Central nervous system manifestations of CO intoxication are well known, but little has been written regarding peripheral neuropathies. Claude was the first author who reported diffuse nerve demyelination in 2 patients . Few cases of CO-induced neuropathies have been described later: isolated radial paralysis, median and facial nerves paralysis, brachial plexus injury secondary to axillar hematoma, sciatic paralysis due to nerve hematoma [3–5].
To our knowledge, 8 reports of neuropathy after CO intoxication have been published last decades [6–13]. Only one series has described CO induced neuropathy [11, 12]. In this study, of 2759 patients admitted to hospital for CO poisoning and examined clinically between 1976 and 1982, neuropathy was diagnosed in 23 subjects. The incidence of neuropathy was 0,8% in all admitted cases. There were 11 men and 12 women with ages ranging from 17 to 52 years old. Among all patients, 14 had sensory symptoms, 8 mixed symptoms and only one exhibited isolated motor symptoms. All cases except two involved the lower extremity. There was one case of facial paralysis. Local swelling of the affected side was found in 20 patients and acute renal failure developed in 7 others. On ENMG, all patients presented mild to moderate denervation potentials while nerve conductions velocities were normal in seven. An asymptomatic extremity was affected in four patients, as suggested by ENMG study. Evidence of lumbosacral radiculopathy was noted in five patients. There were 12 cases of mononeuropathy and 9 of polyneuropathy. In 2 cases, the type of neuropathy was not precised. In two patients, pathologic findings of sural nerve and muscle biopsies were consistent with demyelination and muscle necrosis. The author concluded that from his experience, neuropathy after CO poisoning affects usually young adults of both sexes, is exclusively confined to the lower extremity, has motor and sensory symptoms, occurs in nerve root as well as peripheral nerve, is promoted by localized swelling secondary to rhabdomyolysis and complete recovers after 3 to 6 months [11, 12].
Other articles have reported sporadic peripheral neuropathy: polyradiculonevritis , polyneuritis [9, 14], isolated bilateral facial paralysis , optic neuropathy , phrenic nerve paralysis  and Volkmann’s contracture [6, 11].
More recently, the only detailed electrophysiological study of CO induced neuropathy has been published . ENMG study in this case showed abnormalities compatible with mixed sensory and motor neuropathy in both symptomatic (right) and asymptomatic (left) lower limb. The absence of denervation potentials in right weak tibialis anterior muscle suggested that axonal damage was not the main pathogenic mechanism involved. Patient has completely recovered and electrophysiological study performed 1 year later returned to normal.
Our patient experienced reversible bilateral brachial plexus injury following acute CO poisoning with total improvement after few months. It represents the third case published in literature with isolated involvement of bilateral upper limbs. Choi mentioned one case of bilateral Volkmann’s contracture in his series and Snyder reported a bilateral symmetrical ulnar paralysis in a 25 years old man 4 days after recovering from coma [8, 11]. Paralysis in our patient was caused by bilateral brachial plexus injury. There is no publication until now reporting bilateral involvement of brachial plexus after CO poisoning.
Electrophysiological study after CO intoxication reveals findings compatible with a motor and sensory peripheral neuropathy with mostly radicular damages . Nerve biopsy shows usually demyelination with preservation of axons explaining the excellent prognosis with total improvement often observed [2, 7, 15]. However, Choi in his series hypothesized a concomitant axonal involvement. This nonspecific finding offers little help in determining pathogenesis of CO neuropathy. At least 4 different mechanisms may be responsible: ischemia due to hypoxia induced by CO; petechial hemorrhages; cytotoxic effect of CO itself and direct nerve compression or venous obstruction with ensuing edema and circulatory compromise in an unconscious patient. This last mechanism resulting in a compartment syndrome is usually evoked in case of mononeuropathy or Volkmann’s syndrome. However, interruption of the arterial blood flow due to mechanical pressure while the patient is unconscious for several hours and the increased subfascial edema due to muscle necrosis appear to combine with the already anoxic state produced by CO. The appearance of symmetrical peripheral nerve lesions in our patient is against compressive or petechial hemorrhage mechanisms. Most likely neuropathy resulted from combination of ischemic and toxic factors. Improvement of edema may have contributed to the recovery of the neuropathy.