Intrathecal nicardipine

• Intrathecal nicardipine for cerebral vasospasm after non-traumatic subarachnoid hemorrhage: a meta-analysis
• Earlier onset of cerebral vasospasm in ruptured infectious intracranial aneurysms
• The Clinical Research Landscape of Intracranial Nicardipine for Aneurysmal Subarachnoid Hemorrhage: Insights From Bibliometric Analysis
• Effects of intrathecal administration of sodium nitroprusside and nicardipine on cerebral pial microcirculation, cortical tissue oxygenation, and electrocortical activity in the early post-resuscitation period in a porcine cardiac arrest model
• Intrathecal Nicardipine After Aneurysmal Subarachnoid Hemorrhage: A Scoping Review
• Intrathecal Nicardipine-Time to Treat the Symptom?
• Intrathecal Nicardipine as Treatment for Severe Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Retrospective Clinical Study
• Reply to: Comment: Cerebrospinal Fluid Pharmacokinetics of Nicardipine Following Intrathecal Administration in Subarachnoid Hemorrhage Patients

Data suggest that the intrathecal (IT) delivery of the calcium channel blocker (CCB) nicardipine may have a role in a reactive (rather than a preventative) approach to address cerebral vasospasm treatment and avoid delayed cerebral ischemia (DCI) ¹⁾. This approach has the advantage of avoiding deleterious systemic effects, i.e., decreased blood pressure, that is common with oral and intravenous CCBs ²⁾. An intermittent and titratable IT nicardipine regimen was shown to be associated with proximal vessel vasodilation, reduced risk for DCI, and improved long-term functional outcomes ^{3) 4)}. However, the macrovascular vasodilation itself, as quantified by a reduction in daily TCD blood flow velocity, was not associated with outcomes ⁵⁾

Sathialingam et al. employed a non-invasive optical modality called diffuse correlation spectroscopy (DCS) to quantify the acute microvascular cerebral blood flow (CBF) response to intrathecal nicardipine (up to 90 min) in 20 patients with medium-high grade non-traumatic SAH. On average, CBF increased significantly with time post-administration. However, the CBF response was heterogeneous across subjects. A latent class mixture model was able to classify 19 out of 20 patients into two distinct classes of CBF response: patients in Class 1 (n = 6) showed no significant change in CBF, while patients in Class 2 (n = 13) showed a pronounced increase in CBF in response to nicardipine. The incidence of DCI was 5 out of 6 in Class 1 and 1 out of 13 in Class 2 (p < 0.001). These results suggest that the acute (<90 min) DCS-measured CBF response to IT nicardipine is associated with intermediate-term (up to 3 weeks) development of DCI ⁶⁾.

In this observational study, we prospectively employed a non-invasive optical modality called diffuse correlation spectroscopy (DCS) to quantify the acute microvascular cerebral blood flow (CBF) response to IT nicardipine (up to 90 min) in 20 patients with medium-high grade non-traumatic SAH. On average, CBF increased significantly with time post-administration. However, the CBF response was heterogeneous across subjects. A latent class mixture model was able to classify 19 out of 20 patients into two distinct classes of CBF response: patients in Class 1 (n = 6) showed no significant change in CBF, while patients in Class 2 (n = 13) showed a pronounced increase in CBF in response to nicardipine. The incidence of DCI was 5 out of 6 in Class 1 and 1 out of 13 in Class 2 (p < 0.001). These results suggest that the acute (<90 min) DCS-measured CBF response to IT nicardipine is associated with intermediate-term (up to 3 weeks) development of DCI ⁷⁾.