A cerebral artery occlusion occurs when a blood vessel supplying oxygen and nutrients to the brain becomes blocked, leading to an ischemic stroke. This blockage prevents brain tissue from functioning and causes neurological damage. The Anterior Cerebral Artery (ACA) supplies a specific brain territory, and a blockage results in a highly characteristic set of symptoms. Identifying this pattern is the first step in diagnosing an ACA stroke, as the symptoms directly reflect the functions of the deprived brain regions.
Anatomical Context of the Anterior Cerebral Artery
The ACA originates from the internal carotid artery and becomes part of the Circle of Willis at the base of the brain. It travels into the longitudinal fissure, the deep groove separating the two cerebral hemispheres. The artery supplies the medial surface of the frontal and parietal lobes, which are the parts of the brain situated toward the center line.
The ACA supplies the cortical areas that control movement and sensation for the lower half of the body. These regions include the paracentral lobule and the medial parts of the primary motor and somatosensory cortices. The ACA also provides blood to deep structures, such as the anterior portion of the internal capsule and parts of the basal ganglia, which influence motor and cognitive function.
Primary Motor and Sensory Deficits
The most characteristic physical symptom associated with an ACA occlusion is contralateral hemiparesis, or weakness on the side of the body opposite the stroke. This weakness is distinctly leg-dominant, a pattern known as crural hemiparesis. The lower limb, including the hip and thigh muscles, is significantly more affected than the upper limb or the face.
This differential weakness results from the ACA supplying the motor cortex area dedicated to the leg and foot. This area is located high on the medial surface of the brain, within the ACA’s territory. In contrast, the areas for the face and arm are situated lower on the lateral surface, supplied by the Middle Cerebral Artery (MCA).
Since the MCA remains unaffected in a pure ACA stroke, the facial and arm muscles are often spared or only minimally weakened. Contralateral sensory loss, or hypesthesia, often accompanies the motor deficit, following the same leg-dominant pattern. This occurs because the somatosensory cortex, which processes touch and position sense, is located directly behind the motor cortex and is also supplied by the ACA in the leg representation area.
Behavioral and Executive Dysfunction
ACA occlusion frequently causes non-motor symptoms resulting from damage to the frontal lobe structures. These deficits relate to higher-order cognitive functions and executive control. The most notable symptom is abulia, characterized by an extreme lack of initiative, spontaneity, and drive.
Patients with abulia may appear indifferent, speak very little, or show a profound delay in responding to questions or commands. This symptom arises from injury to the prefrontal cortex and the anterior cingulate gyrus, which are supplied by the ACA and are responsible for motivation and purposeful action. A pervasive apathy, or emotional indifference, often accompanies abulia.
Another common finding is gait apraxia, a difficulty in planning and initiating walking steps despite having the physical strength to move the legs. This results from damage to the supplementary motor area, which is located in the ACA territory and is responsible for motor planning. Severe prefrontal cortex damage may also cause personality changes or disinhibition, leading to inappropriate social behavior.
Associated Signs and Symptom Variability
While leg weakness and abulia form the core presentation, other associated signs can occur, particularly in severe or bilateral strokes. Urinary incontinence is common, linked to the involvement of the paracentral lobule, which controls bladder function. This symptom is often seen in strokes affecting both ACAs or the deep structures of the frontal lobe.
The presence of primitive reflexes, such as the grasp reflex or the sucking reflex, may also be noted. These reflexes indicate a “release” of frontal lobe control over basic motor patterns, suggesting extensive ACA territory damage.
Symptom Variability Based on Location
Symptom presentation varies significantly depending on the precise location of the blockage. If the occlusion occurs proximal to the anterior communicating artery (ACom), symptoms may be minimal or absent due to collateral blood flow from the other hemisphere. Conversely, a blockage of a distal branch, such as the callosomarginal artery, may result in a more isolated deficit, such as weakness only in the contralateral leg, without the broader behavioral changes.