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To describe features in patients admitted to the intensive care unit (ICU) for poor-grade aneurysmal subarachnoid hemorrhage (SAH) and to identify predictors of 12-month outcome. We conducted a controlled observational study of 51 consecutive patients treated with endovascular coiling within 96 h of rupture for poor-grade aneurysmal SAH (20 men and 31 women, age 54 +/- 12 years). We recorded co-morbidities; initial severity; aneurysm location; occurrence of acute hydrocephalus, initial seizures, and/or neurogenic lung edema; troponin values, Fisher grade; computed tomography (CT) findings; treatment intensity; and occurrence of vasospasm. The brain injury marker S100B was assayed daily over the first 8 days. Glasgow Outcome Scores (GOS) were recorded at ICU discharge, at 6 and 12 months. The main outcome criterion was the 1-year GOS score, which we used to classify patients as having a poor outcome (GOS 1-3) or a good outcome (GOS 4-5). Overall, clinical status after 1 year was very good (GOS 5) in 41% of patients and good (GOS 4) in 16%. Neither baseline characteristics nor interventions differed significantly between patients with good outcome (GOS 4-5) and those with poor outcome (GOS 1-3). Persistent intracranial pressure elevation and higher mean 8-day S100B value significantly and independently predicted the 1-year GOS outcome (P = 0.008 and P = 0.001, respectively). Patients in poor clinical condition after SAH have more than a 50:50 chance of a favorable outcome after 1 year. High mean 8-day S100B value and persistent intracranial hypertension predict a poor outcome (GOS 1-3) after 1 year.

Purpose Accurate early anticipation of long-term irreversible brain damage during the acute phase of patients with aneurysmal subarachnoid hemorrhage (aSAH) remains difficult. Using a combination of clinical scores together with brain injury-related biomarkers (H-FABP, NDKA, UFD1 and S100β), this study aimed at developing a multiparameter prognostic panel to facilitate early outcome prediction following aSAH. Methods Blood samples of 141 aSAH patients from two separated cohorts (sets of 28 and 113 patients) were prospectively enrolled and analyzed with 14 months of delay. Patients were admitted within 48 h following aSAH onset. A venous blood sample was withdrawn within 12 h after admission. H-FABP, NDKA, UFD1, S100β and troponin I levels were determined using classical immunoassays. The World Federation of Neurological Surgeons (WFNS) at admission and the Glasgow Outcome Score (GOS) at 6 months were evaluated. Results In the two cohorts, blood concentration of H-FABP, S100β and troponin I at admission significantly predicted unfavorable outcome (GOS 1–2–3). A multivariate analysis identified a six-parameter panel, including WFNS, H-FABP, S100β, troponin I, NDKA and UFD-1; when at least three of these parameters were simultaneously above cutoff values, prediction of unfavorable outcome reached around 70% sensitivity in both cohorts for 100% specificity. Conclusion The use of this panel, including four brain injury-related proteins, one cardiac marker and a clinical score, could be a valuable tool to identify aSAH patients at risk of poor outcome.

Aim/Objective: The Bordeaux Pharmacovigilance center detected potential index case of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors related tendinopathy. The aim of this study was to assess whether querying a hospital CDW could be used to amplify this pharmacovigilance signal. Methods: We searched for tendinopathies occurring in patients treated with PCSK9 inhibitors in the CDW of Bordeaux University Hospital, without any time or age or gender restrictions. To this end, we searched tendinopathies in unstructured data (e.g. hospitalization records or medical consultation reports) using the following keywords: \"tendinitis\" OR \"tendinopathy\" OR \"Achilles tendon\" and in structured data (e.g. main or associated diagnoses' coding) using ICD10 code M76. For medication, we searched at least one prescription of PCSK9 inhibitors in the same unstructured data using the following keywords: \"Praluent\" OR \"alirocumab\" OR \"Repatha\" OR \"evolocumab\" OR \"PCSK9\" and in structured data (e.g. in-hospital prescription database) using Anatomical Therapeutic Chemical C10AX13 and C10AX14. Results: Twenty-seven patients were initially found, with no patients retrieved using structured data only. From this initial dataset, 17 patients were excluded for the following reasons: eleven because they cited a history of tendinopathy, five because of a PCSK9 inhibitor was mentioned in the medical records but was not subsequently prescribed, and one because the actual use of PCSK9 inhibitor was not proven. Among the ten other patients, all were treated with alicorumab, which was formally suspected in three cases; the date of drug initiation or symptoms showed a tendency to be more precisely reported in suspected cases than in others. One positive dechallenge was reported. Conclusion: Through this pilot study, we showed that unstructured data collected in hospital CDW could be useful for finding potential individual case safety reports for signal amplification. Other signals should be investigated to assess whether CDW analyses could be implemented in routine pharmacovigilance practice.

Objective At the acute phase of traumatic brain injury (TBI), brain swelling contributes substantially to the development of secondary neurological lesions. Elucidating the pathophysiology of brain swelling is crucial to improve TBI management. In a previous study, specific gravity (SG) of the noncontused hemisphere, as estimated by computed tomography (CT), was higher in patients with high Marshall CT scores and severe brain swelling. The aim of this study was to investigate the relationship between estimated specific gravity (eSG) and clinical variable suggestive of brain swelling. Design Retrospective study of data from a prospectively established database. Setting Neurology ICU in a teaching hospital in Paris, France. Participants We studied 20 patients with severe traumatic brain injury (TBI), 20 patients with high-grade subarachnoid hemorrhage (SAH) presenting similar brain-swelling criteria, 20 patients with low-grade SAH, and 20 healthy controls. Interventions None. Measurements and Results Estimated brain specific gravity was acquired from CT images obtained at ICU admission. eSG was estimated in the overall intracerebral content and in a region-of-interest composed of white matter and the diencephalon. eSG in the region of interest was significantly higher in the TBI patients than in the high-grade SAH patients (1.0350 ± 0.0041 vs. 1.0310 ± 0.0019 g/ml, P  < 0.05). eSG was similar in the high-grade SAH, low-grade SAH, and control groups. Conclusions Our findings do not support a causal link between brain swelling and eSG elevation. The eSG increase in severe TBI patients is not due to brain swelling.

