Idiopathic Intracranial Hypertension Group Research Articles

Trigeminal Hyperexcitability in Idiopathic Intracranial Hypertension: A Blink Reflex Study.

To compare blink reflex examination findings in patients with idiopathic intracranial hypertension (IIH) with migraineurs and controls and to investigate the role of blink reflex data in the follow-up by evaluating their relationship with clinical symptoms. We included 23 patients with IIH, 15 migraineurs, and 16 controls. Blink reflex was studied with bilateral paired stimulations, and the 2R2/1R2 and 2R2c/1R2c area ratios, 1R2, 2R2, 1R2c, and 2R2c latencies were compared (R2:ipsilateral R2 response, R2c:contralateral R2 response). 2R2/1R2 area ratios at 200, 300, and 500 ms interstimulus intervals were significantly higher in the IIH group compared with the controls, and significantly higher 2R2/1R2 area ratio at 200 ms interstimulus interval was also detected in the IIH group compared with the migraine group. Significantly shorter 2R2 latencies were found at 500 and 800 ms interstimulus intervals in IIH group compared with the migraine group and controls. Significantly higher 2R2/1R2 area ratios at 500, 800 ms, and 2R2c/1R2c area ratios at 300, 500, and 800 ms were detected in patients with IIH in remission compared with patients with attacks. The significant increase in R2 recovery rates in patients with IIH in remission suggests that there is an increased excitability in the trigeminal pathways. Our findings may provide a new perspective for IIH mechanism related to trigeminal hyperexcitability and evaluating new management strategies.

Quantitative Pupillometry for Detection of Intracranial Pressure Changes During Head-Down Tilt.

There is a need to develop noninvasive methods to monitor intracranial pressure (ICP). Pupillary reactivity decreases in patients with elevated ICP with demonstrated cerebral edema. We sought to determine whether pupillary reactivity is affected when ICP is elevated in the absence of brain edema. Healthy subjects and individuals with idiopathic intracranial hypertension (IIH) underwent pupillometry in different positions (upright, supine, and head-down tilt) and during different physiological maneuvers. A separate group of healthy subjects were tested in the upright resting position only. The pupillary dynamics were measured with a pupillometer. Healthy and IIH subjects were enrolled. In the healthy subjects the change from upright to head-down tilt led to a Neurological Pupil Index (NPI) decrease from 4.30 to 4.12, while maximum pupil size and minimum pupil size increased from 4.74 to 5.19 and 3.04 to 3.44, respectively. In the IIH group the maximum pupil size, minimum pupil size, and latency increased in magnitude with a decline in head tilt. The mean NPI of IIH subjects, 4.37, was greater than the healthy mean, 4.25. Also, the mean IIH Max and Min, 5.02 and 3.25, were greater than the healthy mean, 4.62 and 2.92. We observed changes in the pupillary reactivity in all subjects based on changes in position and task. There were also differences between the healthy and IIH subjects. This is consistent with our hypothesis that elevated intracranial pressure may result in decreased pupillary reactivity even in the absence of brain edema.Soeken TA, Alonso A, Grant A, Calvillo E, Gutierrez-Flores B, Clark J, Donoviel D, Bershad EM. Quantitative pupillometry for detection of intracranial pressure changes during head-down tilt. Aerosp Med Hum Perform. 2018; 89(8):717-723.

Cerebrospinal Fluid and Cerebral Blood Flows in Idiopathic Intracranial Hypertension.

