Poisonous Strokes: Understanding The Link Between Toxins And Brain Attacks

Poisoning by certain substances can present with symptoms that mimic an acute stroke. These are known as stroke mimics and can lead to potentially harmful treatments, including thrombolysis. Methyl iodide, Susumber berries, ethylene glycol, and carbon monoxide poisoning can all cause stroke-like symptoms. However, there are often other symptoms not characteristic of a stroke, such as hyperventilation, agitation, and a disturbance of consciousness, that may appear later and indicate intoxication.

Methyl iodide poisoning can mimic an acute stroke

Methyl iodide poisoning can indeed mimic an acute stroke, as evidenced by a case report of a 50-year-old man who developed stroke-like symptoms after exposure to methyl iodide at his workplace. The patient presented with sudden onset of slurred speech, double vision, heaviness on the right side of his body, and unsteadiness of gait. On admission, he had an elevated blood pressure of 180/60 mmHg and a raised temperature of 38°C. Neurological examination revealed a Glasgow Coma Scale of 14-15, bilateral grade 2 nystagmus, slurred speech, and a broad-based ataxic gait.

Methyl iodide poisoning is a rare event, with only a handful of case reports in the literature. It is a monohalomethane used by the pharmaceutical industry and as a fumigant. The population at risk includes workers in the industry, such as tractor drivers and soil sealers, as well as bystanders near the area of fumigation. The exact mechanism of neurotoxicity is not fully understood but is hypothesized to involve glutathione depletion through methyl halide metabolism.

In acute exposure, methyl iodide can cause pulmonary and dermal irritation, pulmonary edema, and alkali burns. Symptoms may include renal failure, cerebellar and Parkinsonian symptoms, seizures, coma, and psychiatric disturbances. A review of documented cases reveals that patients often experience chronic neurological syndromes with delayed psychiatric, behavioral, and cognitive sequelae.

The accurate diagnosis of stroke relies on a detailed patient history and clinical examination, including imaging techniques such as diffusion-weighted MRI. It is crucial to distinguish stroke mimics from true strokes to ensure early and appropriate management, reduce potential harm, and prevent misdiagnosis and inappropriate treatment.

Carbon monoxide poisoning is a suspected risk factor for stroke

Carbon monoxide (CO) poisoning is a suspected risk factor for stroke. However, the association between stroke occurrence and carbon monoxide poisoning remains unclear. A nationwide, population-based longitudinal study in South Korea found that of the 29,301 patients diagnosed with CO poisoning from 2012 to 2018, 984 (3.36%) were diagnosed with stroke after CO poisoning, with approximately 50% occurring within the first year. This indicates that CO poisoning is a high-risk factor for the development of stroke.

The study's findings suggest that CO poisoning can lead to a significantly increased risk of stroke, with the overall stroke hazard ratio (HR) being 2.28 times higher for patients admitted to the Intensive Care Unit (ICU) due to CO poisoning. The risk was higher for both ischemic stroke (HR: 2.35) and hemorrhagic stroke (HR: 1.76). The high incidence of stroke after CO poisoning affects adults of almost all ages and significantly increases the socioeconomic burden.

The pathophysiology of stroke following CO poisoning is complex and involves hypoxic stress, oxidative stress, and lipid peroxidation. CO binds to hemoglobin, reducing oxygen delivery to the tissues and causing tissue hypoxia, which affects the brain and heart, organs with high oxygen demand. This can lead to oxidative stress, cellular necrosis, apoptosis, and inflammation. Resulting pathological changes in the brain include hippocampal necrosis, demyelination of the cerebral white matter, and vacuolar necrosis of the cerebral cortex and globus pallidus.

The incidence of stroke after CO poisoning varies with age, and the risk is not limited to older adults. The study found that the stroke incidence rate was highest in younger patients aged 30-39 years, followed by those aged 40-49 years. This is concerning as CO poisoning tends to occur more frequently in younger individuals, and the high incidence of stroke in this age group contributes significantly to the national socioeconomic burden.

Furthermore, certain premorbid conditions were associated with a higher risk of stroke after CO poisoning. Atrial fibrillation and heart failure were associated with the highest risks, with a standardized incidence ratio (SIR) of 7.12 and 6.94, respectively. Other conditions such as diabetes mellitus, hypertension, ischemic heart disease, and depressive disorders were also recognized as risk factors.

While hyperbaric oxygen therapy (HBOT) is recommended for the treatment of acute CO poisoning, its effectiveness in preventing stroke development after CO poisoning is unclear. The South Korean study found that stroke incidence after CO poisoning did not differ significantly between patients who received HBOT and those who did not. However, HBOT may still be beneficial for reducing stroke occurrence in patients admitted to the ICU for CO poisoning.

In conclusion, carbon monoxide poisoning is a suspected risk factor for stroke, and the high incidence of stroke after CO poisoning highlights the need for practical strategies to prevent stroke in survivors of CO poisoning. Further research is needed to fully understand the association between CO poisoning and stroke occurrence and to develop effective preventive measures.

Ethylene glycol poisoning can present as an acute stroke mimic

Ethylene glycol is a clear, water-soluble, and sweet-tasting toxic alcohol commonly found in antifreeze liquids. Poisoning can occur accidentally or through intentional ingestion as a suicide attempt. The early symptoms of ethylene glycol poisoning include intoxication, vomiting, abdominal pain, and tachycardia, which can be followed by a decreased level of consciousness, headache, and seizures.

