Poison-Induced Strokes: Understanding The Link

Poisoning by certain substances can indeed cause symptoms that mimic a stroke. For example, methyl iodide poisoning can cause symptoms such as slurred speech, double vision, and unsteadiness of gait, which are often associated with a stroke. Similarly, ethylene glycol poisoning may present as an acute stroke mimic, with symptoms including dysarthria, nystagmus, and truncal ataxia. In some cases, poisoning by Jamaican Susumber berries can also lead to neurological symptoms that resemble an acute ischemic stroke, such as dysarthria and unstable gait. Carbon monoxide poisoning is another well-known cause of stroke-like symptoms, and it has been linked to an increased risk of ischemic stroke, particularly in younger individuals. Therefore, it is crucial for medical professionals to carefully evaluate patients presenting with stroke-like symptoms and consider the possibility of poisoning to ensure prompt and appropriate treatment.

Methyl iodide poisoning can mimic acute stroke symptoms

Methyl iodide poisoning can present as a mimic of acute stroke symptoms, as reported in a case study of a 50-year-old Caucasian man who developed symptoms suggestive of a posterior circulation stroke after exposure to methyl iodide at his workplace. The patient exhibited slurred speech, double vision, heaviness on the right side of his body, and unsteadiness of gait. These symptoms, along with headaches, elevated blood pressure, and a raised temperature, led to a diagnosis of cerebrovascular accident (CVA) possibly involving the vertebrobasilar territory.

Further investigations, including computed tomography (CT) and magnetic resonance imaging (MRI) of the brain, yielded normal results. However, the patient's occupational history and the presence of a small alkali burn on his wrist raised suspicions of methyl iodide poisoning, which was later confirmed. Methyl iodide is a monohalomethane used in the pharmaceutical industry and as a fumigant. Its neurotoxicity is believed to be due to glutathione (GSH) depletion and its high lipid solubility.

The accurate diagnosis of stroke relies on a thorough patient history, clinical signs, and imaging techniques such as diffusion-weighted MRI. Stroke mimics, which are often non-vascular disease processes, can be challenging to diagnose in an emergency room setting and may lead to inappropriate treatment. Therefore, it is crucial to distinguish these mimics to provide early and appropriate patient management.

Carbon monoxide poisoning is a high-risk factor for stroke

Carbon monoxide (CO) poisoning is a significant risk factor for the development of strokes. CO poisoning occurs when carbon monoxide enters the human body through inhalation and binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). This reduces the amount of oxygen delivered to the body's tissues, leading to hypoxia, particularly in the brain and heart, which have the highest demand for oxygen.

CO poisoning can cause oxidative stress, cellular necrosis, apoptosis, and inflammation, and can lead to pathological changes in the brain, including hippocampal necrosis, demyelination of the cerebral white matter, and spongy necrosis of the globus pallidus and cerebral cortex. These changes can be observed through brain magnetic resonance imaging (MRI).

Studies have found that CO poisoning is associated with a long-term risk of increased incidence of ischemic stroke, with the relative risk being greatest in the youngest age group of 20-34 years. The overall incidence of ischemic stroke was 2.5 times greater in those exposed to CO poisoning compared to unexposed individuals. Furthermore, CO poisoning was found to be associated with a 1.84 times greater risk of developing a stroke overall, with the risk being highest in the first and second years following CO poisoning.

The development of ischemic stroke following CO poisoning may be due to pro-coagulant tendencies, hypo-fibrinolysis, and cerebrovascular endothelial dysfunction or endothelial cell death induced by oxidative stress. CO poisoning can also lead to an increase in free oxygen radicals, which can cause oxidative stress, endothelial damage, and stenosis of the arteries, further contributing to the risk of stroke.

In summary, carbon monoxide poisoning is a high-risk factor for stroke, with long-term consequences for cardiovascular health. The development of ischemic stroke following CO poisoning is associated with various pathological mechanisms, and the risk is particularly elevated in younger individuals.

Ethylene glycol poisoning can present as an acute stroke mimic

Ethylene glycol is a clear, water-soluble liquid commonly found in antifreeze, air conditioning systems, and radiator fluid. It is toxic to humans and can cause kidney failure, brain damage, and even death. Poisoning can occur accidentally or through intentional ingestion as a suicide attempt, as ethylene glycol has a sweet taste and is easily accessible. The clinical signs and symptoms of ethylene glycol poisoning are often nonspecific and similar to those of alcohol intoxication, making it a rare but possible stroke mimic.

The toxicity of ethylene glycol is mainly due to its metabolic breakdown products, glycolic acid and oxalic acid, which can lead to severe metabolic acidosis and the formation of calcium oxalate crystals in various organs, including the brain. The central nervous system is affected early in ethylene glycol poisoning, with symptoms such as intoxication, slurred speech, nystagmus, ataxia, and confusion. In more severe cases, seizures, coma, and cranial nerve palsy may occur.

The diagnosis of ethylene glycol poisoning can be challenging and is often based on clinical presentation, laboratory findings, and the presence of calcium oxalate crystals in the urine. The measurement of ethylene glycol levels in the blood is definitive but may not be available in all hospitals. The presence of a large osmolal gap and metabolic acidosis with a high anion gap also supports the diagnosis.

