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Background: The recreational use of nitrous oxide is becoming increasingly common among teenagers and young adults. Since 2018, the use of nitrous oxide has increased exponentially and has become a public health problem. Case presentation: A 23-year-old patient was referred to accident and emergency (A&E) by his general practitioner for deterioration in general condition, vomiting, diarrhea and febrile headache at 39 °C. He reported that he had been partying for a month and consuming alcohol, cannabis and nitrous oxide. Three days before the consultation, he reported increased abdominal pain in the right iliac fossa. His homocysteine concentration was 51.9 μmol/L, and his plasma methyl malonate concentration increased to 4.45 μmol/L. A thoracic and abdominal CT scan revealed right iliac venous thrombosis associated with bilateral pulmonary embolism. Conclusion: Nitrous oxide inhibits the activity of methionine synthetase. We therefore observed an increase in plasma homocysteine and 5-methyl-THF. The increase in homocysteine could be responsible for the pro-thrombotic activity resulting from nitrous oxide intoxication. At present, no threshold or duration of exposure has been identified as being particularly likely to cause complications. It is likely that other factors coexist, such as coagulation disorders and polymorphisms of the MHTFR gene, which can lead to hyperhomocysteinaemia, cannabis consumption, inflammatory conditions and others. Treatment is based on vitamin B12 supplementation and curative anticoagulation. Some authors also recommend folate supplementation. Consumption of nitrous oxide could be associated with arterial and venous thromboembolic disease. [ABSTRACT FROM AUTHOR]

Abstract Background The recreational use of nitrous oxide is becoming increasingly common among teenagers and young adults. Since 2018, the use of nitrous oxide has increased exponentially and has become a public health problem. Case presentation A 23-year-old patient was referred to accident and emergency (A&E) by his general practitioner for deterioration in general condition, vomiting, diarrhea and febrile headache at 39 °C. He reported that he had been partying for a month and consuming alcohol, cannabis and nitrous oxide. Three days before the consultation, he reported increased abdominal pain in the right iliac fossa. His homocysteine concentration was 51.9 μmol/L, and his plasma methyl malonate concentration increased to 4.45 μmol/L. A thoracic and abdominal CT scan revealed right iliac venous thrombosis associated with bilateral pulmonary embolism. Conclusion Nitrous oxide inhibits the activity of methionine synthetase. We therefore observed an increase in plasma homocysteine and 5-methyl-THF. The increase in homocysteine could be responsible for the pro-thrombotic activity resulting from nitrous oxide intoxication. At present, no threshold or duration of exposure has been identified as being particularly likely to cause complications. It is likely that other factors coexist, such as coagulation disorders and polymorphisms of the MHTFR gene, which can lead to hyperhomocysteinaemia, cannabis consumption, inflammatory conditions and others. Treatment is based on vitamin B12 supplementation and curative anticoagulation. Some authors also recommend folate supplementation. Consumption of nitrous oxide could be associated with arterial and venous thromboembolic disease.

Abstract Background Nitrous oxide is a medical and household gas that has seen its use drift to recreational purpose among the young population in recent years. Significant neurological, hematological and psychiatric side effects, generally related to an induced functional vitamin B12 deficiency, have been described separately in the literature. Case report A 22-year-old woman of North African origin experienced an exceptional combination of polyneuropathy, bilateral pulmonary embolism and severe pancytopenia related to vitamin B12 deficiency and hyperhomocysteinemia induced by recreational nitrous oxide use. After treatment with vitamin B12 supplementation and intensive rehabilitative management, the patient progressively regained the ability to walk and her biological parameters gradually returned to normal. The pathophysiological mechanisms related to a decrease in vitamin B12 activity are the reduction of products needed for synthesis of deoxyribonucleic acid, carbohydrate or fatty acids, and the increase of hyperhomocysteinemia. Other mechanisms involving a direct action of N2O are also suspected. Conclusion This case report brings elements to support our knowledge about pathological pathway, recovery and prognosis of recreational N2O abuse complications. The general and medical population should be aware to the serious consequences of this type of consumption.

