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|LETTER TO EDITOR
|Year : 2016 | Volume
| Issue : 7 | Page : 116-118
Isolated posterior circulation stroke following honey-bee sting
Rohan Mahale, Anish Mehta, Abhinandan K Shankar, Kiran Buddaraju, Aju Abraham John, Mahendra Javali, Rangasetty Srinivasa
Department of Neurology, MS Ramaiah Medical College and Hospital, Bangalore, Karnataka, India
|Date of Web Publication||3-Mar-2016|
Department of Neurology, MS Ramaiah Medical College and Hospital, Bangalore, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mahale R, Mehta A, Shankar AK, Buddaraju K, John AA, Javali M, Srinivasa R. Isolated posterior circulation stroke following honey-bee sting. Neurol India 2016;64, Suppl S1:116-8
|How to cite this URL:|
Mahale R, Mehta A, Shankar AK, Buddaraju K, John AA, Javali M, Srinivasa R. Isolated posterior circulation stroke following honey-bee sting. Neurol India [serial online] 2016 [cited 2019 Jun 26];64, Suppl S1:116-8. Available from: http://www.neurologyindia.com/text.asp?2016/64/7/116/178053
The venomous sting of honey-bees cause a multitude of medical problems. Manifestations range from local and systemic allergic reactions to serious manifestations such as rhabdomyolysis, disseminated intravascular coagulation (DIC), cerebral hemorrhage, acute pulmonary edema, acute renal failure, and even death.  Strokes following bee stings are reported but are rare. In this report, we present the case of a young male patient who had multiple honey-bee stings with a mild local allergic reaction, and who subsequently developed ataxia within 24 hours. Brain magnetic resonance imaging (MRI) showed acute infarcts in the vertebrobasilar artery territory.
A 36-year-old man was attacked by multiple honey-bees (approximately 30-50 according to the patient), while he was working in the field. He had a local allergic reaction over the face and neck, which was treated with intravenous antihistaminics and steroids at the local hospital. The next day, he was found in an unconsciousness state with no frothing from the mouth or incontinence. After being unconscious for 3 hours, he recovered his consciousness in the local hospital. He noticed that he had unsteadiness on walking along with mild appendicular incoordination. Vomiting, double vision, or speech disturbances were absent. He was normotensive and nondiabetic. On examination, he was conscious and oriented, and his speech was normal. His fundus examination was normal. The extraocular movements and cranial nerves were also normal. Bilateral fine, horizontal jerky, gaze-evoked nystagmus was observed. Motor examination revealed normal muscle tone, power, and reflexes. Sensory examination did not yield any abnormality. Mild appendicular incoordination was observed on both sides along with impaired tandem gait. He had a broad-based ataxic gait. His brain MRI showed acute infarcts in bilateral cerebellar hemispheres, pons, and left occipital lobe [Figure 1]. MR and computed tomography angiography showed no significant abnormality except for a hypoplastic right vertebral artery [Figure 2]. His complete hemogram and renal, hepatic, and thyroid functions were normal. Prothrombin and activated partial thromboplastin times were within normal values. The serological test results were negative for human immunodeficiency virus, hepatitis B virus antigen, and venereal disease research laboratory (VDRL) test. The vertebral artery Doppler, electrocardiography, echocardiography, and electroencephalography scans were normal. Serum homocysteine, antinuclear antibody, lupus anticoagulant, and anticardiolipin antibody tests yielded normal results. He received antiplatelets and intravenous dexamethasone for 3 days. There was improvement in his gait unsteadiness during his hospital stay. At a follow up of 3 months, he had a remarkable improvement in clinical symptoms but persisted with a mildly impaired tandem gait.
|Figure 1: Fluid-attenuated inversion recovery (FLAIR) MRI images of the brain (a and d) show hyperintensities in the bilateral cerebellar hemispheres, pons, and left occipital lobe (red arrow); diffusion-weighted imaging (DWI; b and c) shows hyperintense signals, and apparent diffusion coefficient (ADC; e and f) shows hypointense signals in bilateral cerebellar hemispheres, pons. and left occipital lobe, suggestive of an acute infarct (red arrow)|
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|Figure 2: Computed tomography (CT) angiogram of the brain and neck vessels shows no significant abnormality|
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The quantity of venom injected by a solitary bee sting is approximately 0.33 mg. Neurological complications due to bee stings include aphasia, dysarthria, seizures, ataxia, apraxia, and coma.  Different mechanisms are responsible for the causation of stroke following honey-bee stings. Firstly, hypotension produced by anaphylaxis can cause cerebral ischemia.  The bee venom contains phospholipases, hyaluronidase, thromboxane, leukotrienes, histamine, serotonin, and other vasoactive and inflammatory mediators. These can cause vasoconstriction leading to cerebral ischemia. Disseminated intravascular coagulation secondary to exposure of the blood to the phospholipids from damaged tissue, endothelial damage, and hemolysis causes vessel occlusion due to widespread fibrin thrombi deposition.
A search for the previous reports on strokes following honey-bee stings led to the following reported cases. Bhat et al., in 2002 reported a 35-year-old man who had multiple bee stings all over the body and an onset of neurological deficits within 24 hours. The neurological deficits included dysarthria, tinnitus, gait ataxia, and bilateral cerebellar signs. The patient also had rhabdomyolysis along with acute renal failure. Neuroimaging showed bilateral hemorrhagic cerebellar infarction.  Schiffman et al., in 2004 reported a patient with bilateral ischemic optic neuropathy and stroke consequent to multiple bee stings due to the systemic anaphylaxis causing hypotension.  Rajendiran et al., reported the case of a 25-year-old man with bee stings over the head and neck region and presenting with neurological deficits after 24 hours. He had left brachial monoparesis along with blurring of vision. The brain MRI showed infarcts in the right frontoparietal and occipital region along with hemorrhagic transformation. He had a complete recovery.  Jain et al., in 2012 reported the case of an elderly man who had multiple intracerebral infarcts and hemorrhagic transformation along with acute renal failure and rhabdomyolysis. The postulated cause for the infarcts was disseminated intravascular coagulation (DIC).  Viswanathan et al., in 2012 reported the case of a 59-year-old man with a middle cerebral artery infarct following multiple bee stings.  Bilir et al., (2013) reported a 35-year-old man with a left parieto-occipital infarction following bee stings. 
The possible mechanism for stroke in our patient could be toxin-mediated thromboembolism even though there was no evidence of vasospasm, vertebrobasilar artery thrombosis, cardiac wall motion abnormality, or DIC. This case depicts the rare instance of an isolated posterior circulation stroke following honey-bee stings without any evidence of systemic anaphylaxis.
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[Figure 1], [Figure 2]