Introduction . Arsenic toxicity though rare can affect multiple organs including peripheral nerves. We aim to describe the clinical and electrophysiological characteristics of two patients with arsenic neuropathy Methods . A retrospective chart review of two patients with neuropathy and markedly elevated arsenic levels in blood and hair. Results . Patient 1, a 33-years-old male, developed acute gastroenteritis after consuming locally made liquor, followed by febrile encephalopathy, which improved over one week. Two weeks later, he developed painful ascending paraesthesias involving legs up to knees and hands up to wrists. This was associated with difficulty in walking independently. The patient also used to smoke illicit imported cigarettes. He was provisionally diagnosed to have chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Examination during the fourth week of illness revealed Mee’s lines, hypotonia, and weakness of all limbs distally, global areflexia, and graded sensory loss to all modalities of sensation. Electrophysiological testing showed reduced motor conduction velocities and absent sensory potentials suggesting demyelinating neuropathy. The patient was treated with d-penicillamine. At three month follow up he improved significantly and could resume his job. Patient 2, a 35-year-old gentleman, painter by occupation, developed painful paraesthesias of distal extremities, imbalance while walking in the dark, and slippage of footwear of two months duration. He had a febrile illness 10 days prior to the onset of neurological symptoms. He was provisionally diagnosed to have immune-mediated neuropathy. Examination revealed Mee’s lines, generalised hyperpigmentation, raindrop pigmentation, and palmoplantar hyper-keratosis. He had normal power, but global areflexia, impaired kinesthetic sensation in all limbs and sensory ataxic gait. Electrophysiological testing showed reduced amplitude of sensory potentials suggesting sensory axonopathy Conclusion . Neuropathy arising from arsenic toxicity can have acute/subacute/chronic course and may be mistaken for other acquired inflammatory neuropathies. A high index of suspicion is required to make an early diagnosis and to initiate appropriate preventive measures.