Background: Nitrous oxide is a medical and household gas that has seen its use drift to recreational purpose among the young population in recent years. Significant neurological, hematological and psychiatric side effects, generally related to an induced functional vitamin B12 deficiency, have been described separately in the literature. Case report: A 22-year-old woman of North African origin experienced an exceptional combination of polyneuropathy, bilateral pulmonary embolism and severe pancytopenia related to vitamin B12 deficiency and hyperhomocysteinemia induced by recreational nitrous oxide use. After treatment with vitamin B12 supplementation and intensive rehabilitative management, the patient progressively regained the ability to walk and her biological parameters gradually returned to normal. The pathophysiological mechanisms related to a decrease in vitamin B12 activity are the reduction of products needed for synthesis of deoxyribonucleic acid, carbohydrate or fatty acids, and the increase of hyperhomocysteinemia. Other mechanisms involving a direct action of N2O are also suspected. Conclusion: This case report brings elements to support our knowledge about pathological pathway, recovery and prognosis of recreational N2O abuse complications. The general and medical population should be aware to the serious consequences of this type of consumption. [ABSTRACT FROM AUTHOR]

The recreatinal use of nitrous oxide has become more common in recent years, especially in adolescents and young adults. It has been mainly associated with medical conditions like megaloblastic anemia and (myelo)neuropathy. We report on the thromboembolic complications, a less known side effect, associated with recreational inhalation of nitrous oxide. An extensive literature search was performed for publications reporting on the thromboembolic complications associated with recreational nitrous oxide abuse. Data about sex, age, location of thrombosis, laboratory findings, therapy and outcome were collected. A total of 13 case reports or case series were identified comprising a total of 14 patients. The reported thromboembolic side effects included deep venous thrombosis, pulmonary embolism, mesenterial-, portal and splenic vein thrombosis, cerebral sinus thrombosis, cortical vein thrombosis, stroke, acute myocardial infarction and peripheral artery thromboembolism. These side effects are possibly mediated by the interaction of nitrous oxide with vitamin B12, a cofactor of the methionine synthase complex, which eventually results in elevation of plasma levels of homocysteine. Despite being a known risk factor for cardiovascular disease, the exact pathophysiological mechanism remains unclear. Cessation of nitrous oxide inhalation is necessary to prevent recurrent thrombosis. Nitrous oxide abuse may thus result in a wide spectrum of thromboembolic complications. One should be aware of this etiology, especially in a young person with no obvious risk factors for cardiovascular disease. Spreading awareness is important to inform people about the potentially serious side effects associated with nitrous oxide inhalation. [ABSTRACT FROM AUTHOR]

ObjectiveThe aim of the study was to investigate the clinical, neuropsychological, and regional cerebral blood flow (rCBF) perfusion changes in patients with neuropsychiatric symptoms caused by nitrous oxide (N2O) abuse.MethodsA total of 16 patients with neuropsychiatric symptoms caused by nitrous oxide abuse were recruited for this study. The study was carried out in the withdrawal phase of N2O abuse. A 925–1110 MBq 99mTc-ECD was administered intravenously. SPECT/CT images were collected with a low-energy and high-resolution collimator. The region uptake statistics of different brain regions of interest between patients with N2O abuse and normal people of the databases for younger subjects from the Scenium DB Comparison software were calculated automatically.ResultsThe clinical manifestations of the 16 patients with neuropsychiatric symptoms were mood lability, anxiety, hallucination, delusion, agitation, confusion, and other psychiatric symptoms. In addition, 15 of the patients also complained of memory decline; 14 patients manifested numbness or paresthesia; 14 patients developed limb weakness, and their motor impairments were more severe in the lower limbs than in the upper limbs; and eight patients had urinary and defecation disturbances. In the neuropsychological examination, the BPRS score was 54.69 ± 11.48, the HAMD score was 30.00 ± 11.06, the HAMA score was 18.06 ± 5.77, the MMSE score was 28.06 ± 2.29, and the MoCA score was 25.06 ± 3.40. SPECT showed hypoperfusion in the frontal and temporal lobes, which is consistent with the clinical findings.ConclusionThis was the first study to demonstrate the obvious effect of N2O abuse on CBF in patients with neuropsychiatric symptoms. CBF perfusion imaging is helpful to detect the changes in the local brain functional activity in patients with N2O abuse.

