Version May 2024
INTRODUCTION — Intracranial hypotension occurs when imbalance in the production, absorption, or flow of cerebrospinal fluid (CSF) leads to low intracranial pressure and "sagging" of the brain within the skull. The resultant traction on connected nerves and other structures can cause a clinical syndrome often described by postural headaches, but nonpostural headaches and other neurologic symptoms may also occur.
Intracranial hypotension most commonly occurs from a persistent CSF leak after lumbar puncture but may also be spontaneous.
This topic will review the treatment and prognosis of spontaneous intracranial hypotension. The pathophysiology, clinical features, and diagnosis of spontaneous intracranial hypotension are discussed separately. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis".)
Post-dural puncture headache is reviewed elsewhere. (See "Post dural puncture headache".)
INITIAL TREATMENT — For most patients with spontaneous intracranial hypotension, we suggest lumbar epidural blood patch (EBP) once the diagnosis is established. For selected patients with symptoms <2 weeks duration that are mild to moderate in severity who prefer an initial noninvasive option, we offer a trial of conservative measures for one to two weeks before proceeding with EBP. However, in the authors' experience, conservative therapy is often ineffective and most patients with spontaneous intracranial hypotension subsequently require EBP (algorithm 1). (See 'Trial of conservative treatment' below and 'Lumbar epidural blood patch' below.)
For patients with severe symptoms due to a focal trauma or cerebrospinal fluid (CSF)-venous fistula, targeted therapy is indicated. (See 'Treatment at the site of leak' below.)
Trial of conservative treatment — For patients with acute spontaneous intracranial hypotension who present with mild to moderate symptoms of <2 weeks duration and prefer an initial noninvasive option, we offer an initial one- to two-week trial of conservative treatment, in agreement with consensus clinical guidelines [1]. For such patients whose symptoms persist despite conservative measures for one to two weeks and for other patients with more severe and/or prolonged initial symptoms, we suggest EBP. (See 'Lumbar epidural blood patch' below.)
Our preferred regimen of conservative therapy includes:
●Bedrest to minimize upright positioning
●Oral caffeine intake
Approximately 200 to 300 mg of caffeine, given two to three times daily, generally provides short-term relief. Caffeinated beverages (eg, coffee or soda) or caffeine tablets can be used. With improvement, patients can return to activity gradually, incorporating scheduled rest periods lying flat (eg, five minutes per hour).
However, many patients are unable to comply with strict bed rest, particularly as its benefits can be very short lasting. Other strategies aimed at restoring CSF volume include:
●Oral or intravenous hydration [2]
●High salt intake [3]
●Use of an abdominal binder [4]
●Analgesic medications [5]
●Glucocorticoids [6]
Oral hydration is frequently recommended, but its effectiveness has not been demonstrated in clinical studies [2]. Analgesic medications are often recommended as first-line treatment but generally provide little relief [5].
Conservative therapy may be effective in some cases and can help patients avoid the risks associated with invasive treatment options. In a meta-analysis of data from 17 studies including 748 patients with spontaneous intracranial hypotension, the success rate of conservative treatment was 28 percent [7]. However, by the time that many patients with mild to moderate spontaneous intracranial hypotension present to a neurologist, the symptoms have been present for weeks to months, and conservative measures have failed. For those patients, EBP is recommended as soon as possible. (See 'Lumbar epidural blood patch' below.)
Lumbar epidural blood patch — We suggest EBP as first-line therapy for patients with spontaneous intracranial hypotension who fulfill any of the following conditions [8,9]:
●Symptomatic for two weeks or longer at the time of diagnosis
●Severe headache or other disabling symptoms, regardless of duration
●An aggressive precipitating injury (eg, a water-skiing accident) as compared with a minor or "trivial" trauma (eg, a sudden twist or stretch)
●A history of connective tissue disease or joint hypermobility
●Persisting symptoms after one to two weeks for patients who prefer an initial trial of conservative treatment (see 'Trial of conservative treatment' above)
EBP is an effective treatment for spontaneous intracranial hypotension that can be performed by trained clinicians in the outpatient setting. In a meta-analysis of 33 studies that included treatment of 1758 patients with spontaneous intracranial hypotension, the success of treatment with EBP was 64 percent [7].
