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Carbon Monoxide Poisoning: Neurologic Aspects by K K Jain MD (Dr

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Carbon Monoxide Poisoning: Neurologic Aspects by K K Jain MD (Dr Carbon monoxide poisoning: neurologic aspects By K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.) Originally released June 6, 1997; last updated April 5, 2016; expires April 5, 2019 Introduction This article includes discussion of carbon monoxide poisoning: neurologic aspects and CO poisoning. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations. Overview Carbon monoxide can produce several nonspecific symptoms and can mimic several diseases. Most of the signs and symptoms are due to hypoxia, which affects mainly the brain. The most significant neurologic and psychiatric manifestations of carbon monoxide poisoning are seen as subacute or late sequelae, often following a period of complete recovery from an acute episode. There is a possible interaction between nitric oxide, a ubiquitous molecule in the human body, and carbon monoxide. Carbon monoxide exposure initiates processes including oxidative stress that triggers activation of N-methyl-D-aspartate neuronal nitric oxide synthase, and these events are necessary for the progression of carbon monoxide–mediated neuropathology. The most important diagnostic test for carbon monoxide poisoning is the direct spectroscopic measurement of carboxyhemoglobin level in the blood. Brain imaging findings frequently correlate with clinical manifestations. Hyperbaric oxygen plays an important role in the management of carbon monoxide poisoning. Key points • Carbon monoxide poisoning can produce several nonspecific symptoms and can mimic several diseases. • Most of the effects are due to hypoxia. • Neurologic sequelae are significant and may be delayed in onset. • Hyperbaric oxygen plays an important role in management of carbon monoxide poisoning. Historical note and terminology Human beings have been exposed to carbon monoxide ever since they first made fire inside sheltered caves. In 300 BC, Aristotle stated that, "coal fumes lead to heavy head and death." Obviously, this was a reference to carbon monoxide poisoning. In 1857 Claude Bernard showed that carbon monoxide produces hypoxia by reversible combination with hemoglobin (Bernard 1857), and in 1865 Klebs described clinical and pathologic findings in rats exposed to carbon monoxide (Klebs 1865). The classic bilateral lesions of the globus pallidus and diffuse subcortical demyelination were described and correlated with psychic akinesia by Pineas (Pineas 1924) and with parkinsonism by Grinker (Grinker 1925). In 1895 Haldane showed that rats survived carbon monoxide poisoning when placed in oxygen at a pressure of 2 ATA (Haldane 1895). The effectiveness of hyperbaric oxygen in experimental carbon monoxide poisoning in dogs and guinea pigs was demonstrated in 1942 (End and Long 1942). In 1960 hyperbaric oxygen was first used successfully in treating human cases (Smith and Sharp 1960). Carbon monoxide is produced in small amounts endogenously during the catabolism of heme, resulting in the coproduction of biliverdin and iron. Carbon monoxide is considered to be a signaling molecule because it shares some chemical and biological properties with nitric oxide. Carbon monoxide is a mediator in the autonomic nervous system. Inhalation of subtoxic concentrations of carbon monoxide may have a cytoprotective effect, which is being investigated currently. Actions of carbon monoxide in the nervous system, thus, range from the physiological to the pathological. Clinical manifestations Presentation and course Carbon monoxide can produce several nonspecific symptoms and can mimic several diseases. Most of the signs and symptoms are due to hypoxia, which affects mainly the brain, but other vital organs (ie, the heart) may also be involved. The onset may be acute or it may be insidious if the cause is chronic, low-grade carbon monoxide poisoning. The severity of symptoms is related to the blood carboxyhemoglobin levels, but frequent disparities exist between these. The most frequent neurologic manifestations of mild acute carbon monoxide poisoning (carboxyhemoglobin 10% to 20%) are headache (90%), dizziness (82%), and visual disturbances. These may be accompanied by impairment of higher cerebral function, nausea, weakness, and abdominal pain. With a moderate degree of poisoning (carboxyhemoglobin 20% to 40%), the patient may present with cardiac disturbances, dyspnea, and vomiting. Loss of consciousness may occur. Severe poisoning (carboxyhemoglobin 40% to 60%) may lead to coma, convulsions, and respiratory impairment. The patient may present in a decerebrate state. A vegetative state, extrapyramidal rigidity and movement disorders, Tourette syndrome, or severe memory deficits may follow