The Great Mimicker Carbon Monoxide in Neurology

Special Article - Neurology

Austin Med Sci. 2018; 3(1): 1020.

The Great Mimicker Carbon Monoxide in Neurology

Dubey A1* and Dubey S2

1Department of Neurology, SAIMS Medical College and PG Institute, India

2Department of Medicine, Gandhi Medical College and Hamidia Hospital, India

*Corresponding author: Ayush Dubey, Department of Neurology, SAIMS Medical College and PG Institute, Indore, India

Received: December 04, 2017; Accepted: January 24, 2018; Published: January 31, 2018


Carbon Monoxide is an established acute as well as chronic toxicant which arises from incomplete combustion and occurs in a variety of occupational and environmental situations. It has been known to cause various symptoms including severe neurological ones too. It has got a complex and varied mechanism of cellular toxicity. Delayed neurological deficits are less recognized and often not attributed to the toxicity. Radiological findings are often less specific and sometimes reversible. A comprehensive review on this important yet relatively less reported entity is discussed.

Keywords: Carbon Monoxide; Hyperbaric oxygen therapy


CO: Carbon Monoxide; HBOT: Hyper Baric Oxygen Therapy; NBOT: Normo Baric Oxygen Therapy; CO-Hgb: Carboxyhaemoglobin


Carbon Monoxide (CO) is a colorless, odorless, non irritating gas produced by incomplete burning of carbon containing fossil fuels [1]. It is the leading cause of poisoning related mortality in the United States and is responsible for more than half of all the fatal poisonings occurring worldwide.

CO is often referred to as a “great mimicker” or “great imitator” because the clinical presentations associated with its toxicity are non specific and diverse including headache, chest pain, syncope, seizures and flu like illness. Undiagnosed exposure may often lead to a significant morbidity and mortality [2,3].

Environmental CO exposure is usually less than 0.001% or around 10 ppm [4], but may be higher in urban areas. The amount of CO which is absorbed by the body is dependent on minute ventilation, duration of exposure, and concentrations of CO and oxygen in the surrounding environment [5-8]. After cooking with a gas stove, the indoor air concentrations of CO may reach 100 ppm [9]. Cigarette smokers are exposed to an estimated 400 to 500 ppm of CO while active smoking [10]. Automobile exhaust may contain around 10% (100,000 ppm) CO [11]. Exposure to 70 ppm may lead to Carboxyhemoglobin (CO-Hgb) levels of 10% at equilibrium (approximately 4 hours) [2], while exposure to 350 ppm may lead to CO-Hgb levels of 40% at equilibrium [10]. In addition to these, CO poisoning has been reported in campers using coal stoves in outdoor tents especially during winters, boaters, and people using solvents in paint industry, ice skaters and people using propane-powered resurfacing machines [12].

Neurological manifestations can be acute as well as chronic and depend upon the severity and duration of CO exposure.


Carbon monoxide causes hypoxia by forming carboxyhemoglobin and thereby shifting the oxyhemoglobin dissociation curve to the left [4]. Carbon monoxide’s affinity for hemoglobin is known to be more than 200 times that of oxygen [13], resulting in the formation of carboxyhemoglobin with even relatively low amounts of the inhaled carbon monoxide. Carbon monoxide increases the cytosolic heme levels, which leads to oxidative stress [14], and binds to platelet heme protein and cytochrome c oxidase [13], interrupting cellular respiration [15] and producing reactive oxygen species [16], which in turn leads to neuronal necrosis and finally apoptosis [17]. Impaired cellular respiration provokes stress response, including the activation of hypoxia-inducible factor 1a [18], resulting in neurologic and cardiac protection [19] or injury, dependent on the dose of carbon monoxide, by means of gene regulation. Carbon monoxide exposure also causes inflammation through multiple pathways that are independent of the pathways to hypoxia, resulting in neurologic and cardiac injury.

Clinical features

The clinical manifestations of CO poisoning are variable and severity depends on the concentration of CO in the inspired air, duration of exposure and general health of the involved person. The population at increased risk comprises of infants, elderly, and patients with cardiovascular disorders, lung disorders, anemia and increased basal metabolic rate [20]. The features of acute CO poisoning are better known and more easily recognized than those having chronic exposure. Symptomatology and prognostication correlate poorly with the level of carboxyhaemoglobin measured at the time of presentation. Table 1 shows the clinical features manifested with the varying levels of blood carboxyhaemoglobin concentration [21]. During acute exposure, patients may complain of headache, dizziness, nausea, vomiting, emotional liability, confusion, impaired judgment, clumsiness and syncope. Vomiting may be the only presenting symptom in presenting infants and may be misdiagnosed as gastroenteritis. Coma or seizures can occur in patients with prolonged CO exposure. Elderly people, especially those with coronary disease, may have accompanying myocardial ischemia, which may often result in frank myocardial infarction [22]. CO exposure has deleterious effect on pregnant women because of the greater sensitivity of the foetus to these harmful effects of the gas. The excessive leftwards shift of foetal carboxyhaemoglobin causes more severe tissue hypoxia by releasing comparatively less oxygen to the tissues [23]. Prolonged exposures resulting in altered mental status or coma may be accompanied by retinal hemorrhages and lactic acidosis [24]. Myonecrosis can also occur but it rarely leads to renal failure. Cherry-red colored skin which is associated with severe carbon monoxide poisoning, is seen in around 2-3% of symptomatic cases [25]. Severe poisoning often leads to hypotension and sometimes pulmonary oedema with the former is being the most reliable marker of prognosis.