- MCA most common site
