Hearing impairment after subarachnoid hemorrhage.

Background: Subarachnoid hemorrhage (SAH) survivors experience significant neurological disability, some of which is under-recognized by neurovascular clinical teams. We set out to objectively determine the occurrence of hearing impairment after SAH, characterize its peripheral and/or central origin, and investigate likely pathological correlates. Methods: In a case-control study (n = 41), participants were asked about new onset hearing difficulty 3 months post-SAH, compared with pre-SAH. Formal audiological assessment included otoscopy, pure tone audiometry, a questionnaire identifying symptoms of peripheral hearing loss and/or auditory processing disorder, and a test of speech understanding in noise. A separate cohort (n = 21) underwent quantitative susceptibility mapping (QSM) of the auditory cortex 6 months after SAH, for correlation with hearing difficulty. Results: Twenty three percent of SAH patients reported hearing difficulty that was new in onset post-SAH. SAH patients had poorer pure tone thresholds compared to controls. The proportion of patients with peripheral hearing loss as defined by the World Health Organization and British Audiological Society was however not increased, compared to controls. All SAH patients experienced symptoms of auditory processing disorder post-SAH, with speech-in-noise test scores significantly worse versus controls. Iron deposition in the auditory cortex was higher in patients reporting hearing difficulty versus those who did not. Conclusion: This study firmly establishes hearing impairment as a frequent clinical feature after SAH. It primarily consists of an auditory processing disorder, mechanistically linked to iron deposition in the auditory cortex. Neurovascular teams should inquire about hearing, and refer SAH patients for audiological assessment and management.

Non-invasive measurement of oxygen saturation in the spinal vein using SWI: quantitative evaluation under conditions of physiological and caffeine load.

Susceptibility-weighted imaging (SWI) has been used for quantitative and non-invasive measurement of blood oxygen saturation in the brain. In this study, we used SWI for quantitative measurement of oxygen saturation in the spinal vein to look for physiological- or caffeine-induced changes in venous oxygenation. SWI measurements were obtained for 5 healthy volunteers using 1.5-T MR units, under 1) 3 kinds of physiological load (breath holding, Bh; hyperventilation, Hv; and inspiration of highly concentrated oxygen, Ox) and 2) caffeine load. Oxygen saturation in the anterior spinal vein (ASV) was calculated. We evaluated changes in oxygen saturation induced by physiological load. We also evaluated the time-course of oxygen saturation after caffeine intake. For the physiological load measurements, the average oxygen saturation for the 5 subjects was significantly lower in Hv (0.75) and significantly higher in Bh (0.84) when compared with control (0.80). There was no significant difference between Ox (0.81) and control. Oxygen saturation gradually decreased after caffeine intake. The average values of oxygen saturation were 0.79 (0 min), 0.76 (20 min), 0.74 (40 min), and 0.73 (60 min), respectively. We demonstrated a significant difference in oxygen saturation at 40 and 60 min after caffeine intake when compared with 0 min. In conclusion, we demonstrated the feasibility of using SWI for non-invasive measurement of oxygen saturation in the spinal vein. We showed changes in oxygen saturation under physiological as well as caffeine load and suggest that this method is a useful tool for the clinical evaluation of spinal cord oxygenation.

Brain iron detected by SWI high pass filtered phase calibrated with synchrotron X-ray fluorescence.

PURPOSE: To test the ability of susceptibility weighted images (SWI) and high pass filtered phase images to localize and quantify brain iron. MATERIALS AND METHODS: Magnetic resonance (MR) images of human cadaver brain hemispheres were collected using a gradient echo based SWI sequence at 1.5T. For X-ray fluorescence (XRF) mapping, each brain was cut to obtain slices that reasonably matched the MR images and iron was mapped at the iron K-edge at 50 or 100 microm resolution. Iron was quantified using XRF calibration foils. Phase and iron XRF were averaged within anatomic regions of one slice, chosen for its range of iron concentrations and nearly perfect anatomic correspondence. X-ray absorption spectroscopy (XAS) was used to determine if the chemical form of iron was different in regions with poorer correspondence between iron and phase. RESULTS: Iron XRF maps, SWI, and high pass filtered phase data in nine brain slices from five subjects were visually very similar, particularly in high iron regions. The chemical form of iron could not explain poor matches. The correlation between the concentration of iron and phase in the cadaver brain was estimated as c(Fe) [microg/g tissue] = 850Deltavarpi + 110. CONCLUSION: The phase shift Deltavarpi was found to vary linearly with iron concentration with the best correspondence found in regions with high iron content.