Peripheral neuropathy after carbon monoxide (CO) intoxication is rarely reported. A peripheral nerve dysfunction mimicking a central presentation has never been reported.

To determine the place of nerve conduction studies (NCS) in the assessment of peripheral neuropathy following CO intoxication.

We reported the case of a young patient aged 21 years who was addressed to the electrophysiological department Sahloul to perform NCS one year after a severe CO intoxication. He developed during his hospitalization, a left hemiparesis (lower and upper limbs). The NCS was not performed at this time. The diagnosis was rhabdomyolysis complicated by an acute renal failure due to CO poisoning in a patient with central nervous system complication. Actually the physical examination revealed the left hemiparesis with conserved or even exaggerated reflexes. These clinical features were compatible with a central dysfunction. However, when performing NCS on the left side, sural, superficial peroneal, ulnar, and median sensory nerve action potentials were unobtainable, as well as peroneal and tibial compound muscle action potentials. Such findings evoke a diffuse peripheral neuropathy with axonal dysfunction. This association was not reported after CO intoxication.

Although demyelinating neuropathy is the mostly common reported form of neuropathy after CO intoxication, axonopathy can also be occurred but needs more times to recover. Rhabdomyolysis and CO itself are the major factors leading to peripheral neuropathy.

A peripheral neuropathy mimicking a central presentation can occur after CO intoxication. Clinicians should be aware of the major implication of the peripheral nervous system in this context.