Bariatric Surgery and Pseudotumor Cerebri

| March 1, 2017

Column Editor: Daniel B. Jones, MD, MS, FASMBS Professor of Surgery, Harvard Medical School Vice Chair, Beth Israel Deaconess Medical Center Boston, Massachusetts

This month: Bariatric Surgery and Pseudotumor Cerebri

by Leith Hathout, BS
Medical Student, Harvard Medical School Boston, Massachusetts

Bariatric Times. 2017;14(3):16–22.

Obesity increases risk for several comorbidities, including many common metabolic, cardiovascular, respiratory, musculoskeletal, and gastrointestinal disorders.One important, but less frequently highlighted, condition associated with obesity is idiopathic intracranial hypertension, commonly referred to as pseudotumor cerebri. This article serves as a review of idiopathic intracranial hypertension and its association with obesity The author also discusses the current literature on treatment of idiopathic intracranial hypertension with bariatric surgery.

Obesity, defined as having a body mass index (BMI) of 30kg/m2 or more, is an increasingly prevalent disease. In the United States, 34.9 percent of adults and approximately 20 percent of adolescents have obesity.[1,2] Additionally, it is estimated that the prevalence of obesity in adults in the United States will increase to greater than 44 percent by 2030 and the prevalence of obesity worldwide continues to increase as well.[3,4] As is well known, obesity increases risk for several comorbidities, including many common metabolic, cardiovascular, respiratory, musculoskeletal, and gastrointestinal disorders. These comorbidities not only increase the overall disease burden of obesity in patients but also increase the financial burden on the healthcare system.[5]

It is well established that weight loss surgery can play a significant role in reducing, or even eliminating comorbidities associated with obesity. As such, the current indications for bariatric surgery rely not only on the calculation of BMI but also on the presence of associated comorbidities, and studies have demonstrated significant rates of improvement or resolution of obesity-related diseases following bariatric surgery.[6–8] Currently, more than 340,000 weight loss surgeries are being performed each year.[9–11]

One important, but less frequently highlighted, condition associated with obesity is idiopathic intracranial hypertension (IIH), commonly referred to as pseudotumor cerebri. This article serves as a review of IIH and its association with obesity as well as an overview of the current data for treatment of IIH with bariatric surgery.

What is IIH and Who Does it Affect?
IIH is typically diagnosed based on fulfillment of the clinical criteria known as the modified Dandy criteria. This includes having increased intracranial pressure demonstrated on lumbar puncture but normal cerebrospinal fluid (CSF) composition in the setting of signs and symptoms consistent with increased intracranial pressure without other neurologic abnormalities or decreased consciousness, as well as lack of evidence of any other identifiable cause of increased intracranial pressure, such as mass lesions, venous sinus thrombosis, or meningitis on neuroimaging or other means of evaluation.[12,13] In the general population, the annual incidence of IIH has been estimated to be approximately 1–2/100,000 people.[14,15] However, the rates of IIH are considerably higher in patients with obesity, and particularly women of childbearing age with obesity, in whom annual incidence has been estimated to be up to 21/100,000, (i.e., a 10-fold increase in incidence as compared to the general population).[15,16] In one study of 50 consecutively diagnosed IIH patients, it was found that 94 percent had obesity and 92 percent were women.[17] Several other studies have also demonstrated a strong association between development of IIH and obesity, particularly in women.[18,19] Given the strong relationship between obesity and IIH as well as the increasing prevalence of obesity, it should not be surprising that the worldwide incidence of IIH is also increasing.[20] While female gender and obesity are the most significant risk factors for IIH, it should be noted that IIH can also be observed in other patient populations and there may be other associated risk factors as well. For example, IIH can be observed in prepubertal children, and in this patient population it has not been clearly associated with increased BMI.[21–23] Additionally, there are data to suggest that up to five percent of patients with IIH report a family history of IIH. Given that this is higher than the prevalence of IIH in patients with obesity, there may also be unknown genetic factors associated with the development of IIH.[24]

Clinical Presentation
Patients with IIH present with symptoms suggestive of increased intracranial pressure. In the Idiopathic Intracranial Hypertension Treatment Trial (IIHTT), which is the largest prospective cohort study of untreated patients with IIH, it was found that the most common presenting symptoms of IIH include headache, pulsatile tinnitus, retrobulbar pain, transient visual obscurations (monocular vision loss lasting seconds, associated with positional changes), photopsia and diplopia, as well as possible permanent visual loss.[24] While headache was the single most commonly reported symptom, headache timing, quality, and severity may be highly variable in patients with IIH. For example, many patients reported constant or daily headaches while others reported only intermittent headaches and the median number of days per month with headache was found to be 12, with a range from 1 to 30. Similarly, patient descriptions of visual disturbances and tinnitus as well as other symptoms may vary significantly.[17, 25] Thus, patients with some constellation of the above symptoms may be suspected of IIH in the appropriate clinical and epidemiological setting, but these symptoms are rarely specific for a diagnosis of IIH and other causes of intracranial hypertension must also be considered.

