Any artery or arterial branch may be affected by ischemic stroke, with corresponding symptoms related to the location and size of the infarct. The diagnosis and management of stroke are discussed in Chapter 19.
The MCA territory includes the majority of the cerebral hemisphere, including portions of the frontal, temporal, and parietal lobes with the exception of the anterior, medial, and superior frontal lobes and the medial and superior parietal lobes (supplied by the ACA), and the occipital and inferior temporal lobes (PCA territory) (Fig. 7–8). The functional regions supplied by the MCA therefore include the motor and premotor regions, somatosensory cortex, the frontal eye fields, the language areas (found on the left in the majority of patients), parietal regions responsible for spatial attention (right parietal lesions may cause left-sided neglect), and the superior and inferior radiations of the visual pathways as they pass through the parietal and temporal lobes, respectively. Therefore, a full left MCA syndrome causes right hemiplegia and hemisensory loss, aphasia, gaze deviation toward the left, and right homonymous hemianopia. A full right MCA syndrome causes left hemiplegia and hemisensory loss, left-sided neglect, gaze deviation to the right, and left-sided homonomyous hemianopia. Gaze deviation is discussed in Chapter 11 and visual field deficits in Chapter 6.
MCA infarct. Axial CT scan demonstrating full-territory left MCA infarct. Note spared areas including: A: caudate (supplied by recurrent artery of Huebner), thalamus (supplied by PCA), ACA and PCA territories, as well as the medial temporal lobe (B). Note also hyperdense left MCA in B (see Ch. 19 for explanation of this sign).
The MCA stem is called the M1 segment of the MCA. The MCA stem gives off the lenticulostriate penetrating branches that supply the basal ganglia and internal capsule before dividing into superior and inferior branches known as the M2 segments. The superior M2 branch of the MCA supplies Broca’s area (most commonly on the left), the motor cortex, and the superior visual radiation, whereas the inferior M2 branch supplies Wernicke’s area (most commonly on the left) and the inferior visual radiation. The M2 segments divide into further branches—the smaller and more distal the vessel occluded in ischemic stroke, the smaller the corresponding deficit. However, if a small penetrating (lenticulostriate) branch of the MCA stem is affected, this can affect the convergence of descending motor fibers and lead to a complete contralateral hemiparesis despite a small infarct (pure motor lacunar syndrome; see “Lacunar Strokes” below).
The MCA stem is quite poorly collateralized, and MCA stem occlusion (proximal to the origin of the lenticulostriate branches) can lead to a large subcortical infarct with sparing of more distal regions if there is good collateral flow distally (Fig. 7–9).
MCA stem infarct. Axial diffusion-weighted MRI (DWI) demonstrating ischemic infarct in the territory of the MCA stem on the right.
The ACAs supply the anterior, superior, and medial frontal lobes and the superior and medial parietal lobes—essentially all of the frontal and parietal lobes not supplied by the MCAs (Fig. 7-10). Due to the position of the leg area in the motor homunculus (medial; see Ch. 4), ACA strokes cause contralateral leg weakness and sensory loss more so than face and arm weakness and sensory loss. ACA strokes can also cause cognitive changes such as abulia. The ACAs are connected by the anterior communicating artery. Proximal to the anterior communicating artery, the ACAs are labeled A1 segments; distal to the anterior communicating artery, they are labeled A2 segments.
ACA infarct. Axial diffusion-weighted MRI (DWI) demonstrating ischemic infarct in the territory of the right ACA.
In some patients, both ACAs arise from a common trunk (azygous ACA). Occlusion of both ACAs simultaneously can cause acute paraplegia, mimicking acute spinal pathology. The presence of cognitive symptoms usually distinguishes bilateral ACA infarction from acute spinal cord pathology.
The ACAs can also be compromised by subfalcine herniation (see Ch. 25).
One typically learns that the MCA supplies the face and arm areas on the lateral surface of the homunculus and the ACA supplies the leg area, so that MCA strokes cause contralateral face and arm weakness much more so than leg weakness, and ACA strokes cause contralateral leg weakness much more so than face and arm weakness. This is true for strokes affecting the cortical surface. However, the motor fibers join subcortically and travel together, so a stroke that affects the subcortical white matter pathways can cause a complete contralateral hemiparesis or hemiplegia affecting the face, arm, and leg (e.g., a lacunar stroke in the posterior limb of the internal capsule or a full MCA territory infarct affecting the cortex and subcortical white matter).
Recurrent Artery of Huebner Territory Infarction
The recurrent artery of Huebner is a branch of the ACA that supplies the head of the caudate and the adjacent internal capsule. Infarction can cause contralateral hemiparesis and/or movement disorder, which may be accompanied by cognitive deficits.
