SIH is first described by Schaltenbrand [
1]. SIH is a syndrome of low CSF volume and pressure caused by persistent CSF leakage through a dural defect. This leads to downward migration of the brain, causing various symptoms. Orthostatic headache is the most common and cardinal clinical symptom. In the 50% of patients, other symptoms are accompanied by orthostatic headache; posterior neck pain, neck stiffness, nausea, vomiting, etc. [
2]. Estimates suggest that the annual incidence of SIH is 5 per 100,000 individuals per year [
3]. SIH is typically encountered in middle age (30-50 years of age) and has a predilection for female (female:male=2:1) [
14]. The diagnosis of SIH is not simple. Schievink [
2] reported 17 of 18 patients (94%) were misdiagnosed initially and the median diagnostic delay was 5 weeks despite invasive diagnostic procedures were done in some patients. For this reason, it is essential to carefully check the patient's history and check appropriate diagnostic test. According to the Monroe-Kelly hypothesis, as the intracranial CSF decreases, the intracranial blood volume increases to compensate for this. Due to this, diffuse pachymeningeal enhancement and enlargement and engorgement of pituitary gland appear, which can be confirmed by gadolinium-enhanced brain MRI. Watanabe et al. [
4] reported on the diagnostic usefulness of MRI. However, since brain MRI showed no abnormal findings in about 19% of patients with SIH and can’t give information about the leakage sites, additional spinal imaging is required if active treatment is being considered [
16]. There are no guidelines widely acknowledged for the treatment of SIH yet. According to meta-analysis about SIH, conservative treatment including bed rest, hydration, analgesia, steroids, caffeine was effective in about 24.5% of 881 patients for a period ranging from 7 to 9 weeks [
7,
17]. EBP is commonly used treatment to patients showed no response to conservative treatment. Autologous blood injection to epidural space, aka ‘epidural blood patch’, was first described by Gormley [
16] in 1960. Even though EBP is commonly used for the treatment of SIH, the process how it acts has not been determined, but may involve a temporary increase in epidural pressure, the sealing of a tear by coagulating injected blood, or the initiation of inflammatory reactions that promote dural tear healing [
8,
10-
12]. According to previous studies, the therapeutic effect of EBP showed various improvement rate in 64-93% of patients after first treatment [
7,
13,
18-
20]. There are two methods of EBP, targeted and non-targeted one. There is controversy over which EBP is more effective. Some authors reported the superiority of targeted EBP [
8,
14,
21]. Cho et al. [
8] reported the success rate after the first targeted EBP was 87.1%, as compared with 52% for non-targeted EBP. Targeted EBP may cause serious complications including compression of the spinal cord and nerve roots, chemical meningitis, intrathecal injection of autologous blood, and neck stiffness. Beside, due to the anatomy of the cervical or thoracic level, small amount of blood can be injected relatively as compared with the lumbar level [
8]. Because of these risks, some authors prefer the blind EBP [
22,
23]. Ferrante et al. [
24] reported 90% success rate of blind EBP. In our study, we performed blind EBPs on the L1-2 level according to the hypothesis presented by Franzini et al. [
9]. Franzini et al. [
9] proposed a hypothesis about the pathophysiologic mechanism of SIH between the CSF and the venous drainage of the spinal epidural space. Negative pressure within the inferior vena cava (IVC) will result in overdrainage of venous blood from the epidural spinal vein network via large lumbar collectors through 1-way valves. A decrease in spinal epidural pressure and volume of epidural veins result in modification of the epidural gradient between epidural space pressure (negative) and CSF pressure (positive in orthostatic conduction). This modification results in aspiration of CSF into the spinal space and veins. They proposed the technique aimed to provoke a marked rise in epidural pressure to reverse the CSF-hematic gradient, thus removing the main etiopathogenetic factor that is the epidural hypotension maintained by the epidural venous drainage through the IVC. The L1-2 level is the target for helping reversing the CSF-blood gradient within the epidural space along the entire cord, not for the sealing of leakage point.
We performed all blind EBPs at the L1-2 levels regardless of leakage points for the following reasons.
II. It is technically easier than performing EBP to the epidural space at the thoracic level.
III. As an intermediate point between the lumbar and thoracic region, the locational advantage of being easy to spread patched blood was considered. In fact, considering the postoperative fluoroscopic images that the contrast agents were widely spread in the thoracolumbar area and the symptom improvement rate was high in the cases of applying a high volume of blood, it would be difficult to rule out the possibility that it was not because of Franzini’s hypothesis, but because of the locational advantage.
Our series had a few significant limitations. We performed retrospective chart and image reviews. Therefore, we could not eliminate biases inherent of retrospective reviews. SIHs are not a common disease entity. Thus, we did not experience the sufficient cases to confirm the efficacy of blind EBP. Because the mean follow-up period in our series was short, there is the possibility that the recurrence rate was underestimated. Due to the small size of our study, we could not rule out the chance that the favorable results were somewhat exaggerated. The favorable results of our cases do not necessarily mean that blind EBP is the treatment of choice for SIHs. However, this technique is a safe and technically easy treatment option that physicians should consider when they encounter this disease entity.