Lumbar ("blind") EBP is the preferred initial intervention over either EBP targeted to the site of the leak or surgical options. EBP performed caudal to the terminus of the spinal cord avoids the risk of myelopathic complications associated with targeted EBP at higher spinal segments. Lumbar EBP may also be effective for some patients with a leak remote from the site of the EBP due to the tamponade effect from the epidural blood. In addition, targeted EBP may not be possible if the specific site of the CSF leak is not found. In some cases, spinal imaging identifies a fluid collection or other evidence of intracranial hypotension, but the site of the leak remains inapparent. The overall effectiveness of targeted EBP may be similar to lumbar EBP. (See 'Targeted epidural blood patch at site of leak' below.)
Regimen — The initial EBP treatment typically involves the percutaneous infusion of 10 to 20 mL (up to 40 mL) of autologous blood into the lumbar epidural space [1,4]. An EBP directed at the cervical or thoracic spine may be preferred if the leak site is strongly suspected to be higher; examples include CSF leaks related to athletic activity (eg, swimming, bench pressing, or playing tennis).
The technique for EBP is discussed in greater detail separately. (See "Post dural puncture headache", section on 'EBP technique'.)
EBP is contraindicated in patients with a coagulopathy or taking anticoagulant medications and in patients with an active systemic infection. Adverse effects of EBP are uncommon but include back pain, radiculopathy, leg paresthesias, and fever. Transient bilateral paraplegia and cauda equina syndrome from arachnoiditis have been reported with high-volume EBPs [10].
The mechanism that accounts for the success of EBP is not completely understood but appears to work through initial tamponade of the dural leak followed by fibrin deposition and scar formation, typically occurring within three weeks [4]. The tamponade of the leak often results in an immediate improvement in symptoms.
Repeat EBP treatments — For patients whose symptoms partially or transiently improve after an initial EBP, we repeat the treatment, typically after an interval of two or more weeks, in agreement with clinical guidelines [1]. EBP may be repeated one or more times for optimal benefit. For patients whose symptoms do not improve progressively with repeated EBP, we obtain imaging to identify the site of the leak for targeted therapy. (See 'Management of patients with persistent symptoms' below.)
●Number of treatments – In small studies, up to 57 percent of patients with spontaneous intracranial hypotension require more than one EBP treatment [11-13]. In one series of 25 consecutive patients with spontaneous CSF leaks, a good response was reported in 36 percent after an initial EBP and another 33 percent after a second EBP [11]. Some patients may require up to four to six patches for sustained relief [6,14]. Features associated with a lack of response to a first targeted EBP include the length of anterior epidural CSF collection, the severity of diencephalic-mesencephalic deformity, and an injected blood volume ≤22.5 mL [15].
●Volume of repeat EBP – A larger volume (20 up to 100 mL in some studies) infusion may be used if the initial blood patch is unsuccessful [16]. With use of the higher volume infusion, we delay a minimum of two weeks between blood patches because of the potential for an increased risk of complications including back pain and radiculopathy.
●Site of repeat EBP – Different injection sites may be used for repeated blood patches (eg, first at the upper lumbar region, then in the lower lumbar area) [16]. However, lumbar placement of the EBP can be effective even when the site of CSF leakage is above the site of the blood patch or is unknown due to the tamponade effect of the blood.
Multiple EBP treatments may be needed for durable improvement in symptoms because the efficacy of EBP therapy is generally lower for spontaneous intracranial hypotension than for post-dural puncture headache. In a review of the management of 105 patients with symptomatic intracranial hypotension, EBP was performed more frequently in patients with spontaneous intracranial hypotension than those with post-dural puncture headache (70.5 versus 45.5 percent) and typically occurred more than once (37.7 versus 13.6 percent) [13]. While there is no single explanation for this, several factors may play a role. A lumbar puncture is a site-known "nick" in the posterior aspect of the dura. By contrast, a spontaneous CSF leak site is often site unknown and is commonly above the lumbar region and near the nerve root sleeve and thus distant from the EBP placement. Additionally, a spontaneous CSF leak is not a well-placed hole but rather a dural rent, tear, or connective tissue laxity. Therefore, the healing and "sealing" process following EBP placement is more complex, and the lesion may be more likely to leak again or never fully seal in the first place.
MANAGEMENT OF PATIENTS WITH PERSISTENT SYMPTOMS — For patients with symptoms that do not resolve with initial conservative treatment or lumbar epidural blood patch (EBP), we perform a diagnostic evaluation to locate the site of the cerebrospinal fluid (CSF) leak along the neuraxis and guide targeted treatment (algorithm 2) [3,17].
