Cerebro vascular accident (CVA )
Q1: What are the common causes of CVA?
Cerebrovascular disease can be
- due to a thrombotic process in the vessel
- large vessel disease
- Small vessel disease
- from an embolus from the heart
- from inadequate cerebral blood flow due to decreased perfusion pressure
- from rupture of a vessel.
Q2: What is the consequence to occlusion of cerebral vessel?
- Infarction of brain occurs in the distribution area of the affected vessel.
- Approximately 80% are ischemic infarction and 20% are hemorrhagic infarcts.
Q3: What are the available imaging procedures and their utility for the evaluation of CVA?
- The first diagnostic study which should be performed in patients with suspected stroke is a non contrast CT.
- In the acute setting, CT is used to differentiate ischemia from hemorrhage.
- Evidence of hemorrhage will be a contraindication to the use of thrombolytic or anticoagulant agents.
Q4: What are the advantages and disadvantages of CT?
- Advantages of CT are widespread access, noninvasiveness, and speed of acquisition.
- CT, however, does have several disadvantages:
- it provides limited information about the nature and age of an ischemic stroke during the crucial first three hours
- it has limited capacity to show vascular lesions in the brain stem and cerebellum and small ischemic infarctions deep within the cerebral hemispheres.
Q5: What are the advantages and disadvantages of MRI?
- Advantages
- MRI can also help define intra cerebral hemorrhages, old and new.
- MRI is more sensitive than CT for the early diagnosis of brain infarction.
- With MRI, you can determine the precise location and size of the infarction and follow the lesion over time.
- Lacunar infarcts and small cortical strokes are seen with higher sensitivity.
- MRI scanners with the ability to perform FLAIR images (fluid-attenuated inversion recovery) and DWI (diffusion-weighted images) are very useful in showing infarcts early after onset of symptoms.
- DWI images are useful in distinguishing acute from chronic ischemic changes.
Q6: Does a normal CT or MRI rule out stroke?
- No.
- It is important to remember that in patients with ischemia who do not yet have infarction, both CT and MRI may be normal.
- Repeating the CT in 48 hours will most likely demonstrate the stroke lesion.
Q7: What are the imaging findings of stroke ?
Acute Stroke (up to 7 days):
- MR imaging of the brain is far more sensitive than CT imaging to recognize acute infarction.
- Diffusion wtd. pulse sequence (DW imaging) is the most sensitive MR sequence to demonstrate stroke. This sequence is sensitive to restricted diffusion within the cell from stroke-induced cytotoxic edema and the region of acute stroke is seen as an area of bright signal on DWI . Cytotoxic edema can occur immediately after the initial insult, thus DWI images can reveal the area of acute infarct immediately after the insult.
- Intra vascular contrast enhancement, another sign of early stroke .
- Sulcal effacement, gyral edema , loss of gray-white matter interface can occur within 12 hours of stroke.
- Parenchymal contrast enhancement , mass effect and hemorrhage can occur within 1-7 days of insult.
Sub acute Infarct (1 to 8 weeks):
- Contrast enhancement slowly decreases in time but can persist for 8 weeks, with decreasing mass effect and abnormal signal intensity.
Old Infarct:
- Focal area of encephalomalacia.
- Porencephalic dilatation of adjacent ventricle.
- Residual old blood products may be present.
Q8: Once CVA is confirmed, You must attempt to confirm the pathophysiology behind the CVA.
- This is based largely on history and physical, but also incorporates imaging studies.
- Embolic stroke
- An EKG can exclude atrial fibrillation.
- All patients with suspected embolic stroke should have a TTE.
- Trans esophageal echocardiography (TEE) can exclude ascending aortic atheromatous disease or clot in the left atrial appendage.
- Trans thoracic echocardiography (TTE) can exclude left ventricular thrombi in patients with CHF or a previous MI.
- A TEE should be performed if the TTE, preliminary cardiac and vascular imaging tests do not clarify the cause.
- Furthermore, extra cranial and intra cranial arteries should be studied as possible sources of emboli.
- The anterior circulation can be studied using duplex ultrasound of the neck and trans cranial Doppler of the intra cranial arteries.
- CT angiography or MR angiography can be performed.
- A conventional angiography is warranted when the screening tests do not identify the lesion.
