The most common complications of intracranial surgery in companion animals chiefly consist of brain swelling, hemorrhage, seizures, and worsening of neurologic status, aspiration pneumonia, and anesthetic death. Further dividing these into intraoperative and postoperative complications, postoperative are more common. Preventative measures can include careful surgical planning, cerebro-protective anesthetic regimes, seizure prophylaxis, and postoperative sedation/pain management that allows for an early return to function and ambulation and an adequate and accelerated nutrition.

UNASSIGNED: Grey-white matter ratio (GWR) measured by head computed tomography (CT) scan is known as a neurological prognostication tool for out-of-hospital cardiac arrest (OHCA) survivors. The prognostic value of GWR obtained early (within two hours after return of spontaneous circulation [ROSC]) remains a matter of debate.
UNASSIGNED: We conducted a multicenter, retrospective, observational study at five hospitals. We included adult OHCA survivors who underwent head CT within two hours following ROSC. GWR values were measured using head CT. Average GWR values were calculated by the mean of the GWR-basal ganglia and GWR-Cerebrum. We divided the patients into poor or favorable neurological outcome groups defined by Glasgow-Pittsburgh Cerebral Performance Category scores. The predictive accuracy of GWR performance was assessed using the area under the curve (AUC). The sensitivities and specificities for predicting poor outcome were examined.
UNASSIGNED: Of 377 eligible patients, 281 (74.5%) showed poor neurological outcomes at one month after ROSC. Average GWR values of the poor neurological outcome group were significantly lower than those of the favorable neurological outcome. The average GWR value to predict neurological outcome with Youden index was 1.24 with AUC of 0.799. When average GWR values were 1.15 or lower, poor neurological outcomes could be predicted with 100% specificity.
UNASSIGNED: GWR values measured by head CT scans early (within two hours after ROSC) demonstrated moderate predictive performance for overall ROSC patients. When limited to the patients with GWR values of 1.15 or lower, poor neurological outcomes could be predicted with high specificity.

BACKGROUND: Spontaneous intracerebral hemorrhage (ICH) with large hematomas is commonly treated with craniotomy combined with decompressive craniectomy, procedures that involve huge trauma and require subsequent cranioplasty. Recently, endoscopic surgery has shown significant promise in treating ICH, but its feasibility for large hematomas remains uncertain. Therefore, this study aims to compare endoscopic surgery with craniotomy and to evaluate the efficacy and safety of endoscopic surgery in treating large hematomas ICH.
METHODS: A retrospective analysis was conducted on the clinical data from patients with spontaneous supratentorial ICH and hematoma volumes exceeding 50 mL who underwent either endoscopic surgery or craniotomy. Propensity score matching analysis was employed to reduce selection bias. The efficacy and safety of endoscopic surgery were evaluated by analyzing blood loss, postoperative edema, mortality rate, complications, and the Glasgow Outcome Scale (GOS) at 6-month follow-up.
RESULTS: A total of 113 cases that met the criteria were collected, with 65 in the endoscopic surgery group and 48 in the craniotomy group. After propensity score matching, each group contained 34 cases. The mean hematoma volume was 64.84 ± 11.02 mL in the endoscopy group and 66.57 ± 12.77 mL in the craniotomy group (p = 0.554). Hematoma evacuation rates were 93.27% in the endoscopy group and 89.34% in the craniotomy group (p = 0.141). The endoscopy group exhibited lower blood loss, shorter surgical time, and reduced postoperative edema volume at 24 h compared to the craniotomy group. The rate of pulmonary infection was slightly lower in the endoscopy group compared to the craniotomy group (70.59% vs. 91.18%, p = 0.031), but there were no statistically significant differences in overall complications and mortality rate between the two groups. GOS scores were similar in both groups at the 6-month follow-up.
CONCLUSIONS: Endoscopic surgery is safe and feasible for treating spontaneous supratentorial ICH with large hematomas, demonstrating efficacy similar to that of craniotomy with decompressive craniectomy.

Pathogenic CACNA1A mutations can result in paroxysmal attacks of encephalopathy, hemiplegia and cerebral edema. We report two patients with CACNA1A-associated encephalopathy, hemiplegia and contralateral hemispheric cerebral edema treated successfully with intravenous magnesium sulfate and dexamethasone. One patient met the clinical criteria for familial hemiplegic migraine. There is a paucity of guidance in the literature on how to manage these patients. Despite some discrepancies in the treatment protocols in our two cases, they indicate that magnesium and dexamethasone could be part of the treatment algorithm for these patients. Further research to delineate appropriate dosing and duration of therapy is needed.

