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Show Primary Spontaneous Cerebrospinal Fluid Leaks and Idiopathic Intracranial Hypertension Mario A. Pérez, MD, Omer Y. Bialer, MD, Beau B. Bruce, MD, MS, Nancy J. Newman, MD, Valérie Biousse, MD Introduction: Idiopathic intracranial hypertension (IIH) is increasingly recognized as a cause of spontaneous cere-brospinal fluid (CSF) leak in the otolarnygological and neurosurgical literature. The diagnosis of IIH in patients with spontaneous CSF leaks typically is made a few weeks after surgical repair of the leak when symptoms and signs of elevated intracranial pressure (ICP) appear. Methods: Case reports and literature review. Two young obese women developed spontaneous CSF rhinorrhea related to an empty sella in one and a cribriform plate encephalocele in the other. Both patients underwent surgical repair of the CSF leak. A few weeks later, they developed chronic headaches and bilateral papilledema. Lumbar punctures showed elevated CSF opening pressures with normal CSF contents, with temporary improvement of headaches. A man with a 3-year history of untreated IIH developed spontaneous CSF rhinorrhea. He experienced improvement of his head-aches and papilledema after a CSF shunting procedure, and the rhinorrhea resolved after endoscopic repair of the leak. Results: These cases and the literature review confirm a definite association between IIH and spontaneous CSF leak based on: 1) similar demographics; 2) increased ICP in some patients with spontaneous CSF leak after leak repair; 3) higher rate of leak recurrence in patients with raised ICP; 4) patients with intracranial hypertension secondary to tumors may develop CSF leak, confirming that raised ICP from other causes than IIH can cause CSF leak. Conclusions: CSF leak occasionally may keep IIH patients symptom-free; however, classic symptoms and signs of intracranial hypertension may develop after a CSF leak is repaired, exposing these patients to a high risk of recurrence of the leak unless an ICP-lowering intervention is performed. Journal of Neuro-Ophthalmology 2013;33:330-337 doi: 10.1097/WNO.0b013e318299c292 © 2013 by North American Neuro-Ophthalmology Society Cerebrospinal fluid (CSF) leaks traditionally have been classified as traumatic or nontraumatic (1,2). Non-traumatic CSF leaks may be spontaneous in the absence of obvious cause, such as skull base abnormalities or bone erosion related to a mass lesion or hydrocephalus (1-3). Spontaneous CSF leaks sometimes are referred to as high-pressure leaks when increased intracranial pressure (ICP) is a contributing factor (2,3). Idiopathic intracranial hyperten-sion (IIH) is increasingly recognized as a cause of sponta-neous CSF leak in the otolaryngological and neurosurgical literature. There are reports suggesting that the so-called primary spontaneous CSF leaks might be due to IIH (2-8). Some of these patients are asymptomatic or only have symp-toms attributable to the CSF leak (such as rhinorrhea, CSF hypotension-related headaches, or bacterial meningitis) while the leak is active. The diagnosis of IIH is typically made weeks or months after surgical repair of the leak (9). At times, pa-tients with a known diagnosis of IIH may develop a spontane-ous CSF leak, presumably secondary to the chronically raised ICP with skull base erosion and meningoceles (2). MATERIALS AND METHODS Medical records and neuroimaging of the illustrative cases were reviewed. PubMed was searched for English-language articles published before January 2013 using the search terms "idiopathic intracranial hypertension," "encephalocele," "skull-base defect," "spontaneous cerebrospinal fluid leak," "CSF rhinorrhea," and "CSF otorrhea." The reference lists of identified articles were searched for further relevant articles. Departments of Ophthalmology (MAP, OYB, BBB, NJN, VB), Neu-rology (BBB, NJN, VB), and Neurological Surgery (NJN), Emory University, Atlanta, Georgia. The authors report no conflicts of