17 Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

Clinical Presentation

A 39-year-old HIV-positive man was admitted to the infectious diseases unit after developing mild speech disturbance and hypesthesia of his right face. An opportunistic infection or lymphoma was suspected, but MRI revealed an ischemic cortical stroke in the left middle cerebral artery (MCA) territory. An intracranial MR angiogram (MRA) demonstrated a proximal M2 branch occlusion of the left MCA (Fig. B17.1 and Fig. B17.2). There were no known vascular risk factors. His symptoms improved spontaneously and a diagnostic workup was initiated. No heparin or antiplatelet therapy was given. Five days later his condition acutely worsened, with severe right-sided hemiparesis and marked aphasia. He was then transferred to the stroke unit for further evaluation and treatment (National Institute of Health Stroke Scale [NIHSS] score: 10).

Initial Neuroradiologic Findings

Following transfer to the stroke unit, a cerebral MRI revealed a large left-sided infarct in the striatum extending into the parietal lobe. The intracranial MRA now demonstrated a left proximal M1-MCA occlusion (Fig. B17.3 and Fig. B17.4).

Suspected Diagnosis

Ischemic reinfarction in the left MCA territory caused by M1-MCA occlusion.

Questions to Answer by Ultrasound Techniques

Was there evidence of atherosclerotic change or vasculitis in the extracranial brain-supplying arteries?
Was there a sustained left M1-MCA occlusion?
If so, was there evidence of collateral leptomeningeal blood flow via the anterior (ACA) and/or posterior (PCA) cerebral arteries?

Initial Neurosonologic Findings (Day 1)

Extracranial Sonography

B-mode sonography revealed a single echogenic atherosclerotic plaque in the left carotid bifurcation at the origin of the internal carotid artery (ICA). Doppler spectrum analysis showed a flow signal with marked reduced flow velocity in the left ICA (flow velocity 24/8 cm/s). Flow signals in the right ICA (flow velocity 58/23 cm/s) as well as in both external carotid arteries (ECAs) and the vertebral arteries (VAs) were normal (Fig. B17.5, Fig. B17.6, Fig. B17.7).

Transcranial Duplex Sonography

In projection of the left M1-MCA segment within the sylvian fissure no flow signal was detectable. The terminal left C1-ICA segment showed a flow pattern similar to the extracranial ICA (31/16 cm/s). In the left A1-ACA (flow velocity 147/70 cm/s) and proximal P2-PCA (flow velocity 94/47 cm/s) segments there was increased nonturbulent flow indicating leptomeningeal collateralization. Normal flow velocities were seen in all the right cerebral arteries and in both ophthalmic arteries (OAs) (Fig. B17.8–Fig. B17.13; see also Video B17.1).

Conclusion

Left proximal M1-MCA occlusion of unknown origin. Leptomeningeal collateral blood flow via the left ACA and PCA.

Conventional Angiography (Day 3)

Digital subtraction angiography (DSA) was performed to exclude or confirm cerebral vasculitis. Proximal occlusion of the left M1-MCA segment was seen. Smooth borders at the contrast block were suggestive of thrombotic occlusion. There was distinct leptomeningeal collateralization via the left anterior and posterior cerebral arteries (Fig. B17.14, Fig. B17.15, Fig. B17.16).

Fig. B17.17 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries.

Fig. B17.1 Cerebral MRI, apparent diffusion coefficient (ADC) map, axial plane. Territorial MCA infarct in the left-sided temporal lobe and anterior insula 2 days after the initial event (arrowheads).

Fig. B17.2 Intracranial contrast-enhanced MRA, axial maximal intensity projection (MIP). Absent signal in a prominent M2-MCA branch suggestive of left proximal MCA branch occlusion (arrowhead).

Fig. B17.3 Cerebral MRI, ADC map, axial plane. Acute infarction predominantly in the left striatum 7 days after the initial event. Note the isointense residual temporal infarct (arrowhead).

Fig. B17.4 Intracranial 3D TOF-MRA, axial MIP. In contrast with the first MRA, there was a proximal left M1-MCA occlusion (arrowhead). Note the fetal-type PCA in the contralateral side and the increased vessel signal of the left PCA main stem indicating collateral flow.

Clinical Course

In view of the recent cerebral infarction, no systemic thrombolysis was performed. Considering the underlying immunosuppressive disease, absence of vascular risk factors (no thrombophilia, no findings predisposing for cardiac embolism), infective cerebral vasculitis was suspected. However, cerebrospinal fluid (CSF) analysis did not support this hypothesis, revealing only an intrathecal IgG synthesis, consistent with the known HIV infection. A mild hyperlipidemia was thought to be due to the antiretroviral therapy, but this was not sufficient to be the only causal factor. Cardiac embolism was ruled out as far as possible. An artery-to-artery embolism from the extracranial left ICA plaque was considered to be a potential trigger of the initial vessel occlusion that then led to progressive in-situ thrombosis with an adjacent extension of the clot. Besides the two-step embolism from the ICA plaque, primary HIV-related in-situ thrombosis with secondary extension also seemed possible. Secondary stroke prevention was started with aspirin. The patient was transferred to another hospital for rehabilitation. Over the next few weeks his neurologic deficits improved only marginally. The patient was then lost to follow-up.

Fig. B17.5 Extracranial duplex, longitudinal plane. B-mode imaging reveals a mildly hyperechoic atherosclerotic plaque in the left carotid bifurcation with extension to the proximal ICA (arrows).

Fig. B17.6 Extracranial duplex, longitudinal plane. Markedly reduced flow in the left ICA (flow velocity 24/8 cm/s).

Fig. B17.7 Extracranial duplex, longitudinal plane. Normal flow signal in the right ICA (flow velocity 58/23 cm/s).

Fig. B17.8 TCCS (transtemporal approach), left-sided insonation, upper pontine plane. Left terminal C1-ICA with flow signal, similar to the extracranial ICA (flow velocity 31/16 cm/s). Absent signal within the unusual bright sheath of the left M1-MCA (arrowheads).