Cerebrovascular diseases & some problems with similar consequences

(= Brain disorders caused by pathologic processes involving blood vessels)

Basic problems important for us

• Thrombosis in a vessel Ischemia of the region supplied by that vessel

• Embolus in a vessel Ischemia of the region supplied by that vessel

• Rupture of a vessel Direct damage of the brain tissue + accompanying ischemia

• Generalized hypoperfusion (Shock) Global ischemia

• Severe hypoxia (high altitude, anemia, CO, cyanide…etc.)

• Severe hypoglycemia

Injury

Necrosis (Infarction)

…due to severe systemic hypotension (usually <50 mm Hg)

Introduction

• If the injury (or necrosis) occurs

acutely due to a vascular problem CVA (Cerebrovascular accident)

The clinical manifestations of CVA: -Stroke…the symptoms are irreversible -Transient ischemic attack (TIA)…the symptoms are reversible within 24 hours …in fact: less than 1 hour

Global cerebral ischemia

…if the insult is mild and short in duration: transient post

ischemic confusional state, with eventual complete

recovery

…if severe generalized ischemia: widespread neuronal

death…persistent vegetative state or more than this

(brain death)

…What is respirator brain?

…remember that neurons are more susceptible than glial

cells

…the most susceptible neurons:

-pyramidal cells of the hippocampus and neocortex

-Purkinje cells of the cerebellum

If you hear about “watershed” infarcts:

Focal cerebral ischemia …due to occlusion (thrombosis/embolus) or vessel rupture (hemorrhage)

*Embolic infarctions are more common than thrombotic ones

…most common source for emboli: mural thrombi (due to MI,

atrial fibrillation, valvular diseases)…also carotid artery, aortic

arch…etc.

…most common affected artery: middle cerebral artery

*Thrombotic occlusion:

…most common: carotid bifurcation, origin of middle cerebral

artery and either end of basilar artery

…Lacunar infarct: small infarcts only few millimeters…due to

damage of small penetrating arteries due to long-standing HTN

*Infarction due to thrombosis/embolus (occlusion) =

Nonhemorrhagic infarct…may evolve into hemorrhagic infarct

due to reperfusion (collateral flow or dissolution of embolus for

example)

Sequence of morphological changes in non hemorrhagic infarct: -first 6 hours: no change -12 hours: red neurons, cytotoxic edema -neutrophils then replaced by macrophages during 2-3 weeks -for months or even years: macrophages in a cavity (cyst) (remember that it is a liquefactive necrosis) -surrounding gliosis

We must differentiate between hemorrhagic and non hemorrhagic infarcts by imaging (significant difference in management)

Intracranial hemorrhage

The most common cause of spontaneous non traumatic intraparenchymal hemorrhage

…also can cause cortical microhemorrhages (<1mm)

Deposition of A beta amyloid that weakens vessel wall

Most common casue of nontraumatic SAH

Other causes: coagulopathies, tumors…etc.

Elsevier. Kumar et al. Robbins basic pathology 10th

More about subarachnoid hemorrhage (SAH)

*Adult polycystic kidney disease *Ehler-Danlos syndrome

*In the early period after a

subarachnoid hemorrhage, there is an

additional risk for ischemic injury from vasospasm of other vessels

The second most common cause of SAH after rupture of saccular aneurysm is arteriovenous malformation (AVM) …especially in males <40 years

Elsevier. Kumar et al. Robbins basic pathology 10th

Hypertensive cerebrovascular disease

• Hyaline arteriolar sclerosis of the deep penetrating arteries and arterioles

...supply the basal ganglia, the

hemispheric white matter, and

the brain stem

…affected arteriolar walls are

weakened and are more

vulnerable to rupture

• Minute aneurysms (Charcot-Bouchard microaneurysms)

…in vessels less than 300 μm in

diameter

Pathogenesis Complications *Massive intracerebral hemorrhage *Lacunar infarcts …due to occlusion of a single penetrating vessel …few mms …mostly: deep gray matter (basal ganglia and thalamus) …also internal capsule, deep white matter, pons …may be silent or clinically significant *Rupture of small-caliber penetrating vessels …this leads to small hemorrhages …these bleeds resorb, leaving a slit-like cavity (slit hemorrhage) surrounded by brownish discoloration *Acute hypertensive encephalopathy …sudden sustained increased diastolic pressure …increased intracranial pressure with headache, confusion, vomiting…may also: convulsions and coma …edema +/- transtentorial or tonsillar herniation

Brain trauma • Contusion…rapid tissue displacement and disruption of vascular

channels

• Concussion…reversible loss of consciousness,

temporary respiratory arrest, and loss

of reflexes

…neurologic recovery is the norm

…amnesia for the event persists

…if recurrent may end in chronic traumatic

encephalopathy…initially described in boxers

(dementia pugilistica)…cognitive impairment, parkinsonism and later

development of neurodegenerative processes

• Laceration…tissue tearing

• Diffuse axonal injury…due to angular acceleration, even in the absence

of impact…responsible for 50% of coma cases after

trauma…swollen axons

• Intracranial hemorrhage

Check https://en.wikipedia.org/wiki/Coup_contrecoup_injury for references

modified

Brain trauma, intracranial hemorrhage

• Epidural (extradural)

…always skull fracture (except

infants)

…dural vessels (middle

meningeal artery)

…lucid interval: patient can be

normal for several hours

before signs appear

• Subdural…bridging veins…thin-walled in infants and stretched in brain atrophy

• Subarachnoid

• Intraparenchymal