Cerebrovascular diseases

10.1.3.1.1. Stroke

Acute neurologic deficit syndromes that result from brain parenchyma infarction have ischemic origin in 80% of the cases. These can occur as a result of embolisation or vessel occlusion.

Hemorrhagic infarcts make up 15% of strokes. The underlying cause is usually hypertension, but vascular malformation, aneurysm rupture, cerebral amyloid angiopathy, tumor bleeding and the hemorrhagic transformation of ischemic infarcts can all lead to cerebral hemorrhage.

Moreover - as a rather common cause - patients with coagulopathies (mostly the ones receiving antithrombotic therapy) can also suffer hemorrhagic stroke.

The remaining (5%) of the patients can suffer spontaneous subarachnoid hemorrhage that most often results from brain aneurysm (on the branches of Circle of Willis) or from vascular malformations.

Etiological differentiation of ischemic infarcts:

Infarcts of microangiopathic origin can be lacunar infarcts that develop due to the complete or the partial occlusion of the cerebral arterioles. They predominantly occur at the basal ganglia, thalamus, internal capsule and the pons.

Biswanger’s disease (subcortical arteriosclerotic encephalopathy) is also results from microangiopathy.

Infarcts due to hemodynamic changes can occur as a result of perfusion reduction at the end-arteries or at the border-zone (watershed) regions.

Thromboembolic infarcts show a territorial distribution restricted to the supplied areas of certain arteries.

1: Lacunar infarcts MRI, FLAIR.

2: Binswanger's disease, CT

3: Left posterior border-zone infarct, CT

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Cerebral infarcts (ischemic)

CT:The primary goal of the diagnostics is to rule out hemorrhage, for which CT is very sensitive. It is essential to differentiate ischemic stroke from hemorrhagic stroke because their therapeutic approaches and consequences are fundamentally different. When bleeding is excluded, based on the neurologic assessment of the patient (deficit, age of stroke etc.) thrombolytic therapy can be initiated by the neurologist either as a generalized (intravenous) or a local procedure (selective thrombolysis – perormed by a radiologist -).

In hyperacut infarctus(12 órán belül) . A CT kép normálisnak tűnhet ez esetek 50-60 %-ában. A hyperdens arteria jel (Gács jel), melyet az arteria lumenén belűli thrombus

hyperdensitása okoz a folyó vérhez képest kb az esetek 25-50 % -ában látható az érben. Ez leggyakrabban az a. cerebri media főága, néha kisebb ágai is, de a. basilaris thrombosis esetén is látható lehet az érben a hyperdensitás. Igen korai jel lehet a nucleus lentiformis határainak elmosódása.

CT angiographiával jól ábrázolódik az érelzáródás okozta telődési hiány MRI vizsgálattal a diffusió súlyozás (DWI) igen korán mutatja az infarctus kiterjedését.

In acute phase (12-24 hours after the occlusion of the middle cerebral artery) on CT hypodense basal ganglia, the loss of cortical white-grey matter differentiation and sulcal effacement are the characteristic imaging findings. On MRI, diffusion restriction causes hyperintense signal on T2W images. The leptomeningeal border of the infract zone will show contrast enhancement.

After 1-3 days the ―mass-effect‖ of the infarct increases. It is more apparent in case of large territorial infarcts, the sulcal effacement completes, the loss of cortical white matter and grey matter differentiation is more pronounced (especially in the white matter) due to the increased hypodensity. Hemorrhagic transformation in the grey matter (cortex, basal ganglia) can also occur at this stage. It is worth to note, that for hemorrhagic transformation one should not always blame thrombolytic therapy; it rather occurs spontaneously in a great majority of the cases.

After 4-7 days the edema and the ―mass-effect‖ persist, there is a marked hypodensity and even contrast enhanced CT can detect enhancement at the leptomeningeal border of the infarct zone.

Within 1-8 weeks contrast enhancement and mass-effect still persist. Later a slow regression in the mass-effect can be noted. In children (transient) calcification can also occur.

In the chronic phase of the infarct (months to years) the hypodensity of the lesion (CT) reaches the level of the cerebrospinal fluid. There is no more contrast enhancement, the lesion is well differentiated and it degenerates into a cyst secondary to encephalomalacia. The brain parenchyma experiences a volume decrease due to the degeneration (sometimes calcifications can occur at the marginal border of the infarct).

Diffuse arterial sclerosis and elevated hematocrit may increase the arterial density, both mimicking hyperdense media sing, and leading to differential diagnostic problems.

 For the record: acute and chronic stages of the ischemic infarct may differ in various educational centers.

113 4. a-c: CT: territorial infarction of the left MCA. Hypodensity progression from early acute to

later subacute stages

5. Chronic right MCA infarction CT.

6. Right hyperdense MCA sing, CT.

7. Hyperacute infarction in the right basal ganglia, DWI.

10.1.3.1.2. Cerebral venous sinus thrombosis:

Usually, cerebral sinus thrombosis occurs secondary to the propagation of a local infection.

