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Abstract After spinal cord injury (SCI), patients face many physical and psychological issues including intestinal dysfunction and comorbidities, strongly affecting quality of life. The gut microbiota has recently been suggested to influence the course of the disease in these patients. However, to date only two studies have profiled the gut microbiota in SCI patients, months after a traumatic injury. Here we characterized the gut microbiota in a large Italian SCI population, within a short time from a not only traumatic injury. Feces were collected within the first week at the rehabilitation center (no later than 60 days after SCI), and profiled by 16S rRNA gene-based next-generation sequencing. Microbial profiles were compared to those publicly available of healthy age- and gender-matched Italians, and correlated to patient metadata, including type of SCI, spinal unit location, nutrition and concomitant antibiotic therapies. The gut microbiota of SCI patients shows distinct dysbiotic signatures, i.e. increase in potentially pathogenic, pro-inflammatory and mucus-degrading bacteria, and depletion of short-chain fatty acid producers. While robust to most host variables, such dysbiosis varies by lesion level and completeness, with the most neurologically impaired patients showing an even more unbalanced microbial profile. The SCI-related gut microbiome dysbiosis is very likely secondary to injury and closely related to the degree of completeness and severity of the lesion, regardless of etiology and time interval. This microbial layout could variously contribute to increased gut permeability and inflammation, potentially predisposing patients to the onset of severe comorbidities.

Abstract The authors present a case of atlantoaxial instability associated with C1–C2 inflammatory tissue leading to subarachnoid hemorrhage. A 65-year-old male patient arrived in June 2011 to the emergency unit for cervical pain and fever. Imaging studies documented periodontoid pseudotumor at C1–C2 level. Infective disease was suspected; the patient was therefore hospitalized and treated with antibiotics. Subsequent computed tomographic (CT) scans revealed C1–C2 instability. In August, the patient showed acute neurological deterioration and coma. Urgent brain CT revealed a hemorrhagic lesion which caused compression on the medulla oblongata, subarachnoid hemorrhage, and ventricular dilatation. An external ventricular drainage was positioned. Angio-CT and angiography did not show any vascular abnormalities. Cervical magnetic resonance imaging documented a solid tissue lesion between the atlas arch and axis. The lesion was associated with an epidural and subdural hematoma, exerting compression on brainstem. The patient underwent posterior decompression and C1–C2 fusion according to Harms technique in October, with significant clinical improvement. The authors present a case of atlantoaxial instability associated with a periodontoid pseudotumor at C1–C2 level determining dural sac compression. The patient showed an acute neurological deterioration caused by bleeding of the solid component of the cervical lesion. Hemorrhage of the solid component of periodontoid masses linked to atlantoaxial instability has not yet been reported in literature. To the best of our knowledge, this is the first case of C1–C2 instability with periodontoid pseudotumor leading to subarachnoid hemorrhage.