Imaging evaluation to identify site of leak — Spinal imaging to assess for the site of CSF leak is performed by myelography. Multiple techniques have been used to locate a CSF leak including computed tomography (CT) myelography, magnetic resonance (MR) myelography, and digital subtraction myelography (DSM). Noninvasive options that avoid risk of worsening symptoms as a complication of intrathecal injection may be preferred before attempting more invasive options (algorithm 2).
Noninvasive MR myelography — We suggest noncontrast, noninvasive MR myelography using heavily T2-weighted three-dimensional sequences without gadolinium as the initial study to identify a CSF leak (image 1). This procedure is typically used to confirm the diagnosis of spontaneous intracranial hypotension but may also be used to detect the level of CSF leaks [7,18,19]. Noninvasive MR myelography may also be appealing as it does not expose patients to radiation, does not require gadolinium contrast, and is typically a quicker study than myelography performed with intrathecal injection. In addition, it does not carry the adverse risks of causing a CSF leak or potential toxic reaction to intrathecal gadolinium associated with myelography performed with intrathecal injection. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis", section on 'Noninvasive MR myelography'.)
Noninvasive MR myelography has been used to identify the specific site of a CSF leak only in small case series [18,19]. In many cases, it may identify an extradural CSF collection but not the specific site of the leak [7]. In these cases, further testing is required.
Myelography with intrathecal contrast — We suggest CT myelography with intrathecal contrast to identify the site of a CSF leak when noninvasive studies are nondiagnostic. For most patients with symptomatic spontaneous intracranial hypotension undergoing imaging evaluation, myelography with intrathecal contrast is needed to identify the site of a CSF leak (image 2) [7]. Contrast is infused via dural puncture, allowed to distribute through the spinal subarachnoid space, and then imaging is performed.
We generally prefer CT myelography over MR myelography based on clinical experience and the more extensive data supporting its use. In addition, CT myelography avoids the risk of a potential toxic reaction or cerebral retention that may occur with the off-label administration of intrathecal gadolinium-based contrast agent. However, at some centers, MR myelography may be preferred over CT myelography due to local protocol and experience.
CT myelography historically was the preferred study to identify a CSF leak [16], but contemporary experience in some centers has shown the utility of MR myelography [20,21]. In a meta-analysis of studies assessing the proportions of positive findings of myelography with intrathecal contrast, the rate of positive findings with MR myelography was similar to CT myelography (60 versus 62 percent) [7]. However, the certainty of these results is limited by the smaller number of patients and studies using MR myelography.
CT myelography — CT myelography with intrathecal contrast has been the most common technique used to localize the level of the spinal leak when treatment beyond EBP (such as surgery or fibrin glue injection) is contemplated (image 2) [22]. CT myelography involves use of ionizing radiation and requires a dural puncture.
Specific protocols may be performed to enhance the diagnostic yield of CT myelography:
●Both early and delayed imaging should be obtained at each spinal level since CSF leaks may be rapid or slow. In cases where radioisotope cisternography or MRI has identified the approximate level of the leak, focused CT cuts can be used to locate the source more precisely.
●Prone patient positioning during image acquisition may improve diagnostic yield for patients suspected of having a ventral dural defect such as those with a ventral collection of extradural CSF [23].
●Dynamic CT myelography, where images are obtained during intrathecal contrast injection while the patient is in the CT scanner, has improved temporal and spatial resolution compared with routine CT myelography, where intrathecal contrast is given prior to moving the patient to the CT scanner [24]. Thus, dynamic CT myelography is better suited than routine CT myelography to detect rapid or high-flow CSF leaks [25]. In several cases when routine CT myelography showed no evidence of a CSF leak through a dural defect, positive-pressure or lateral decubitus dynamic CT myelography has revealed direct CSF flow through a CSF-venous fistula as the cause of spontaneous intracranial hypotension [23,26].
Despite the utility of CT myelography for determining the site of CSF leak, the results can occasionally be misleading. As an example, retrospinal CSF collections at the C1-C2 level and CSF extravasation into surrounding tissues at the cervicothoracic junction may be false localizing signs [27,28].
MR myelography — MR myelography with intrathecal gadolinium may be performed to identify the specific site of a CSF leak [7,22,29,30]. MR myelography is an alternative to CT myelography typically performed for patients unable to tolerate CT myelography or according to institutional protocol. The technique does not involve use of ionizing radiation but requires a dural puncture. Intrathecal use of gadolinium has been associated with the risk of toxic adverse effects such as encephalopathy and seizures in some [31-34] but not all studies [35,36]. Associated bony features such as a vertebral microspur may not be as easily identified on MR myelography as on CT myelography.
