Self-study | Nitrous Oxide Use: It’s No Laughing Matter [Active June 30, 2025 - June 5, 2026]

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* 1. End code

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* 2. The primary proposed mechanism of action of nitrous oxide in the body, which accounts for its anesthetic and analgesic properties is:

a. Post-synaptic NMDA (glutamate) receptor blockade

b. Cannabinoid receptor agonism

c. Dopamine release into the nucleus accumbens

d. Selective serotonin reuptake inhibition

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* 3. Nitrous oxide has several industrial applications, such as an additive/propellant for whipped cream and as an oxidizing agent added to combustion engine fuel to enhance combustion/engine power. Additionally, nitrous oxide continues to be used in certain medical settings, such as dentistry. These industrial applications, in particular, have the unfortunate consequence of increasing the availability of nitrous oxide because:

a. Most individuals who misuse nitrous oxide work in the culinary industry and therefore have access to culinary whipped cream canisters

b. Since most individuals who misuse nitrous also huff gasoline, the exposure to nitrous oxide is incidental to gasoline huffing

c. Due to its industrial applications, nitrous oxide falls under the federal through the Food, Drug, and Cosmetic Act, which allows for largely unregulated sale of nitrous oxide as long as the retail sale is not specifically marketed as producing a high. This results in easy retail purchasing through online vendors such as Amazon

d. The industrial applications of nitrous oxide increase the atmospheric nitrous oxide concentrations that results in “second hand exposure” that causes deleterious consequences to individuals in proximity to their industrial use.

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* 4. Nitrous Oxide-Induced Subacute Combined Degeneration of the Cord (N2O-SACD) is a serious neurological condition resulting from nitrous oxide use, which was first described in 1978 in a series of 14 dentists. Symptoms include: parasthesias (starting distally), gait ataxia sometimes with falls and/or inability to walk altogether, increased lower extremity deep tendon reflexes, sometimes with delirium/psychosis. The primary cause of N2O-SACD is:

a. Spinal column infarcts secondary to asphyxia caused by nitrous oxide use

b. High concurrence of neurosyphilis in individuals who misuse nitrous oxide

c. Low thiamine ingestion due to restrictions in diet while individuals are actively using nitrous oxide

d. Inactivation of vitamin B12 through the irreversible oxidation of the cobalt ion in cobalamin.

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* 5. The typical treatment approach to N2O-SACD can include all of the following except:

a. Hemodialysis

b. Cessation of nitrous oxide use/exposure

c. B12 supplementation (Either IM 1000micrograms daily or every other day x 1 week, then once a week x4-6 weeks, then monthly thereafter until symptoms no longer improve, OR oral 1000-2000micrograms daily until symptoms no longer improve)

d. Methionine supplementation (1g 3x/day for 4-6 weeks)

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* 6. EMG/nerve conduction studies on individuals with N2O-SACD are likely to show axonal predominant, length dependent peripheral neuropathy. MRI of the brain/spine is likely to show the classic “inverted V” pattern of dorsal column spinal demyelination. Serum Vitamin B12 levels may be low or normal. Serum homocysteine and methylmalonic acid levels are likely to be (respectively):

a. Low, Low

b. Low, High

c. High, Low

d. High, High

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