10-31 NeuroPATH: Infarction and Hemorrhage Flashcards
epidural hematoma
—between skull and closely applied dura
—2° to head trauma (except qqf in kids)
—arterial bleed usu from MMA
—doesn’t usually cross suture lines?
subdural hematoma
—bleeding of bridging veins into potential space between dura and arachnoid
—usu slower but can be acute w/ severe trauma
Diffuse Brain Injury: DAI
Diffuse Axonal Injury —tearing of (usu. WM) axons —often in setting of MVA —due to acceleration/deceleration (worse when in coronal plane) —causes Wallerian degeneration —often leads to coma/PVS
Diffuse Brain Injury: Diffuse edema
complication of several forms of head injury
—For unknown reasons, swelling of one hemisphere may accompany an acute subdural hematoma on the same side.
—Bi- hemispheric swelling after head trauma appears in young children; thought to result from loss of normal vasoregulation which then leads to an increased cerebral blood flow
—incr ICP seen in this setting is due to increased intracranial blood volume
Diffuse Brain Injury: Diffuse Hypoxic Brain Damage
common in patients dying as a result of non-impact head injury
—A proportion of this damage is clearly related to a combination of one or more of the following, namely: brain shifts, raised intracranial pressure, systemic hypoxia and arterial spasm.
—Ischemic changes are often seen in the arterial boundary zones.
Diffuse Brain Injury: diffuse vascular injury
multiple small hemorrhages throughout the brain, associated with rapid death.
Focal Brain Injury types
- skull fx
- Contusions and Lacerations
- hemorrhages
most common cause of open injury
GSW!
penetrating vs. perforating GSWs
- penetrating: enters skull and does not leave (can ricochet though)
- perforating: goes in one side of head and out the other (exit wound in the skull is characteristically larger than the entry site)
Shaken Baby Syndrome
- s/sx
- long-term sequelae
- autopsy findings
S/SX: retinal hemorrhage, subdural and/or subarachnoid hemorrhages, and sometimes little or no external injury. Most subdural hematomas in infants are the result of abuse.
—SEQUELAE: seizures, vomiting, lethargy, coma, mental retardation, motor dysfunction, and death.
—AUTOPSY: Pathologic findings may also include white matter tears and DAI.
What’s the most common cause of spontaneous cerebral hemorrhage?
1 = hypertensive vascular disease
—Congenital (berry) aneurysms and vascular malformations are next in frequency
—Blood neoplasms and infections make up the remaining.
What is the pathogenesis of hypertensive cerebral vasulopathy?
The wall of a normal cerebral artery, unlike muscular arteries, lacks an external elastica and its media and adventitia are thinner.
—In long-standing ‘benign’ hypertension, the arteries respond by muscular hypertrophy which is often overshadowed by degenerative changes in the media and excess deposition of collagen in the adventitia.
—As these degenerative changes set in, the arteries lose their elasticity, elongate and acquire a tortuous course becoming prone to focal thrombosis.
—[[[[In accelerated or ‘malignant’ hypertension, on the other hand, the characteristic change is fibrinoid necrosis of arterioles.]]]]
Microaneurysms
—46% of HTN pts patients vs 7% normotensives. —(average 20 in number)
—basal ganglia along the smaller branches of the lenticulostriate aa, subcortical WM, pons and cerebellum, in that order of freeq.
—diameter is usually about 500 um; rarely up to 2 mm.
—wall formed by variable amounts of collagen and the rest is made up of hyaline amorphous material and blood clot in various stages of organization.
Lacunae
occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%). [WIKI]
Quickly: CNS consequences of systemic HTN
1) vascular changes (loss of elasticity)
2) microaneurysms
3) Hypertensive hemorrhages
4) lacunes.
Where do Berry Aneurysms bleed into?
subarachnoid space
Telangiectasias
—for the most part of no clinical importance.
—consist of multiple widened capillaries separated by normal neural tissue, an arbitrary point of distinction between telangiectasia and cavernous hemangioma.
—often seen in the pons.
Cavernous Hemangiomas
These not uncommonly result in recurrent hemorrhages (subarachnoid or intraparenchymatous) and focal seizures.
—consist of large, closely packed channels with no intervening neural tissue.
—Thick collagen bands lined with a single layer endothelium form the wall of these abnormal channels
—subcortical tissue in the region of the central fissure is frequently involved.
AVMs
-tortuous vascular masses usually in the leptomeninges though the brain itself may also be affected
—Unlike cavernous hemangiomas, the main arteries and veins leading to and from the mass are also enlarged.
—The abnormal channels consist of variable sized arteries and ‘arterialized’ veins.
Where does atherosclerosis occur most often in cerebrovascular disease?
more proximally: carotids, basilar aa., circle of willis/base of brain
—Not usually distal to that
autopsy finding with cerebrovascular dementia
granular atrophy of the cortex
Which parts of brian are exhibit “selective vulnerability” to ischemia?
—hippocampal and cerebellar Purkinje cells
—some neurons in certain layers of the cortex
**brain stem motor neurons & pontine neurons quite resistant
red neuron
most acute specific ∆ seen in the brain following ischemic event that is lethal to neurons
—6-8hrs to develop
Gross Path ∆s w/ Time s/p large infarct
2-3 days: swelling and discoloration
3-4 days: massive edema and early dissolution
~1 week: brain break down
3-4 wks: oatmeal
>1 mo: shrinking/clear/shiny
years: complete cavitation w/ no fibrosis
Microscopic Path ∆s w/ Time s/p infarct
0-6 hrs: minimal ∆s; ?edema
6-12: red neurons
12-24: endothelial cells react—>decr BBB effect —> pericellular edema; PMNs appear
24-36: BIG influx of PMNs
36-72: MOs replace neutrophils
72-mos: MOs remove dead tissue
7-9 days: astrocytes become reactive and begin forming gliosis ("glial scar")
weeks-months: CSF-filled cystCauses of Wallerian Degen
ischemia transecting white matter tract
—trauma—>DAI
NBTE
Nonbacterial thrombotic endocarditis
infarction due to local thrombosis vs. embolus
embolism causes hemorrhagic infarct b/c:
—embolism lodges, causes infarct
—gets dissolved
—distal area reprofused
Don’t lower BP too QUICKLY!
SERIOUSLY DON’T DO IT.
—cerebral autoregulation is out of whack; normal BP can cause hypoperfusion—> boundary zone (“Watershed”) infarct /
—can be laminar or cortical necrosis
consider looking up laminar vs cortical necrosis
don’t have time
venous infarctions of CNS
rare —cause horrible szs, herniation, death —venogram shows seemingly obliterated sup. sag. sinus —build-up of pressure causes hemorrhage –What Hillary Clinton had?
Hypertensive hemorrhages almost always occur in one of three sites:
1 Basal Ganglia
2 Cerebellar White Matter
3 Pons
germinal matrix hemorrhage
occurs in premature infants