recovery from coma. According to a study, the concept of relating specific symptoms to specific carboxyhemoglobin levels is invalid as none of the symptoms of carbon monoxide poisoning can be related to a specific carboxyhemoglobin level (Hampson et al 2012). The patient may present in a state of delirium associated with neurologic involvement; this may be prolonged in 20% of the cases. Other neurologic manifestations of acute carbon monoxide poisoning are hemiplegia with aphasia, focal epileptiform seizures, hearing loss due to auditory nerve hypoxia, optic neuritis, and peripheral neuropathy. Carbon monoxide toxicity can induce a visual agnosia of apperceptive type, with well-defined characteristics seldom seen with other types of injury and a poor prognosis for recovery. Unilateral involvement of the phrenic nerve may lead to diaphragmatic paralysis. Various disturbances of cardiac rhythm and conduction are identified by abnormalities on ECG. The patient may suffer from angina pectoris and myocardial ischemia. A combination of cerebral symptoms and a non-Q/non-ST elevation myocardial infarction, with enzyme elevations and electrocardiographic abnormalities, has been described in carbon monoxide poisoning (Johnson 2005). Other manifestations in comatose patients include neurogenic pulmonary edema and acute renal failure due to muscle necrosis or carbon monoxide-induced rhabdomyolysis without pressure necrosis. Children seem to have a lower threshold for toxicity of carbon monoxide. Lethargy and syncope may occur at a mean carboxyhemoglobin concentration of 25%, whereas these symptoms are seen in adults at a level of about 40% carboxyhemoglobin. Symptoms of chronic exposure to carbon monoxide are vague. A more subtle form of subacute carbon monoxide poisoning has been termed "occult carbon monoxide poisoning," used when the exposure is initially unknown to the patient and the physician. Chronic occult carbon monoxide poisoning can produce a syndrome of headache, fatigue, dizziness, paresthesias, chest pain, palpitation, and visual disturbances. “Warehouse worker headache” is the term used for carbon monoxide poisoning from industrial exposure to exhausts in unventilated indoor environments. Among patients presenting with the complaint of headache to an emergency department during winter-heating months are those who have raised carboxyhemoglobin levels in blood that could be traced to carbon monoxide exposure. Elevated carboxyhemoglobin levels are found in a small percentage of patients presenting to the emergency department with neurologic complaints of nontraumatic origin other than headache or dizziness and in whom carbon monoxide poisoning is not suspected. The most significant neurologic and psychiatric manifestations of carbon monoxide poisoning are seen as subacute or late sequelae, often following a period of complete recovery. These are also referred to as "interval form of carbon monoxide poisoning," "secondary syndromes," or "delayed postanoxic encephalopathy," and may develop 1 to 3 weeks after exposure to carbon monoxide. Late sequelae of carbon monoxide poisoning include dementia, parkinsonism, and psychoses. In some instances, there has been repeated exposure to carbon monoxide. The incidence of secondary syndromes, as described in the older literature, varies from 15% to 40% of the survivors of acute carbon monoxide poisoning. Delayed neurologic sequelae occur several years following the initial exposure. The most frequent neuropsychiatric sequelae of carbon monoxide poisoning are apathy, disorientation, memory impairment, hypokinesia, mutism, irritability, and bizarre behavior. Rare complications include amnesic syndrome, psychic akinesia, akinetic mutism, depression and psychoses, Klüver-Bucy syndrome, perceptual disorders, and cortical blindness. Several movement disorders occur as late sequelae of carbon monoxide poisoning, mostly in association with neuropsychiatric deficits (Table 1). Delayed movement disorders are the most prominent of these. Of the 242 patients with carbon monoxide poisoning examined between 1986 and 1996 in Korea, parkinsonism was diagnosed in 23 patients (9.5%) and developed within 1 month in the majority of the patients (Choi 2002). A retrospective study of case records of patients with carbon monoxide poisoning found that the Glasgow Coma Scale and MMSE scores and positive findings in brain CT scans were predictors of the development of delayed neuropsychological sequelae but carboxyhemoglobin level was not (Ku et al 2010). Another retrospective study found that predictive risk factors for delayed neuropsychological sequelae after carbon monoxide poisoning that can be assessed in the emergency department include the following: carbon monoxide exposure duration of more than 6 hours, a Glasgow Coma Scale score less
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