Chapter 2 Clinical-Anatomical Syndromes of Ischemic Infarction
Ischemic stroke can be defined as a sudden focal neurological deficit corresponding to a vascular distribution. Brain imaging techniques allow us to visualize lesions with great anatomical precision. However, optimal interpretation of the information provided by neuroimaging requires having detailed knowledge of the arterial anatomy (Figures 2-1 through 2-4) and the vascular territories of the brain (Figure 2-5).
CAROTID BIFURCATION OCCLUSION
A 61-year-old man with history of coronary artery disease, previous myocardial infarction, and multiple vascular risk factors presented to the emergency department with global aphasia and right hemiplegia for more than 6 hours. On examination, he was drowsy and exhibited forced left gaze deviation, right hemianopia, right flaccid hemiplegia involving the arm and the leg to similar degree, and absent response to pain on the right side. Diffusion-weighted imagery (DWI) of the brain revealed a large area of ischemia in the left hemisphere, including the territories of the anterior and middle cerebral arteries (Figure 2-6). Fluid-attenuated inversion recovery (FLAIR) sequence showed no parenchymal hyperintensity but disclosed extensive hyperintense signal in the left middle cerebral artery consistent with fresh thrombus (Figure 2-7). Magnetic resonance angiography (MRA) of the intracranial circulation confirmed the presence of a left carotid terminus occlusion (Figure 2-7). The patient was subsequently diagnosed with acute myocardial infarction and a left ventricular mural thrombus. His neurological condition deteriorated over the following 48 hours, and he expired after care was restricted to palliative measures.
MIDDLE CEREBRAL ARTERY OCCLUSION
A 65-year-old man with history of hypertension presented with acute global aphasia and right flaccid hemiplegia involving the lower face, the arm, and, to a lesser degree, the leg. He also had a dense right visual field deficit and profound right sensory loss. Magnetic resonance imaging (MRI) with DWI revealed extensive ischemia in the territory of the left MCA (Figure 2-13). T2* sequence disclosed a hypointense signal in the left MCA indicative of acute vessel thrombosis and MRA confirmed the left M1 occlusion (Figure 2-14). Atrial fibrillation was noted on cardiac telemetry. Over the following 48 hours, the patient developed fatal brain swelling (see Figure 2-14).
Territorial MCA Infarction
Deep Middle Cerebral Artery Infarction
Superficial Divisional Middle Cerebral Artery Infarction
Superficial Cortical Infarctions
Hemispheric Border-Zone Infarctions
ANTERIOR CEREBRAL ARTERY OCCLUSION
A 65-year-old man presented to the hospital with acute onset of left crural paresis. He had suffered a myocardial infarction 2 weeks before and was taking aspirin and clopidogrel for secondary prevention of coronary events. Examination revealed left leg weakness predominantly involving the proximal flexor muscles and associated with hyperreflexia. MRI demonstrated acute infarction in the right ACA distribution (Figure 2-24). Echocardiogram disclosed a mural thrombus overlying a hypokinetic segment of the left ventricle. The patient was anticoagulated and recovered well with physical therapy.
ANTERIOR CHOROIDAL ARTERY OCCLUSION
POSTERIOR CEREBRAL ARTERY OCCLUSION
A 68-year-old woman with a history of atrial fibrillation on chronic anticoagulation presented to the hospital with acute behavioral changes, visual disturbances, and right hemiparesis. On examination, she was somnolent, had poor short-term recollection, dense right hemianopia, mild right hemiparesis, and profound right hypoesthesia. Her INR was subtherapeutic because the patient had recently stopped taking warfarin for a dental procedure, and she had opted not to replace it with subcutaneous low-molecular-weight heparin. MRI of her brain showed a large left PCA infarction and MRA disclosed proximal occlusion of this vessel (Figure 2-28). Despite some functional recovery over the following 6 months, her visual and cognitive disturbances remained disabling.
TABLE 2-2 Visual field disturbance caused by PCA infarction.
Bilateral PCA infarction |
Cortical blindness |
Bilateral altitudinal hemianopia |
Unilateral PCA infarction |
Macular sparing hemianopia |
Temporal crescent paring hemianopia |
Quadrantanopia |
Isolated macular hemianopia (rare) |
VERTEBROBASILAR DISEASE

Figure 2-33 Computed tomography scan of the brain showing a massive infarction in the vertebrobasilar territory.