Cerebrospinal fluid (CSF) and blood flows have a strong relationship during a cardiac cycle. Idiopathic intracranial hypertension (IIH) is a pathology that seems to present hemodynamic and hydrodynamic disturbance. The aim of this study was to establish CSF and blood interaction in IIH. We retrospectively studied cerebral hydrodynamic and hemodynamic flows by phase-contrast MRI (PCMRI) in 13 IIH subjects (according Dandy's criteria) and 16 controls. We analyzed arterial peak flow, pulsatility index, and resistive index in arterial and venous compartments (PFart, PIart, RIart, PFvein, PIvein, RIvein) and measured arteriovenous and CSF peak flow and stroke volume (PFav, SVVASC, PFCSF, SVCSF). We found no significant difference between IIH and control groups in arterial and venous parameters. Arteriovenous flow analysis showed higher PFav and SVVASC in the IIH group than in the control group (respectively 369 ± 27 mL/min and 286 ± 47 mL/min, p = 0.02; and 1085 ± 265 μL/cardiac cycle and 801 ± 226 μL/cardiac cycle, p = 0.007). PFCSF and SVCSF were higher in the IIH group than in the control group (respectively 206 ± 50 mL/min and 126.6 ± 24.8 mL/min, p = 0.04; and 570 ± 190 μL/cardiac cycle and 430 ± 100 μL/cardiac cycle, p = 0.0007). Although no significant change was found in arterial and venous flows, we showed that a small phase shift of venous outflow might cause an increase in the arteriovenous pulsatility and an increasing brain expansion during the cardiac cycle. This arteriovenous flow increase would result in an increase of CSF flushing through the foramen magnum and an increased ICP.

Is cerebral edema effective in idiopathic intracranial hypertension pathogenesis?: Diffusion weighted MR imaging study

The aim of this study is to research whether cerebral edema is effective in the pathogenesis of patients with idiopathic intracranial hypertension (IIH) by using diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC) measurements. Was changed into thirty-six IHH patients who received DWI and 36 age- and sex-matched healthy control group were assessed retrospectively. ADCmin, ADCmean, and ADCmax values were measured from different regions of the brain for both IHH patients and the control group. The StudentÂ’s t-test was used to compare the ADCmin, ADCmax, ADCmean values acquired from distinct parts of the brain parenchyma of IIH patients with the values of control group. No significant difference was found between ADCmin, ADCmax, and ADCmean values of IIH and control group in bilateral frontal, parietal temporal and occipital lobe cortical and subcortical white matter, caudate nucleus head, putamen, thalamus, corpus callosum splenium and genu (P>0.05). This study showed that cerebral edema cannot be a significant mechanism in the pathogenesis of IIH.

Intracranial elastance is increased in idiopathic intracranial hypertension.

To date, no pathophysiological model has sufficiently accounted for all the findings encountered in patients with idiopathic intracranial hypertension (IIH). Intracranial elastance is an index of volume-buffering capacity known to play a role in certain disorders of cerebrospinal fluid (CSF) dynamics, which has not been previously investigated in relation to IIH patients. This was a single-center retrospective cohort study from 1 July 2011 to 1 July 2016. Values for opening pressure (PO ), closing pressure (PC ) and volume (V) of CSF removed were collected, as well as demographic and clinical covariates. Intracranial elastance (E) and pressure-volume index (PVI) were calculated according to established equations: E = (PO -PC )/V and PVI = V/log10 (PO /PC ), respectively. Those with an alternative central nervous system pathology, including meningitis, encephalitis and normal pressure hydrocephalus were excluded. Eligible patients were subdivided into two groups based on final diagnosis: a control group and an IIH group. In our cohort (n = 49), a significant association of both E (P < 0.0001) and PVI (P = 0.005) with a diagnosis of IIH was observed. Median E was 0.45 [interquartile range (IQR) 0.29-0.63] in the control group and 1 (IQR 0.59-1.29) in the IIH group, and median PVI was 98.07 (IQR 59.92-135.86) in the control group and 64.1 (IQR 42.4-91.7) in the IIH group. Neither E nor PVI were significantly associated with age, gender or body mass index. PVI was independent of opening pressure. As calculated by clinically accessible indices, our study provides evidence that intracranial elastance is increased in IIH, reflecting a novel insight into disease pathogenesis.

Sigmoid Sinus Diverticulum, Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension?

Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group. CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (n = 42), without pulsatile tinnitus (n = 37), and controls (n = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence. Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (P < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (P = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group. While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension.

Increased Curvature of the Tentorium Cerebelli in Idiopathic Intracranial Hypertension.