Aim/Objective: To analyze CARs diagnosis recorded in the French pharmacovigilance database (FPVD). Methods: We performed a retrospective analysis of CARs registered in FPVD with EV from 1st July 2021 to 30 December 2023. Data collection included demographic characteristics (age, gender) and skin disorders characteristics (time to onset, clinical features, severity, biopsy results, associated systemic signs, outcome, management, terms used for coding). Results: Our study included 83 patients with an average age of 70 years (standard deviation 8.5), and a sex-ratio M/F of 2.8. Half of the cases were serious including 8 deaths. Despite various clinical features (46 different terms used), most included erythema (24 cases) and blistering (10 cases). The mean time to onset was 12 days. Systemic involvement was associated in 36% of CARs, such as blood disorders (11%) or acute renal failure (8%). Nearly half of cases (53%), displayed signs of direct cutaneous toxicity from EV. Misdiagnoses were found in 6 cases: 3 cases considered as symmetrical drug-related intertriginous and flexural exanthema and 3 cases considered as toxic epidermal necrolysis. Most cases (68%) resolved, often with dermocorticoids. Whereas EV dosage was often reduced in non-serious cases, EV treatment was stopped in serious cases. Conclusion: Misdiagnosis of EV-induced toxic CARs was frequent. Most of CARs shared stereotyped features and similar time to onset. Skin detachment associated with keratinocyte necrosis, and dysmaturation on histology argue for direct cutaneous toxicity of EV. This is a form of chemotherapy skin toxicity observed with other cytotoxic anticancer drugs defined as \"toxic erythema of chemotherapy\". [1] However, CARs appear to be more severe with EV and potentially life-threatening. [2] Our study highlights the importance of a multidisciplinary decision when facing these complexes CAR. Indeed, a recent clinical trial demonstrated the benefits of combining EV with pembrolizumab, but with increased rates of CARs. [3]

PurposePCSK9 might affect central nervous system development, neuronal apoptosis, and differentiation. We investigate the neurocognitive adverse events associated with the use of PCSK9 inhibitors (alirocumab and evolocumab) using pharmacovigilance reports.MethodsWe used the World Health Organization pharmacovigilance database (VigiBase) to perform a disproportionality analysis comparing the proportion of neurocognitive adverse events reported with PCSK9 inhibitors versus the proportion of these effects reported since August 14, 2015 (date of first post-marketing report suspecting a PCSK9 inhibitor), for all drugs in the database. Associations between PCSK9 inhibitor use and neurocognitive adverse events were assessed using both proportional reporting ratio (PRR) and information component (IC). Complementary analyses were performed on other neurologic events, and different sensitivity analyses were conducted to evaluate the robustness of results.ResultsAmong the 81,108 reports involving at least one PCSK9 inhibitor, 1,941 concerned the occurrence of neurocognitive disorders. Most of patients (52.3%) were aged 45–74 years, and 58.0% were women. Signals of disproportionate reporting were found for PCSK9 inhibitors (PRR 1.22, 95% CI 1.17; 1.28; IC 0.28, IC025 0.21) and for each drug individually. No signal of disproportionality was found for any of the other neurologic events investigated. Signals of disproportionate reporting were found for the positive control (benzodiazepines), but not for the negative control (aspirin). The results of the main analysis were confirmed by sensitivity analyses.ConclusionsThis study identified a signal of neurocognitive disorders associated with PCSK9 inhibitors and encourages paying attention to at-risk populations.

Delirium is a frequent complication of traumatic brain injury, especially during the weaning period. Antipsychotic drugs are often used in this case. Loxapine is a tricyclic antipsychotic drug with sedating properties. The effects of intravenous loxapine on EEG as well as on systemic and cerebral hemodynamics after traumatic brain injury are unknown. Seven sedated and mechanically ventilated traumatic brain injured patients were studied 11 +/- 5 days after trauma. They were on continuous perfusion of sufentanil and midazolam. Left and right spectral edge frequency (SEFl, SEFr) of continuous EEG recording, intracranial pressure (ICP), mean flow velocity of the middle cerebral artery (MFV(MCA)) and mean arterial pressure (MAP) were simultaneously recorded and digitalized before and after loxapine infusion (10 mg in 10 min of continuous infusion). Loxapine induced no significant change on MAP, MFV. On the contrary, it decreased ICP and both SEFl, SEFr. ETCO(2 )and the dose of vasopressors were not altered during the study period. 10 mg of loxapine administered intravenously over 10 min decreased brain electrical activity. There is a concomitant reduction in ICP without any significant change in cerebral blood flow velocity. The use of intravenous loxapine to control agitation is not accompanied by deleterious hemodynamic or systemic effects in ICU's traumatic brain injured patients.

As for the majority of antiepileptic drugs, encephalopathy, manifested by transient somnolence, mood and motor disorders, is a possible side-effect. To our knowledge, there is little information about gabapentin-induced coma. We report a third case of gabapentin-induced coma where magnetic resonance-spectrometry was performed in diagnosis assessment.