Sinus thrombosis can be caused by mastoiditis or extradural cervical infections, but also it can occur as the complication of intradural infections (meningitis or abscess). Sometimes

dehydration, coagulopathies and cerebrospinal trauma can be the cause of the thrombosis. In sinus thrombosis 2/3rds of the patients are female, in half of the recurring cases the use of oral contraceptives is reported and 1/3rd of the women have thrombophilia. The most common location for thrombosis is the superior sagittal sinus followed by the transversal sinus and the sigmoid sinus. The thrombosis of the carvernous sinus (usually infectious origin:

thromboplebitic complication) is a very dangerous condition. Internal venous thrombosis usually results in the bilateral necrosis of the basal ganglia (+ thalamus, hypothalamus, or cerebellum can also be involved).

The CT appearance of a thrombotic vein/sinus, similarly to an occluded artery, is hyperdense.

A very characteristic sign is the loss of enhancement in the thrombotic segment (―empty delta sign‖), that can only be confirmed unequivocally if the slice is perpendicular to the sinus (MDCT reconstruction). The infarct edema shows a delayed appearance and it is a frequent complication of cerebral venous/sinus thrombosis. It shows a different

localization/distribution than the ones seen in arterial territorial occlusion. Hemorrhages occurring adjacent to the sinus can also cause an obstruction in the blood flow of the sinus.

Non contrast enhanced MRI shows loss of signal void, while a loss of contrast enhancement can be noted in contrast enhanced examinations.

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8. Empty delta sign in the left sigmoid sinus, CTA

9. Left transverse and sigmoid sinus thrombosis MR (PC sequence)

10.1.3.1.3. Hemorrhages

Parenchymal hemorrhage most often occurs in patients with hypertension, after malignant hypertensive states. The initial localization for its occurrence is at the basal ganglia

(putaminal-claustral hemorrhage) that can extend into the ventricles or to the subarachnoid space. The mean age of these patients is usually younger than that of the ones with ischemic infarcts.

Bleeding usually originates from saccular ―berry‖ aneurysms (on the branches of the Circle of Willis). Aneurysm rupture besides subarachnoid hemorrhage can also cause intraparenchymal bleeding when it breaks into the parenchyma.

The so called lobar hemorrhage is usually caused by tumor bleeding, hemorrhagic vascular malformations, rebleeding of ischemic infarcts. Bleeding secondary to cerebral amyloid angiopathy frequently occurs in the elderly without prevalent hypertension. It often presents as a sequential hemorrhage, each bleeding following one another, resulting in various ages of hemorrhages.

On CT images acute bleeding always presents as hyperdensity. (One has to keep it mind that hyperdensity of the blood is affected by the hematocrit levels, hence making the diagnosis more difficult.) Intraparenchymal blood is dominated by a destructive appearance (mass-effect) and it is surrounded by hypodensity as a sign of perifocal edema. It often breaks into the ventricles. In patients lying in a supine position they collect (sediment) at the occipital horn of the lateral ventricles, creating a hyperdense liquid-to-liquid levels. Later on, the density of blood decreases and shows a peripheral ring or rim-like contrast enhancement without mass-effect.

Although, subarachnoid hemorrhage (SAH) is most often caused by the rupture of a berry aneurysm, arteriovenous malformation (AVM) and trauma can also lead to it. SAH is typically located at the basal subarachnoid spaces, which then propagates along the lateral fissures or it fills up the interhemispheric fissure till the convexities. The main collection of the blood is usually indicative of the source of origin. In cases of parenchymal spread the mechanism, whether it broke in, or it broke out from the parenchyma could represent a differential diagnostic challenge. When accompanied by brain edema, the consequent herniation can result in parenchymal infarcts as well.

CT angiography examination is usually advisory in order to confirm the site of the bleeding. It is also effective when a hemorrhagic tumor is in the differentials, although complete

differentiation might only be achieved by follow-up examinations. CTA is also essential in the diagnostics of multiple aneurysms (which are prevalent in 20-30% of the cases based on autopsy reports.) In case of a subarachnoid hemorrhage the consequently developing

115 hydrocephalus and its degree might only be detected on follow-up CT examinations. It is very important to note that an initial brain aneurysm rupture might be followed by a second one within the first 7 – 10 days and the resulting vasospasm carries a much higher risk of mortality than the one at the time of the first SAH. This is why the scrutonius review of the acute diagnostic imaging is essential and it plays a fundamental role in patient treatment.

Open brain surgery of the aneurysm (clipping) has been replaced by catheter angiography (DSA) nowadays. The aneurysm is either filled up with thrombogenic coils through its neck or recently bypassing stents are inserted to exclude the aneurysm from the cerebral

circulation. of ischemic infarction in the right

MCA territory.

Central nervous system tumors can be of various origins:

Neuroepithelial cell tumors: astrocyte, oligodendrocyte, ependyma, cells of the pineal gland, neurons and ill- differentiated, embryonic tissue cell tumors

Nerve sheath cell tumors: neurilemmoma, neurofibroma, neurosarcoma Mesenchymal cell tumors: meningioma, meningiosarcoma, melanoma

Other tumors and tumor-like masses: primary lymphomas, vascular tumors, other

neuroepithelial tumors (craniopharyngioma, dermoid, epidermoid), vascular malformations, adenohypophyseal tumors, regional tumors with local infiltration (glomus tumor,

paraganglioma, chordoma).

Metastases