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These studies suggest that anterior cerebral artery stroke can cause hemiplegia, sensory neglect, micrographia, and executive dysfunction, with atherosclerosis being a common cause and mechanical thrombectomy as a potential treatment.
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Anterior cerebral artery (ACA) strokes are relatively rare, accounting for only 1-2% of all cerebral infarctions. These strokes can result from various mechanisms, including local atherosclerosis, cardiogenic embolism, and internal carotid artery embolism . The clinical presentation and outcomes of ACA strokes are influenced by the specific regions of the brain affected and the underlying stroke mechanisms.
Patients with ACA strokes often present with motor dysfunction, which is the most common symptom, occurring in approximately 91% of cases. Severe motor dysfunction is particularly associated with involvement of the supplementary motor area and paracentral lobule. Other notable symptoms include hypobulia or apathy, which are linked to lesions in the frontal pole, corpus callosum, and superior frontal gyrus. Urinary incontinence and grasp reflex are also observed, with the latter being related to corpus callosum involvement.
Infarctions in the ACA territory can also lead to contralateral hemiparesis, urinary incontinence, transcortical aphasia, agraphia, apraxia, and executive dysfunction . In some cases, patients may exhibit complete hemiplegia, profound sensory neglect, and micrographia . Bilateral ACA infarctions, although rare, can result in severe outcomes such as akinetic mutism and significant sphincter dysfunction .
ACA strokes are most commonly caused by local atherosclerosis, particularly at the A2 segment of the artery . Detailed mechanisms include local branch occlusion, in situ thrombotic occlusion, artery-to-artery embolism, and combinations of these factors. Cardiogenic embolism and internal carotid artery embolism are also significant contributors to ACA strokes .
Variability in the diameter of the ACA (A1 segment) and its ratio to the middle cerebral artery (M1 segment) can predict the likelihood of ACA strokes. Larger ipsilateral A1 diameters and higher A1D/M1D ratios are associated with an increased risk of ACA strokes. Additionally, a hypoplastic A1 segment may facilitate embolism in the ACA.
Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) are crucial in diagnosing ACA strokes and understanding their mechanisms. Angiographic studies often reveal occlusive changes, segmental dilatation, and hypoplasia of the ACA . Diffusion-weighted imaging (DWI) is particularly useful in the early phase of stroke to delineate the boundaries of the lesion.
Computer models have shown that the circle of Willis (CoW) and leptomeningeal anastomoses play significant roles in modifying infarct topography following ACA occlusion. While the CoW is helpful in redirecting flow after proximal occlusions, leptomeningeal anastomoses are crucial for distal occlusions, influencing motor outcomes by altering the extent of infarct topography.
Mechanical thrombectomy (MT) has been established as a safe and effective treatment for thromboembolic occlusions in various arteries, including the ACA. Studies have shown that MT for ACA occlusions achieves a high rate of recanalization (80%) and has a relatively low rate of procedural complications (23%). However, the rate of good functional outcomes at three months post-treatment is lower compared to other stroke types, highlighting the need for further research.
ACA strokes, though uncommon, present a unique set of clinical features and challenges. Understanding the mechanisms, anatomical factors, and effective treatment options is crucial for improving patient outcomes. Continued research and advanced imaging techniques will play a vital role in enhancing our knowledge and management of ACA strokes.
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