Middle Cerebral Artery Infarct following Multiple Bee Stings

Middle Cerebral Artery Infarct following Multiple Bee Stings

Case Report Middle Cerebral Artery Infarct following Multiple Bee Stings Stalin Viswanathan, MD,* Vivekanandan Muthu, MD,* Ajai P. Singh, MD, DM,† Ra...

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Case Report

Middle Cerebral Artery Infarct following Multiple Bee Stings Stalin Viswanathan, MD,* Vivekanandan Muthu, MD,* Ajai P. Singh, MD, DM,† Rajarajan Rajendran, MBBS,* and Robin George, MBBS*

Neurologic events following bee stings are very rare. We report a 59-year-old man who became drowsy with slurred speech following multiple bee stings. In the hospital, he was found to have left-sided hemplegia, seventh cranial nerve palsy, and left conjugate gaze palsy. Further investigation revealed dyslipidemia, impaired glucose tolerance, and a middle cerebral artery territory infarct. His limb weakness and speech improved before his discharge from the hospital. Key Words: Strokedneurologic eventsdbeedwasp. Ó 2012 by National Stroke Association

Hospitalization arising from bee stings is generally due to anaphylactic and systemic allergic manifestations. Vascular events of coronary and cerebral circulation due to bee stings are very rare, with only 4 cases of bee stingrelated stroke reported in the literature. We report a middle cerebral artery (MCA) stroke in a 59-year-old right-handed man following multiple bee stings.

Case Report The patient, a farm laborer, was brought to the emergency department with a history of alleged multiple (.5) bee stings sustained after he had prodded a beehive with a staff. He had been stung on the face, neck, scalp, and anterior chest and had been taken to a local dispensary within 1/2 hour of the sting, where he had been given intravenous antihistamines and hydrocortisone. There it was found that he was unable to speak and could only communicate by signs. He had indicated he was feeling dizzy and wanted to lie down. About 2 hours later, he From the *Department of Internal Medicine, and †Neurology, Pondicherry Institute of Medical Sciences, Pondicherry. Received May 7, 2010; accepted June 10, 2010. Address correspondence to Stalin Viswanathan, MD, Department of Internal Medicine, Pondicherry Institute of Medical Sciences, Pondicherry 605014. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2010.06.003

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was brought to our hospital. He had never smoked and drank (,5 g of alcohol) only during festivals. On examination, he was drowsy and disoriented, with normal pulse, blood pressure, and respirations. He had multiple erythematous wheals over his anterior scalp, face and neck. Neurologic exam revealed slurred speech, leftsided upper motor neuron facial nerve palsy, left conjugate gaze palsy, depressed gag reflex, left-sided hemiplegia, unelicitable deep tendon jerks and bilaterally mute plantar reflexes. Computed tomography (CT) of the brain performed approximately 3-1/2 hours after the stings revealed narrowing of right MCA territory gyri (Fig 1). Lipid profile revealed elevated low-density lipoprotein (146 mg/dL), total cholesterol (222 mg/dL), triglycerides (146 mg/ dL), and high-density lipoprotein (47 mg/dL). Serum electrolyte values were normal, but serum creatinine was 1.5 mg/dL, which dropped to 0.7 mg/dL before discharge. His hemogram, liver function tests, prothrombin time, activated prothromboplastin time, and IgE level were normal. D-dimer analysis, thrombin-antithrombin complex evaluation, and a workup for other hypercoagulable states could not be performed due to financial constraints. Electrocardiography, chest radiography, and carotid artery Doppler ultrasonography were normal. Treatment was started with aspirin, atorvastatin, heparin, and limb physiotherapy. On day 2 after admission, the patient exerienced an episode of left upper limb focal seizures, for which sodium valproate was given. Magnetic

Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 2 (February), 2012: pp 148-150

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Figure 1. Brain CT scans done about 3-1/2 hours after the bee stings showing (A) effacement of sulci and gyri and (B) mild narrowing of the gyri in the right MCA cortex.

resonance imaging (MRI) done on day 3 after admission (approximately 70 hours after the stings) revealed diffuse altered signal intensity along perisylvian, peri-insular, and parietal cortices (Fig 2). The patient’s financial status precluded magnetic resonance angiography or 3-dimensional CT intracranial angiography. On day 3 of admission, the patient began tolerating oral semisolid feeding, was talking coherently, and his lower limb power had improved to 3/5. His blood pressure remained normal throughout his hospital stay. On an out patient department (OPD) follow-up visit 2 weeks later, he had 41/5 power on his affected side and demonstrated no cranial nerve deficits.