The destruction of the blood-brain barrier and damage to the gastrointestinal mucosa after intracerebral hemorrhage (ICH) are important reasons for its high disability and mortality rates. However, the exact etiology is not yet clear. In addition, there are currently no effective treatments for improving cerebral edema and gastric mucosal damage after ICH. Trefoil factor 1 (TFF1) is a secretory protein that plays a crucial role in maintaining the integrity and barrier function of the gastric mucosa, and it has been reported to have a protective effect on brain damage induced by various causes. This study utilized a rat model of ICH induced by type IV collagenase was utilized, and intervened with recombinant TFF1 protein from an external institute to investigate the protective mechanisms of TFF1 against brain edema and gastric mucosal damage after ICH. The results demonstrated that TFF1 alleviated the neurological function and gastric mucosal damage in the rat model of ICH induced by type IV collagenase. TFF1 may ensure the integrity of the blood-brain and gastric mucosal barriers by regulating the EGFR (epidermal growth factor receptor)/Src (non-receptor tyrosine kinase)/FAK (focal adhesion kinase) pathway. Clearly, the disruption of the blood-brain barrier and the destruction of the gastric mucosal barrier are key pathological features of ICH, and TFF1 can improve the progression of blood-brain barrier and gastric mucosal barrier disruption in ICH by regulating the EGFR/Src/FAK pathway. Therefore, TFF1 may be a potential target for the treatment of ICH.

The peri-hematomal area (PHA) emerges as a key but puzzling interface where edematous and neuroinflammatory events co-occur after intracerebral hemorrhage (ICH), while being considered either as deleterious or protective. We aimed at unraveling the pathogeny and natural history of PHA over time after experimental ICH. Male and female rats were longitudinally followed up to day 7 using multimodal brain MRI. MRI measures were compared to neuropathological and behavioural results. While the peak of PHA volume at day 3 was predictive for spontaneous locomotor deficit without sex-effect, its drop at day 7 fitted with locomotor recovery and hematoma resorption. The PHA highest water density was observed at onset despite microvascular hypoperfusion, taken over by blood-brain barrier (BBB) leakage at day 3. Water density dropped at day 7, when vascular integrity was normalized, and the highest number of reactive astrocytes, microglial cells, and siderophages found. This study shows that the PHA with edematous component is hematoma-driven at onset and BBB-driven at day 3, but this excess neuroinflammation enabled PHA volume reduction and significant hematoma resorption as soon as day 7. Therapeutic interventions should consider this pathogeny, and be monitored by multimodal MRI in preclinical ICH models.

BACKGROUND: Hemorrhagic transformation (HT) and cerebral edema (CED) are both major complications following ischemic stroke, but few studies have evaluated their overlap. We evaluated the frequency and predictors of CED/HT overlap and whether their co-occurrence impacts functional outcome more than each in isolation.
METHODS: 892 stroke patients enrolled in a prospective study had follow-up CT imaging evaluated for HT and CED; the latter was quantified using the ratio of hemispheric CSF volumes (with hemispheric CSF ratio < 0.90 used as the CED threshold). The interaction between HT and CED on functional outcome (using modified Rankin Scale at 3 months) was compared to that for each condition separately.
RESULTS: Among the 275 (31%) who developed HT, 233 (85%) manifested hemispheric CSF ratio < 0.9 (CED/HT), with this overlap group representing half of the 475 with measurable CED. Higher baseline NIHSS scores and larger infarct volumes were observed in the CED/HT group compared with those with CED or HT alone. Functional outcome was worse in those with CED/HT [median mRS 3 (IQR 2-5)] than those with CED [median 2 (IQR 1-4)] or HT alone [median 1 (IQR 0-2), p < 0.0001]. Overlap of CED/HT independently predicted worse outcome [OR 1.89 (95% CI: 1.12-3.18), p = 0.02] while HT did not; however, CED/HT was no longer associated with worse outcome after adjusting for severity of CED [adjusted OR 0.35 (95% CI: 0.23, 0.51) per 0.21 lower hemispheric CSF ratio, p < 0.001].
CONCLUSIONS: Most stroke patients with HT also have measurable CED. The co-occurrence of CED and HT occurs in larger and more severe strokes and is associated with worse functional outcome, although this is driven by greater severity of stroke-related edema in those with HT.