interest. Supported in part by an unrestricted departmental grant (Depart-ment of Ophthalmology) from Research to Prevent Blindness, Inc, New York, and by National Institutes of Health/National Eye Insti-tute (NIH/NEI) core grant P30-EY06360 (Department of Ophthal-mology). B. B. Bruce receives research support from the NIH/NEI (K23-EY019341). N. J. Newman is a recipient of the Research to Prevent Blindness Lew R. Wasserman Merit Award. M. A. Pérez re-ceives support from a scholarship-loan program by COLFUTURO (Bogotá DC, Colombia). Address correspondence to Valérie Biousse, MD, Neuro-Ophthalmology Unit, Emory Eye Center, The Emory Clinic, 1365-B Clifton Road NE, Atlanta, GA 30322; E-mail: vbiouss@emory.edu 330 Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. CASE REPORTS Case 1 A 49-year-old obese African American woman developed isolated CSF rhinorrhea, which initially was mistaken for sinusitis. One year later, she developed bacterial meningitis, and computed tomography (CT) demonstrated a skull-base defect in the right cribiform area causing meningocele with CSF leak (Fig. 1A). She underwent endoscopic sinus surgery with repair of the leak. Three months later, she complained of headaches and transient visual obscurations and was found to have bilat-eral papilledema (Fig. 1B). Automated perimetry showed enlarged blind spots and nasal visual field loss (Fig. 1C). Lum-bar puncture revealed increased CSF opening pressure (OP) of 37 cm H2O and resulted in temporary resolution of the head-aches. She underwent a ventriculoperitoneal shunt with imme-diate resolution of her symptoms of raised ICP; papilledema resolved within 1 month. The CSF leak did not recur. Case 2 A 32-year-old obese Caucasian woman was found to have isolated CSF rhinorrhea after presenting with postural headaches. Brain imaging showed an empty sella and intrasellar bone erosion (Fig. 2A, B). She underwent endo-scopic surgical repair of the CSF leak, and her headaches resolved after the procedure. A few weeks later, persistent headaches developed, and she experienced transient visual obscurations. She was found to have bilateral optic disc edema (Fig. 2C) with enlarged blind spots on visual field examination. Lumbar puncture showed elevated CSF OP of 42 cm H2O and resulted in temporary resolution of head-aches. The patient subsequently underwent a CSF shunt-ing procedure with complete resolution of all symptoms of intracranial hypertension; at 6 weeks of follow-up, papilledema had resolved. The CSF leak did not recur. Case 3 A 43-year-old mildly overweight Caucasian man was followed for 3 years for symptomatic IIH treated intermittently with acetazolamide. He had moderate bilateral papilledema with enlarged blind spots in his visual fields but only mild headaches, and generally did well without treatment. He was reevaluated for worsening headaches, which were occurring daily and associated with tinnitus and transient visual obscurations. Repeat neuro-ophthalmic examination showed persistent, bilateral papilledema (Fig. 3A) and stable visual fields. Repeat lumbar puncture showed elevated CSF OP of 33.5 cm H2O. His headaches improved, but he developed CSF rhinorrhea. Neuroimaging showed a right cribriform plate defect (Figs. 3B & 3C), an empty sella, and bilateral transverse sinus stenoses (Fig 3D). The patient was placed on prophylactic antibiotics and underwent a ventricu-loperitoneal shunt. CSF rhinorrhea markedly decreased, and endoscopic repair of the leak was subsequently performed, with immediate resolution of the leak. However, 6 weeks later, the leak recurred in the setting of recurrent increased ICP secondary to proximal shunt obstruction. The shunt was revised, and the CSF leak resolved. One month later, he remained asymptomatic, with improvement of his papilledema. Review of the Literature Table 1 presents a summary of reports in the English liter-ature of spontaneous CSF leaks associated with presumed or diagnosed IIH (2-24). DISCUSSION IIH is increasingly recognized