Laughing gas is becoming increasingly popular as a recreational drug of choice, particularly among young adults. Nitrous oxide, the toxic component of laughing gas, can cause neuronal injury when used in high doses. Through multiple mechanisms, nitrous oxide leads to B12 depletion and subsequent demyelination, particularly in the spinal cord. Here, we present the case of a 27-year-old female who presented with ataxia and was found to have laughing gas-induced subacute combined degeneration from nitrous oxide. After aggressive vitamin B12 repletion and laughing gas cessation for three months, the patient improved., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Rao et al.)

The abuse of inhalants like nitrous oxide (N 2 O), readily available worldwide, has remained a prominent public health problem during the last few decades. Literature reveals increased use during the previous pandemic, particularly regarding recreational use. There is limited evidence-based data available to relate the abuse of N 2 O with psychosis. Therefore, this case report of a 22-year-old adult with no previous psychiatry history, reportedly abusing 75-100 canisters of N 2 O per day during the last pandemic COVID-19 lockdown, highlights the relationship between (N 2 O) abuse and the symptoms evolved including delusions, auditory hallucinations, and disorganized cognition. All the laboratory findings and results from imaging modalities were inconsistent for any organic cause of the symptoms. The case then underwent treatment with antipsychotic medications and a multidisciplinary model, which improved the symptoms gradually. The case, in particular, discusses N 2 O abuse, which is widespread in European Union countries, including the UK and the Republic of Ireland, and its chronic use puts one at a higher risk of developing psychosis, personality changes, affective lability, anxiety, depression, cognitive impairment, and myeloneuropathy. The sale of N 2 O for its psychoactive properties is prohibited in many countries, including the Republic of Ireland, as per legislation. However, N 2 O is not a controlled drug, meaning it is not a crime to possess N 2 O. This case report manifests the psychopathy caused by abuse of N 2 O, which would further attract specialists in the field to conduct epidemiological studies for prevention at the primary level., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Raaj et al.)

Background The recreational abuse of nitrous oxide (N 2 O) is becoming increasingly prevalent within the United Kingdom and across the globe. Chronic abuse can cause nerve and spinal cord damage through the functional inactivation of vitamin B12. We present six cases from a single centre in the United Kingdom between 2016 and 2020 with neurological complications from N 2 O abuse, ranging from paraesthesia to subacute combined degeneration of the spinal cord. Methodology A retrospective review of all neurology admissions to Queen Elizabeth Hospital Birmingham (QEHB) between 2016 and 2020 was conducted to identify patients admitted with a diagnosis of neurological dysfunction (neuropathy or myelopathy) in association with chronic N 2 O misuse. The Prescribing Information and Communication System was used to collect data on demographics, reported N 2 O misuse, presenting symptoms, results of blood tests, nerve conduction studies and treatment regimens. All patients gave verbal consent for inclusion in the case series. Data were anonymised and analysed by the corresponding author. Results All patients were males aged between 22 and 28 years. In all cases, the patients were admitted with the abuse of N 2 O whippet  canisters (ranging from 20 to 500 canisters per session), presenting with a combination of sensory and motor disturbance. Clinical suspicion, in the context of a history of N 2 O abuse, along with elevated blood concentrations of methylmalonic acid (MMA) and homocysteine, and nerve conduction studies, was the cornerstone of the diagnosis. All patients were treated with parenteral vitamin B12, though individual regimens differed, with no standardisation in the duration or frequency of treatment. All patients received intramuscular (IM) vitamin B12 injections during admission, with one patient receiving oral vitamin B12 before being switched to IM vitamin B12 injections. One patient received additional folic acid as a treatment adjunct. Prescriptions were most varied on discharge with huge discrepancies in duration and frequency of vitamin B12 replacement, ranging from no B12 replacement at all to IM injections once weekly for eight weeks.  Conclusions The variability in route, dose and duration of vitamin B12 treatment, along with the variable use of adjunctive therapy reported in the literature, highlights the current lack of consensus in managing N 2 O neurotoxicity., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Crisp et al.)

