Objective Coronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators. Methods In this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2–specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/− sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS). Results We detected anti–SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10). Conclusions Our results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.

Human coronaviruses are known for their tropism for central nervous system and to be associated with neurological complications. SARS-CoV-2 pandemy represent a major health issue and if respiratory symptoms are at the forefront, neurological symptoms should be expected. Here we report the case of two patient that developed encephalitic symptoms with neuropsychological impairment and pathologic cerebrospinal fluid features concomitantly to SARS-CoV-2 documented infection. Both patient recovered promptly without treatment. This report raises the question of central nervous system involvement in SARS-CoV-2 infection and the need for investigation of neuropsychological complications in infected patient.

We read with great interest the article by Pouclet-Courtemanche and colleagues¹ published recently in Brain Communications. The article reported an increased prevalence of idiopathic normal pressure hydrocephalus (iNPH) among patients with a behavioural variant frontotemporal dementia (bvFTD) (7.25%) in comparison with those with Alzheimer’s disease (1.1%).¹ Therefore, we proposed to evaluate this high prevalence of iNPH in patients with FTD (not only focusing on bvFTD) followed at the Leenaards Memory Center of the Lausanne University Hospital between January 2013 and December 2022.

Purpose: This study examines GPT-4o’s ability to communicate effectively with relatives of patients undergoing decompressive hemicraniectomy (DHC) after malignant middle cerebral artery infarction (MMCAI). Methods: GPT-4o was asked 25 common questions from patients’ relatives about DHC for MMCAI, twice over a 7-day interval. Responses were rated for accuracy, clarity, relevance, completeness, sourcing, and usefulness by board-certified intensivist* (one), neurologists, and neurosurgeons using the Quality Analysis of Medical AI (QAMAI) tool. Interrater reliability and stability were measured using ICC and Pearson’s correlation. Results: The total QAMAI scores were 22.32 ± 3.08 for the intensivist, 24.68 ± 2.8 for the neurologist, 23.36 ± 2.86 and 26.32 ± 2.91 for the neurosurgeons, representing moderate-to-high accuracy. The evaluators reported moderate ICC (0.631, 95% CI: 0.321–0.821). The highest subscores were for the categories of accuracy, clarity, and relevance while the poorest were associated with completeness, usefulness, and sourcing. GPT-4o did not systematically provide references for their responses. The stability analysis reported moderate-to-high stability. The readability assessment revealed an FRE score of 7.23, an FKG score of 15.87 and a GF index of 18.15. Conclusions: GPT-4o provides moderate-to-high quality information related to DHC for MMCAI, with strengths in accuracy, clarity, and relevance. However, limitations in completeness, sourcing, and readability may impact its effectiveness in patient or their relatives’ education.

Cerebral hemosiderosis is a condition resulting from recurrent or extensive intracranial hemorrhages, leading to hemosiderin deposition in central nervous system structures and affecting cranial nerves. The classic clinical triad includes sensorineural hearing loss, cerebellar ataxia, and pyramidal signs, with less frequent involvement of other cranial nerves. In our case however, we report a unique presentation of multiple lower cranial nerve involvement following a right-myelencephalic subarachnoid hemorrhage secondary to hemorrhagic ventricular effraction in a 58-year-old male patient. We aim to highlight the implications of atypical cranial nerve hemosiderosis on swallowing and tracheotomy weaning and demonstrate the importance of tailored rehabilitation approaches. The patient presented a coma after hemorrhagic stroke and was later diagnosed with hemosiderosis affecting cranial nerves IX, X, and XII, leading to severe dysphagia and delayed tracheotomy weaning. Magnetic resonance imaging with susceptibility-weighted sequence confirmed the diagnosis. Neurorehabilitation was adjusted to incorporate specific swallowing techniques addressing pharyngeal motor deficits. Despite the tracheotomy weaning delay (31 vs 12.75 days average), a specific adaptation of cervical posture during the swallowing, that is, anterior flexion combined with a rotation ipsilateral to the affected side helped to secure swallowing and promote tracheotomy weaning. This case emphasizes that hemosiderin deposits can affect cranial nerves beyond the typical vestibulocochlear nerve, possibly influenced by cerebrospinal fluid flow patterns near Magendie’s foramen. This case underscores the need for early diagnosis and tailored rehabilitation in cerebral hemosiderosis with atypical cranial nerve involvement to optimize functional outcomes. Further research is essential to guide management in such rare presentations.