Transverse sinus effacement is detectable on MRV examinations in almost all patients with idiopathic intracranial hypertension. This effacement of the transverse sinus is presumed to be mediated by elevation of intracranial pressure, resulting in compression and inward collapse of the dural margins of the sinus. We sought to establish whether supratentorial broad-based downward deformity of the tentorium might explain transverse sinus effacement in idiopathic intracranial hypertension. MRV examinations of 53 adult patients with idiopathic intracranial hypertension were reviewed retrospectively and compared with 58 contemporaneously acquired controls. The curvature of the tentorium with reference to a line connecting the transverse sinus laterally with the confluence of the tentorial leaves medially was calculated as a segment of a circle. The height and area of the segment and the angle subtended by the midpoint of the tentorium from the falx were calculated. The height and area of the segment described by the chord connecting the transverse sinus with the apex of the tentorial confluence and subtended midtentorial angle were greater in the idiopathic intracranial hypertension group; this finding supports the hypothesis that increased tentorial bowing is present in idiopathic intracranial hypertension. Increased bowing of the tentorium in patients with idiopathic intracranial hypertension compared with controls is a new observation, lending itself to new hypotheses on the nature and localization of elevated intracranial pressure in idiopathic intracranial hypertension. Bowing of the tentorium may play a part in distorting the contour of the transverse sinuses, resulting, at least in part, in the effacement of the transverse sinuses in idiopathic intracranial hypertension.

High-resolution transbulbar ultrasonography helping differentiate intracranial hypertension in bilateral optic disc oedema patients.

The enlargement of optic nerve sheath diameter (ONSD) has been proven to be related with raised intracranial pressure (ICP). No prospective study has been focused on utilizing retrobulbar ultrasonography in optic disc oedema patient presented to ophthalmologist. High-resolution transbulbar ultrasonography was performed in a cohort of patient presented with bilateral optic disc oedema. The subarachnoid space of optic nerve (SAS), ONSD and optic nerve diameter (OND) was measured prior to other ancillaries including lumbar puncture. Subjects were classified into increased intracranial pressure (IIP) and normal intracranial pressure (NIP) group according to the open cerebrospinal fluid pressure more than 200mm H2 0. The SAS, ONSD and OND were compared between groups and with normal control. The sensitivity of SAS or ONSD change for predicating intracranial hypertension was assessed. A total of 20 IIP, 25 NIP patients and 25 normal controls were evaluated. The mean SAS and ONSD measured in idiopathic intracranial hypertension group was significantly increased than that of NIP and controls (p<0.001), whereas the OND showed no statistic difference between each group. The sensitivities using the SAS and ONSD for differentiating increased ICP in optic disc oedema patients were 0.99 and 0.97, respectively. The enlarged SAS and ONSD measured by high-resolution transbulbar sonography are very sensitive parameters to predicate increased ICP in bilateral optic disc oedema patients.

Neuron-specific enolase levels as a marker for possible neuronal damage in idiopathic intracranial hypertension.

Although formerly considered as a "benign" disease, the presence of some important problems such as vision loss, resistance to appropriate medical treatment and relapses suggests that neuronal damage might play a role in the pathophysiology of IIH. In order to demonstrate possible neuronal damage/dysfunction participating in IIH pathophysiology, we aimed to investigate the relationship between serum neuron-specific enolase (NSE) levels and clinical features in patients with idiopathic intracranial hypertension (IIH). Thirty-six patients with IIH, diagnosed according to the revised criteria, and 40 age, gender and body mass index-matched healthy controls were enrolled in this study after their consent. Serum samples were evaluated for NSE via enzyme-linked immunosorbent assay method. NSE levels were higher in the IIH group (23.7±14.53ng/ml) compared to the control group (22.7±13.11ng/ml), but the difference was not statistically significant (p=0.824). There were also no statistically significant differences in NSE levels in IIH patients regarding the presence of visual loss, relapse, oligoclonal bands and papilledema. We could not demonstrate any correlations between NSE levels and age, body mass index, cerebrospinal fluid opening pressure and disease duration. The present study is the first to analyze NSE levels in IIH patients and showed no significant difference between patients and controls, and also between different clinical subgroups of IIH patients.

