13.1.1 Clinical Presentation

A 61-year-old male patient presented with a headache and visual disturbance for 3 days. On arrival to the emergency department (ED), the patient had an episode of seizures with tongue bite. Associated comorbidities include hypertension and moderate valvular aortic stenosis.

13.1.2 Imaging Workup and Investigations

The patient underwent CT angiography and perfusion. CT images were unremarkable with no evidence of loss of gray-white differentiation or hypodensity in the posterior fossa (Fig. 13.1). Postcontrast CT images showed atheromatous plaque causing near-total stenosis of the V4 segment of the left vertebral artery.

MR imaging performed later showed infarction involving left cerebellar hemisphere confirming to superior cerebellar artery territory (Fig. 13.2), multiple punctate infarcts involving thalami, and bilateral parieto-occipital region (Fig. 13.3). Susceptibility-weighted imaging (SWI) showed the absence of hemorrhagic transformation. Diffusion-weighted imaging–fluid-attenuated inversion recovery (DWI–FLAIR) mismatch suggestive of hyperacute nature of infarction was present.

3D time of flight (TOF) MR angiography revealed significant stenosis involving V4 segment of the left vertebral artery with significant stenosis involving proximal basilar artery (i.e., exaggerated stenosis due to flow-dependent nature of TOF angiography). Postcontrast MR angiography revealed similar findings as in TOF angiography.

Conventional angiography confirmed stenosis involving the V4 segment of the left vertebral artery with mild stenosis of the proximal basilar artery. The stenosed segment of the vertebral artery was treated with thromboaspiration and stent placement.

13.1.3 Diagnosis

Severe stenosis involving left vertebral artery with mild stenosis involving proximal basilar artery.

13.1.4 Treatment

Mechanical thrombectomy by thromboaspiration and stenting.

13.1.5 Outcome

The patient showed significant improvement of motor weakness, cerebellar ataxia, and left superior quadrantanopia.

13.2.1 Clinical Presentation

A 77-year-old female patient presented with right faciobrachiocrural hemiplegia and motor aphasia. Clinical examination revealed an NIHSS score of 20. The patient was a case of paroxysmal atrial tachycardia and dyslipidemia. The patient was not a candidate for thrombolysis due to the recent history of surgery and established stroke.

13.2.2 Imaging Workup and Investigations

MR imaging performed at the peripheral hospital showed ischemic changes involving the left parietal region, insular cortex, head of the caudate nucleus, and posterior aspect of the lentiform nucleus. Axial FLAIR showed hyperintense vessel sign involving cortical branches of the left MCA suggestive of slow arterial flow along with multiple foci of encephalomalacic changes involving right parietotemporal and left frontal region. 3D TOF MR angiography showed abrupt cutoff involving M1 segment of the left MCA with gradient images showing susceptibility vessel sign. No evidence of hemorrhagic transformation on gradient recalled echo images. CT angiography showed occlusion at the level of M1 MCA on the left side along with significant mismatch on perfusion imaging. The patient underwent mechanical thrombectomy with complete recanalization of MCA (TICI 3).

13.2.3 Diagnosis

Left middle cerebral artery thrombosis.

13.2.4 Treatment

Mechanical thrombectomy with complete recanalization (TICI 3).

13.2.5 Outcome

MR imaging performed postthrombectomy showed no increase in the size or extent of ischemic changes (Fig. 13.4).

The patient was treated with speech, physio, and ergotherapy. The patient showed partial improvement of motor weakness with an NIHSS score of 7 and modified Rankin scale of 4 at the time of discharge.

13.3.1 Background

The radiologists in training are the ones to perform an initial evaluation of stroke imaging in emergencies usually. Hence, the awareness of early signs of ischemia becomes necessary for accurate and reliable diagnosis especially in challenging situations such as imaging on low strength magnets (≤1.5 T) using fast imaging sequences (time is brain).

