Nitrous Oxide-Induced Cerebral Venous Thrombosis: A Case Report, Potential Mechanisms, and Literature Review

Abstract

Cerebral venous thrombosis can result from hypercoagulation, either genetic or acquired. Hyperhomocysteninemia was previously thought to be linked with thrombophilia, although this is still controversial to this present day. In recent years, there has been a notable surge in the recreational use of nitrous oxide, which could potentially lead to hyperhomocysteinemia. We present a case of a 19-year-old female who was diagnosed with cerebral venous thrombosis with intracerebral hemorrhage. She had a history of nitrous oxide abuse, which is known to cause dysfunction of vitamin B12. Additionally, we conducted a literature review of cerebral venous thrombosis following nitrous oxide usage. Investigation showed that her serum vitamin B12 level was <100 pg/mL (reference range 197-771 pg/mL), and homocysteine level was 100.6 µmol/L (reference range 5.0-15.0 µmol/L). After receiving a vitamin B12 supplement, both serum vitamin B12 and homocysteine levels returned to normal. No other risk factors for thrombophilia were detected. Previously reported cases predominantly demonstrated hyperhomocysteinemia. The most likely mechanism of her cerebral venous thrombosis was hyperhomocysteinemia due to vitamin B12 deficiency caused by nitrous oxide abuse. This finding supports the hypothesis that hyperhomocysteinemia can induce cerebral venous thrombosis.

Keywords: cerebral venous thrombosis; cobalamin; homocysteine; nitrous oxide; vitamin b12.

Figure 1. Several intraparenchymal hematomas involving the left frontal, right parietal, and right parietotemporal lobes, with perilesional edema

Figure 2. Thrombosis of internal cerebral veins, the vein of Galen, and straight sinus

Figure 3. Thrombosis of bilateral transverse sinus and left sigmoid sinus

Figure 4. Cobalamin, in the form of cob(I)alamin, carries a methyl group from 5-methyltetrahydrofolate and transfers it to homocysteine in the form of methylcobalamin. This methionine cycle is affected by nitrous oxide, which reduces cob(I)alamin and methylcobalamin, leading to an increase in homocysteine levels.

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