An 18-year-old female who studied abroad in Australia and recently returned presented at our inpatient department with numbness and weakness in all four limbs, disturbance of orientation, and memory impairment for 5 days. She also presented with abnormal sensation in the lower limbs, difficulty walking, trouble speaking, and irritation. She was found lying on the ground in her house in Sydney and was unable to identify her brother. They also found thousands of steel bulbs (each of which contained 10 mL of pressurized N2O) in the house. She admitted that she had used N2O bulbs recreationally for >5 months. She used at least 50 bulbs during the past 5 months, one bulb every other day. During the last 4 days, she used more frequently than before, but she could not remember the exact number of bulbs she used.
Vital signs (temperature [T] 36.6 C, pulse [P] 80/min, respiratory rate [R] 20/min, and blood pressure [BP] 112/62 mmHg) were normal, and the physical examination was notable for a weakly positive Babinski sign, enhanced sensation in all four limbs, and ataxia. The upper limbs exhibited stage 4 muscle strength, while the lower limbs exhibited stage 3 muscle strength. The patient's past history of medical and psychiatric diseases were unremarkable, and there was no family history of psychiatric disorders. A full blood examination showed hemoglobin (Hb) 112 g/L, platelet count 174x109/L, white cell count 7.95x109/L, and mean corpuscular volume (MCV) 93.2 fL. Vitamin B12 was <1,500 pmol/L. The results of a urine toxicology screen were all negative, including methylam-phetamine, heroin, morphine, ketamine, and methylene-dioxyphenethylamine. Blood gas (arterial blood) analysis showed partial pressure of oxygen in the alveolar (PAO2) 97.5 mmHg, partial pressure of oxygen in the artery (PaO2) 80.0 mmHg, PCO2 37.0 mmHg, pH 7.48, and base excess (BE) 3.4 mmol/L. Liver function, renal function, and electrolyte tests showed total bilirubin (TBIL) 4.2 mumol/L, direct bilirubin (DBIL) 2.4 mumol/L, indirect bilirubin (IBIL) 1.8 mumol/L, alanine aminotransferase (ALT) 21 IU/L, aspartate aminotransferase (AST) 20 IU/L, AST/ALT 0.95, total protein (TP) 66.0 g/L, albumin (ALB) 41.8 g/L, glucose (GLU) 4.96 mmol/L, alkaline phosphatase (ALP) 40 IU/L, lactate dehydrogenase (LDH) 380 IU/L, amylase (AMY) 83 IU/L, lipase (LIP) 36 IU/L, creatinine (CREA) 46.0 mumol/L, sodium (Na) 142.7 mmol/L, potassium (K) 4.43 mmol/L, and chlorine (Cl) 104.0 mmol/L. Due to concerns regarding a potential spinal cord compromise and cerebral disease, an enhanced spinal and cerebral magnetic resonance imaging (MRI) was implemented. Figure 1A shows gyrus atrophy and broadened anfractuosity compared to the normal state on a T1-weighted image. Table 1 (before the treatment) shows the results of motor nerve conduction velocity (MCV). The motor conduction amplitude of bilateral tibial nerves, peroneal nerves, median nerves, and ulnar nerves decreased, and motor conduction velocity of bilateral median nerves and ulnar nerves similarly slowed down. Table 2 (before the treatment) shows the result of sensory nerve conduction velocity (SCV). Sensory conduction amplitude of bilateral peroneal nerves decreased, and sensory conduction velocity of bilateral median nerves, ulnar nerves, and peroneal nerves slowed down. Bilateral anterior tibial muscles showed a large amount of spontaneous potential (positive sharp wave and fibrillation wave), and the right abductor hallucis brevis showed multiple spontaneous potential (positive sharp wave and fibrillation wave), small contraction, and huge motor unit action potentials (MUAPs) in a quiet state. The patient was unable to complete the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) due to the poor medical condition.
The patient did not use N2O recreationally again, and we prescribed vitamin B12 to improve neurological symptoms and an atypical antipsychotic drug, quetiapine, to help control irritation. The patient also received HBOT with a treatment pressure of 2 atm in an air-pressurized chamber and was given 100% oxygen for a period of 90-120 minutes at a time, a procedure that was repeated three times a session for 20 sessions. The dysfunction in sensory ataxia, numbness, and impaired cognitive functioning gradually improved with treatment by hyperbaric oxygenation. The MoCA and MMSE scores after treatment were in the normal range. A subsequent MRI to re-examine the cranium showed (Figure 1B) improvement in the encephalatrophy compared with the previous MRI. The results of motor (Table 1, after the treatment) and sensory (Table 2, after the treatment) NCV showed peripheral nerve impairment improved, as indicated by increased NCV values.
Written informed consent for the publication of her clinical details and clinical images was obtained from the patient. A copy of the consent from is available for review from the editor of this journal.