Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic complications. CO poisoning has previously been related to central nervous system, cardiovascular system, respiratory system, hematological system, metabolic and endocrinological system, musculoskeletal system and changes in perception of the visual and auditory systems, especially the cardiovascular system and central nervous system such as amnesia, encephalopathy, dysarthria, parkinsonism and peripheral neuropathy. Among them, little has been reported regarding peripheral neuropathies.
To our knowledge, there was a large-scale clinical study about neuropathy after CO poisoning. Among 2759 patients with acute CO poisoning examined clinically between 1976 and 1982, peripheral neuropathy was diagnosed in 23 subjects( 11 men and 12 women, mean age was 29.3) by electrophysiological detection. Of all patients, 14 subjects had sensory symptoms, 8 subjects had mixed symptoms and only one had isolated motor symptoms. All are involve in the lower extremity except 2 subjects. The study also show that peripheral neuropathy after CO poisoning commonly affected young people and all recovered within 3–6 months[2]. Rahmani et al reported a 42-year-old man with reversible bilateral brachial plexus injury after acute CO poisoning, who had good prognosis after hyperbaric oxygen therapy[3]. Gi-Young Park et al reported unilateral brachial plexopathy with impaired cognitive function after CO intoxication. Electrophysiological interpretation was left incomplete total brachial plexopathy with axonal involvement. The 45-year-old patient had poor prognosis with no significant change of left upper extremity weakness and impaired cognitive function when 11 months after CO intoxication[4]. Other articles have also reported peripheral neuropathy after
CO intoxication: Sciatic neuropathy and rhabdomyolysis, motor and sensory peripheral neuropathy, unilateral diaphragmatic paralysis.
The precise pathogenesis of peripheral neuropathy following CO intoxication remains in doubt. However, 4 possible mechanisms may be responsible for this: hypoxia due to CO and subsequently ischemia, nerve compression, cytotoxic effect of CO and petechial hemorrhages. CO causes hypoxia through the formation of COHb and binding to heme-containing proteins, particularly cytochrome c oxidase and myoglobin. In addition, CO binds to platelet heme protein, causing the release of NO. Increased NO produces peroxynitrite (ONOO), which impairs mitochondrial function and worsens tissue hypoxia[5]. The central nervous system are most vulnerable to the effects of ischaemia and hypoxia. The thoracic spinal cord was feed by the radiculomedullary arteries, which originate from a few intercostal arteries (from the subclavian artery and aorta), compromise of blood flow from these arteries potentially creates a great risk of ischemia because of poor collateralization in the thoracic vascular region. Besides, The watershed effect is common in the vascular system of the spinal cord. It occurs when 2 streams of blood flowing in opposite directions meet. The watershed effect is at its maximum in the midthoracic area because the distance between radicular arteries is the greatest[6]. In the case, we found that Long strip T2 high signal was shown in the left part of the cervical medulla at the level of the 4/5 intervertebral space. Abnormal signal intensity of the left cervical spinal cord is present at MRI at a level suggestive of a correlation with the clinical symptoms and signs. At that level there is also a disk protrusion. However, it is clear that this lumbar disk protrusion did not compress the spinal cord of patient, so it was not sufficient to cause brachial plexus injury. The patient’s wife found him lying in the driver's seat with his head tilted to the left. It is possible that it is a spondilogenic compression myelopathy (ischemic pathomechanism?) possibly related to the position of the unconscious patient in the car. So we suspect that the ischemia of spinal cord caused by CO intoxication may be a key mechanism of left brachial plexopathy. Besides, nerve compression and cytotoxic effect of CO should also be considered. The young man in our case experienced isolated unilateral brachial plexus injury following acute CO poisoning with incomplete improvement after nearly 3 months, which is the second case on unilateral brachial plexopathy following CO intoxication in literature so far. Ischemia of spinal cord caused by CO may be the main mechanism about unilateral brachial plexopathy. Therefore, correct hypoxia caused by CO (hyperbaric oxygen and normobaric 100% oxygen) as soon as possible is necessary to prevent peripheral neuropathy after acute CO intoxication. In addition, persisting in rehabilitation training might be important to treat peripheral neuropathy after acute CO intoxication.