as a cause of primary sponta-neous CSF leaks. Over the past 2 decades, several articles on this topic have been published mostly in the otolaryngo-logical and neurosurgical literature (2-25). These reports highlight the similarities between the demographics of pa-tients with IIH and those with spontaneous CSF leaks suggesting a causal relationship between IIH and the so-called spontaneous CSF leak (Table 1). Similar to IIH patients, reported cases of spontaneous CSF leak are often young or middle-age obese women, with a mean body mass index (BMI) greater than 30 kg/m2 FIG. 1. Case 1. A. Coronal computed tomography of the brain without contrast reveals dehiscence of the right cribiform plate with soft tissue in the right olfactory recess (arrow) consistent with a meningocele. B. Following repair of the cerebrospinal fluid leak, the patient developed bilateral papilledema. C. Automated visual fields, performed on the SITA-fast 24-2 program, show an enlarged blind spot and nasal field loss in each eye. Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 331 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. (4,24) (Table 1). Such demographic overlap also is shared by patients with primary empty sella syndrome, an endo-crinologic entity in which chronically increased ICP may be a contributing factor (26,27). In a retrospective study of 11 patients with b-2 transferrin-proven spontaneous CSF leaks, 72% of patients met the criteria for the diagnosis of IIH (5). Obesity has been suggested as an independent risk factor for the development of spontaneous CSF leaks and spontaneous encephaloceles, and the BMI of these patients is significantly higher than in those of patients developing CSF leaks for other reasons. In 1 study specifically per-formed to evaluate the role of obesity (BMI $ 30 kg/m2) in spontaneous encephaloceles and CSF leak, the mean BMI of the patients with spontaneous encephaloceles was 33.4 kg/m2 vs 27.0 kg/m2 in the group of nonspontaneous encephaloceles (28). The presenting symptoms of spontaneous CSF leaks vary greatly depending on multiple factors, including the FIG. 2. Case 2. A. Postcontrast sagittal T1 magnetic resonance imaging shows an empty sella (arrow). B. Coronal computed tomography reveals intrasellar bone erosion (asterisk). C. After repair of the cerebrospinal fluid leak, there is bilateral papilledema. OD, right eye; OS, left eye. FIG. 3. Case 3. A. Bilateral papilledema is seen on funduscopic examination. B. Noncontrast coronal computed tomography shows dehiscence of the right cribiform plate (arrow) with soft tissue in the right olfactory recess, consistent with me-ningocele. C. Coronal T2 magnetic resonance imaging demonstrates fluid and soft tissue in the right olfactory recess (arrowhead) and distension of the perioptic nerve subarachnoid space (arrows). D. Bilateral transverse sinus stenoses (arrows) are present on coronal magnetic resonance venogram. 332 Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. TABLE 1. Reports in the English literature of patients with CSF leaks associated with symptoms and signs of presumed idiopathic intracranial hypertension Case Series (Reference) Number of Cases % Women Mean age (Years) BMI (kg/m2) CSF OP (cm H2O) Clinical Presentation Site of Leakage (Number of patients) Treatment Diagnosis of IIH Brisman et al*(10) 1 100 44 ? "Elevated" Rhinorrhea Cribiform plate Surgical (craniotomy + sealing of the cribiform plate with muscle) Yes Applebaum and Desai (11) 1 100 52 "Moderately obese" ? Rhinorrhea, previous meningitis Sella turcica Surgical repair Maybe Eljamel and Foy (12) 2 ? ? ? "High" Rhinorrhea ? LP shunt in one of the patients, unknown for the other patient Yes Clark et al (2) 4 100 38 ? 32 Rhinorrhea Cribiform plate Surgical repair/lumbar punctures/diuretics Yes Camras et al (13) 1 100 46 "Obese" 25 Rhinorrhea, headaches Anterior cranial fossa Bifrontal craniotomy + fascia lata graft Yes Mokri (9) 4 100 27 ? 