A new index for the assessment of transverse sinus stenosis for diagnosing idiopathic intracranial hypertension

Background and purposeTo assess the role of MR venography (MRV) for detecting transverse sinus stenosis, to determine the importance of this finding in idiopathic intracranial hypertension (IIH), and to propose...

Comparative observational study on the clinical presentation, intracranial volume measurements, and intracranial pressure scores in patients with either Chiari malformation Type I or idiopathic intracranial hypertension.

OBJECTIVE Several lines of evidence suggest common pathophysiological mechanisms in Chiari malformation Type I (CMI) and idiopathic intracranial hypertension (IIH). It has been hypothesized that tonsillar ectopy, a typical finding in CMI, is the result of elevated intracranial pressure (ICP) combined with a developmentally small posterior cranial fossa (PCF). To explore this hypothesis, the authors specifically investigated whether ICP is comparable in CMI and IIH and whether intracranial volumes (ICVs) are different in patients with CMI and IIH, which could explain the tonsillar ectopy in CMI. The authors also examined whether the symptom profile is comparable in these 2 patient groups. METHODS The authors identified all CMI and IIH patients who had undergone overnight diagnostic ICP monitoring during the period from 2002 to 2014 and reviewed their clinical records and radiological examinations. Ventricular CSF volume (VV), PCF volume (PCFV), and total ICV were calculated from initial MRI studies by using volumetric software. The static and pulsatile ICP scores during overnight monitoring were analyzed. Furthermore, the authors included a reference (REF) group consisting of patients who had undergone ICP monitoring due to suspected idiopathic normal-pressure hydrocephalus or chronic daily headache and showed normal pressure values. RESULTS Sixty-six patients with CMI and 41 with IIH were identified, with comparable demographics noted in both groups. The occurrence of some symptoms (headache, nausea, and/or vomiting) was comparable between the cohorts. Dizziness and gait ataxia were significantly more common in patients with CMI, whereas visual symptoms, diplopia, and tinnitus were significantly more frequent in patients with IIH. The cranial volume measurements (VV, PCFV, and ICV) of the CMI and IIH patients were similar. Notably, 7.3% of the IIH patients had tonsillar descent qualifying for diagnosis of CMI (that is, > 5 mm). The extent of tonsillar ectopy was significantly different between the CMI and IIH cohorts (p < 0.001) but also between these 2 cohorts and the REF group. Pulsatile ICP was elevated in both cohorts without any significant between-group differences; however, static ICP was significantly higher (p < 0.001) in the IIH group. CONCLUSIONS This study showed comparable and elevated pulsatile ICP, indicative of impaired intracranial compliance, in both CMI and IIH cohorts, while static ICP was higher in the IIH cohort. The data did not support the hypothesis that reduced PCFV combined with increased ICP causes tonsillar ectopy in CMI. Even though impaired intracranial compliance seems to be a common pathophysiological mechanism behind both conditions, the mechanisms explaining the different clinical and radiological presentations of CMI and IIH remain undefined.

Evidence for potential involvement of pro-inflammatory adipokines in the pathogenesis of idiopathic intracranial hypertension.