13.3.2 Early Signs

The early and useful signs of hyperacute stroke to be recognized on MR imaging include the presence of hyperintensity on trace images with low apparent diffusion coefficient (ADC) values (i.e., restricted diffusion); FLAIR hyperintense vessel (FHV; Fig. 13.5) sign in involved vascular territory (i.e., ACA, MCA, and PCA territories); susceptibility vessel sign suggestive of thrombosis with prominence of deep medullary veins on T2*GRE or SWI; vascular stenosis or occlusion on 3D TOF angiography; and the presence of intramural T1 hyperintensity on 3D VISTA suggestive of dissection; abnormalities including decreased cerebral blood volume (CBV), cerebral blood flow (CBF), and increased mean transit time (MTT) and time to peak (TTP) on perfusion-weighted imaging (PWI). ^{1 ,​ 2 ,​ 3 ,​ 4 ,​ 5 ,​ 6 ,​ 7}

13.4.1 Diffusion-Weighted Imaging

DWI is a technique based on spin echo echoplanar imaging which utilizes different gradient strengths and magnitude (b-value) to look for tissue differences in the rate of diffusion. It comprises imaging at different b-values (i.e., 0 and 1,000 for routine clinical imaging). Although the b-values can be varied from 1,000 to 3,000, high b-value DWI only accentuates the hyperintense signal on trace images without any significant change in sensitivity to diagnose an infarction. ^{8 ,​ 9} The DWI comprises of b = 0, trace, and ADC images for each slice position. Calculation of the ADC values helps in the quantification of the degree of restriction of water motion. The presence of restricted diffusion is suggested by hyperintensity on trace images with the corresponding hypointensity on ADC images (i.e., low ADC values). The presence of significantly low ADC values is usually associated with the irreversible nature of infarct, tissue necrosis, and increased risk of hemorrhagic transformation post intravenous or endovascular management. ¹⁰

DWI shows a sensitivity of 75 to 95% in the detection of lacunar stroke. However, DWI can be negative in large arterial stroke and lacunar infarction due to imaging performed either before the appearance of changes on DWI or because of hypoperfusion severe enough to cause symptoms in lacunar strokes but not enough to cause restricted diffusion or due to its size smaller than the slice thickness and interval. ^{11 ,​ 12} In cases with suspected stroke showing the absence of restricted diffusion, the lack of flow-related enhancement on TOF involving cerebral vasculature; the presence of thrombus along with prominent deep medullary veins on T2*GRE/SWI involving M1–M4 segments of MCA, A1 and A2 segments of ACA, P1 and P2 segments of PCA; and the presence of FHV sign on 2D FLAIR along with perfusion abnormalities should highlight the presence of ischemia. In addition, the presence of FHV sign on FLAIR, visualization of deep medullary and cortical veins on gradient, and SWI with perfusion abnormalities also indicate the presence of salvageable cerebral parenchyma (i.e., penumbra).

Along with depicting early signs of ischemia, DWI also throws some light on the likely etiology of stroke depending on the distribution of the vascular lesions. Involvement of multiple vascular territories and diffuse nature suggests embolic origin; involvement pertaining to a vascular territory suggests thrombotic etiology; unilateral involvement and infarcts in border zone territory suggests hypoperfusion as in ICA stenosis and bilateral diffuse watershed infarcts with involvement of basal ganglia and hippocampus with or without cerebral cortical involvement; and predominantly perirolandic involvement is suggestive of hypoxia–hypoperfusion complex.

The radiologist needs to be aware of imaging findings in hyperacute stroke as they are subtle and can be missed easily. Stroke onset shows a diurnal variation with the majority of them presenting early in the morning. ¹³ In cases with wakeup stroke, the presence of DWI–FLAIR mismatch serves as a reliable marker in the identification of hyperacute stroke less than 4.5 hours which aids in the selection of patients for reperfusion therapy since the hyperintense signal on FLAIR is visualized in all patients after 7 hours. ¹⁴

The presence of susceptibility artifacts in the basifrontal and temporal region can mimic areas of restricted diffusion in some cases. The knowledge of the occurrence of such artefacts and comparison with available previous imaging helps us avoid the misdiagnosis.

13.4.2 Fluid-Attenuated Inversion Recovery

FLAIR is an inversion recovery-based sequence which suppresses the signal from cerebrospinal fluid and accentuates visualization of signal intensity changes involving cerebral parenchyma.

The predominant role of FLAIR imaging in stroke is in the identification of DWI–FLAIR mismatch, the presence of FHV sign, to differentiate between coexisting hyperacute and subacute infarct and depict parenchymal changes of differential etiology. However, early visualization of altered signal intensity (<6 hours) involving cerebral parenchyma is associated with increased risk of hemorrhagic transformation of infarct due to posttherapeutic intervention. ¹⁵

The presence of FHV sign is attributed to large vessels occlusion and retrograde leptomeningeal collaterals. It serves as an indirect marker of the penumbra, associated with smaller lesions, decreased rate of infarct progression, and better prognosis, and disappears spontaneously about 10 days after reperfusion. ^{16 ,​ 17 ,​ 18}