On physical exam, one of the most common findings in patients with IIH is papilledema, a condition in which increased pressure in or around the brain causes the part of the optic nerve inside the eye to swell. While it is generally bilateral and symmetric, unilateral or asymmetric papilledema may also be noted.[26­–28] In addition to offering diagnostic information, the finding of papilledema is also of prognostic value as patients with more severe papilledema have been shown to be at higher risk of permanent visual loss and patients without papilledema are at lower risk for loss of vision.[27, 29-31] Thus, evaluation for visual loss, which is perhaps the most important cause of morbidity in IIH, is a critical component of assessing patients with IIH. Visual loss in IIH may manifest as decreased visual acuity as well as visual field loss (particularly of peripheral vision although the physiological blind spot may also be pathologically enlarged). The latter is considered to be a somewhat more sensitive indicator of visual loss in IIH at the time of presentation.[24, 32, 33] Various studies have suggested that anywhere from 6 to 24 percent of patients may develop severe visual impairment or blindness.[34–37] The typical course of untreated IIH consists of chronic symptoms lasting months to years with gradual symptomatic progression over time. However, there is a subset of patients who present with a more rapidly progressive course leading to permanent visual loss within weeks of onset.[38–41]

The visual loss observed in IIH is thought to be caused by axoplasmic stasis within the optic nerve. Transmission of increased intracranial pressure causes increased pressure of the optic nerve within its intracranial sheath, and thus the axons traveling within the intracranial portion of the optic nerve experience a much higher pressure than the cell bodies located within the globe because IIH does not increase the pressure within the globe. This difference in pressure along the course of the neurons interferes with normal axonal transport thereby causing axoplasmic stasis, which underlies the development of both papilledema and visual loss in patients with IIH.[42–44]

Pathophysiology of IIH
As its name suggests, the pathophysiology of IIH is not entirely understood. Several mechanisms have been proposed to explain the development of IIH and to attempt to account for the increased incidence in patients with obesity, particularly women of childbearing age (Figure 1). The most commonly cited proposed mechanism for pathogenesis of IIH relates to development of intracranial venous hypertension, as patients with IIH have a similar clinical presentation to patients with conditions such as cerebral venous thrombosis and other causes of obstructed venous outflow. Several reports have described cerebral venous outflow abnormalities on magnetic resonance venography (MRV) in patients diagnosed with IIH, although the frequency and implications of these findings have been controversial.[45–47] In one case-control study, 29 patients diagnosed with IIH were evaluated with MRV and bilateral sinovenous stenosis was found by blinded readers in 27 of the 29 patients as compared to 4 of 59 control patients.[48] While this suggests that increased intracranial venous pressure caused by venous sinus stenosis may play an important role in the development of IIH, this proposed mechanism leaves multiple unanswered questions. For example, it is unclear whether venous sinus abnormalities, such as stenosis, are a primary cause of IIH or if such abnormalities are secondary changes caused by venous compression due to other causes of increased CSF pressure, such as increased CSF production or impaired CSF absorption. Additionally, this mechanism does not directly explain how the pathogenesis of IIH relates to obesity, though theories have been proposed to link the two. For example, it has been suggested that microthromboses of venous sinuses below imaging thresholds for detection may prevent CSF absorption via arachnoid granulations, thereby leading to increased intracranial pressure.[49,50]

The increased intracranial pressure could directly cause IIH as well as secondarily lead to venous sinus stenosis, which would further exacerbate intracranial hypertension.  Given the generally hypercoaguable state associated with obesity, this mechanism would theoretically explain the increased incidence of IIH in patients with obesity. However, impaired absorption of CSF as suggested in this mechanism might reasonably be expected to produce imaging findings of hydrocephalus as do most other causes of CSF overproduction or decreased absorption. However, IIH is not associated with hydrocephalus on neuroimaging.[51]

Other mechanisms to explain the association between obesity and IIH have also been considered. For example, it has been postulated that in addition to increasing intra-abdominal pressure, central obesity may also increase pleural pressure, cardiac filling pressures, and possibly lead to increased intracranial venous pressure.[52] While there is a small amount of evidence to support this premise, there is a paucity of studies done to fully evaluate this theory and, furthermore, this mechanism would not account for cases of IIH in patients without obesity or for the lack of increased incidence of IIH due to other causes of increased intra-abdominal pressure, such as pregnancy.[53–55]

