Virtual monoenergetic dual-energy CT reconstructions at 80 keV are optimal non-contrast CT technique for early stroke detection

Background Virtual monoenergetic (VM) dual-energy computed tomography (DE-CT) enables grey-to-white matter contrast-to-noise ratio optimization, potentially increasing ischaemic brain oedema visibility. The aim of this study was to compare the diagnostic accuracy of VM and standard DE-CT reconstructions for early stroke detection. Methods Consecutive patients with non-contrast DE-CT of the brain scanned within 12 h of stroke symptom onset were prospectively included in the study. Patients with other significant brain pathology were excluded. Two radiologists jointly evaluated standard and VM reconstructions (from 40 to 190 keV at increments of 10 keV) for early stroke signs on a four-point Likert scale: (a) stroke definitely present, (b) stroke probably present, (c) probably no stroke, and (d) definitely no stroke. Follow-up imaging and clinical data served as the standard of reference. Diagnostic accuracy was evaluated by receiver operating characteristic analysis. Results Stroke incidence among 184 patients was 76%. In 64 patients follow-up imaging served as the standard of reference: ischemic brain oedema detection was significantly more accurate on VM reconstructions at 80 keV compared with standard DE-CT reconstructions (area under the curve (AUC) = 0.821 vs. AUC = 0.672, p = 0.002). The difference was most prominent within the first 3 h after symptom onset (at 11%, AUC = 0.819 vs. AUC = 0.709, p = 0.17) and in patients with National Institutes of Health Stroke Scale above 16 (at 37.5%, AUC = 1 vs. AUC = 0.625, p = 0.14). Conclusion VM DE-CT reconstructions at 80 keV appear to be the optimal non-contrast CT technique for diagnosing early ischaemic stroke, particularly within the first 3 h after symptom onset and in severely ill patients.

Aquaporins in GtoPdb v.2021.3

Aquaporins and aquaglyceroporins are membrane channels that allow the permeation of water and certain other small solutes across the cell membrane, or in the case of AQP6, AQP11 and AQP12A, intracellular membranes, such as vesicles and the endoplasmic reticulum membrane [16]. Since the isolation and cloning of the first aquaporin (AQP1) [20], 12 additional mammalian members of the family have been identified, although little is known about the functional properties of one of these (AQP12A; Q8IXF9) and it is thus not tabulated. The other 12 aquaporins can be broadly divided into three families: orthodox aquaporins (AQP0,-1,-2,-4,-5, -6 and -8) permeable mainly to water, but for some additional solutes [4]; aquaglyceroporins (AQP3,-7 -9 and -10), additionally permeable to glycerol and for some isoforms urea [14], and superaquaporins (AQP11 and 12) located within cells [12]. Some aquaporins also conduct ammonia and/or H2O2 giving rise to the terms 'ammoniaporins' ('aquaammoniaporins') and 'peroxiporins', respectively. Aquaporins are impermeable to protons and other inorganic and organic cations, with the possible exception of AQP1, although this is controversial [14]. One or more members of this family of proteins have been found to be expressed in almost all tissues of the body [reviewed in Yang (2017) [26]]. AQPs are involved in numerous processes that include systemic water homeostasis, adipocyte metabolism, brain oedema, cell migration and fluid secretion by epithelia. Loss of function mutations of some human AQPs, or their disruption by autoantibodies further underscore their importance [reviewed by Verkman et al. (2014) [23], Kitchen et al. (2105) [14]]. Functional AQPs exist as homotetramers that are the water conducting units wherein individual AQP subunits (each a protomer) have six TM helices and two half helices that constitute a seventh 'pseudotransmembrane domain' that surrounds a narrow water conducting channel [16]. In addition to the four pores contributed by the protomers, an additional hydrophobic pore exists within the center of the complex [16] that may mediate the transport through AQP1. Although numerous small molecule inhibitors of aquaporins, particularly APQ1, have been reported primarily from Xenopus oocyte swelling assays, the activity of most has subsequently been disputed upon retesting using assays of water transport that are less prone to various artifacts [5] and they are therefore excluded from the tables [see Tradtrantip et al. (2017) [22] for a review].

Two-step staged resection of giant olfactory groove meningiomas

Background The surgical treatment of giant olfactory groove meningiomas (OGMs) with marked perilesional brain oedema is still a surgical challenge. After tumour resection, increase of brain oedema may occur causing dramatic neurological deterioration and even death of the patient. The objective of this paper is to describe surgical features of a two-step staged resection of these tumours performed to counter increase of postoperative brain oedema. Methods This two-step staged resection procedure was carried out in a consecutive series of 19 patients harbouring giant OGMs. As first step, a bifrontal craniectomy was performed followed by a right-sided interhemispherical approach. About 80% of the tumour mass was resected leaving behind a shell-shaped tumour remnant. In the second step, carried out after the patients’ recovery from the first surgery and decline of oedema, the remaining part of the tumour was removed completely followed by duro- and cranioplasty. Results Ten patients recovered quickly from first surgery and the second operation was performed after a mean of 12.4 days. In eight patients, the second operation was carried out later between day 25 and 68 due to surgery-related complications, development of a trigeminal zoster, or to a persisting frontal brain oedema. Mean follow-up was 49.3 months and all but one patient had a good outcome regardless of surgery-related complications. Conclusions Our results suggest that a two-step staged resection of giant OGMs minimizes the increase of postoperative brain oedema as far as possible and translates into lower morbidity and mortality.