BACKGROUND: Our aim was to determine whether the Apparent Diffusion Coefficient is able to predict the presence of a symptomatic pineal cyst by detecting cerebral edema.
METHODS: We retrospectively analyzed MRIs of 45 patients with pineal cysts before and after resection and 51 patients without pineal cysts, comparing ADC values of thalamus, central, periventricular and subcortical white matter. Furthermore we evaluated cyst size and morphology and analyzed its correlation to ADC values in corresponding patients.
RESULTS: Differences between patients with symptomatic pineal cyst and control group were not significant (p = 0.200 - 0.968). ADC ratios did not change significantly after resection of the cyst (p = 0.575 - 0.862). Cyst size showed no significant correlation to ADC ratios (p = 0.071 - 0.918). Raw data analyses revealed more significance, especially periventricularly and in central white matter, which resulted in significant interhemispheric differences in ADC ratios in both subgroups (p < 0.001 and p = 0.031). MRI of 1.5T showed consistently higher values than 3T but mostly insignificant.
CONCLUSIONS: Our analysis revealed no evidence that pineal cysts lead to intracerebral edema caused by venous compression. Since variability was higher than the differences seen, ADC sequences do not appear to be an appropriate diagnostic tool for symptomatic pineal cysts.

BACKGROUND: Cerebral edema is a common, potentially life-threatening complication in critically ill patients with acute brain injury. However, uncertainty remains regarding best monitoring and treatment strategies, which may result in wide practice variations.
METHODS: A 20-question digital survey on monitoring and management practices was disseminated between July 2022 and May 2023 to clinicians who manage cerebral edema. The survey was promoted through email, social media, medical conferences, and the Neurocritical Care Society Web site. We used the χ2 test, Fisher\'s exact test, analysis of variance, and logistic regression to report factors associated with practice variation, diagnostic monitoring methods, and therapeutic triggers based on practitioner and institutional characteristics.
RESULTS: Of 321 participants from 160 institutions in 30 countries, 65% were from university-affiliated centers, 74% were attending physicians, 38% were woman, 38% had neurology training, and 55% were US-based. Eighty-four percent observed practice variations at their institutions, with \"provider preference\" being cited most (87%). Factors linked to variation included gender, experience, university affiliation, and practicing outside the United States. University affiliates tended to use more tests (median 3.87 vs. 3.43, p = 0.01) to monitor cerebral edema. Regarding management practices, 20% of respondents\' preferred timing for decompressive hemicraniectomy was after 48 h, and 37% stated that radiographic findings only would be sufficient to trigger surgery. Fifty percent of respondents reported initiating osmotic therapy based on radiographic indications or prophylactically. There were no significant associations between management strategies and respondent or center characteristics. Twenty-seven percent of respondents indicated that they acquired neuroimaging at intervals of 24 h or less. Within this group, attending physicians were more likely to follow this practice (65.5% vs. 34.5%, p = 0.04).
CONCLUSIONS: Cerebral edema monitoring and management strategies vary. Features associated with practice variations include both practitioner and institutional characteristics. We provide a foundation for understanding practice patterns that is crucial for informing educational initiatives, standardizing guidelines, and conducting future trials.

Mitochondrial function is tightly linked to morphology, and fragmentation of dendritic mitochondria during noxious conditions suggests loss of function. In the normoxic cortex, spreading depolarization (SD) is a phenomenon underlying migraine aura. It is unknown whether mitochondria structure is affected by normoxic SD. In vivo two-photon imaging followed by quantitative serial section electron microscopy (ssEM) was used to monitor dendritic mitochondria in the normoxic cortex of urethane-anesthetized mature male and female mice during and after SD initiated by focal KCl microinjection. Structural dynamics of dendrites and their mitochondria were visualized by transfecting excitatory, glutamatergic neurons of the somatosensory cortex with bicistronic AAV, which induced tdTomoto labeling in neuronal cytoplasm and mitochondria labeling with roGFP. Normoxic SD triggered rapidly reversible fragmentation of dendritic mitochondria alongside dendritic beading; however, mitochondria took significantly longer to recover. Several rounds of SD resulted in transient mitochondrial fragmentation and dendritic beading without accumulating injury, as both recovered. SsEM corroborated normoxic SD-elicited dendritic and mitochondrial swelling and transformation of the filamentous mitochondrial network into shorter, swollen tubular, and globular structures. Our results revealed normoxic SD-induced disruption of the dendritic mitochondrial structure that might impact mitochondrial bioenergetics during migraine with aura.