11.1.1 Clinical Presentation

A previously healthy 69-year-old, right hand–dominant woman was brought to the emergency department (ED) with sudden-onset right middle cerebral artery (MCA) syndrome while driving. She was last seen well 45 minutes prior to arrival in the ED. Initial vital signs show a blood pressure of 168/72 mm Hg and a regular heart rate of 86 beats per minute, and were otherwise normal. Neurological examination was notable for right gaze preference, left homonymous hemianopsia, dysarthria, left hemiparesis, hemibody sensory loss affecting the face, upper and lower extremities, and left hemineglect with somatagnosia. Total National Institutes of Health Stroke Scale (NIHSS) score was 10.

On further history, she denied headache, nausea, or vomiting. A detailed review of systems was negative. She had no known past medical history and did not take regular medications. She was a lifelong nonsmoker, rarely drank alcohol, and there was no recreational drug use history.

11.1.2 Imaging Workup and Investigations

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  Noncontrast computed tomography (NCCT) of the head showed absence of hemorrhage. The ASPECTS score was 9, with 1 point deducted for loss of gray-white matter differentiation in the right insular ribbon. CT angiography (CTA) of the head and neck was significant for an abrupt cutoff of the right MCA in the distal M1 segment (Fig. 11.1a, b).

  
  
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  CT perfusion (Fig. 11.1c–f) demonstrated a small area of severely decreased relative cerebral blood volume (rCBV) and relative cerebral blood flow (rCBF) in the right parietal lobe. There was, however, a large area of increased mean transit time (MTT) and time to maximal residue (Tmax) noted in the right lateral frontal, temporal, and parietal lobes, with sparing of the right lentiform nucleus. Appearances therefore indicated a large area of perfusion mismatch in the right MCA territory.

  
  
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  Laboratory investigations were normal, including complete blood count, creatinine, and coagulation profile. Electrocardiography demonstrated no evidence of cardiac ischemia.

  

11.1.3 Diagnosis

Right MCA territory ischemic stroke secondary to acute right M1 occlusion.

11.1.4 Treatment

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  In the absence of contraindications, intravenous (IV) thrombolysis was initiated in the ED and the patient was promptly transported to the angiography suite for intra-arterial thrombectomy.

Technique

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  An 8-Fr vascular sheath was placed following groin access, and a 6-Fr Shuttle sheath was advanced over a 5-Fr diagnostic catheter. The 5-Fr catheter was used to select the right internal carotid artery, and a diagnostic injection demonstrated filling defect consistent with thrombus in the distal right M1 segment (Fig. 11.2a).

  
  
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  The 6-Fr shuttle sheath was positioned in the distal cervical internal carotid artery. The angiographic catheter was removed and the intermediate aspiration catheter was advanced over a coaxial system of the 0.027″ Marksman microcatheter over a 0.016″ Fathom microwire.

  
  
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  The right MCA was selected using the microwire and the microcatheter tip was positioned distal to the thrombus in the inferior M2 segment. The guidewire was removed and a 4 × 20 mm stent retriever was introduced. The device was deployed across the thrombus (Fig. 11.2b) and the microcatheter was removed. The aspiration catheter was advanced to the face of the thrombus and connected to the aspiration system.

  
  
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  The stent retriever was then partially withdrawn into the aspiration catheter until flow arrest, signaling capturing of the thrombus between the stent retriever and the aspiration catheter. The stent retriever and aspiration catheter were then removed as a unit. The guide catheter was allowed to back-bleed, and when no thrombus was seen, it was flushed forward. Follow-up angiography of the right anterior circulation demonstrated complete recanalization and reperfusion (Fig. 11.2c, d).

  

Follow-up

Follow-up MRI on postoperative day 1 demonstrated limited infarct burden, with patency of the right MCA. Perfusion-weighted imaging shows normalization of the previously seen perfusion mismatch (Fig. 11.3).

Paroxysmal atrial fibrillation was diagnosed on extended cardiac monitoring following discharge, and was felt to be the most likely stroke etiology in this patient.

11.2.1 Clinical Presentation

A 77-year-old, right hand–dominant woman was brought to the emergency department with moderate aphasia, right facial droop, and right upper extremity paresis and numbness. She was last seen well 5 hours prior. Initial blood pressure was 93/65 mm Hg, with a regular heart rate of 116 beats per minute. Neurological exam, with head-of-bed at 60 degrees, was remarkable for decreased verbal expression and intermittent ability to follow single-step commands, inability to move right arm against gravity, a prominent right lower facial droop, and right arm numbness. Total NIHSS score was 8. Repeat examination after IV fluid administration, at a systolic blood pressure of 150 mm Hg, with head-of-bed at 5 degrees, showed improved fluency and comprehension of speech as well as right arm pronator drift and improvement in facial droop, with persistent arm numbness. Repeat NIHSS was 4. Past medical history was notable for medically controlled hypertension and dyslipidemia. The patient has no prior history of stroke.