Impact of hyperglycaemia on complications in patients who had a stroke after thrombolysis

BackgroundWe sought to investigate whether admission hyperglycaemia is associated with complications in patients who had an acute ischaemic stroke (AIS) treated with intravenous recombinant tissue plasminogen activator and, if so, whether complications during hospitalisation modify the effect of hyperglycaemia on 3-month poor outcome after thrombolysis.MethodsPatients who were diagnosed with AIS after thrombolysis between July 2016 and January 2019 were enrolled in this study. Five prespecified complications, including infections, brain oedema, deep vein thrombosis (DVT), haemorrhagic transformation (HT) and gastrointestinal bleeding, were recorded during hospitalisation.ResultsOf 388 patients, 143 (36.86%) presented with hyperglycaemia. Patients with hyperglycaemia were more likely to experience one or more complications than patients without hyperglycaemia. After adjustment for potential confounders, hyperglycaemia was associated with brain oedema (OR 2.39; 95% CI 1.08 to 5.30), HT (OR 2.16, 95% CI 1.06 to 4.41), symptomatic intracerebral haemorrhage (sICH) (OR 7.32, 95% CI 2.35 to 22.80) and gastrointestinal bleeding (OR 3.62; 95% CI 1.93 to 6.80), but was not linked to infections (OR 1.48, 95% CI 0.76 to 2.9) and DVT (OR 0.60, 95% CI 0.23 to 1.5). Additional adjustment for the complications in the clinical outcome analysis, done to assess these complications as an intermediate in the pathway from admission hyperglycaemia to clinical outcome, did not substantially change the model (all p for interaction >0.05).ConclusionHyperglycaemia is an independent predictor of complications following stroke after thrombolysis, especially for brain oedema, gastrointestinal bleeding, HT and sICH. Complications during hospitalisation did not modify the effect of hyperglycaemia on the poor outcome at 3 months in ischaemic stroke.

Glucocorticoid In Cytotoxicity Followed by Delayed Edema

Background: Cytotoxicity is the toxicity to cell. Any type of brain oedema producing raised intracranial pressure (ICP) which may be a fatal pathological state. Corticosteroid is contraindicated in cytotoxic brain oedema but in vasogenic oedema, it is beneficial. Cytotoxic oedema in its consequences induces vasogenic oedema where the corticosteroid may helpful. Objectives: To determine the effects of corticosteroid on tertiary vasogenic brain oedema from cytotoxic edema. Methods: Total of 328 patients was diagnosed as brain oedema and they had been first time reported & all were admitted in Combined Military Hospital (CMH) Dhaka, between Jan 2017 to Jun 2019. Out of 328 patients, brain oedema due to spontaneous ICHs was 219 (66.77%) and traumatic ICHs were 109(33.33%). Diagnosis was based upon history, clinical examination and non-contrast Computed Tomography (CT) scan of brain. Results: Total 328 admitted patients in CMH Dhaka from Jan 2017-Jun 2019 were included in our study who full-fill the criteria. Males were 231 (70.43%); females were 97(29.57%) and were aged between 1 to 95 year. Intracranial haemorrhage rate among age group less than 55 years old being 76 (34.70%) and 55 years or above 143 (65.30%) of total 219 patients. Traumatic ICHs were 109 and 1 to 44 years age is most vulnerable, 69(63.30%) and 45 years and above 40 (36.70%) patients. Corticosteroid was used after vasogenic brain oedema formation following cytotoxic oedema which was diagnosed mainly radiologically. Cytotoxic oedema induced by 24 hours and vasogenic oedema in two to four days of brain insult. Vasogenic oedema developed in 24 -48 hours, 65 (19.82%) patients and 117 (35.67 %) by 48-72 hours and above 72 hours rest 146 (44.51%) patients after brain insult. After vasogenic oedema formation, out of 164 patients that is 50% patients were treated with corticosteroid and GOS was assessed- GOS 4,5 -103(62.80%), GOS 3-34 (20.73%), GOS 2- 23(14.02%) and GOS 1-4(2.44%) whereas without corticosteroid treatment of rest vasogenic oedema 164 (50%) , GOS was- GOS 4,5 -85(51.83%), GOS 3-43 (26.22%), GOS 2- 27(16.46%) and GOS 1-9(5.49%) at 30 days of incidence. There is more than two times mortality without corticosteroid therapy than with steroid therapy. Conclusion: Cytotoxic brain oedema is contraindicated for steroid but we observed that corticosteroid gives better GOS in vasogenic oedema which develops after cytotoxic brain oedema. Outcome in cytotoxic oedema followed by vasogenic oedema is beneficial for corticosteroid. Bang. J Neurosurgery 2020; 10(1): 45-51

Management of raised intracranial pressure

Normal intracranial pressure is between 5 and 15 mm Hg in supine subjects. Intracranial hypertension (ICP >20 mm Hg) is common in many central nervous system diseases and in fatal cases is often the immediate cause of death. Increases in intracranial volume and hence—given the rigid skull—intracranial pressure may be the consequence of brain oedema, increased cerebral blood volume, hydrocephalus, and space-occupying lesions. Brain perfusion depends on the cerebral perfusion pressure which is mean arterial pressure minus intracranial pressure. The normal brain autoregulates cerebral blood flow down to a lower limit of cerebral perfusion pressure of about 50 mm Hg in healthy subjects, and perhaps 60–70 mm Hg in disease. Cerebral perfusion pressure reduction to below these values results in cerebral ischaemia.