Background Although specific role players are currently unknown, contribution of inflammatory mediators has been suggested in the pathophysiology of idiopathic intracranial hypertension (IIH), which is a disease more prevalent in obese female individuals of childbearing age. We aimed to investigate the levels of adipokines and cytokines to demonstrate possible markers for inflammation that participate in IIH pathophysiology and their association with clinical features of IIH. Methods IIH patients, diagnosed according to the revised criteria, and age-, gender- and body mass index (BMI)-matched healthy controls were enrolled in this study. Serum samples were evaluated for insulin-like growth factor 1, insulin, nesfatin, adiponectin, interleukin (IL)-1β, IL-6, IL-8, leptin, plasminogen activator inhibitor type-1, resistin, tumour necrosis factor-alpha (TNF-α) and monocyte chemotactic protein 1 via enzyme-linked immunosorbent assay or multiplex immunoassays. Results IL-1β level was significantly higher ( p = 0.012), and IL-8 and TNF-α levels were significantly lower in the IIH group ( p < 0.001 and p = 0.008, respectively) compared to the control group. There were no correlations between the cytokine/adipokine levels and age, BMI, disease duration, and cerebrospinal fluid oligoclonal bands. There were also no significant differences in cytokine and adipokine levels between IIH patients regarding visual impairment. However, statistically significant differences were found between IIH patients with relapse versus healthy controls regarding IL-1β ( p = 0.007), IL-8 ( p = 0.001) and TNF-α ( p = 0.017) levels. Other investigated cytokines and adipokines showed no significant alterations in IIH patients investigated in the remission period. Conclusion Altered serum levels of IL-1β, IL-8 and TNF-α seem to be associated with IIH pathogenesis, and these cytokines may be used as prognostic markers in IIH to predict relapse.

HEADACHE DETERMINES QUALITY OF LIFE IN IIH

BackgroundThere have been no previous studies assessing quality of life (QOL) in idiopathic intracranial hypertension (IIH). Our previously published prospective cohort study confirmed that weight loss, significantly reduced intracranial pressure...

Automated Quantitation of the Posterior Scleral Flattening and Optic Nerve Protrusion by MRI in Idiopathic Intracranial Hypertension

Subjective determination of the posterior sclera flattening and optic nerve protrusion in MRI is challenging because of the 3D nature of the globe morphology. This study aims to develop and compare quantitative measures of globe flattening and optic nerve protrusion with subjective rating, and assess relationships with papilledema grade and intraocular and CSF pressures. Data of 34 globes from 7 overweight female patients with idiopathic intracranial hypertension and 6 age- and weight-matched healthy female control subjects were assessed, as well as a subcohort of 4 of the patients with idiopathic intracranial hypertension who underwent follow-up MR imaging 2 weeks after lumbar puncture and initiation of treatment with acetazolamide. MR imaging examination included a 3D CISS sequence on 1.5T and 3T scanners with 0.6-mm isotropic resolution. Subjective ratings of globe flattening were obtained by experienced and inexperienced readers. Quantitative measures of globe flattening, nerve protrusion, and maximal deformation were derived by use of a 2D map of the distances from the globe center to the posterior wall. Contingency coefficients for globe flattening agreements with subjective rating by the experienced and inexperienced readers were 0.72 and 0.56, respectively. Mean values of the 3 deformation measures were significantly poorer in the idiopathic intracranial hypertension group, with nerve protrusion demonstrating the strongest difference (P = .0002). Nerve protrusion was most strongly associated with papilledema grade with a contingency coefficient of 0.74 (P = .01), whereas globe flattening was negatively correlated with intraocular pressure (R = -0.75, P < .0001). Maximal deformation was negatively associated with CSF opening pressure (R = -0.86, P = .0001). After treatment, only the changes in nerve protrusion and maximal deformation were significant. Automated measures of globe deformation improve reliability over subjective rating. Of the 2 globe deformation measures, nerve protrusion had the strongest predictive value for papilledema grade and had the highest sensitivity for assessment of treatment efficacy in idiopathic intracranial hypertension.

Factors Determining the Clinical Significance of an “Empty” Sella Turcica

Although often incidental, the "empty" sella turcica can reflect chronically elevated intracranial pressure (ICP). It is particularly common in the setting of idiopathic intracranial hypertension (IIH). This study evaluated which clinical and MRI findings could be used to differentiate patients with chronically elevated ICP from those with incidental empty sella turcica. Forty-five patients with definite IIH and 92 patients with "empty sella" reported on brain MRI were evaluated. Measurements of the sella turcica, diaphragm sella, pituitary gland, infundibulum, and scalp and neck soft tissues were made on MR images. These measurements, age, sex, clinical symptoms, and frequency of previously reported orbital findings of IIH were compared between the IIH and incidental empty sella turcica groups. Measurements on MRI were correlated with patient age in each group. The IIH and incidental empty sella turcica groups had statistically similar sellar, pituitary, and infundibular measurements. The patients with IIH were significantly younger than the patients with incidental empty sella turcica (mean age, 36.1 vs 54.3 years, respectively; p < 0.05); were more likely to report headache (93.3% vs 32.6%; p < 0.05) and visual complaints (66.2% vs 28.3%; p < 0.05); showed greater mean scalp thickness (9.0 vs 6.4 mm; p < 0.05) and neck soft-tissue thickness (19.5 vs 13.8 mm; p < 0.05); and were more likely to have an orbital finding suggestive of IIH (93% vs 14%). Age modestly correlated with the width of the diaphragm sella (r = 0.53) in the IIH group only. The significance of the MRI finding of an empty sella turcica can be determined using a combination of clinical and imaging findings.