Anterior Choroidal Artery Territory Infarction
The anterior choroidal artery branches directly from the internal carotid artery and supplies the posterior thalamus (including the lateral geniculate nucleus) and the internal capsule (including descending motor and ascending thalamocortical pathways). Infarction in the territory of the anterior choroidal artery can cause contralateral visual field defects, contralateral hemiparesis, and/or contralateral hemisensory loss, and can also cause cortical signs (e.g., neglect if the right hemisphere is affected) due to interruption of thalamocortical pathways.
The PCAs supply the occipital lobes, inferior medial temporal lobes, and the thalami (Fig. 7–11). Depending on the extent of infarction in the PCA territory, deficits can include contralateral homonymous hemianopia or superior quadrantanopia (see Ch. 6), impaired short-term memory (if there is medial temporal/hippocampal involvement), inability to read with spared ability to write (alexia without agraphia) (if there is left inferior temporal involvement), decreased ability to recognize faces (prosopagnosia) (if there is right inferior temporal involvement), and/or changes in cognition and/or level of arousal (if there is thalamic involvement).
PCA infarct. Axial diffusion-weighted MRI (DWI) demonstrating ischemic infarct in the territory of the left PCA. Note that this territory involves not only the posterior occipital lobe but also the thalamus (A) and medial temporal lobe (B).
The PCAs are connected to the anterior circulation by the posterior communicating arteries. Proximal to each posterior communicating artery, the PCA is called the P1 segment, and distal to the posterior communicating artery, it is called the P2 segment. In some patients, one or both PCAs arise from the internal carotids rather than the top of the basilar artery, a variant referred to as a fetal PCA (see Fig. 7–5). Although strokes in the PCA territory are generally considered posterior circulation strokes, if a patient has a PCA stroke in the setting of a fetal PCA, the stroke would be considered to have arisen from the anterior circulation. This is important to recognize in patients with PCA stroke and ipsilateral carotid stenosis: A fetal PCA on the side of a PCA stroke and carotid stenosis suggests that the stenotic carotid is symptomatic (see Ch. 19).
In some patients, the left and right thalami are both supplied by a single artery that arises from the PCA, referred to as the artery of Percheron. Occlusion of this artery can lead to bithalamic infarction causing acutely altered mental status, a rare global, rather than focal, stroke syndrome (Fig. 7–12).
Artery of Percheron infarct. Axial diffusion-weighted MRI (DWI) demonstrating ischemic infarct in the bilateral thalami due to occlusion of the artery of Perceheron.
Lacunar strokes are caused by occlusion of small penetrating arteries affecting the subcortical white matter (internal capsule), subcortical gray matter (basal ganglia, thalamus [Fig. 7–13]), or anterior pons. Lacunar stroke syndromes include:
Pure motor stroke: unilateral hemiparesis/hemiplegia due to involvement of the posterior limb of the internal capsule or the anterior pons.
Pure sensory stroke: unilateral hemisensory loss due to involvement of the VPL/VPM nuclei of the thalamus.
Ataxia-hemiparesis: unilateral hemiparesis/hemiplegia (due to involvement of the corticospinal tract) with ataxia in the weak limb(s) (due to interruption of the corticopontocerebellar fibers destined for the middle cerebellar peduncles (see Ch. 8)). This can occur due to lacunar stroke in either the internal capsule or the anterior pons, both of which are places where the corticospinal tract and corticopontocerebellar fibers run together.
Dysarthria–clumsy hand: dysarthria and unilateral upper limb ataxia; localization is the same as for ataxia-hemiparesis (internal capsule or anterior pons).
Lacunar infarct. Axial diffusion-weighted MRI (DWI) demonstrating lacunar infarction in the right thalamus.
Infarction in the Watershed (Borderzone) Territories
The MCA-ACA watershed regions span the “stripes” at the border of the two territories (Fig. 7-14). Recalling the homunculus (Fig. 4–1), the part of the motor homunculus supplied by the MCA-ACA watershed region includes the proximal arm and leg, which are joined at the shoulder and hip in the homunculus. Therefore, infarction in the MCA-ACA borderzone can cause proximal arm and leg weakness with preserved strength distally in the hands and feet. When this occurs bilaterally, it causes what is called the “person in a barrel” syndrome since the distal arms and legs function well but the proximal limbs are weak (simulating a person in a barrel with the hands and feet sticking out).
Watershed (borderzone) infarcts. Axial diffusion-weighted MRI (DWI) demonstrating ischemic infarction in the borderzones. A: Bilateral MCA-ACA borderzone infarctions. B: Bilateral deep borderzone infarctions. C: Bilateral MCA-PCA borderzone infarctions.
The MCA-PCA watershed region is at the parieto-occipital junction. When the MCA-PCA watershed region is affected bilaterally, the patient will often have deficits in visual attention that can include some or all of the elements of Balint’s syndrome: optic ataxia, ocular apraxia, and simultanagnosia (see Ch. 6).
The evaluation and management of patients with cerebral infarction is discussed in detail in Chapter 19.