The diagnosis of ethylene glycol poisoning can be confirmed by identifying metabolic acidosis, an elevated anion or osmolar gap, the presence of calcium oxalate crystals in the urine, and toxicological detection of ethylene glycol in the serum or urine. Treatment includes the administration of ethanol or fomepizole to prevent the formation of toxic metabolites, along with hemodialysis to enhance the removal of ethylene glycol and its metabolites from the body.

Jamaican Susumber Berry Poisoning can cause neurological symptoms that mimic an acute stroke

Case Reports

Case 1 and Case 2 (Brooklyn):

Two women, aged 72 and 67, presented to the ED with progressively worsening slurred speech, difficulty swallowing, blurry vision, nausea, vomiting, and gait instability. Both had normal vital signs and blood glucose levels. Neurologic examination revealed left gaze deviation, nystagmus, dysarthria, and dysphagia. Their gait was unstable with left lateropulsion. A stroke code was activated, but head CT scan and CT angiography were normal, and tPA was withheld. It was later discovered that these patients lived together and had shared a meal containing SB imported from Jamaica 12-18 hours prior to symptom onset.

Case 3 and Case 4 (Bronx):

A 48-year-old man presented to the ED with blurred vision, dysarthria, and generalized weakness. His symptoms began with blurred vision and a sensation of things moving side-to-side, followed by headache, vomiting, diarrhea, slurred speech, and weakness. Neurological examination revealed slurred speech, opsoclonus, and finger-to-nose dysmetria. He was unable to walk due to subjective weakness. A stroke code was activated, but head CT and CT angiography were normal, and tPA was withheld. The patient had eaten SB imported from Jamaica 12 hours before symptom onset and reported that the berries tasted more bitter than usual.

A 69-year-old woman, the mother of Case 3, presented with weakness and blurry vision shortly after her son. She had shared the same meal containing SB and reported initial symptoms of flickering vision, slurred speech, and leg weakness. Neurological examination revealed mild generalized weakness. A stroke code was not activated, and her head CT was unremarkable.

Systematic Review

A systematic review of the literature identified 13 previously reported cases of SB intoxication, in addition to the 4 new cases presented here. Of the 17 total patients who became ill, 16 (94%) presented with acute neurological manifestations, including dysarthria, unstable gait, nystagmus/gaze deviation, blurry vision, and autonomic symptoms. Six (35%) required ICU admission, and 3 (18%) were intubated. The majority of patients (82%) had a rapid complete recovery, while 3 were hospitalized for up to one month.

Pathophysiology and Clinical Implications

SB contains steroidal glycoalkaloids (SGA), which are normally innocuous but can become toxic when berries are exposed to variations in growing conditions, post-harvest stressors, and temperature changes. In cases of toxicity, the berries may taste more bitter than usual. Chromatography studies have identified two toxins, solasonine and solamargine, which may stimulate muscarinic/nicotinic cholinergic receptors or inhibit acetylcholinesterase.

When multiple patients present simultaneously to the ED with stroke-like symptoms or when stroke-like symptoms fail to localize, a toxicological etiology, such as SB toxicity, should be considered. A thorough toxicologic history may reveal responsible ingestions, including Solanum torvum. Clinicians should be aware of the possibility of SB toxicity, particularly in the Afro-Caribbean population, where Susumber berries are commonly consumed.

The risk of stroke was also higher in patients admitted to the ICU due to carbon monoxide poisoning

Carbon monoxide (CO) poisoning is a suspected risk factor for stroke. In a South Korean study, 3.36% of patients diagnosed with CO poisoning from 2012 to 2018 were subsequently diagnosed with stroke. The study found that the overall stroke hazard ratio (HR) for patients admitted to the ICU for CO poisoning was 2.28, compared with 2.35 for ischemic stroke and 1.76 for hemorrhagic stroke.

CO poisoning can lead to massive ischemic tissue necrosis due to the formation of carboxyhemoglobin (COHb) by binding to hemoglobin (Hb) in the blood. This reduces oxygen delivery to the tissues, particularly the brain and heart, which have the highest demand for oxygen. As a result, hypoxia, oxidative stress, cellular necrosis, apoptosis, and inflammation can occur.

The South Korean study found that the incidence of stroke after CO poisoning was highest during the first and second years, with about 50% of strokes occurring within the first year. The risk of stroke was also higher in younger patients, with the highest rates of CO poisoning observed in females aged under 20 and over 70. The study concluded that CO poisoning is a high-risk factor for the development of stroke and that practical strategies are needed to prevent stroke in these patients.

In addition to the South Korean study, there have been case reports of ischemic stroke following CO poisoning. In one case, a 29-year-old male patient with cerebral palsy was transferred to the emergency service for hyperbaric oxygen therapy after being diagnosed with CO poisoning. His computerized cranial tomography revealed a hypodense area with irregular boundaries adjacent to the posterior horn of the left lateral ventricle. Diffusion-weighted MRI (DWI) confirmed the presence of acute ischemia in the left occipitoparietal region. Another case involved a 22-year-old female patient who was transferred to the emergency department in need of intensive care and hyperbaric oxygen therapy. Her cranial CT showed a suspicious hypodense area in the frontal region, and DWI obtained seven days later confirmed the presence of an acute-subacute phase infarct area in the frontoparietal region.

Overall, CO poisoning is a significant risk factor for stroke, and the risk is particularly high for patients admitted to the ICU. The pathophysiology of stroke following CO poisoning involves hypoxic stress, oxidative stress, and lipid peroxidation, which can lead to cerebral injuries and demyelination of white matter. The incidence of stroke is highest in the first two years after CO poisoning and affects patients of all ages, with a significant socioeconomic burden.

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