韓正恩的部落格

. After the initial aneurysm hemorrhage, multiple pathological mechanisms account for neuronal injury including: hydrocephalus,
apoptosis, cerebral edema, loss of blood–brain barrier, abnormal cerebral autoregulation, microthrombosis, cortical spreading depression
and vasospasm.
. Current treatment of delayed cerebral ischemia (DCI) involves nimodipine, maintenance of euvolemia, induced hypertension for
symptomatic DCI and possible endovascular treatment for patients with DCI symptoms refractory to induced hypertension.
. Cortical spreading depolarization is the latest mechanisms targeted for in DCI after aneurysmal subarachnoid hemorrhage and future
trials will use ketamine to suppress cortical spreading depolarizations.
. Other future therapy for DCI will include agents to block apoptotic pathways, agents to prevent smooth muscle cell contraction and
proliferation and low-dose anticoagulation to prevent microthrombosis.

血管痙攣的治療

 —Hypertension/hypervolemia/hemodilution (triple H治療)可用來預防及治療因 血管痙攣而引起的腦缺血，接受此類治療的病人應儘可能將動脈瘤夾除， 且於加護病房中緊密監測其hemodynamic function。

—Nimodipine可口服或靜脈給藥，建議早期使用連續性 靜脈注射，前兩小時建議用量5cc/hr，如血壓穩定可調整至最高劑量10cc/ hr來減少因血管痙攣產生的不良預後。==> 目前不建議!!!!!!!

 其它種類的鈣離子阻斷劑效果仍未 有明確價值。而Intra-arterial Nimodipine注射，被報告有效。

—如嚴重之血管痙攣，可以考慮使用Transluminal angioplasty。

—腦池內注射 fibrinolysis、antioxidant及anti-inflammatory藥物其效果仍未 明。
 

Nimodipine was developed to reduce angiographic vasospasm after aSAH. At tolerable doses, there was minimal effect on angiographic vasospasm. Current theory is that multiple processes contribute to delayed cerebral ischemia  and delayed infarction, including angiographic vasospasm, cortical spreading ischemia, microthromboembolism, loss of autoregulation, and capillary transit time heterogeneity. Nimodipine may have improved outcome because it inhibits these deleterious processes, but at tolerable doses has only a small effect on the most widely measured process (angiographic vasospasm). Evidence consistent with this is that at some doses, nimodipine and other dihydropyridines reduce angiographic vasospasm, cortical spreading ischemia, and microthromboembolism. Nimodipine may have improved outcome because it inhibits these deleterious processes, but at tolerable doses has only a small effect on the most widely measured process (angiographic vasospasm). NEWTON tested the hypothesis that intracranial delivery of Intraventricular EG-1962, which achieved high and sustained CSF concentrations in preclinical studies, would increase efficacy without compromising safety.