Abstract
We report a 22 year-old finance student with progressive sub-acute gait disturbance and lower limb sensorimotor neuropathy. She disclosed a 6-month history of daily recreational nitrous oxide ‘laughing gas’ inhalation via large cylinders ordered online (A$4000 monthly).
Examination [SEE VIDEO] demonstrated a broad-based, high-stepping sensory ataxia with positive Romberg test. She had bilateral lower limb hypertonia and distal-predominant lower limb weakness with bilateral foot-drop and 4/5 hip flexion (left>right). There was symmetrical spreading hyperreflexia throughout all limbs. Patellar and ankle jerks were brisk with clonus. Adductor reflexes were crossed. Plantar responses were upgoing. Pain and temperature sensation was reduced distally to the shins. Proprioception was impaired distally and vibration sense preserved above the medial malleoli. There was no sensory level. She had normal upper limb sensation and no cerebellar signs.
Biochemistry revealed low B12 (84pmol/L), high methylmalonic acid (0.37umol/L) and high homocysteine (>50umol/L) levels. Neurophysiology demonstrated a length-dependent sensorimotor neuropathy with absent (right) and near-absent (left) sural sensory SNAPs. Spinal cord MRI demonstrated cervical and thoracic T2-hyperintensity restricted to the lateral cord, with no visible dorsal column involvement (figure 1).
The neurological complications secondary to nitrous oxide toxicity and B12 deficiency are well recognised, however the radiological findings we report have not been described before.1 In addition, our case offers a clinical reminder that preserved, or even brisk tendon reflexes (mediated by type-1a muscle afferents) do not exclude the presence of a severe large fibre sensorimotor peripheral neuropathy.2
References
Mair D, et al. Neurol.Neurosurg.Psychiatry 2023;94:681–688.
Burke D, et al. Neurol.Sci. 2018;387:75–79.