30.8 Orthostatic headaches-after repair: elevated ICP related-symptoms Spinal Surgical repair Maybe Owler et al (14) 1 100 38 ? ? Rhinorrhea, visual disturbances, headaches Anterior cranial fossa Craniotomy + LP shunt; transverse sinus stenting Yes Schlosser et al (4) 16 81 49.6 35.9 26.5 Rhinorrhea, symptoms of elevated ICP Lateral sphenoid recess (8), central sphenoid (4), ethmoid roof (4), cribiform (2), supraorbital/posterior frontal recess (2), frontal sinus (2) Surgical repair Yes Schlosser and Bolger (15) 16 81 49.6 35.9 28.3 Rhinorrhea, symptoms of elevated ICP Lateral sphenoid recess (8), central sphenoid (4), ethmoid roof (4), cribiform (2), supraorbital/posterior frontal recess (2), frontal sinus (2) Surgical repair Yes Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 333 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. (Continued ) Case Series (Reference) Number of Cases % Women Mean age (Years) BMI (kg/m2) CSF OP (cm H2O) Clinical Presentation Site of Leakage (Number of patients) Treatment Diagnosis of IIH Mirza et al (16) 11 ? ? ? ? Rhinorrhea, meningitis Sinonasal Surgical repair (+ CSF shunting in 3 patients) Yes Rudnick and Sismanis (8) 1 100 33 48.8 26 Rhinorrhea Cribiform plate Gastric bypass (weight loss) Yes Dunn et al (17) 15 93 50 "Obese" ? ? Roof of the ethmoid (6), sphenoid (5), cribiform plate (4) Endoscopic repair Maybe Schlosser et al (5) 16 81 49.6 35.9 31.1 Rhinorrhea, symptoms of elevated ICP Lateral sphenoid recess (8), central sphenoid (4), ethmoid roof (4), cribiform (2), supraorbital/posterior frontal recess (2), frontal sinus (2) Surgical repair Yes Prichard et al (18) 8 50 58 34.9 ? Hearing loss, meningitis, otorrhea, rhinorrhea Posterior fossa Surgical repair; LP shunt (in 1 patient) Maybe Ransom et al (19) 1 100 53 ? "Elevated" Postural headaches, rhinorrhea Roof of the ethmoid sinus Revision of VP shunt Maybe Suryadevara et al (6) 2 100 47 "Obese" 26 Rhinorrhea, headaches, rhinorrhea, meningitis Cribiform plate Surgical repair Yes Woodworth et al (20) 55 78 61 43 patients: .30, only one was ,25 27 ? Lateral sphenoid sinus (23), ethmoid roof (17), cribiform plate (12), central sphenoid (7), frontal sinus (7) Surgical Maybe Stangherlin et al (21) 1 100 45 48 ? Rhinorrhea Left posterior ethmoidal cell Gastric banding (weight loss) Maybe 334 Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. (Continued ) Case Series (Reference) Number of Cases % Women Mean age (Years) BMI (kg/m2) CSF OP (cm H2O) Clinical Presentation Site of Leakage (Number of patients) Treatment Diagnosis of IIH Seth et al (22) 39 85 57.7 38.5 24 ? Cribiform plate, sphenoid lateral pterygoid recess, ethmoid roof Surgical repair (+acetazolamide in 9 patients) (+CSF shunting in 6 patients) Maybe Reh et al (23) 12 92 ? 40 Monitoring: .25 (at least 4% of the time) Rhinorrhea, headaches, tinnitus Sphenoid, ethmoid, cribiform Endoscopic repair + lumbar drain with continuous CSF pressure monitoring Maybe Yang et al (3) 21 86 53 31.2 25.5 Rhinorrhea Ethmoid sinus (13), lateral sphenoid sinus (7), frontal sinus (1) Surgical repair + oral diuretics (in some cases) Yes Brainard et al (7) 9 89 57 41 24.5 Otorrhea ? ? Yes Rosenfeld et al (24) 4 100 42 34.7 30.6 Rhinorrhea, otorrhea Cribiform plate, middle ear Surgical repair in 2 patients and CSF shunting in 2 patients Yes *This study also reports 4 additional women with spontaneous CSF leaks and empty sella, but no diagnosis of IIH. BMI, body mass index; CSF OP, cerebrospinal fluid opening pressure; ICP, intracranial pressure; IIH, idiopathic intracranial hypertension; LP, lumboperitoneal; VP, ventriculoperitoneal; ?, not known/undetermined. Pérez et al: J Neuro-Ophthalmol 2013; 33: 330-337 335 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. location and activity of the leak, and the presence of con-current signs of raised ICP. If the leak is active, symptoms and signs of intracranial hypotension (e.g., orthostatic headaches, neck stiffness) may occur (9). Depending on the location of the leak, CSF otorrhea and