Methods: Bedside instruments that can be used includes a measuring tape, compass, goniometer, inclinometer and cervical range of motion (CROM) instrument.
Discussion: Cervical flexion-extension, lateral flexion and rotation will be assessed with bedside instruments. This would aid in increasing accuracy and precision of objective measurement while conducting clinical examination to determine the cervical range of motion.
METHODS: A double-blinded, randomised, placebo-controlled study was carried out among adults with non-traumatic ICH. Eligible study subjects were randomly assigned to receive placebo, 2-g TXA treatment or 3-g TXA treatment. Haematoma volumes before and after intervention were measured using the planimetric method.
RESULTS: A total of 60 subjects with 20 subjects in each treatment group were recruited for this study. Among the 60 subjects, the majority were male (n = 36, 60%), had known cases of hypertension (n = 43, 71.7%) and presented with full Glasgow coma scale (GCS) (n = 41, 68.3%). The results showed that there was no statistically significant difference (P = 0.315) in the mean changes of haematoma volume when compared with three study groups using ANCOVA, although the 3-g TXA group was the only group that showed haematoma volume reduction (mean reduction of 0.2 cm3) instead of expansion as in placebo (mean expansion 1.8 cm3) and 2-g TXA (mean expansion 0.3 cm3) groups. Good recovery was observed in all study groups, with only three subjects being moderately disabled. No adverse effects were reported in any of the study groups.
CONCLUSION: To the best of our knowledge, this is the first clinical study using 3 g of TXA in the management of non-traumatic ICH. From our study, 3 g of TXA may potentially be helpful in reducing haematoma volume. Nonetheless, a larger-scale randomised controlled trial should be carried out to further establish the role of 3 g of TXA in non-traumatic ICH.
METHODS: A prospective cohort study was conducted over a 2-year period (May 2013-May 2015) to investigate the levels of NOx in the CSF and serum of patients with radiologically confirmed aneurysmal SAH. NOx samples and all relevant data were collected from the patients on admission and serially over 5 days. On admission, NOx levels were compared between the groups of patients, who were divided as per the World Federation Neurosurgeons Score (WFNS) grading scale, Fisher scale, occurrence of vasospasm on transcranial doppler (TCD), and Glasgow outcome scale (GOS) upon discharge and at 6 months follow-up. The ratios of CSF-to-serum were calculated and correlated with SAH severity and the outcome parameters listed above.
RESULTS: The patients (N = 40) had a mean (SD) age of 58.2 (11.8) years old. The majority (65%) had a higher severity of SAH (WFNS score 3-5). On evaluation of the CT scan findings, 74% had outcomes equivalent to 4 on the Fisher scale. Vasospasm was detected via TCD in nearly half (45%) of the cohort during the study period; 80% were noted to have a poor outcome (GOS 1-3) at discharge; this persisted at 6 months follow-up. Comparison of NOx levels in the CSF/serum ratio was based on the incidence of vasospasm and severity of outcome (GOS) for day-1 and day-4. Statistically significant results were evident for patients with better outcomes, high severity grading, and the presence of vasospasm (P-values: 0.031, 0.034 and 0.043, respectively).
CONCLUSION: Elevated NOx levels in CSF and serum and reductions in the ratio of NOx in CSF/serum were found to be associated with severity, occurrence of vasospasm and clinical outcome in aneurysmal SAH patients. This indicates the possible role of NOx as a biomarker to assess severity and prognosis in patients with SAH.
METHODS: The Trypan blue viability assay used to examine cell death. Immunofluorescence assay, glial fibrillary acidic protein (GFAP) was used to portray the morphology of astrocytes. The hypoxia-inducible factor 1 (HIF-1) staining was performed to confirm hypoxia induced cell death and there was a dramatic expression of HIF-1α displayed in exposed astrocyte cells compared to the control. In molecular level, genes were chosen, such as glyceraldehyde 3-phosphate dehydrogenase (GAPDH), GFAP, HIF-1α and B-cell lymphoma 2 (Bcl-2) and ran the reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS: Microscope revealed a filamentous and clear nucleus appearance in a control whereas the rupture nuclei with no rigid structure of the cell were found in the 3% oxygen. The control and hypoxia cells were also stained with the annexin V-fluorescein isothiocyanate (annexin V-FITC). Fluorescence microscope reveals astrocyte cells after hypoxia showed higher expression of nuclei but not in control. Merging PI and FITC showed the differences of nuclei expression between the control and hypoxia. In the molecular analysis, there were significant changes of GFAP, HIF-1α and Bcl-2 in hypoxia exposed cells when compared to the control group.
CONCLUSION: Cells that were exposed to hypoxia (3% oxygen for 15 min) clearly showed damage. General view of human hippocampal astrocyte genomic response to hypoxia was obtained.
Methods: We performed diffusion magnetic resonance imaging with probabilistic tractography on four Malay males to parcellate the hippocampus according to its relative connection probability to the six subdivisions of the PFC.
Results: Our findings revealed that each hippocampus showed putative connectivity to all the subdivisions of PFC, with the highest connectivity to the orbitofrontal cortex (OFC). Parcellation of the hippocampus according to its connection probability to the six PFC subdivisions showed variability in the pattern of the connection distribution and no clear distinction between the hippocampal subregions.
Conclusion: Hippocampus displayed highest connectivity to the OFC as compared to other PFC subdivisions. We did not find a unifying pattern of distribution based on the connectivity-based parcellation of the hippocampus.