Faculty Bibliography

Cerebrovascular ischaemia is potentiated by hyperthermia, and even mild temperature elevation has proved detrimental to ischaemic brain. Infarction progression following endovascular reperfusion relates to multiple patient-specific and procedural variables; however, the potential influence of mild systemic temperature fluctuations is not fully understood. This study aims to assess the relationship between systemic temperatures in the early aftermath of acute ischaemic stroke and the loss of at-risk penumbral tissues, hypothesizing consumption of the ischaemic penumbra as a function of systemic temperatures, irrespective of reperfusion status. A cross-sectional, retrospective evaluation of a single-institution, prospectively collected endovascular therapy registry was conducted. Patients with anterior circulation, large vessel occlusion acute ischaemic stroke who underwent initial CT perfusion, and in whom at least four-hourly systemic temperatures were recorded beginning from presentation and until the time of final imaging outcome were included. Initial CT perfusion core and penumbra volumes and final MRI infarction volumes were computed. Systemic temperature indices including temperature maxima were recorded, and pre-defined temperature thresholds varying between 37°C and 38°C were examined in unadjusted and adjusted regression models which included glucose, collateral status, reperfusion status, CT perfusion-to-reperfusion delay, general anaesthesia and antipyretic exposure. The primary outcome was the relative consumption of the penumbra, reflecting normalized growth of the at-risk tissue volume ≥10%. The final study population comprised 126 acute ischaemic stroke subjects (mean 63 ± 14.5 years, 63% women). The primary outcome of penumbra consumption ≥10% occurred in 51 (40.1%) subjects. No significant differences in baseline characteristics were present between groups, with the exception of presentation glucose (118 ± 26.6 without versus 143.1 ± 61.6 with penumbra consumption, P = 0.009). Significant differences in the likelihood of penumbra consumption relating to systemic temperature maxima were observed [37°C (interquartile range 36.5 - 37.5°C) without versus 37.5°C (interquartile range 36.8 - 38.2°C) with penumbra consumption, P = 0.001]. An increased likelihood of penumbra consumption was observed for temperature maxima in unadjusted (odds ratio 3.57, 95% confidence interval 1.65 - 7.75; P = 0.001) and adjusted (odds ratio 3.06, 95% confidence interval 1.33 - 7.06; P = 0.009) regression models. Significant differences in median penumbra consumption were present at a pre-defined temperature maxima threshold of 37.5°C [4.8 ml (interquartile range 0 - 11.5 ml) versus 21.1 ml (0 - 44.7 ml) for subjects not reaching or reaching the threshold, respectively, P = 0.007]. Mild fever may promote loss of the ischaemic penumbra irrespective of reperfusion, potentially influencing successful salvage of at-risk tissue volumes following acute ischaemic stroke.

Saccadic eye movement abnormalities are among the earliest manifestations of Huntington's disease (HD) but are difficult to quantify at the bedside. Similarly, afferent visual pathway involvement in HD is poorly characterised. The objective was to evaluate afferent and efferent visual function in HD. Participants with manifest HD (n = 19) and healthy controls (n = 20) performed the King-Devick test, a timed test of rapid number naming. Binocular high and low-contrast (2.5% and 1.25%) acuities were measured using low-contrast Sloan letter charts, and pupillometric recordings were made using a handheld NeurOptics PLR-3000 pupillometer. The NEI-VFQ-25 questionnaire with 10-item neuro-ophthalmic supplement were also completed. Unified Huntington's Disease Rating Scale (UHDRS) motor score and other clinical and demographic variables were collected. Comparisons between manifest HD and controls were performed using linear regression adjusted for confounders. Mean King-Devick time scores were 102.9 seconds in patients with manifest HD and 48.2 seconds in controls (p < .01, t-test). In unadjusted analyses, binocular high contrast acuity was seven letters (one Snellen line equivalent) lower in manifest HD than controls (p = .043). This effect was similar for low-contrast acuity, but only low-contrast acuity remained statistically significant after adjusting for covariates. Low-contrast acuity also correlated with UHDRS motor score. There were no differences in pupillary reactivity or self-reported vision-related quality of life. In conclusion, HD is associated with reduced low-contrast acuity and abnormal performance on the King-Devick test of rapid number naming. These tests are easy to administer, providing an objective quantitative measure of visual function which could be incorporated into optimised rating scales.