B114 Cerebrovascular diseases Flashcards
What are the 3 major types of cerebrovascular events
Thrombotic occlusion of vessels
Embolic occlusion of vessels
Vessel rupture
When does generalized cerebral ischemia occur?
With cariac arrest, shock, severe hypotension. Occurs once systolic pressure is less than 55 mmHg
Or when there is severe systemic hypoxia, due to inadequate respiration, ventilation, oxygen transfer, etc.
Symptoms of mild and severe generalized CNS hypoxia.
Mild:
-
Transient postichemic confusional state. Usually complete recovery. Neuronal death may occur in susceptible regions
- Hippocampal pyramidal neurons
- Purkinje cells of the cerebellum
- Neocortical pyramidal cells.
-
Border-zone, aka Watershed infarcts
- regions lying between the regions supplied by major arteries have the lowest perfusion, and may infarct during generalized hypoxia.
- The infarcts are wedge shaped at the most distal ends of the perfusion zones.
- These infarcts are hemorrhagic - encephalomalacia rubra, since flow is maintained by one of the two arteries of the border zone
Severe:
- Widespread neuronal death of all kinds
- If patients survive they often remain in coma’s or in PVS
- May awake with permanent deficits, or have clinical brain death, requiring artifical survival and isoelectric, flat EEG waves
- Brain dead patients on artificial life support will undergo progressive brain autolysis
Describe the progression of a CNS infarct, and all the terms for encephalomalacia
Encephalomacia: Softening of the brain after ischemia (osteomalacia softening of bone, encephalomalacia softening of brain)
Encephalomalacia alba: Pale white infarcted area devoid of blood
Encephalomalacia flava: Liquifactive necrosis gives the area a yellow color
Cysta post encephalomalacia: pseudocyst formation with astrocytes forming a reactive gliotic scar around the border.
Encephalomalacia rubra: only occurs in specific situations, in watershed regions, if reperfusion occurs.
What are the types and causes of focal ichemic events in the brain?
Transient ischemic attacks
Lacunar infarcts
Focal cerebral ischemia
What are the causes and risk factors for focal ischemia of the brain
Causes:
Embolus - these are most common.
- Arise from cardiac mural thrombi
- valvular disease/endocarditis
- atrial fibrillation
- healed myocardial infact and myocardial aneurysm.
- Ruptured plaques in the ascending aorta/carotids.
Thrombosis, especially Sinus venous thrombosis
- associated with hypercoagulable states
- polycytemia
- Oral contraceptives
- Paraneoplastic hypercoagulability
Rupture
- causing intracranial hemorrhage, next topic
Vasculitis
Describe the histological changes of an area of focal ischemia
Gross morphology:
- Up to 6 hours, no visible change
- 48 hours, tissue is soft, pale, and swollen encephalomalacia alba
- days 2-10, necrosis and autolysis is occuring, encephalomalacia flava
- day 10 thru 3 weeks, pseudocyst forma. csyta post encephalomalacia
Histology:
- for first 12 hours,
- ischemic neurons shrink and become very eosinophilic so called ‘red neurons.’
- cytotoxic and vasogenic edema also occur
- Endothelial and glial cells swell
- Myelinated fibers disintegrate
- up to 48 hours,
- neutrophils begin to infiltrate begining from the border of the infarct from the regions of in tact vasculature
- Following weeks
- macrophages and mononuclear cells invade, along with activated microglia
- phagocytosis and liquefaction occurs, cyst forms
- astroglial scar forms around the border of the peudocyst.
Describe the gross morphology and histology of brain affected by global ischemia
morphology:
- brain is swollen, wide gyri, narrow sulci
- poor demarcation between the gray and white matter on cut surface
Histology:
- Early changes: 12-24 hours
- acute neruonal change, shrinking and eosinophilia
- nuclear pyknosis and karyorrhexis
- similar changes occur to a lesser degree in astrocytes and oligos
- Subacute changes: 1 day - 2 weeks
- neutrophils invade areas of damaged tissue
- vascular proliferation
- reactive gliosis
- Repair
- replacement of infarcted regions by fibrotic glial scar.
Types of vasculitis that can cause focal CNS ischemia
Usually by oportunistic infections in immunocompromised patients:
- aspergillosis
- herpes zoster
- CMV
Or as part of polyarteritis nodosa.
Primary angiitis of the CNS: A vasculitis that affects small and medium sized subarachnoid vessels. Chronic inflammation causes diffuse encephalopathy and cognitive dysfunction.
Venous thrombosis
Symptoms are highly variable, depending on the location,
venous thrombosis near an end artery may produce ischemia, thrombosis of a venous sinus can range from totally asymptomatic to causing severe symptoms, coma, and death
chronic/subacute thrombosis of a dural venous sinus may produce hydrocephalus
What causes lacunar infarcts? What are their symptoms?
They are the most common type of CNS infarct. They are related to hypertensive cerebrovascular disease
i. Hypertension → hyaline arteriolar sclerosis of the deep
penetrating arterioles supplying the basal ganglia
ii. Arteriolar walls weaker and vulnerable to rupture.
iii. An important clinical and pathologic outcome of arteriolar
sclerosis is the development lacunar infarcts.
iv. These small localized infarcts are just a few millimeters wide
and are most commonly found in the deep gray matter, basal
ganglia and thalamus and internal capsule.
Depending on where exactly the infarct occurs, they can cause:
- Ataxia and hemiparesis
- Body sensory deficits
- Asymptomatic
What is hypertensive cerebrovascular disease and its major risks
The effects of hypertension on the brain. Increased risk for:
a. Intracerebral hemorrhage
b. Acute Hypertensive encephalopathy
c. Lacunar infarcts
Acute hypertensive encephalopathy:
- A sudden and sustained rise in diastolic blood pressure greater than 130 mmHg.
- Causes increased ICP.
- Global CNS dysfunction
- headaches
- confusion
- vominting
- seizures
- coma
- Brain edmea with or without herniations
- petechiae and fibrinoid necrosis of arterioles.
What is a Transient Ischemic Attack
A transient episode of neurologic dysfunction.
It is caused by ischemia, but is not severe or long enough to cause infarction and necrosis.
Symptoms: sudden focal neurologic deficits, paralysis, pareisis, numbness or loss of sensation.
TIAs by definition resolve within 24 hours.
No morphological or histological changes occur from TIA, but it is considered a serious warning sign for future strokes. 1/3rd of TIA patients have strokes within 5 years.