Static and pulsatile intracranial pressure in idiopathic intracranial hypertension

Objective The aim of this observational study was to characterize the static and pulsatile intracranial pressure (ICP) in conservatively (medically) treated idiopathic intracranial hypertension (IIH) patients in need of shunt surgery, and also in patients with chronic daily headache (CDH) without visual disturbances. Methods The material includes 14 IIH patients and 7 CDH patients in whom ICP was monitored continuously over-night. Static ICP was characterized by mean ICP, pulsatile ICP was characterized by the wave amplitude, rise time, and rise time coefficient. Results In the IIH group all 14 had headache and visual disturbances. Mean ICP was high ( >15 mmHg) in only 7 patients (50%), while mean ICP wave amplitude was high (≥4 mmHg) in all 14 (100%). All IIH patients were shunted and improved clinically thereafter (i.e., relief from visual disturbances and/or headache). None in the CDH group had high mean ICP or mean ICP wave amplitude, and none were shunted. Conclusions In this cohort of 14 conservatively treated IIH patients with lasting and shunt-responsive headache and visual disturbances, the mean ICP wave amplitude was elevated (≥4 mmHg) in all patients despite normal mean ICP (<15 mmHg) in 7 patients (all but one on medication). Therefore, the pulsatile ICP may be more relevant than the static ICP in the diagnostic setting for patients with IIH. Further prospective standardized approaches are warranted.

Cup-to-Disc Ratio in Patients With Idiopathic Intracranial Hypertension Is Smaller Than That in Normal Subjects

A small cup-to-disc (C:D) ratio is an established risk factor for nonarteritic anterior ischemic optic neuropathy. We sought to determine if a small C:D ratio was present in patients with idiopathic intracranial hypertension (IIH) as a potential risk factor for visual loss in that disorder. We performed a retrospective review of 52 charts of patients diagnosed with IIH at Michigan State University from 1990 to 2003. Twenty-eight patients (55 eyes) met diagnostic inclusion criteria and had undergone fundus photography of sufficient quality to allow assessment of the C:D ratio after optic disc edema had become minimal or resolved. C:D ratio was measured from the digitized photographs. The data were placed into rank order categories (0.1 unit intervals) and compared to published normative C:D data. The average vertical C:D ratio was 0.143 (SD 0.061) in the right eye and 0.127 (SD 0.056) in the left eye. The average horizontal C:D ratio was 0.145 (SD 0.053) in the right eye and 0.133 (SD 0.053) in the left eye. The IIH group rank distribution data were compared to published normative C:D ratio data (chi-square test). In each case, the IIH population had a statistically significantly smaller C:D ratio (P < 0.0001) compared to normal subjects. The C:D ratio in our IIH population was smaller than that in published control populations. A small C:D ratio may lower the threshold for developing optic disc edema from ischemia, increased intracranial pressure, or other mechanisms. Additional studies are needed to confirm these findings.

