Neurology Department
Conditions
Keywords
nitrous oxide poisoning
Brief summary
N2O inactivates vitamin B12, impairing its ability to act as a cofactor of methionine synthase. In addition, the elimination of vitamin B12 is increased. Neurological damage is similar to that described in combined sclerosis of the marrow, and are probably related to induce vitamin B12 deficiency. The use of N2O can then precipitate the rapid appearance of signs (neurological, psychiatric and hematological) related to a true and/ or functional vitamin B12 deficiency. In 1978, RB Layzer described the first 3 cases of peripheral neuropathy secondary to nitrous oxide (N2O) consumption. In 2016, a team collected the 91 published cases: among these, 72 had neurological complications, and 52 had a concentration of vitamin B12 considered low or normal-low Since then, consumption patterns seem changed due to: an increasing ease of access, the change of container (packaging in cartridge 8 grams versus bottle of 600 grams) and a usually occasional and festive consumption that seems to become solitary and regular, This change in consumption patterns is explained by an increased incidence of neurological complications, although no epidemiological work is yet available. The objective of this work is to describe the epidemiology of this condition, to correlate it with major recent social phenomena (confinement related to the SARS-Cov2 pandemic), and finally to compare the incidence of myelopathies secondary to N2O with the incidence of other frequent inflammatory neurological diseases (autoimmune myelitis and Guillain-Barré syndrome).
Interventions
None listed
Sponsors
Centre Hospitalier de Saint-Denis
Study design
Observational model
COHORT
Time perspective
RETROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
16 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Adult patient (≥16 years) * Hospitalized or having consulted with the departments of Neurology or Internal Medicine for neurological phenomena related to the consumption of N2O. The neurological phenomena included are usually: neuropathies or myelopathies, However, the existence of other neurological or psychiatric signs is not a factor of exclusion: for example, headaches or cognitive or psychiatric disorders with acute onset. * Exposure to N2O for recreational or medical reasons (Meopa anesthesia). * Lack of alternative diagnosis other than N2O poisoning * Consultation for neurological disorders between 01/01/2018 and 31/12/2021
Exclusion criteria
* Minor subjects or subjects subject to a legal protection measure (guardianship, curators) during the consultation. * Refusal to include in a study explained in the file * Absence of N2O consumption during the 6 months preceding the appearance of signs
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| consumption of toxic substances (alcohol, tobacco, cannabis) | Day 1 | describe the epidemiology of neurological complications to nitrous oxide poisoning |
| age | Day 1 | describe the epidemiology of neurological complications to nitrous oxide poisoning |
| place to live | Day 1 | describe the epidemiology of neurological complications to nitrous oxide poisoning |
| Occupational status | Day 1 | describe the epidemiology of neurological complications to nitrous oxide poisoning |
| sexe | Day 1 | describe the epidemiology of neurological complications to nitrous oxide poisoning |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Date and nature of first symptoms | Day 1 | correlate epidemiology with major recent social phenomena |
| consumption mode and quantity | Day 1 | correlate epidemiology with major recent social phenomena |
Other
| Measure | Time frame | Description |
|---|---|---|
| detail of symptoms, origin and consequences | Day 1 | compare the incidence of myelopathies secondary to N2O with the incidence of other frequent inflammatory neurological diseases |
Countries
France
Contacts
Primary ContactMickael BONNAN, MD
Backup ContactThomas DE BROUCKER, MD
Outcome results
None listed