CNS Pathology

Part 3. Trauma and cerebrovascular diseases

A. Trauma
a. Epidural hematoma rupture of middle meningeal artery as result
of trauma
i. branch of maxillary artery
ii. commonly with skull fracture at pterion of temporal bone
iii. rapid expansion with high arterial pressure
1. can lead to transtentorial herniation
iv. Presentation
1. momentary loss of consciousness
2. lucid period usually 30 minutes or so
3. headache, nausea, hemiparesis
v. physical exam CN III palsy
vi. imaging "biconvex disk" on CT
vii. Treatment evacuation of blood/lower intracranial pressure

b. Subdural hematoma rupture of bridging veins where they enter

the superior sagittal sinus results in slow venous bleeding below the
dura mater
i. slow expansion with low venous pressure delayed symptoms
ii. populations at greatest risk: elderly individuals, alcoholics
1. atrophied brain makes veins more vulnerable
2. blunt trauma, shaken baby
iii. Presentation: nausea, headache
iv. Imaging: "crescent-shaped" on CT
v. Treatment evacuation of blood/lower intracranial pressure

Epidural (biconvex) Subdural

(crescent)

B. 85% infarction vs. 15% hemorrhage

a. Infarction causing liquefactive necrosis, leading to cyst formation

b. Subarachnoid hemorrhage rupture of an aneurysms

i. commonly berry aneurysm (lack of media layer)
 1. MC location is anterior cerebral or anterior
communicating
2. At the bifurcation
ii. populations at greatest risk
1. Marfan's, Ehlers-Danlos, APCKD or an AVM
iii. complaints of "worst headache of my life"
iv. Lumbar puncture blood/yellow spinal tap
v. Complications hydrocephalus, further hemorrhage, permanent
neurologic deficits
vi. Treatment
1. evacuation of blood/lower intracranial pressure
2. calcium channel blockers
a. mediates risk of vasospasm following breakdown of
blood
b. 2-3 days post rupture
c. Parenchymal hematoma
i. cause/contributing factors
1. hypertension
2. amyloid angiopathy
3. diabetes mellitus
ii. MC location is basal ganglia and internal capsule
iii. Symptom based on mass effect of surrounding structures

C. Global hypoxic injury

a. Due to cardiac arrest, shock, chronic CO poisoning
b. Complications cerebral atrophy, watershed infarcts, and stroke

Apoptotic (red) neurons: w. pyknotic nuclei within space

D. Ischemic brain diseasestroke

a. Acute onset of focal neurologic deficits resulting from
i. diminished blood flow (ischemic stroke)
ii. hemorrhage (hemorrhagic stroke)
iii. irreversible damage after 5 minutes
b. Most vulnerable brain regions
i. hippocampus, cortex (layer 3,5,6), cerebellum, and
watershed areas (dual-supply)
c. Risk factors
i. Diabetes
ii. Smoking
iii. atrial fibrillation
iv. cocaine
d. Etiology
 i. 35% - atherosclerosis of the extracranial vessels (carotid
atheroma)
ii. 30% - cardiac and fat emboli, endocarditis
iii. 15% - lacunar
iv. 10% - parenchymal hemorrhage
v. 10% - subarachnoid hemorrhage

e. Types of stroke
i. thrombotic/atherosclerotic infarct
1. most common type of stroke
2. most preceded by a transient ischemic attack
a. focal neurologic dysfunction
3. anemic/pale (liquefactive necrosis)
a. not re-perfused
b. forms cystic cavity with reactive gliosis
4. usually at periphery of cortex supplied by MCA
ii. embolic infarcts
1. hemorrhagic/red infarct
2. due to reperfusion once embolus is degraded
3. commonly from left heart (atrial fibrillation) or
atherosclerotic plaques
4. middle cerebral artery at greatest risk
iii. lacunar infarcts
1. occur in areas supplied by small perforating vessels
2. mainly basal ganglia
3. caused by hyaline arteriolosclerosis
4. risk factors
a. atherosclerosis
b. hypertension
c. diabetes

f. Imaging

i. CT without contrast for acute presentation

1. important to diagnose as ischemic or hemorrhagic

2. bright on diffusion weighted MRI in 3-30 minutes and

remains bright for 10 days

3. dark on CT in 24 hours

ii. MRI for subacute

iii. vascular studies of intra and extracranial vessels

g. Histology

i. red neurons (12-28 hours)

 ii. necrosis + neutrophils (24-72 hours)

iii. macrophages (2-3 days)

iv. reactive gliosis + vascular proliferation (1-2 weeks)

v. glial scar (> 2 weeks)

h. treatment
i. For occlusive disease give tPA if within 3 hrs
ii. For embolic disease and hypercoagulable states give
warfarin/aspirin once the hemorrhagic stroke has been ruled out
i. hemorrhage
i. hemorrhagic stroke
1. intracerebral bleeding often due to aneurysm rupture
2. may be secondary to ischemic stroke following
reperfusion
ii. watershed infarcts
1. occurs at areas at border of two arterial supplies
2. often follow prolonged hypotension
3. damage is usually bilateral, deep cortical areas

Carotid/Ophthalmic Monocular Blindness

MCA Aphasia, neglect, hemiparesis, gaze preference, and homonymous
hemianopsia
ACA Leg paresis, hemiplegia, and urinary incontinence
PCA Homonymous hemianopsia
Basilar Artery Coma, cranial nerve palsies, apnea, drop attack, and vertigo
Lacunar stroke
Pure motor (internal capsule affected) or sensory stroke (thalamus
affected), dysarthria, and ataxic hemiparesis