Chapter 22 Flashcards
symptoms of CNS pathologies
degeneration inflammation infection neoplasia *SELECTIVE VARIABILITY*
patterns of neuronal injury
neuronal astrocytes oligodendrocytes microglia ependymal cells
decrease in axonal transport
SWELLING of soma
displacement of Nissl substance
reversible neuronal injury
result of acute-hypoxic injury
- SHRINKING* of soma (but axonal swelling)
- RED NEURONS*
irreversible neuronal injury
shrinking of cell body/soma
red neurons
CNS fibrosis - astroglia or gliosis
injury –> hypertrophy and hyperplasia
enlarged nucleus
atscrocytes (neuronal injury pattern)
glial filament sprout; activated and change shapes
type of astrocyte injury pattern
gemistocytic astrocyte
produce myelin in CNS
acquired demyelinating disorders and leukodystrophies
ENLARGED nucleus
oligodendrocytes (neuronal injury pattern)
resident PHAGOCYTES of CNS
proliferate and enlarge: injury, infection, trauma
demyelination, infarction, hemmorhage
microglia (neuronal injury pattern)
line ventricles and spinal cord
infections: cytomegalovirus (CMV)
irregularities of ventricular surface (ependymal GRANULATIONS)
may involve CHOROID plexus
ependymal cells (neuronal injury pattern)
3 types of intracellular inclusions
viral infections
neurodegernative diseases
lipofusion
rabies: NEGRI BODY
CMV: owl’s eye
types of which intracellular inclusion
viral infections
Parkinson’s Disease: LEWY BODIES
Alzheimer disease: B AMYLOID PLAQUES
neurodegenerative disease
lewy bodies
parkinson’s disease
negi body
rabies
owl’s eye
CMV
accumulation of lipids in neuronal areas, aging
lipofusion
fluid accumulation within the brain tissue
limited expansion, increase ICP (blood, pus, edema)
cerebral edema
BBB disruption
increase in permeability
localized: tumors, infection
generalized: severe trauma
vasogenic (edema)
neuronal/glial membrane injury
intracellular edema
hypoxic-ischemic injury, toxic exposure
cytotoxic (edema)
3 characteristics of cerebral edema are _____ GYRI, ____ SULCI, and ______
flatten gyri
narrowed sulci
ventricular compression
disturbance in CSF flow/resorption/overproduction
increase CSF volume in ventricles
communicating
noncommunicating (localized)
* 2 y.o. = increase ICP, ventricular enlargement
hydrocephalus
MC type of hydrocephalus
disturbed flow/resorption
MC treatment for hydrocephalus
shunting
hydrocephalus with infarction and neurodegeneration
hydrocephalus ex vacuo
cerebrum shifts across dura or through foramen magnum
tissue compression:
decrease blood (infarction)
injury (swelling/vasculature)
brain herniation
MC form of brain herniation with displaced cingulate gyus, under falx cerebri
abnormal posturing, coma
subfalcine (cingulate)
brain herniation with displaced temporal lobe, under anterior tentorium
involves CN III
hemiparesis, brainstem compression
DURET HEMORRHAGE
transtentoral (uncinate)
brain herniation with displaced cerebellar tonsils, through foramen magnum
cardiorespiratory arrest, hydrocephalus, headaches
tonsillar
vessels that enter the PONS are disrupted by herniation
“flame shaped” hemorrhage
duret hemorrhage
3rd leading cause of mortality in US & MC cause of NEUROLOGIC morbidity
cerebrovascular disease (CVA)
Stroke: acute dysfunction, infarction steps (3)
thrombotic occlusion
embolic occlusion
vascular rupture
temporatory neurological dysfunction (<24 hours)
transient ischemic attack (TIA)
SPOT A STROKE acronym
F (face drooping)
A (arm weakness)
S (speech difficulty)
T (time to call)
liquefactive necrosis
ischemia/hypoxia
decrease in O2, partial pressure (hypoxemia)
decrease in O2 availability (CO, anemia, cyanide)
functional hypoxia
hypotension
occlusion
TRANSIENT (temporary)
STROKE (permanent)
ischemia
widespread ischemic-hypoxic injury
decrease perfusion
mild confusion (TIA) –> severe (stroke)
global cerebral ischemia
widespread NEURONAL death
cerebral EDEMA
RED NEURONS
neurological impairment: COMA
severe global cerebral ischemia
arterial occlusion–> localized ischemia
collateral flow limits injury: circle of Willis
*emboli
*thrombi
focal cerebral ischemia
deep tissues have ___ collateral supply (thalamus, basal ganglia, deep white matter)
minimal
MC form of focal cerebral ischemia
cardiac mural thrombi
valave disease
emboli
atherosclerotic plaques
carotid artery, aortic arch, middle cerebral artery
thrombi
intercranial hemorrhage injury that is MC due to HTN
vessel wall injury
SPONTANEOUS hemorrhage that leads to CLOT and then to cavity formation
MC cause= HTN
can be clinically SILENT to DEVASTATING (severe)
Avg age= 60 y.o.
cerebral MICROBLEEDS
primary brain parenchymal hemorrhage
blood fills the subarachnoid space
patient says “this is the worst headache I’ve ever had” (abrupt)
TUNIA MEDIA defect –> aneurysm
commonly recur
subarachnoid hemorrhage
ruptured saccular (BERRY) aneurysm is MC for _______ and in the _______ circulation
subarachnoid hemorrhage
anterior circulation