Other researchers have suggested that development of IIH may be related to another comorbidity of obesity, namely obstructive sleep apnea (OSA). It is theorized that the nocturnal hypercarbia in patients with OSA may promote vasodilation of cerebral blood vessels leading to increased cerebral blood flow and, thereby, elevated intracranial pressure.[56–58]

Thus, several mechanisms have been proposed for the pathogenesis of IIH as well as the association between IIH and obesity. Nevertheless, the underlying causes of IIH have yet to be fully elucidated and remain under investigation.

Treatment of IIH
The primary treatment goals in IIH are the resolution of presenting symptoms as well as the preservation of vision. Potentially efficacious treatment strategies include medical management, surgical intervention, and weight loss with or without bariatric surgery. Several classes of medications may be considered in the treatment of IIH. For example, carbonic anhydrase inhibitors, such as acetazolamide and topiramate, are thought to work by reducing the rate of CSF production.[59] While studies such as the NORDIC trial have reported statistically significant, albeit small, improvements in visual field testing and decreased CSF pressure in patients treated with acetazolamide as opposed to placebo, the true clinical significance of these improvements as well as the effect of acetazolamide on long-term prognosis remain unclear.[60–63] Nevertheless, acetazolamide remains an important part of medical management of IIH. Furthermore, loop diuretics have been considered a useful adjunctive therapy to acetazolamide and may help normalize CSF pressure and reduce papilledema.[64,65] Indomethacin has also been explored as a possible treatment for IIH and has been shown to help reduce CSF pressure and produce symptomatic relief. It is thought to exert these effects by causing cerebral vasoconstriction, thereby reducing cerebral blood flow.[66,67]

While serial lumbar punctures are theoretically an effective treatment, CSF volume quickly recovers. Serial lumbar punctures are an impractical primary treatment strategy due to adverse effects, including pain associated with the procedure as well as risk for complications like headache, CSF leak, or infection. Historically, lumbar punctures had a role in IIH treatment as a temporizing measure until more definitive treatment could be offered, but these are no longer recommended.[55,68,69]

The main nonbariatric surgical interventions employed in the treatment of IIH are CSF shunting procedures and optic nerve sheath fenestration (ONSF). The primary indication for surgery is worsening vision despite maximal medical therapy, but surgery may also be indicated for resolution of other symptoms, such as intractable headaches. With regards to CSF shunting, available procedures include ventriculoperitoneal shunting (VPS) and lumboperitoneal shunting (LPS). The efficacy of shunting procedures in IIH treatment remains controversial. While most studies demonstrate headache relief shortly after shunting procedures, the effect on visual loss is far less clear as some studies report up to 95-percent remission or stabilization of visual disturbances while others report progressively worsening visual symptoms in up to one-third of patients after shunting procedures.[58,70–75] Furthermore, shunting procedures can have high rates of complications. The most common complication is the need for shunt revision and this can occur in up to 86 percent of patients, while some will require multiple revisions.[58,72–76] Shunt infection and CSF leak are other common complications.[77] In contrast to the somewhat more controversial data on efficacy of shunting procedures, several studies have demonstrated the benefit of ONSF in preserving visual function in patients with IIH-associated papilledema.[71] As noted above, papilledema and visual loss in IIH are caused by axoplasmic stasis within the neurons that compose the optic nerve. Fenestration of the optic nerve sheath decreases the pressure of the optic nerve within the optic nerve sheath, thereby relieving the mechanism underlying development of axoplasmic stasis and associated papilledema and visual loss. As evidence of this, in one of the largest available data sets, ONSF led to stabilization or improvement of visual fields and acuity in 88 percent and 94 percent of patients, respectively.[78] Thus, while ONSF can be effectively used to manage the visual loss associated IIH, it must also be noted that this procedure does not address the underlying intracranial hypertension and so it cannot be used to address other symptoms of IIH, such as headache. This is in contrast to CSF shunting procedures, which may address both headache and visual loss as discussed above.

Weight loss is another essential component to the treatment of IIH and may be even more beneficial than medical or surgical management, especially among patients with severe obesity (BMI > 35kg/m2). All patients with overweight and obesity diagnosed with IIH should be counseled regarding weight loss.[79] Strategies for promoting weight loss include lifestyle modifications, such as regular exercise and dietary modification as well as bariatric surgery. With regards to bariatric surgery, common surgical procedures include Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and laparoscopic adjustable gastric banding (LAGB). The expected loss of excess weight after two years from RYGB, SG, and LAGB are approximately 70 percent, 60 percent, and 50 percent respectively.[63, 80–83] Given the potential for bariatric surgery to produce significant and sustained weight loss, it is reasonable to consider the role of bariatric surgery in the treatment of IIH.