Discussion Reactions to bee stings may include local pain and swelling; a large regional allergic reaction involving contiguous body parts near the sting site; immediate hypersensitivityrelated systemic features, such as urticaria, anaphylactic shock, or delayed type hypersensitivity-related like serum

Figure 2. Brain MRI done approximately 70 hours after the bee stings showing a hypointense signal on T1-weighted imaging (A) and a hyperintense signal on T2-weighted imaging (B).

sickness; and Guillian-Barre syndrome.1,2 Reports from the Unites States and Europe note a 3%-4% incidence of systemic reactions in adults after a bee sting.1 Unusual, even rarer reactions to bee stings include myocardial infarction, optic neuropathy, and stroke.3-5 The venom of the common honey bee, Apis mellifera, and other bees contains phospholipase A2, mellitin, which causes histamine release; hyaluronidase, a mast cell- degranulating peptide; and vasoactive amines, including dopamine and noradrenaline.2 Mellitin and phospholipase, which exert a concerted actions in intravascular hemolysis,2 constitute about 50% and 12% of bee venom, respectively.6 Mellitin disrupts cell membranes, and the neurotoxin apamine acts on the spinal cord.7 Elderly males may be more susceptible to the hypotensive effects of bee venom because of preexisting cardiorespiratory disease.2 Hypotension due to histamine release or hypertension due to increased catecholamine release may occur.2 Neurologic vascular events resulting from bee stings are due to either hemorrhage or infarction.2 Bee venom includes epinephrine, dopamine, leukotrienes,

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and thromboxanes. These substances can cause platelet aggregation. Platelet aggregation, hypotension, and coronary spasm causing acute coronary syndrome have been associated with bee stings.3 Cerebral infarction and stroke have been more commonly reported in wasp stings.8 Cerebellar infarction due to bee sting has been reported.5 As of 2009, only 7 cases of wasp sting-related and 4 cases of bee stingrelated strokes had been reported.4,8-10 One of the cases of bee sting-related stroke was from an Africanized (killer) honey bee.4 Africanized honey bees are aggressive, unlike the social honeybees, solitary bees, and bumblebees, all of which belong to the family Apoidea. Similar to bee sting-related acute coronary syndrome, the hypothesized pathophysiology of stroke includes hypotension, platelet aggregation, vasoconstriction and a prothrombotic state,4 hypertension, hemorrhage, and hypoxia.10 Our patient was normotensive, but he was older and had dyslipidemia, an impaired glucose tolerance test, and possibly an undocumented hypotension in the first health care center, and bronchospasm-related hypoxia could have predisposed him to hemiplegia, left gaze palsy, and left focal seizure after the bee stings. A complete workup for a prothrombotic state could not be performed due to financial constraints. Other neurologic symptoms that have been attributed to bee stings include apraxia, ataxia, aphasia, and coma.4 In conclusion, bee sting-related neurologic events like stroke are very rare, with no proven pathophysiologic mechanisms. Multiple factors can contribute to the etiology in persons who may be predisposed to cerebrovascular

events. Two of the 4 previously reported patients with bee sting-related stroke were under 40 years old.4 One of these patients, who had bilateral cerebellar infarction, died, and the other 3 improved with minimal residual deficits, like our patient.

References 1. Heinig JH, Engel T, Weeke ER. Allergy to venom from bee or wasp: The relation between clinical and immunological reactions to insect stings. Clin Allergy 1988;18:71-78. 2. Riches KJ, Gillis D, James RA. An autopsy approach to bee sting-related deaths. Pathology 2002;34:257-262. 3. Erbilen E, Gulcan E, Albayrak S, et al. Acute myocardial infarction due to a bee sting manifested with ST wave elevation after hospital admission [Letter to Editor]. South Med J 2008;101:448. 4. Schiffman JS. Bilateral ischaemic optic neuropathy and stroke after multiple bee stings. Br J Ophthal 2004;88: 1596-1597. 5. Bhat R, Bhat KR, Shivashankar, et al. Bilateral haemorrhagic cerebellar infarction following honey bee sting. J Assoc Physicians India 2002;50:721-722. 6. LoVecchio F, Cannon RD, Algier J, et al. Bee swarmings in children. Am J Emerg Med 2007;25:931-933. 7. Fitzgerald KT, Flood AA. Hymenoptera stings. Clin Tech Small Anim Pract 2006;21:194-204. 8. Chen DLP, Chou K, Fang H, et al. Descending aortic thrombosis and cerebral infarction after massive wasp stings. Am J Med 2004;116:567-569. 9. Temizoz O, Celik Y, Asil T, et al. Stroke due to bee sting. Neurologist 2009;15:42-43. 10. Sachdev A, Mahapatra M, D’Cruz S, et al. Wasp stinginduced neurological manifestations. Neurol India 2009; 50:319-321.