Digital subtraction myelography — DSM may identify the site of a CSF leak when other myelographic studies are nondiagnostic. Retrospective reports suggest that DSM using intrathecal injection of contrast material is useful to detect the site of spinal dural tears in select patients with rapid CSF leaks [7,37-39]. The temporal resolution of CT and MR myelography can be inadequate in the setting of rapid CSF leaks because the contrast can spread over many spinal levels during the time needed to obtain the CT or MRI images, obscuring the exact site of the dural defect [39]. Such rapid CSF leaks typically appear on CT and MRI as longitudinally extensive extradural fluid collections that are ventral to the spinal cord.
The superior temporal resolution of DSM may also be useful for the detection of direct CSF-venous fistulas, which have been implicated as the cause of spontaneous intracranial hypotension in cases where routine CT myelography and MRI myelography failed to identify a dural defect [26,40].
The presence or absence of spinal longitudinal extradural CSF collection on MRI may be useful to guide patient positioning (prone or lateral decubitus) for DSM for patients with spontaneous intracranial hypotension that is refractory to initial EBP [41]:
●For patients with spinal longitudinal extradural collections, prone positioning may assist in localizing the site of dural tears.
●For patients without spinal longitudinal extradural CSF collections, lateral decubitus positioning may improve detection of a CSF-venous fistula, which is relatively common in this population. DSM in the lateral decubitus position may be performed with patients on the left and right sides, often over two days, to assess the dependent nerve roots.
Treatment at the site of leak — For patients with spontaneous intracranial hypotension and a CSF leak with persistent symptoms despite treatment with lumbar blood patching, we suggest targeted EBP at the spinal level of the site of the leak, in agreement with consensus guidelines [1]. For patients with a structural source to the leak unlikely to resolve with a blood patch, such as CSF-venous fistula, and for patients whose symptoms do not improve after a targeted EBP, we suggest interventional or surgical options for definitive treatment (algorithm 2).
Targeted epidural blood patch at site of leak — A targeted EBP may be performed at the spinal level of CSF leak, typically with fluoroscopic guidance. Targeted EBP may be effective for symptomatic patients with a CSF leak due to a dural tear or meningeal diverticula. For other patients with a CSF leak due to a CSF-venous fistula, we suggest interventional or surgical repair. (See 'Interventional options for patients with refractory symptoms' below.)
Repeated targeted EBP may be performed for patients with partial or transient improvement after initial treatment. In addition, repeat targeted EBP may be attempted for patients who undergo surgical or other interventional therapy if symptoms persist.
Some data have suggested targeted EBP may provide a better seal of the CSF leak than a lumbar (blinded) EBP, especially when the site of the leak is in the cervical or upper thoracic region. However, data to support this view are sparse. In one series of 56 patients, clinical improvement was higher in those who received targeted EBP (27 of 31 patients; 87 percent) than those who received nontargeted EBP because the CSF leak site was not found (13 of 25 patients; 52 percent) [42]. By contrast, in a 2021 meta-analysis of studies assessing the effects of EBP, the rate of successful targeted EBP among 14 studies and 816 patients was 70 percent (effect size 95% CI 0.59-0.80), similar to the rate of successful non-targeted EBP among 10 studies and 264 patients (69 percent, 95% CI 0.61-0.76) [7]. Results are limited by observational nature of studies, small numbers in some cases, and selection bias.
Interventional options for patients with refractory symptoms — Surgical or endovascular repair is performed when symptoms do not resolve after targeted epidural blood patch. In addition, endovascular or surgical repair may be performed when a CSF leak is due to a CSF-venous fistula [17,23].
If surgical or endovascular options are unsuccessful or if the patient is unable to undergo surgery, repeat targeted EBP may be attempted. (See 'Targeted epidural blood patch at site of leak' above.)
Surgical repair — Surgical repair of a CSF leak is indicated for patients with a structural cause not amenable to EBP, such as a CSF-venous fistula. Surgical repair may also be required for some patients with an identified CSF leak if nonsurgical therapies fail [16,43,44].
Surgical methods involve the use of suture or metallic clips to ligate leaking meningeal diverticula or CSF-venous fistula [16,43,45,46]. Dural tears and defects can be repaired with suture or with placement of a muscle pledget and/or Gelfoam.
