Cerebral vasospasm (CV) following spontaneous subarachnoid hemorrhage is a serious complication that can lead to delayed cerebral ischemia, significantly increasing both morbidity and mortality. This article offers an in-depth examination of the pathophysiological mechanisms, risk factors, diagnostic strategies, and currently available treatment options concerning CV. Several distinct yet interconnected processes contribute to the development of vasospasm, such as oxidative stress driven by oxyhemoglobin, increased endothelin-1 activity, diminished nitric oxide availability, endothelial dysfunction, vascular inflammation, and sympathetic overactivation. In symptomatic cases, digital subtraction angiography remains the most reliable modality for diagnosis, offering detailed vascular visualization and the opportunity for concurrent therapeutic intervention. Among pharmacological agents, oral nimodipine is the only drug with proven efficacy in enhancing functional outcomes and is strongly endorsed by current clinical guidelines (Class I, Level A). In cases of refractory vasospasm, endovascular treatments such as transluminal balloon angioplasty and intra-arterial vasodilator infusion play a critical role. The management of CV requires an individualized, time-sensitive, and multimodal approach in both diagnosis and therapy. There remains a need for advanced randomized controlled trials and standardized treatment protocols in this field.

Internuclear ophthalmoplegia (INO) is characterized by impaired adduction in the ipsilateral eye and horizontal jerk nystagmus in the contralateral eye, resulting from a lesion in the medial longit...