Somnolence and amantadine treatment in anterior cerebral artery (ACA) infarction
Year: 2026
Type: article
Abstract: Introduction: ACA (anterior cerebral artery) infarcts can cause dysarthria, aphasia, contralateral motor paresis, minimal sensory paresthesia, incontinence, and impaired alertness. Infarcts in the ACA territory are less common.Case: An 81-year-old woman was evaluated for weakness, left leg weakness, and inability to walk. On admission neurological examination she was alert and oriented and followed simple commands; the pupils were isocoric with direct and indirect light reflexes present in both eyes, eye movements were full, and she had hemiparesis with 4-/5 strength in the left lower extremity and 4+/5 in the left upper extremity. Brain CT showed no acute hemorrhage or marked edema. Diffusion MRI (magnetic resonance imaging) showed an acute infarct in the right anterior communicating artery territory. CT angiography showed an occlusion in the distal A2 segment of the right ACA. During follow-up, her somnolence deepened. For the impaired alertness, infarct progression/cerebral edema, nonconvulsive status epilepticus (NCSE), hypoxia, metabolic disturbances, infection, and drug effects were evaluated, and pulmonary embolism was found. Follow-up cranial imaging showed that the ischemic area had progressed to a total right ACA infarct, with mass effect consistent with minimal subfalcine shift. Anti-edema treatment was given. Amantadine treatment was started, taking into account that its use for somnolence is off-label. Because no marked and sustained increase in alertness was achieved during five days of treatment, amantadine was discontinued. In patients who present with somnolence or develop it during follow-up, ACA infarction, NCSE, metabolic disturbances (hypoglycemia/hyperglycemia), hypoxia, toxic exposure, and sedative use must be considered in the differential diagnosis. Amantadine can be used as a neurostimulant, but the evidence specific to stroke is limited and heterogeneous. Amantadine should therefore not be regarded as standard treatment for disturbance of consciousness after stroke, and the decision to use it should be individualized (Figure 1 and 2).Discussion/Conclusion: In our patient, the disturbance of consciousness can be explained by the combined effect of structural damage from the ACA infarct and hypoxia secondary to pulmonary embolism. Reversible causes should be excluded first. Stronger prospective studies are needed on the efficacy of amantadine in the treatment of post-stroke somnolence, because patient selection, optimal dose, and duration of treatment remain uncertain.Keywords:
Authors: Aygül Güneş, Melisa Yapıcı
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W7225808849
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