Bariatric Times

MAR 2017

A peer-reviewed, evidence-based journal that promotes clinical development and metabolic insights in total bariatric patient care for the healthcare professional

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18 The Medical Student Notebook Bariatric Times • March 2017 with IIH were evaluated with MRV a nd 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 v enous pressure caused by venous sinus stenosis may play an important role in the development of IIH, this proposed mechanism leaves multiple unanswered q uestions. For example, it is unclear whether venous sinus abnormalities, such as stenosis, are a primary cause of IIH or if such abnormalities are secondary c hanges caused by venous compression due to other causes of increased CSF pressure, such as increased CSF production or impaired CSF absorption. A dditionally, this mechanism does not directly explain how the pathogenesis of IIH relates to obesity, though theories have been proposed to link the two. For e xample, it has been suggested that microthromboses of venous sinuses below imaging thresholds for detection may prevent CSF absorption via arachnoid g ranulations, thereby leading to increased intracranial pressure. 49,50 The increased intracranial pressure could directly cause IIH as well as secondarily lead to venous sinus s tenosis, which would further exacerbate intracranial hypertension. Given the generally hypercoaguable state associated with obesity, this mechanism would t heoretically explain the increased incidence of IIH in patients with obesity. However, impaired absorption of CSF as suggested in this mechanism might reasonably be e xpected to produce imaging findings of hydrocephalus as do most other causes of CSF overproduction or decreased absorption. However, IIH is not a ssociated with hydrocephalus on neuroimaging. 51 Other mechanisms to explain the association between obesity and IIH have also been considered. For e xample, it has been postulated that in addition to increasing intra- abdominal pressure, central obesity may also increase pleural pressure, cardiac filling pressures, and p ossibly 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 f ully 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 d ue 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

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