In one report of 14 patients with intractable symptoms, exploratory microsurgery allowed visualization and treatment of CSF leaks originating from longitudinal dural slits located on the ventral (n = 10), lateral (n = 3), or dorsal (n = 1) aspects of the dura [44]. All 10 of the ventral slits were caused by calcified microspurs that protruded from the intervertebral disc. However, an earlier report found that surgical exploration had a low yield for detecting the source of a CSF leak [43]. We suggest obtaining surgical treatment from surgeons or centers with expertise in spinal surgery for spontaneous intracranial hypotension.
Epidural fibrin glue — Epidural patching with fibrin glue at the site of the CSF leak has been used successfully in small numbers of patients [47-49]. Anecdotal evidence suggests that this percutaneous method is effective, and thereby avoids surgery, in approximately one-third of patients who have failed EBP treatment [16]. Further evidence of benefit in larger studies is needed before this technique can be routinely recommended [47]. Nevertheless, some experts favor the use of epidural fibrin glue to avoid surgery for patients with a clearly identified site of CSF leak who have failed an adequate trial of blinded and targeted EBP.
Some commercially available fibrin sealant products contain bovine aprotinin, an antifibrinolytic agent. (See "Fibrin sealants", section on 'Components'.)
The use of fibrin sealant is associated with a very low risk of anaphylaxis. However, repeated treatment with fibrin sealant containing bovine aprotinin appears to be associated with a substantially increased risk of hypersensitivity reaction [50]. Thus, patients selected for epidural fibrin glue treatment should be asked about possible previous exposure to aprotinin or fibrin sealant, since these agents have been used for hemostasis in various types of surgery (eg, cardiac, transplantation, joint replacement, repair of splenic injury) and hemostatic disorders [51].
Measures that may reduce the risk of anaphylaxis, although unproven, include treating multiple sites of CSF leak together rather than as staged procedures, waiting three to six months before repeating fibrin sealant treatment, and performing repeat treatment after prophylactic administration of glucocorticoids, H1 receptor antagonists, and hospital admission for observation [50].
Endovascular therapy — Interventional therapy with endovascular embolization may be an alternative to surgical ligation for some patients with CSF leak due to a CSF-venous fistula. Embolization of a CSF-venous fistula has been successful in small case reports and series [52-54]. Liquid or mechanical embolic agents are used at the site of the fistula to close the site of the leak. It is typically performed at centers experienced with spinal angiography and the treatment of arteriovenous fistulas.
Treatment options when site of leak is not found — For patients with spontaneous intracranial hypotension and persistent symptoms and an uncertain site of CSF leak, treatment options are limited.
●Continuous epidural infusion – One method of restoring the intracranial CSF volume, and thereby reducing headache, is a continuous epidural infusion of saline or dextran [55]. This method has limited success, but it may be attempted for patients who fail EBP if the site of the CSF leak cannot be identified [56].
In addition, epidural infusion may be useful as a temporizing measure when urgent treatment is needed (eg, because of stupor or coma) for those who fail EBP and are awaiting permanent repair of a CSF leak [16,57-59].
●Repeat imaging to identify source of leak – We typically repeat spinal imaging if symptoms worsen or after a several-month interval to reevaluate for an intermittent leak not found on initial testing. (See 'Imaging evaluation to identify site of leak' above.)
●Diagnostic reevaluation – Patients with persisting symptoms refractory to treatments without evidence of a specific site of CSF leak should undergo diagnostic reevaluation. Some CSF leaks may resolve spontaneously. The clinical features of spontaneous intracranial hypotension can mimic other neurologic conditions. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis", section on 'Differential diagnosis'.)
PROGNOSIS — The prognosis of spontaneous intracranial hypotension is favorable for most patients whose symptoms resolve spontaneously or with initial treatment. For many patients with persistent symptoms, the prognosis is variable, depending on the identification and repair of the leak as well as the duration and severity of symptoms.
●Symptom duration – Spontaneous intracranial hypotension may resolve spontaneously within two to four weeks [7,60]. In some cases, it may last months or, in rare cases, years. However, intermittent headaches have been reported at intervals of weeks, months, or years, probably caused by intermittent cerebrospinal fluid (CSF) leaks [16]. Furthermore, some patients have persistent symptoms despite documented resolution of CSF leakage with therapy [61].
