What is the treatment for vessel spasm on the left side of the head?

Treatment of Cerebral Vessel Spasm

The primary treatment for cerebral vasospasm is oral nimodipine 60 mg every 4 hours for 21 days, combined with hemodynamic optimization through hypertensive therapy to maintain adequate cerebral perfusion and prevent delayed cerebral ischemia. 1, 2

Pharmacological Management

Nimodipine - First-Line Therapy

• Nimodipine is the only medication proven in randomized controlled trials to reduce poor outcomes from vasospasm across all patient grades. 1, 3
• The FDA-approved dosing is 60 mg orally every 4 hours for 21 days, starting as soon as possible after subarachnoid hemorrhage (SAH). 1
• Nimodipine reduces the severity of neurological deficits resulting from vasospasm, with studies showing significant reductions in severe deficits (1 vs 8 in U.S. trial, 2 vs 10 in French trial). 1
• The drug crosses the blood-brain barrier effectively due to high lipophilicity, with cerebrospinal fluid concentrations reaching 12.5 ng/mL. 1
• Critical caveat: Nimodipine must be given orally or via nasogastric tube—never administer intravenously as this can cause fatal hypotension. 1
• Reduce dose to 30 mg every 4 hours in patients with hepatic cirrhosis, as bioavailability doubles in this population. 1

Hemodynamic Therapy ("Triple-H" Therapy)

• Hypertensive therapy is the mainstay for managing symptomatic vasospasm, though it lacks high-quality randomized trial evidence. 2, 3
• The goal is to augment cerebral blood flow by increasing mean arterial pressure, particularly after the aneurysm has been secured surgically or endovascularly. 2
• Avoid hypovolemia, hypotension, and hemoconcentration, as these are clearly detrimental. 2
• Important distinction: Prophylactic hypervolemia (before symptoms) has NOT been shown superior to normovolemia in preventing vasospasm onset. 2
• Maintain euvolemia as baseline, then escalate to induced hypertension only when symptomatic vasospasm develops. 2

Monitoring and Detection

Clinical Surveillance

• Vasospasm typically occurs 7-10 days after hemorrhage, with maximal narrowing at 5-14 days and spontaneous resolution by day 21. 2, 4
• Monitor for new focal neurological deficits, unexplained increases in mean arterial pressure (autoregulatory response), or subtle examination changes in comatose patients. 2
• Critical pitfall: Symptomatic vasospasm can occur without obvious symptoms in poor-grade patients—maintain high index of suspicion. 2

Diagnostic Imaging

• Transcranial Doppler (TCD) with Lindegaard ratios of 5-6 indicates severe spasm requiring treatment. 2
• TCD ratios (brain vessel velocity/ipsilateral extracranial internal carotid velocity) are more reliable than absolute velocities, especially during hemodynamic therapy. 2
• CTA head detects vasospasm with 80% sensitivity and 93% specificity, providing less invasive screening before catheter angiography. 2
• CT perfusion shows 74% sensitivity and 93% specificity for detecting vasospasm, though using it to guide treatment decisions has not improved outcomes. 2
• Conventional catheter angiography remains the reference standard for characterizing vasospasm severity and enables potential endovascular intervention. 2

Endovascular Interventions

When Medical Management Fails

• Balloon angioplasty is effective for reversing vasospasm in large proximal vessels (supraclinoid ICA, proximal MCA, ACA, basilar artery) but not safe in distal perforating branches beyond second-order segments. 2, 3
• Early intervention (<2 hours from symptom onset) may provide better sustained clinical improvement. 2
• Intra-arterial papaverine infusion (3 mg/mL at 6-9 L/min, up to 300 mg per territory) can reach smaller vessels not amenable to balloon angioplasty. 2
• Critical limitation: Intra-arterial treatment of vasospasm lacks high-quality evidence of improved outcomes despite angiographic improvement. 2
• Risks include vessel occlusion, rupture, thrombus formation, and aneurysm clip displacement. 2

Ineffective Therapies to Avoid

• Aspirin, enoxaparin, and tirilazad have been shown ineffective in improving outcomes or reducing vasospasm. 2
• Clot removal and intrathecal fibrinolytic agents have complications that offset any benefit. 2
• Using CT perfusion to guide treatment decisions in symptomatic patients does not improve outcomes compared to treating all patients without imaging guidance. 2

Prognostic Considerations

• Vasospasm causes 10-20% increase in morbidity and mortality after SAH, accounting for nearly 50% of deaths in patients surviving to treatment. 2
• Only 50% of patients with angiographic large-vessel vasospasm develop clinical ischemic symptoms. 2
• Conversely, 3% of patients develop infarction without angiographic evidence of vasospasm. 2
• Symptoms are frequently irreversible once delayed cerebral ischemia develops, emphasizing the importance of prevention with nimodipine. 2

Essential Supportive Care

• Aggressively avoid systemic insults: hyperglycemia, acidosis, electrolyte fluctuations, hypoxia, hyperthermia, and sepsis. 2
• Control intracranial pressure and decrease metabolic oxygen demand. 2
• Early aneurysm securing (surgical or endovascular) allows more aggressive vasospasm management without rebleeding risk. 2