Nitrous oxide poisoning can lead to hypoxia followed by syncope, heart attack, and even fatal events such as suffocation[3].Nitrous oxide does not bind hemoglobin in the blood but only dissolves in physical form in the blood.Inhaled nitrous oxide with vitamin B12 (also known as cobalamin) after contact, cobalt atoms are oxidized and inactivated, and the inactivated cobalamin recovers slowly[4]. Patients with normal vitamin B12 levels usually develop neurological syndromes after prolonged, repeated exposure to nitrous oxide, while patients with subclinical vitamin B12 deficiency may develop myelopathy after only one abuse of nitrous oxide [5]. The neuropathologic changes in the spinal cord involved area mainly include initial swelling of the myelin sheath around the axons of nerve cells, followed by demyelination and axonal degeneration.It has been reported in many literatures that the nerve damage caused by nitrous oxide is mainly SCD affecting the posterior cord of the spinal cord, which may include ataxia, loss of sense of posture and vibration, and unstable gait[6]. The corticospinal tract may also be involved, leading to weakness, spasms, hyperreflexia, clonus, and positive Babinski sign[7]. Peripheral and optic nerves may also be involved. MRI of the spine showed T2-weighted posterior cord reverse v-shaped high signal characteristics[8], and similar cases of nitrous oxide poisoning with syringomyelia have not yet been reported.
Syringomyelia (SM) is a chronic, progressive disease characterized by tubular cavity formation and gliosis in the spinal cord. Its lesions are mostly found in the cervical spinal cord. Most lesions are located between C2 and T9, but may extend down to the medullary cone or up to the brain stem (the bulb). The onset is insidious and progressive. At present, the causes and pathogenesis of SM are not completely clear. There are congenital developmental abnormality, cerebrospinal fluid dynamics abnormality, blood circulation abnormality and other theories. The pathogenesis can be divided into congenital SM and acquired SM.The most common congenital causes are neural tube defects (myelomeningocele and tetanus syndrome) and Chiari malformations. Acquired SM is thought to be caused by disturbance of normal cerebrospinal fluid circulation. There are many causes of acquired SM, including hydrocephalus, infection, inflammation, trauma, spinal cord tumors, extramedullary tumors, arachnoid cysts, spinal stenosis, etc.[9]. In this case, syringomyelia is thought to be associated with nitrous oxide poisoning, but cannot be determined. Since nitrous oxide with syringomyelia has not been previously reported, this paper provides some evidence for the possibility of abuse of nitrous oxide with syringomyelia.
To sum up, Inhaled nitrous oxide abuse is common and should be given high clinical attention because it is a treatable and possibly reversible cause of myelopathy. While healthy young people in subacute or chronic have disease of the nervous system performance, a history of nitrous oxide abuse should be considered, such as the symmetry of the distal limb numbness, weakness, tendon reflex disappears, pathological character, etc. At the same time, the physician should give patients with cervical and thoracic MRI in order to make clear its related to whether the acquired syringomyelia.In order to avoid irreversible damage of the nervous system, the patient should stop contact with harmful substances and be treated with drugs as soon as possible.