A 64-year-old woman was found unresponsive in her bathroom by her husband. She was intubated by the paramedics and transported to our emergency department. On arrival, she was comatose and breathing at a rate of 40 to 45 per minute. She was tachycardic and hypertensive. Her pupils were slightly anisocoric (3.5 mm on the left and 3 mm on the right), and responses to light were minimal on the left and absent on the right. Corneal and oculocephalic reflexes were preserved. Best motor responses to pain were in the form of withdrawal. DWI showed restricted diffusion in the midcerebellum and mesencephalon (Figure 2-34). A hyperintense signal in the basilar artery indicative of acute thrombosis was visualized on FLAIR. Conventional angiography confirmed occlusion of the basilar trunk. She underwent successful basilar recanalization by intra-arterial thrombolysis combined with mechanical disruption of the clot. Despite reperfusion, the patient failed to improve neurologically. Repeat MRI showed established infarction throughout the midbrain. Patient expired shortly after her family requested withdrawal of artificial life support.
Combination of ophthalmoplegia with motor, sensory, or coordination deficits |
Crossed motor or sensory findings |
Acute ataxia with inability to walk |
Sequential appearance of bilateral Babinski signs* |
Sequential appearance of bilateral weakness |
Acute reduction in the level of consciousness |
* It can also be seen in patients with incipient craniocaudal herniation from massive supratentorial infarctions.
CEREBELLAR INFARCTIONS
Posterior Inferior Cerebellar Artery Infarction
A 38-year-old woman presented with severe neck and posterior head pain, dizziness, gait imbalance, and right-hand clumsiness. Her examination predominantly demonstrated right appendicular ataxia. Brain imaging disclosed a large right PICA stroke with incipient mass effect (Figure 2-38). Vascular imaging revealed a right vertebral artery occlusion, most likely due to dissection. The patient was carefully monitored in the stroke unit, and as she developed mild confusion and restlessness, repeat imaging was performed showing worsening swelling with displacement of the fourth ventricle, effacement of the subarachnoid cisterns, distortion of the brainstem, and dilatation of the temporal horn of the right lateral ventricle. The patient immediately underwent suboccipital craniectomy. She improved substantially after surgery and achieved good functional recovery over the ensuing 6 months.
Anterior Inferior Cerebellar Artery Infarction
Superior Cerebellar Artery Infarction
Cerebellar Border-Zone Infarctions
BRAINSTEM INFARCTIONS
Medullary Infarctions
The main ischemic medullary syndromes are illustrated in Figure 2-42.
A 75-year-old man was admitted with sudden onset of dysphagia, dysarthria, and gait imbalance. He had long-standing history of hypertension and poorly controlled type 2 diabetes. On examination, he had left miosis and ptosis, dysarthria, difficulty swallowing his saliva, left ataxia, and decreased sensation to pain and temperature on the right side. He developed uncontrollable hiccups in the emergency department. CT scan was not informative, but DWI demonstrated a left lateral medullary infarction with associated ischemia of the left cerebellum (Figure 2-43). The PICA was not seen on noninvasive angiogram and considered to be occluded. Irregularities in other intracranial vessels indicated widespread intracranial atherosclerosis. The patient required temporary placement of a percutaneous gastrostomy tube for safe feeding but subsequently made a favorable recovery with moderate residual dysarthria and ataxia.
Wallenberg’s Syndrome
Pontine Infarctions
The main ischemic pontine syndromes are illistrated in Figure 2-44.
A 63-year-old man developed acute onset of slurred speech, gait imbalance, left-sided weakness, and horizontal diplopia. Initially he did not seek medical attention because “he did not like doctors who always found something wrong with him,” but after more than 12 hours of persistent deficits, his family convinced him to go to the hospital. On examination, he had mild dysarthria, right abducens palsy, right facial weakness, left arm and leg weakness, and mild axial and right appendicular ataxia. CT scan showed an area of possible hypoattenuation of the right pons, which was subsequently confirmed by MRI with DWI (Figure 2-45). MRA of the intracranial vessels disclosed atherosclerotic midbasilar stenosis (see Figure 2-45), which was likely the culprit for the pontine stroke by occluding a paramedian penetrating branch. During the hospitalization the patient was diagnosed with hypertension, diabetes mellitus, and hyperlipidemia. He was discharged on antiplatelet therapy, a statin, an angiotensin-converting enzyme (ACE) inhibitor, and an oral hypoglycemic agent. He achieved fair functional recovery with the help of intensive physical and occupational therapy. He remained compliant with the medications and has not had recurrent symptoms of posterior circulation ischemia.
Midbrain Infarctions
The main ischemic midbrain syndromes are illustrated in Figure 2-46.
A 60-year-old man with history of hypertension and heavy smoking was acutely evaluated in the emergency department for sudden onset of diplopia and right hemiparesis. On examination, he was hypertensive and had a left oculomotor nerve palsy and right hemiparesis with upper motor neuron pattern. CT scan was suspicious for an area of hypoattenuation in the middle aspect of the midbrain, and MRI scan confirmed the diagnosis of acute mesencephalic infarction (Figure 2-47). No significant intracranial stenosis was noted on MRA. The patient was kept on antiplatelet therapy, and measures to control his vascular risk factors. The deficits remained stable and moderately disabling at 4 months. He has continued to smoke.
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