The treatment of ethylene glycol poisoning includes stabilization, decontamination, and the use of antidotes such as ethanol or fomepizole to inhibit further metabolism of ethylene glycol. Hemodialysis is also an important treatment modality, especially in cases of organ damage or severe acidosis. Prompt diagnosis and treatment are crucial to prevent severe morbidity and mortality associated with ethylene glycol poisoning.

In summary, ethylene glycol poisoning can present as an acute stroke mimic due to its neurological symptoms, but it is important to consider alternative diagnoses when atypical symptoms such as agitation, hyperventilation, or disturbance of consciousness are present. Close monitoring of patients is essential to facilitate early recognition and effective treatment of ethylene glycol intoxication.

Jamaican Susumber Berry poisoning can cause neurological symptoms that mimic acute stroke

Poisoning can indeed cause neurological symptoms that mimic an acute stroke. Susumber berry (SB) toxicity, in particular, is a rare cause of stroke mimic, with limited case reports available in the literature. Here is a detailed discussion of four new cases of SB toxicity presenting as a stroke mimic.

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. The older woman was right-handed, while the younger one was agitated and incomprehensible. Both had normal vital signs and blood glucose levels. Neurological examinations revealed left gaze deviation, horizontal left-beating nystagmus, dysarthria, and dysphagia. Their gait was unstable with left lateropulsion. A stroke code was activated, but tPA was withheld due to the patients' conditions. It was discovered that these patients lived together and had shared a meal containing SB imported from Jamaica 12-18 hours prior to symptom onset. The second patient reported eating significantly more berries and exhibited higher CK levels. Both patients were discharged after 5 days of observation and supportive care.

Case 3 and Case 4 (Bronx): A 48-year-old right-handed man presented to the ED with blurred vision, dysarthria, and generalized weakness. He had consumed SB 12 hours before symptom onset and reported that the berries tasted more bitter than usual. The patient was admitted to the ICU for monitoring and was discharged on day 4 with complete resolution of symptoms.

A 69-year-old right-handed woman, the mother of Case 3, presented with weakness and blurry vision. She had shared a meal containing SB with her son (Case 3) the previous evening. Her initial symptoms started 12 hours after ingestion and included flickering vision, slurred speech, and leg weakness. She was admitted for monitoring and discharged 12 hours later with complete resolution of symptoms.

Discussion

SB toxicity can cause neurological symptoms that mimic an acute stroke, typically with a posterior circulation symptom complex. The toxins in SB, solasonine and solamargine, may stimulate muscarinic/nicotinic cholinergic receptors or inhibit acetylcholinesterase, leading to gastrointestinal, neurological, and autonomic symptoms. In cases of multiple patients presenting 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.

SB toxicity is a rare cause of stroke mimic, and altered SB toxins may be responsible for the neurological symptoms observed. Clinicians should be aware of the possibility of SB toxicity, especially when multiple patients present with stroke-like symptoms or when symptoms fail to localize.

Stroke mimics can lead to unnecessary treatments and patient harm

Stroke mimics can be dangerous and lead to unnecessary treatments and patient harm. A stroke mimic is a disease or condition that presents with a stroke-like clinical picture but without neurologic tissue infarction. Several clinical syndromes can present with symptoms or signs that resemble an acute ischemic stroke. These include processes that can occur within and outside the central nervous system. Distinguishing these non-cerebrovascular stroke mimics from stroke is increasingly important in this era of interventional stroke therapies with potential adverse effects.

The rate of treatment of stroke mimics with intravenous tissue plasminogen activator (tPA) ranges from 1.4% to 16.7%. The risk of symptomatic intracranial hemorrhage remains a real and potentially dangerous complication of IV tPA. A large study showed symptomatic intracranial hemorrhage rates of up to 1.0% in mimics treated with IV tPA. Although this is less than the approximate 6% hemorrhage rate in stroke patients receiving thrombolytics, it remains a significant and possibly avoidable cause of morbidity and mortality.

The diagnosis of stroke is not always straightforward. Differentiation between a stroke and a stroke mimic is difficult due to the wide variety of overlapping clinical presentations. The presence of historical risk factors for cerebrovascular disease and the abrupt onset of symptoms may be the best clues available to the acute care physician to make this distinction.

The two factors most strongly predictive of a stroke mimic are younger age and the absence of stroke risk factors. On the other hand, the abrupt onset of symptoms and/or the presence of atrial fibrillation are features more suggestive of an actual stroke.

Stroke mimics can be particularly difficult to differentiate from acute stroke when symptoms are brief and resolve before the patient is examined, especially when advanced brain imaging, including MRI, is normal. Prompt identification that symptoms are secondary to a stroke mimic and appropriate treatment of the underlying condition will lead to the avoidance of potential misdiagnosis and the unnecessary long-term use of antithrombotic and other stroke prevention medication.

Misdiagnosis and inadvertent treatment with tPA in stroke mimics can also sometimes be dangerous and lead to serious injury or death. Aortic arch dissection can present with focal neurological symptoms from occlusion of the carotid or vertebral artery. Similarly, trauma can result in epidural, subdural, and brain hematoma that can, at times, be difficult to diagnose even with careful imaging. If the history of trauma is not evident, especially in patients with cognitive dysfunction, speech abnormalities, or hemiplegia, the patient may be treated with tPA with serious complications.

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