Competing Interests: None

Vitamin B12 deficiency causes skin hyperpigmentation, subacute combined degeneration of the spinal cord, and megaloblastic anemia. Although vitamin B12 deficiency rarely occurs in well-nourished, healthy, young people, nitrous oxide (N2O) intoxication is an important cause of vitamin B12 deficiency in this cohort. N2O, a colorless gas used as an anesthetic since the late 19th century because of its euphoric and analgesic qualities, is now used as a recreational drug and is available via the Internet and at clubs. Here, we describe the case of a 29-year-old woman presenting with skin hyperpigmentation as her only initial symptom after N2O abuse for approximately 2 years. N2O intoxication-induced vitamin B12 deficiency was diagnosed based on the skin pigmentation that had manifested over the dorsa of her fingers, toes, and trunk, coupled with myeloneuropathy of the posterior and lateral columns, a low serum vitamin B12 level, an elevated serum homocysteine level, and the N2O exposure revealed while establishing the patient's history. Symptoms improved significantly with vitamin B12 treatment. We recommend that dermatologists consider N2O intoxication-induced vitamin B12 deficiency as a potential cause of skin hyperpigmentation and myeloneuropathy of the posterior and lateral columns in young, otherwise healthy patients. Failure to recognize this presentation may result in inappropriate treatment, thus affecting patients' clinical outcomes.

Background and Purpose: The electrophysiologic characteristics of peripheral neuropathy secondary to nitrous oxide (N 2 O) abuse remain unclear. The paper therefore aimed to summarize the electrophysiologic characteristics of N 2 O-associated peripheral neuropathy and identify the risk factors of severe nerve injury., Methods: The electrophysiologic results and clinical data of patients with peripheral neuropathy secondary to N 2 O abuse at our hospital between 2018 and 2020 were analyzed retrospectively, and their electrophysiologic changes were summarized., Results: Most patients exhibited decreased sensory and motor nerve conduction velocities (75% and 76%), decreased sensory nerve and compound motor action potentials (57% and 59%), and prolonged distal motor latency (59%), while a response was absent in 36%. These findings indicate that N 2 O abuse can result in generalized injury to sensory and motor nerves. Electrophysiologic results indicated axonal neuropathy in 37 cases (49%), demyelinating peripheral neuropathy in 4 (5%), and mixed neuropathy in 12 (16%). Peripheral nerve injury was more common in the lower limbs (72%) than in the upper limbs (42%, p <0.0001). The upper and lower limbs were primarily affected by sensory nerve demyelination (35%) and motor axonal injury (67%), respectively. Subgroup analysis indicated that longer N 2 O exposure and longer disease course were associated with more-severe motor axonal injury in the lower limbs., Conclusions: N 2 O-associated peripheral neuropathy can lead to sensory and motor nerve injury, with axonal injury being the most common. Injuries were more severe in the lower limbs. Prolonged N 2 O exposure and disease course increased the severity of motor axonal injury in the lower limbs., Competing Interests: The authors have no potential conflicts of interest to disclose., (Copyright © 2023 Korean Neurological Association.)

