Marked olfactory impairment in idiopathic intracranial hypertension.

OBJECTIVE: Many long-duration astronauts develop signs of elevated intracranial pressure and have neuro-ophthalmological findings similar to idiopathic intracranial hypertension (IIH) patients. Some also present with nasal congestion and subjective olfactory impairment. We prospectively evaluated olfactory function in IIH patients and the effect of 6° head-down tilt, which simulates the headward fluid shifting in microgravity, as spaceflight analogues. DESIGN: Olfaction was tested for all subjects in upright and 6° head-down tilt positions using two different measures: University of Pennsylvania Smell Identification Test and Olfactory Threshold Sniffin' Sticks with phenylethyl alcohol. RESULTS: IIH patients (n=19) had significant impairment on both olfactory measures compared with matched controls (n=19). The olfactory threshold dilution levels were 9.07 (95% CI 1.85 to 5.81) and 3.83 (95% CI 7.04 to 11.10), p=0.001, and smell identification scores were 35.61 (95% CI 34.03 to 37.18) and 32.47 (95% CI 30.85 to 34.09), p=0.008, for control and IIH subjects, respectively. The threshold detection was mildly impaired in head-down tilt compared with upright position in the combined subjects (6.05 (95% CI 4.58 to 7.51) vs 6.85 (95% CI 5.43 to 8.27), p=0.004). CONCLUSIONS: We demonstrated that IIH patients have marked impairment in olfactory threshold levels, out of proportion to smell identification impairment. There was also impairment in olfactory threshold in head-down tilt compared with upright positioning, but not for smell identification. The underlying mechanisms for olfactory threshold dysfunction in IIH patients need further exploration.

Optical coherence tomography of the optic nerve head detects acute changes in intracranial pressure.

We aimed to determine if there are measurable objective changes in the optic nerve head (ONH) immediately after cerebrospinal fluid (CSF) drainage in a prospective case-series of five patients undergoing a clinically indicated lumbar puncture (LP) for diagnosis of idiopathic intracranial hypertension. A Cirrus high-definition optical coherence tomography machine (Carl Zeiss Meditec, Dublin, CA, USA) was used to acquire images in the lateral decubitus position. Optic disc cube and high-definition line raster scans centered on the ONH were obtained immediately before and after draining CSF, while the patient maintained the lateral decubitus position. Measured parameters included retinal nerve fiber layer (RNFL) thickness, peripapillary retinal pigment epithelium/Bruch's membrane (RPE/BM) angulation, transverse neural canal diameter (NCD) and the highest vertical point of the internal limiting membrane from the transverse diameter (papillary height). The mean (±standard deviation) opening and closing CSF pressures were 34.3±11.8 and 11.6±3.3cmH2O, respectively. Mean RNFL thickness (pre LP: 196±105µm; post LP: 164±77µm, p=0.1) and transverse NCD (pre LP: 1985±559µm; post LP: 1590±228µm, p=2.0) decreased in all subjects, but with non-significant trends. The RPE/BM angle (mean change: 5.8±2.0degrees, p=0.003) decreased in all subjects. A decrease in papillary height was seen in three of five subjects (mean: pre LP: 976±275µm; post LP: 938±300µm, p=0.9). Our results show a measurable, objective change in the ONH after acute lowering of the lumbar CSF pressure, suggesting a direct link between the lumbar subarachnoid space and ONH regions, and its potential as a non-invasive method for monitoring intracranial pressures.

Epilepsy spectrum disorders: A concept in need of validation or refutation.

Episodic psychiatric symptoms are not uncommon and range from panic attacks to repeated violent acts. Some evidence has accumulated over the years that at least in a subset of patients exhibiting these symptoms there may be evidence for the presence of focal cortical/subcortical hyperexcitability. In these cases the condition could be conceptualized as an epilepsy spectrum disorder (ESD) with significant treatment implications. There is currently no clear demarcation of this category of symptoms, their prevalence, an understanding of how these symptoms occur, what is appropriate work up and possible treatments. In this article, we propose that milder degrees of increased neural excitability (i.e., a subthreshold excitation insufficient to cause seizures) may nonetheless be capable of causing observable phenotypic changes. The observable phenotypic changes depend on the degree of hyperexcitability and the location of the hyperexcitable neural tissue. The location of the abnormal neural tissue may dictate the initial manifestation of an attack resulting from activation of the hyperexcitable tissue, but the anatomical connectivity of the abnormal region will dictate the breadth of manifestations. We provide some evidence, derived mainly from either electroencephalography studies of these populations or clinical reports of response to anti-epilepsy treatment, for the assumption and propose methods to test the advanced hypothesis.

Intracranial pressure modulates distortion product otoacoustic emissions: a proof-of-principle study.

BACKGROUND: There is an important need to develop a noninvasive method for assessing intracranial pressure (ICP). We report a novel approach for monitoring ICP using cochlear-derived distortion product otoacoustic emissions (DPOAEs), which are affected by ICP. OBJECTIVE: We hypothesized that changes in ICP may be reflected by altered DPOAE responses via an associated change in perilymphatic pressure. METHODS: We measured the ICP and DPOAEs (magnitude and phase angle) during opening and closing in 20 patients undergoing lumbar puncture. RESULTS: We collected data on 18 patients and grouped them based on small (<4 mm Hg), medium (5-11 mm Hg), or large (≥15 mm Hg) ICP changes. A permutation test was applied in each group to determine whether changes in DPOAEs differed from zero when ICP changed. We report significant changes in the DPOAE magnitudes and angles, respectively, for the group with the largest ICP changes and no changes for the group with the smallest changes; the group with medium changes had variable DPOAE changes. CONCLUSION: We report, for the first time, systematic changes in DPOAE magnitudes and phase in response to acute ICP changes. Future studies are warranted to further develop this new approach. ABBREVIATIONS: DPOAE, distortion product otoacoustic emissionICP, intracranial pressureIIH, idiopathic intracranial hypertensionLP, lumbar punctureTBI, traumatic brain injury.