11.2.2 Imaging Workup and Investigations

NCCT of the head showed a focus of calcification in vicinity of proximal left MCA. CTA of the head and neck demonstrated a calcified and stenotic M1 segment of the left MCA, with no significant extracranial carotid disease (Fig. 11.4a, b). Left MCA territory distal to the stenosis demonstrated CT perfusion abnormality, with increased Tmax and MTT, reduced rCBF, and relatively normal rCBV (Fig. 11.4c–e).

11.2.3 Diagnosis

Hemodynamically significant proximal M1 segment of MCA stenosis due to intracranial atherosclerotic disease.

11.2.4 Treatment

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  The patient was placed on bedrest and initiated on antiplatelet and statin therapy. She was admitted to the neurocritical care unit for neuromonitoring and hypertensive therapy. Transthoracic echocardiogram confirmed normal cardiac function.

  
  
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  IV fluids and vasopressors were administered, with close volume status and blood pressure monitoring. Postural and activity tolerance gradually improved over subsequent days under careful medical supervision.

  
  
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  Systolic blood pressure target to >160 mm Hg was maintained for more than 3 months as the patient had recurrent intermittent and transient right upper limb numbness lasting several minutes at a time.

  
  
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  Blood pressure target was subsequently gradually normalized. The patient was asymptomatic at 9-month follow-up.

11.3.1 Clinical Presentation

A 57-year-old, right hand–dominant woman with poorly controlled vascular risk factors presented with a history of slurred speech and mild right hemiparesis on awakening. She was last seen well 9 hours previously. Neurological examination showed mild dysarthria, right facial droop, and right pronator drift, for a total NIHSS score of 4.

Past medical history was significant for long-standing, uncontrolled systolic hypertension, insulin-dependent type 2 diabetes mellitus, obstructive sleep apnea, and obesity. She was a current smoker, with a 20-pack-year history of tobacco use. She did not consume alcohol or take recreational drugs.

11.3.2 Imaging Findings

MRI demonstrated a small diffusion-restricting lesion involving the posterior limb of the internal capsule on the left (Fig. 11.5a). MR angiogram showed no evidence of intracranial large artery occlusion or atherosclerotic disease (Fig. 11.5b).

11.3.3 Diagnosis

Lacunar infarct involving the posterior limb of the left internal capsule.

11.3.4 Treatment

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  After confirming safety to swallow, aspirin (ASA) 325 mg was administered orally in the ED, followed by ASA 81 mg daily.

  
  
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  Three antihypertensive agents were then sequentially initiated, titrated over days to achieve a blood pressure target of 110 to 140/60 to 90 mm Hg. High-dose statin was initiated, with target low-density lipoprotein (LDL) level of < 80 mg/dL (2 mmol/L).

11.4.1 Background

The three cases discussed earlier illustrate the common presentation of an MCA syndrome due to three different etiologies: M1 occlusion such as from an embolic source, hemodynamic stroke with M1 stenosis, and perforator stroke. However, only the patient with acute MCA occlusion is a candidate for acute endovascular therapy. Consideration of the physiology and pathophysiology associated with cerebral ischemia is important to understand these differential diagnoses.

Impaired regional perfusion is at the basis of symptoms and signs associated with cerebral ischemia. Normal physiology ensures cerebrovascular autoregulation over a large range of mean arterial pressure, to ensure maintenance of blood flow (CBF) above ischemic threshold. In general, normal cerebral function is maintained at a mean CBF of approximately 50 mL/min/100 g of brain tissue. Below this threshold, transient loss of function of the affected cerebral region may become clinically apparent, with chance of normalization with early reestablishment of normal CBF. However, if CBF falls and remains under 10 to 12 mL/min/100 g of brain tissue at any time, infarction occurs. The threshold for irreversible infarction increases over time, and stabilizes at 17 to 18 mL/min/100 g of the brain tissue by 3 hours.

This physiological basis of regional cerebral ischemia implies that clinical presentations are almost exclusively reflective of hypoperfused parenchymal neuroanatomical structures, but may not directly relate to stroke etiology. Therefore, an MCA syndrome may result from loss of anterograde blood flow in an acute M1 segment occlusion, from relative hypoperfusion distal to a high-grade MCA stenosis, or from a perforator vessel occlusion resulting in a lacunar stroke. In other words, any ischemic insult to the frontoparietal motor and sensory cortices or tracts may result in a clinical syndrome of hemiparesis, numbness, and dysarthria. Therefore, appropriate triage and emergent neuroimaging is essential in differentiating between stroke etiologies, and allowing appropriate case selection for emergency endovascular treatment through early identification of large-vessel occlusions. A similar situation exists in the posterior circulation, where, for example, differentiation between a basilar artery occlusion, basilar stenosis with hypoperfusion, and perforator infarction is essential in order to instigate appropriate management.