Objective: The aim of the study was to investigate the clinical, neuropsychological, and regional cerebral blood flow (rCBF) perfusion changes in patients with neuropsychiatric symptoms caused by nitrous oxide (N 2 O) abuse., Methods: A total of 16 patients with neuropsychiatric symptoms caused by nitrous oxide abuse were recruited for this study. The study was carried out in the withdrawal phase of N 2 O abuse. A 925-1110 MBq 99m Tc-ECD was administered intravenously. SPECT/CT images were collected with a low-energy and high-resolution collimator. The region uptake statistics of different brain regions of interest between patients with N 2 O abuse and normal people of the databases for younger subjects from the Scenium DB Comparison software were calculated automatically., Results: The clinical manifestations of the 16 patients with neuropsychiatric symptoms were mood lability, anxiety, hallucination, delusion, agitation, confusion, and other psychiatric symptoms. In addition, 15 of the patients also complained of memory decline; 14 patients manifested numbness or paresthesia; 14 patients developed limb weakness, and their motor impairments were more severe in the lower limbs than in the upper limbs; and eight patients had urinary and defecation disturbances. In the neuropsychological examination, the BPRS score was 54.69 ± 11.48, the HAMD score was 30.00 ± 11.06, the HAMA score was 18.06 ± 5.77, the MMSE score was 28.06 ± 2.29, and the MoCA score was 25.06 ± 3.40. SPECT showed hypoperfusion in the frontal and temporal lobes, which is consistent with the clinical findings., Conclusion: This was the first study to demonstrate the obvious effect of N 2 O abuse on CBF in patients with neuropsychiatric symptoms. CBF perfusion imaging is helpful to detect the changes in the local brain functional activity in patients with N 2 O abuse., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Wang, Yin, Wang, Wang, Liu, Dong, Duan, Zheng, Hong, Liu and Tie.)

Nitrous oxide (N 2 O) toxicity is a concern common to several medical fields. Here, retrospective study of four N 2 O abuses with neurological signs in the emergency practice provides a preliminary basis for a metabolic Discussion/Review. This latter highlights N 2 O abuse as pathology of DNA/RNA/protein methylations, for instance consistent with impairments of protein arginine methyltransferases involved in myelinogenesis and myelopathy in patients. Basically, pathogenesis starts with oxidation by N 2 O of coordinated cobalamine cobalt ions at enzyme sites with impairments of vitamin-B12-dependent pathways. Methionine synthase (methylcobalamine) and methymalonyl-CoA mutase (adenosylcobalamine) are inactivated and cofactor-depleted, respectively. The number of impacted pathways (folate cycle, methylation cycle, S -adenosylmethionine-dependent methyltransferases, transulfuration pathway, Krebs cycle fueling by methylmalonyl-CoA, glutathione synthesis) explains the variety of potential research/laboratory markers, and may provide new clues and future angles to explore N 2 O toxicity. Overall, homocysteine measurements obviously help diagnosis of N 2 O abuses. Additional markers may include vitamin-B12, methionine, methylmalonate, dimethylglycine, sarcosine, S -adenosylmethionine to S -adenosylhomocysteine ratio, various S -adenosylamino acids, S -adenosylmethionine-dependent cellular methylations, and additional analytes (propionylcarnitine, propionylglycine, cystathionine and derived metabolites, methylated amino acids [eg arginine], betaine). • Recreational use of N 2 O can reach 100 to 300 cartridges/day, and cause neurological deterioration. • N 2 O by oxidising the coordinated cobalt ion disrupts cobalamin (vitamin B12)-dependent pathways. • N 2 O disrupts folate, methylation cycles; DNA, RNA, protein methylations; glutathione synthesis. • Laboratory markers include increased plasma homocysteine and numerous metabolites reviewed. • Treatment of abuse is cessation of N 2 O consumption and supplementation with vitamins B12 and B6. [ABSTRACT FROM AUTHOR]

MicroCog test results and supplemental neuropsychological test findings are reported concerning a male health professional who had abused nitrous oxide (N2O) on a regular basis for more than 20 years. At the time of the examination, the health professional had abstained from N2O use for 12 months. Test findings indicate that the patient had suffered a general decrement in cognitive functioning. Spatial functioning and reaction times were better preserved than attention, mental control, verbal and arithmetic reasoning, and verbal memory. His verbal memory loss was particularly severe, but abstract reasoning and practical social judgment remained intact. Marked visual memory and construction deficits were identified with supplemental clinical tests. Since 12 months of abstinence had elapsed prior to the examination, it may be reasonably assumed that cognitive recovery was nearly complete and the findings reported are stable. [ABSTRACT FROM AUTHOR]