Topic 17-19 Neuroradiology and CVA Flashcards
Define cerebrovascular accident (CVA/stroke)
Stroke definition
Rapidly developing clinical signs and symptoms of focal and/or global loss of cerebral function, caused by vascular dysfunction. Symptoms last longer then 24 hours.
Define transient ischaemic attack (TIA)
• Transient Ischemic Attack (TIA) – focal neurological deficit that lasts less than 24hrs
o an embolus lodges in a cerebral artery causing temporary ischemia, a brief interval when normal neuronal functions are disrupted
o the embolus breaks up soon after, and neurological function is restored
o NO permanent damage
S&S include blurred vision, slurred speech, loss of coordination, weakness/numbness in arm or leg (same as an actual stroke)
List the mechanisms that may be responsible for cerebral infarction
MECHANISMS OF BRAIN DAMAGE
A critical shortage of energy (energy crisis)
Excitatory Amino Acid Injury
Cerebral Oedema
Explain these mechanisms of brain damage
A critical shortage of energy (energy crisis)
Excitatory Amino Acid Injury
Cerebral Oedema
A critical shortage of energy (energy crisis)
- A drop in cerebral perfusion, hypoxia, protracted hypoglycemia and severe anemia can cause a critical shortage of energy (energy crisis)
- Blood glucose levels below normal limits for 10-20 minutes and seizures lasting 1-2 hours also cause permanent brain damage
- Lack of energy initially causes electrical failure and, if it lasts long enough, arrest of all cellular functions and cell death
Excitatory Amino Acid Injury
• Glutamate is the principle excitatory neurotransmitter
• Responsible for many higher level funcitons
• Prolonged ischaemia results in an accumulation of extracelluar glutamate
• Resulting in an increase in calcium in cells (calcium cascade results) leading to cell death
• Neuroprotectants can reduce the amount of cell death
Cerebral Oedema
• Vasogenic oedema (integrity of blood brain barrier is disrupted allowing fluid from capillaries to escape into extracellular fluid that surrounds brain cells)
• Cytotoxic oedema (increase in fluid in intracellular space
List the major risk factors of cerebrovascular disease.
- Hypertension – stress, familial
- Diabetes
- Heart Disease – particularly atrial fibrillation
- Smoking
- Increased blood fat levels
- Obesity
Explain the pathophysiology of a stroke
also explain the penumbra
Pathophysiology of damage to brain following a stroke
• Without oxygen and sufficient nutrients (glucose) the neurons become energy depleted, and are unable to generate ATP
Critical shortage of energy( ENERGY CRISIS)
• Consequently, they are unable to fuel the ionic pumps (NA+ K+ pump) which maintain the ionic gradient across the neuronal membrane.
• This leads to depolarisation of the neuronal membrane ceasing synaptic function and conductivity.
o Depolarisation causes the release of glutamate (neurotransmitter)into the synaptic cleft
o In an energy depleted state, the glutamate is unable to be cleared from the extracellular space, thus an excessive amount is left - toxic
• Causes the opening of Ca channels, with an INFLUX of Ca, Na and Cl
• Extra intracellular Ca (Ca cascade) activates a series of destructive enzymes that allow the release of cytokines and mediators
o Loss of cellular integrity (cell wall destroyed)
• Inflammatory response is initiated and eventually cell death.
Pathology involved in the penumbra area following a stroke
Penumbra: the area of brain tissue at the periphery of the ischemic region.
• Here neuronal damage develops much slower as collateral flow from adjacent blood vessels keep cerebral perfusion above the threshold for immediate cell death
• Ischemia is severe enough to cause electrical failure
o Prompt medical management with thrombolytic agents to break down the clot will restore circulation in the penumbra, hopefully preventing structural damage in the area to limit neurological deficit.
Describe briefly the pathologies of
cerebral infarction and
intracranial haemorrhage (subarachnoid and intracerebral)
Ischaemic Stroke (80% of strokes)
• A cerebral artery becomes blocked from either thrombosis or an embolism.
• An embolus may travel from either the heart (or extracranial vasculature (carotid arteries), lodging in a cerebral artery.
• As blood flow is obstructed, the brain tissue supplied by the artery becomes ischemic and deprived of nutrients. Rapid effects as brain does not store glucose and is incapable of anaerobic metabolism
Haemorrhagic Stroke (10-15% of strokes) • Intracerebral 10%: weak deep penetrating arteries burst, spilling blood into and around the brain tissue • Subarachnoid 5-10%: weak blood vessel bursts, leaking blood into the subarachnoid space
• Haemorrhage (irritant to brain cells), ischemia (of intended tissue) and oedema (causing localised pressure injury) cause destruction of the brain tissue
• Most commonly caused by aneurysms which occur at branching points of blood vessels
o Here the blood vessel walls are subject to increased stress which over time can gradually weaken them, causing them to balloon
o Aneurysms form (Saccular most common), others include fusiform, dissecting and giant
Describe briefly the loss of function consequent to Stroke/ occlusion of the internal carotid artery, middle cerebral artery, anterior cerebral artery, posterior cerebral artery and vertebral and basilar arteries
EDIT THIS
Internal carotid artery
Supplies:
• optic nerves and retina;
• cortex and deep white matter of frontal and parietal lobes;
• lateral aspects of temporal and occipital lobes;
• corpus callosum (except posterior portion);
• most of basal ganglia and internal capsuleternal carotid artery
Bifurcates into ACA & MCA therefore a stroke here would be a
TACS (Total anterior circulation stroke)
Involves all 3 of the following:
Unilateral weakness and or sensory deficit of face arm and leg
Homonymous hemianopia (contralateral)
Higher cerebral dysfunction
*may experience other symptoms as well
Describe various neuroradiological findings for CVA
CT: can quickly rule out Hemmorage , may show penumbra
MRI: can diagnose ishemic hemmoragic stroke and other problems involving the brainstem ect
PET: Detects early stage of disease
Define completed stroke
and stroke in evolution
Completed stroke – the signs and symptoms of the stroke become stable.
• Stroke in evolution – other symptoms such as tingling in the face or hands persist. Medical management is required.
Pathology of a lacunar stroke
Pathology of a lacunar stroke (20% of all strokes)
- Occlusion of deep penetrating arteries of major cerebral arteries
- Result in small infarcts in the deeper structures of the brain (eg basal ganglia, thalamus, white matter) and brain stem
- can cause as severe neurological deficit as a much larger hemispheric infarct, without the life threatening cerebal oedema
Define and discuss TACS stroke
Total anterior circulation stroke
Large cortical stroke to ACA & MCA
All 3 of the following:
Unilateral weakness(and or sensory deficit) Face,arm,leg Homonymous hemianopia Higher cerebral dysfunction
Define and discuss PACS stroke
Partial anterior circulation stroke
Cortical stroke to ACA OR MCA
Two of the following:
Unilateral weakness(andor sensory defecit) face,arm,leg
Homonymous hemianopia
Higher cerebral dysfunction
Define and discuss POCS stroke
Posterior circulation syndrome
(vertibro-basilar artery territory)
One of the following:
Cerebellar or brainstem syndromes
Loss of conciousness
Isolated homonymous hemianopia
Define and discuss LACS stroke and symptoms
Lacunar syndrome
Subcortical stroke due to small vessel disease
No evidence of higheer cerebral dysfunction but
One of:
Unilateral weakness ( and or sensory deficit)
(Face+ arm , Arm+leg or all 3)
Pure sensory stroke
Ataxic hemipariesis
