Background Pneumorrhachis (PR) describes the rare presence of intraspinal air, mainly following traumatic or iatrogenic procedures. According to the localization of air in the spinal canal, PR has been classified into internal (subdural) and external (epidural). PR rarely manifests in neurological deficits and usually resolves spontaneously without recurrence, with air being passed directly into the bloodstream. Here, we report a case of external PR occurring spontaneously (without any underlying trauma or surgical interventions) manifesting as neurological deficits. This is an extremely rare finding with only a limited number of cases in the literature. Case presentation We report a case of spontaneous external PR manifesting as neurological symptoms in a 62-year-old male diabetic patient with chronic low backpain who developed numbness in his perineal region mainly on the left side. His medical history was normal, without trauma or surgical intervention. Magnetic resonance imaging (MRI) and computed tomography (CT) in the past 2 years demonstrated degenerative changes in the lumbar spine, including end plates and disc spaces, with intervertebral disc vacuum phenomenon (VP); the CT additionally showed intraspinal air in the epidural space at L5-S1 levels compressing the cauda equina. A diagnosis of spontaneous external PR was made. A follow-up MRI upon exacerbation of neurological deficits showed an increase in air locule size. Our patient was managed conservatively on a nonsteroidal anti-inflammatory agent (NSAID) and was advised for regular follow-ups. No aspiration or surgery has been performed to date. Conclusions Spontaneous external pneumorrhachis manifesting as neurological symptoms is extremely rare. Due to degenerative disc disease producing vacuum phenomenon, we propose that spontaneous PR secondary to intradiscal VP be considered as part of the differential for radicular symptoms, especially with increasing age. The most effective noninvasive investigation for the diagnosis of PR is CT. MRI is less beneficial in the case of PR as gas and calcifications are hard to distinguish, both being of low-intensity signals on all MR sequences.

Axonal regeneration and functional recovery are poor after spinal cord injury (SCI), typified by the formation of an injury scar. While this scar was traditionally believed to be primarily responsible for axonal regeneration failure, current knowledge takes a more holistic approach that considers the intrinsic growth capacity of axons. Targeting the SCI scar has also not reproducibly yielded nearly the same efficacy in animal models compared to these neuron-directed approaches. These results suggest that the major reason behind central nervous system (CNS) regeneration failure is not the injury scar but a failure to stimulate axon growth adequately. These findings raise questions about whether targeting neuroinflammation and glial scarring still constitute viable translational avenues. We provide a comprehensive review of the dual role of neuroinflammation and scarring after SCI and how future research can produce therapeutic strategies targeting the hurdles to axonal regeneration posed by these processes without compromising neuroprotection.

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