- The posterior circulation can also be studied with duplex Doppler.
Q9: What do you expect to assess from the imaging procedures in the evaluation of CVA?
- The most important initial distinction is differentiating ischemic from hemorrhagic stroke utilizing non contrast CT.
- Once it has been determined that the patient has an acute ischemic stroke, consideration should be given to the use of thrombolysis.
- Patients must meet very specific criteria in order to receive thrombolytic therapy.
- After completing this initial assessment, the subsequent evaluation focuses on determining the underlying pathophysiology of the stroke in order to further direct therapy.
- This step incorporates the use of carotid and trans cranial Doppler ultrasonography, TTE, MRA, CT angiography, and conventional angiography.
- In ischemic stroke, you need to distinguish between embolic and thrombotic stroke.
- In patients with thrombotic stroke, it is important to assess whether it is large or small vessel disease.
- The location and size of a brain infarct on CT or MRI can aid in distinguishing between stroke subtypes.
- Small sub cortical infarcts are commonly in the basal ganglia, internal capsule, thalamus, and pons and are caused by lacunar infarctions.
- Large sub cortical infarcts are commonly caused by thrombosis or embolism.
Q10: Describe the evolution of changes in CT following CVA.
- An infarcted brain is pale initially.
- Within hours to days, the gray matter becomes congested with engorged, dilated blood vessels and minute petechial hemorrhages.
- The development of edema within the brain produces subtle parenchymal hypo density changes and mass effect.
- These initial edematous changes are characterized as a loss of distinction between gray and white matter (blurring of the gray-white interface).
- As the ischemic insult continues, there is mounting cellular death and a combination of cytotoxic and vasogenic edema occurs.
- This produces areas of parenchymal hypo attenuation in the region of the affected artery.
- Finally, as the infarct progresses, mass effect develops and progresses to sulcal effacement and ventricular compression.
- When an embolus blocking a major vessel migrates, lyses, or disperses within minutes to days, re circulation into the infarcted area can cause a hemorrhagic infarction and may aggravate edema formation due to disruption of the blood-brain barrier.
- After 24 hours, a cerebral or cerebellar infarct is usually a hypo dense area involving both the gray and white matter in a typical vascular distribution.
- The mass effect initially increases due to edema and is at its maximum 3-5 days post infarct.
- The mass effect usually resolves within 7-10 days.
- This hypo attenuation may regress completely and is related to the breakdown of infarcted tissue, cell wall lysis, leaking of intracellular proteins, and reduction of the edema.
- Chronic ischemic infarcts are characterized by hypo density and sharply demarcated margins.
- As the tissue continues to break down and phagocytosis occurs, the parenchyma is replaced with a cystic CSF-filled space.
- A primary intra cerebral hemorrhage damages the brain directly at the site of the hemorrhage by compressing the surrounding tissue.
- Clot formation occurs within 1-2 hours in this area.
- The brain is unable to repair itself, forming only fibrogliotic scar tissue at the site of infarction or hemorrhage.
Q11 What are the CT findings of plain infarct?
- Three early CT signs of acute cerebral infarction are
- blurring of the clarity of the internal capsule
- loss of distinctness of the insular ribbon cortex
- loss of differentiation between the cortical gray and subjacent white matter.
- Accumulation of intracellular fluid causes swelling of the cortical gyri resulting in sulcal effacement.
- Parenchymal hypo density can be detected in 45-85% of cases with larger lesions associated with a worse prognosis.
- Early focal brain swelling occurs in 40% of patients.
- Interestingly, hyper density of a major cerebral vessel can be detected by CT within minutes of vessel thrombosis and hours before parenchymal changes occur.
- Acute
- Sub acute
- ICH commonly occurs in the putamen/internal capsule, caudate nucleus, thalamus, pons, or cerebellum.
- Acute intraparenchymal bleeding is readily seen as a white density located within the brain tissue.
- Occasionally, intraparenchymal hemorrhage will extend into the subarachnoid space and ventricles.
- Intraparenchymal bleeding (especially if supratentorial) will cause a shifting of the adjacent structures away from the area of hemorrhage.
- Importantly, in adults, the falx cerebri can be calcified, leading to confusion about whether or not blood is present in the inter hemispheric fissure.