It is important to note, however, that isolating the effects of weight loss in patients with IIH has proven difficult as most studies include patients simultaneously engaged in other treatment modalities. Nonetheless, several studies have sought to measure the efficacy of weight loss, with and without bariatric surgery, in resolution of IIH symptoms and preservation of vision.
One recent systematic review compared eight studies comprised of a total of 277 patients who underwent weight loss programs without surgical intervention with seven studies comprised of a total of 65 IIH patients who underwent weight loss surgery, including LAGB, SG, and RYGB.[84]

With regards to weight loss, patient in the nonsurgical groups had an average reduction in BMI of 4.2 kg/m2 whereas patients undergoing bariatric surgery had an average reduction in BMI of 17.5 kg/m2. Patients undergoing surgery had 100-percent resolution of papilledema in all reported results. Additionally, surgery was associated with clinically significant decreases in CSF pressure. In two of the surgical studies analyzed, for example, average CSF pressure decreased by 185mm and 196mm H2O, respectively. For reference, the maximum opening pressure considered normal in the general population is approximately 200mm H2O, whereas a slightly higher maximal normal opening pressure of 250mm H2O may be more appropriate in patients with obesity.[85,86] These results are clearly indicative of decreased intracranial pressure in patients who undergo bariatric surgery. Furthermore, bariatric surgery was associated with resolution of headaches in 90.2 percent of patients. With regards to resolution of visual disturbances, only two out of the seven studies of patients undergoing bariatric surgery reported outcome data from visual field examination, making evaluation of the effect of bariatric surgery on preservation of vision incomplete. However, one study of eight patients who underwent RYGB with a decrease in mean BMI from 49 to 27.5kg/m2 reported improvement of visual field deficits in every patient.[85] The other study that reported data on visual field deficits included four patients who underwent LAGB, two of whom had pre-operative visual field deficits. Both experienced improvement, but not full resolution, of visual field deficits postoperatively.[87] In comparison, patients in the nonsurgical group experienced improvement of papilledema in 66.7 percent of cases, visual field deficits in 75.4 percent of cases, headache in 23.2 percent of cases, and an average decrease in CSF opening pressure of 61.0mmHg.

Comparing these outcomes between the surgical and nonsurgical groups demonstrates superior efficacy of bariatric surgery in alleviating disease burden of IIH. This is in keeping with the well-established evidence that bariatric surgery leads to greater and more sustained weight loss as well as higher remission rates of several other obesity related comorbidities than nonoperative management.[7,88]

Limitations. While this systematic review suggests a prominent role for weight loss in the treatment of IIH, and specifically the potential efficacy of bariatric surgery, there are several important limitations. First, the surgical studies are relatively small and comprise a total of only 65 patients. Second, the individual studies included are generally observation rather than prospective, randomized, control trials. Third, bariatric surgery would not be an appropriate treatment in the subset of patients with IIH who do not have obesity or overweight or who are not suitable surgical candidates. Additionally, bariatric surgery is not appropriate in the subset of patients with rapidly progressive visual loss, given that it entails a lengthy pre-operative process as well as postoperative time required for significant reduction in BMI. Nevertheless, bariatric surgery remains a promising component of IIH treatment that directly intervenes on one of the presumed underlying disease processes of IIH rather than simply treating the downstream effects of these processes as do other interventions, such as nonbariatric surgical interventions like CSF shunting procedures.

Several authors have suggested that IIH be formally and consistently included in worldwide clinical practice guidelines for indications for bariatric surgery.[83,89] While the theoretical basis for benefit of bariatric surgery in patients with IIH is clear and the available data supports the notion of significant clinical improvement following bariatric surgery, further research is necessary to answer several remaining questions, including which bariatric procedure is most beneficial for these patients as well as the most appropriate BMI and symptomatic criteria such that the expected benefits outweigh the risks of surgery.

The author of this article would like to thank Nurhan Torun, MD for her invaluable assistance with reviewing this article. Dr. Torun is on staff in the Division of Ophthalmology at Beth Israel Deaconess Medical Center (BIDMC) and serves as Assistant Professor of Ophthalmology at Harvard Medical School, Boston, Massachusetts.

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FUNDING: No funding was provided.

FINANCIAL DISCLOSURES: The author reports no conflicts of interest relevant to the content of this article.

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