●Complications – Some patients may develop transient intracranial hypertension following successful treatment of a CSF leak [62]. In these patients, headache may be retroorbital and worsen with recumbency. Nausea and blurry vision may occur but papilledema is often absent even when CSF pressure is very high. Symptoms typically resolve in weeks to months, but some may require symptomatic treatment. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Prognosis and treatment".)
Persistent CSF leak may be associated with a long-term risk of superficial siderosis (image 3) [63,64]. The proposed mechanism for superficial siderosis is recurrent hemorrhage from friable vessels at the site of the CSF spinal leak or from cerebellar bridging veins that are stretched due to brain sagging. The duration and ventral site of a CSF leak and an associated osteophyte may be risk factors for these complications [65,66]. In a single-center registry of nearly 1600 patients with spontaneous intracranial hypotension, superficial siderosis was identified on imaging in 3.6 percent of patients [67]. The prevalence of superficial siderosis was higher among patients with ventral CSF leaks (10.3 percent) compared with those with other types of CSF leaks including dural ectasia (3.9 percent), CSF-venous fistulas (2.6 percent), or meningeal diverticula (0.9 percent). The median interval from onset of spontaneous intracranial hypotension to development of superficial siderosis was approximately 10 years. In this series, intracranial hypotension symptoms resolved in 88 percent following interventional or surgical repair and superficial siderosis stabilized or improved in all patients. (See "Superficial siderosis".)
Bibrachial amyotrophy developed in two patients in a cohort of 51 patients with a persistent ventral CSF leak [63]. (See "Brachial plexus syndromes", section on 'Neuralgic amyotrophy'.)
●Recurrence – Although only anecdotal data are available, spontaneous spinal CSF leakage is estimated to recur in approximately 10 percent of patients regardless of treatment [16].
Initial brain magnetic resonance imaging (MRI) findings may be helpful for predicting the outcome of spontaneous intracranial hypotension. In a referral center series of 33 patients with spontaneous spinal CSF leaks and intracranial hypotension, a good outcome was reported in 25 (97 percent) of 26 patients with an abnormal MRI versus 1 (14 percent) of 7 patients with a normal MRI, and the difference between these groups was statistically significant [61]. However, it is unclear why a normal MRI was associated with a worse prognosis, and larger studies in more diverse patient populations are needed to confirm this finding.
SUMMARY AND RECOMMENDATIONS
●Epidural blood patch – For patients with spontaneous intracranial hypotension, we suggest treatment with an epidural blood patch (EBP) (algorithm 1) (Grade 2C). (See 'Lumbar epidural blood patch' above.)
A trial of conservation therapy with bed rest and generous caffeine intake is a reasonable alternative for patients who may wish noninvasive treatment. (See 'Trial of conservative treatment' above.)
For patients whose symptoms partially or transiently improve after an initial EBP, we repeat the treatment one or more times. (See 'Repeat EBP treatments' above.)
●Management for patients with persistent symptoms – For patients with symptoms that do not resolve with initial conservative treatment or lumbar EBP, we perform a diagnostic evaluation to locate the site of the cerebrospinal fluid (CSF) leak along the neuraxis and guide targeted treatment (algorithm 2). (See 'Management of patients with persistent symptoms' above.)
•Myelography to identify the site of leak – We suggest noncontrast, noninvasive magnetic resonance (MR) myelography using heavily T2-weighted sequences as the initial myelographic study to identify a CSF leak. When noninvasive studies are nondiagnostic, we suggest CT or MR myelography with intrathecal contrast to identify the site of a CSF leak. Digital subtraction myelography may be performed when other myelographic techniques are nondiagnostic and for patients with a suspected CSF-venous fistula. (See 'Myelography with intrathecal contrast' above.)
•Treatment at site of leak – Treatment options for patients with spontaneous intracranial hypotension and a CSF leak and persistent symptoms despite treatment with lumbar EBP include a targeted EBP at the spinal level of the site of the leak and surgical or endovascular repair. (See 'Targeted epidural blood patch at site of leak' above and 'Interventional options for patients with refractory symptoms' above.)
●Prognosis – Spontaneous intracranial hypotension may resolve spontaneously within two weeks. In some cases, it may last months or, in rare cases, years. Some patients have persistent symptoms despite documented resolution of CSF leakage with therapy. (See 'Prognosis' above.)
Some patients may develop transient intracranial hypertension following successful treatment of a CSF leak. Persistent CSF leak has been associated with a long-term risk of superficial siderosis and bibrachial amyotrophy.
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