conductive hypoacusia may be a presenting sign in patients with bone defects in the posterior fossa (24), whereas CSF rhinorrhea usually devel-ops in patients with defects of the cribiform plate (6,8,29). Bacterial meningitis may be the initial presentation leading to the discovery of the CSF leak. Some patients may have symptoms of increased ICP even when the leak is active (including headache, tinnitus, visual disturbances, and pap-illedema) (2), but most often, patients develop symptoms and signs of intracranial hypertension only after the CSF leak has been repaired (9,30). The factors predisposing some IIH patients to develop spontaneous CSF leaks remain unclear, although it is likely that chronically elevated ICP is necessary, as demonstrated by our third patient. Some patients with increased ICP secondary to intracranial tumors (distant from the skull base) or hydrocephalus may also develop CSF leak, confirming that raised ICP in itself can cause CSF leaks, possibly through remodeling of the skull base and resultant encephaloceles (1,2,31,32). CT and MRI of the brain are required to identify skull base defects. Often, these studies show imaging findings associated with increased ICP (32). A retrospective study showed that 100% of patients with spontaneous CSF leaks had a completely or partially empty sella compared with 11% of patients with nonspontaneous CSF leaks and 5%-6% of the general population (15). Tortuosity of the optic nerves, increased CSF around the optic nerves, arachnoid pits and dural ectasias are other radiological findings often observed in patients with both IIH and spontaneous CSF leaks (31). The most frequent site of skull basal defects includes the ethmoid sinuses and lateral wall of the sphenoid sinus (3). In addition, there are reports that spinal CSF leak might be associated with increased ICP (9). Given the overlapping clinical and neuroimaging profiles, it has been proposed that patients with primary spontaneous CSF leaks may have a variant of IIH (5). Spontaneous CSF leak patients may develop raised ICP once the leak is repaired (9,25), as did 2 of our patients. In a small prospective study measuring ICP through lumbar catheters after surgical repair of spontaneous CSF leaks, elevated ICP was observed in 7 of 8 patients and in none of 3 patients with traumatic CSF leaks (30). Although spontaneous resolution of spontaneous CSF leak may occur after treatment of increased ICP, the high risk of bacterial meningitis usually requires endoscopic surgical repair of the skull base defect (33). Interestingly, following skull base surgical repair in patients with spontaneous CSF leak, the leak recurrence rate is high, ranging from 25% to 87% (2,3,20). This high rate of recurrence likely reflects excessive elevation of ICP that occurs after leak repair in those patients with presumed IIH (30). Obesity (common in IIH) is also associated with the failure of the CSF leak repair (21). Appropriate ICP-lowering management usually is the first step in managing patients with CSF leak. Reh et al (23) proposed monitoring of CSF pressure through a lumbar drain to assess response to a therapeutic trial of acetazol-amide before surgical intervention. Once there is appropri-ate control of ICP, the rate of success of the spontaneous CSF leak repair approaches 95% and is similar to that of repair of CSF leaks due to other causes (2). It has been proposed that interventions to lower the ICP including medical therapy (weight loss, acetazolamide) or a CSF diver-sion procedure be performed before or at the time of surgical repair of the skull base (20, 25). Our patients underwent CSF shunting procedures as the first-line treatment due to concern that medical management alone might not result in an immediate and dramatic decrease in ICP, necessary to prevent visual loss from papilledema. Indeed, recurrence of the leak occurred in the patient who had shunt malfunc-tion soon after surgery. 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