Rarebit Perimetry in the Evaluation of Visual Field Defects in Idiopathic Intracranial Hypertension

Rarebit perimetry (RBP) is a new perimetric technique that has been reported as a sensitive test for the evaluation of the neural structure of the visual system. The aim of this study was to compare RBP with standard automated perimetry in detecting the visual field defects of patients with idiopathic intracranial hypertension (IIH). Twenty-five patients with IIH and 16 healthy controls were considered. Visual fields were analyzed with Marco automated static perimeter with threshold and central 30-2 programs (MP 30-2) and rarebit perimetry. A visual field was classified into 3 zones for both tests as central, paracentral, and peripheral zones. Mean sensitivity (MS) recorded by the MP 30-2 was compared with the mean hit rate (MHR) recorded by RBP for each zone. MS recorded by MP 30-2 and MHR recorded by RBP for each zone were significantly lower in the IIH group than in healthy control eyes (p < 0.001). Good correlation was present between the visual fields recorded by both tests. Although the sensitivity and specificity values for each zone were lower in the RBP group than the MP 30-2 group, RBP was found to be efficient to differentiate between the visual fields of normal and IIH-affected eyes. The average RBP test duration was significantly shorter than the MP 30-2 test duration (p < 0.001). CONCLUSIONS. RBP is a rapid, comfortable, and widely accessible perimetric test giving reliable results in detecting visual field defects in IIH.

Retinol-Binding Protein and Retinol Analysis in Cerebrospinal Fluid and Serum of Patients With and Without Idiopathic Intracranial Hypertension

Several studies have implicated vitamin A-related compounds in the pathogenesis of idiopathic intracranial hypertension (IIH). The goal of this study was to compare cerebrospinal fluid (CSF) and serum concentrations of retinol and retinol-binding protein (RBP) in subjects with and without IIH. CSF and serum samples were collected from 87 subjects. The study population was composed of subjects with IIH (IIH group, n = 28), subjects with non-IIH neurologic conditions (neurology controls, n = 42), and subjects undergoing preoperative lumbar puncture but with no known neurologic conditions (anesthesia controls, n = 17). RBP levels (nM) were determined using radial immunodiffusion, and retinol levels (nM) were determined using high-performance liquid chromatography. The retinol/RBP ratio was greater in CSF than in serum, especially in subjects with IIH. The finding of increased levels of unbound retinol in the CSF of subjects with IIH provides further evidence that vitamin A may be involved in the pathogenesis of IIH. Comparative statistical analyses revealed multivariate relationships that demonstrate the need to further investigate correlations between vitamin A and RBP levels in CSF and serum.

The Relation of Brain Ouabain‐Like Compounds and Idiopathic Intracranial Hypertension

To determine the relationship between levels of ouabain-like compounds (OLC) in the cerebrospinal fluid (CSF) and the occurence of idiopathic intracranial hypertension (IIH). OLC are naturally occurring inhibitors of the sodium-potassium ATPase that are found in the CSF of mammals. Since the production of CSF is dependent upon sodium-potassium ATPase activity, and since there is evidence that the increased intracranial pressure found in the condition of IIH may be the result of increased CSF production, we hypothesized that the level of endogenous OLC would be reduced in the CSF of patients with IIH. CSF samples were obtained from n = 7 patients with IIH and n = 31 patients with neurological disorders other than IIH ("control" patients) who had lumbar puncture as part of their routine evaluation or treatment. The concentration of OLC in the CSF samples was measured using an established ELISA. Patients with IIH exhibited a concentration of OLC in the CSF of 0.11 +/- 0.03 ng/mL. In comparison, the concentration of OLC in CSF samples from non-IIH control patients was 0.12 +/- 0.01 ng/mL. These values were not statistically different when compared with a t-test (P= 0.31). However, the concentration of OLC did negatively correlate to the opening pressure on lumbar puncture, but only in the IIH group (r=-0.80, P= .03). Furthermore, IIH patients who were newly diagnosed or who were unsuccessfully treated (n = 5 of 7 IIH patients) exhibited OLC concentrations of 0.06 +/- 0.1 ng/mL, which is nearly lower than that of the control group (P= .06). The average concentration of OLC in IIH patients (treated and untreated) is unlikely to be distinguishable from that in non-IIH control patients with other neurological conditions. However, the concentration of OLC may be inversely related to the intracranial pressure in patients with IIH, and it may prove to be lower in the subgroup of untreated and unsuccessfully treated IIH patients.