Journal of the Neurological Sciences 301 (2011) 104–106

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Journal of the Neurological Sciences

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Bilateral cavernous sinus syndrome and bilateral cerebral infarcts:

A rare combination after wasp sting
Mukund R. Vidhate a,⁎, Pawan Sharma a, Rajesh Verma a, Rajesh Yadav b
a
Department of Neurology, Chhatrapati Shahuji Maharaj Medical University, Lucknow, Uttar Pradesh, India
b
Department of Radiodiagnosis, Chhatrapati Shahuji Maharaj Medical University, Lucknow, Uttar Pradesh, India

a r t i c l e i n f o a b s t r a c t

Article history: Neurologic manifestations of wasp sting are uncommon and delayed in onset (Sachdev et al. [1]). Various
Received 11 August 2010 central and peripheral nervous system presentations have been described including wasp sting
Received in revised form 16 October 2010 encephalopathy, cerebral infarction, optic neuropathy, polyradiculopathy, neuromuscular junction disorders,
Accepted 22 October 2010
etc [1]. Cerebral infarction is a rare manifestation and sequential bilateral hemiparesis has been reported in
Available online 4 December 2010
only one case (Riggs [2]). We report a case of a young boy presented with bilateral cavernous sinus thrombosis
Keywords:
with bilateral cerebral infarcts, a rare combination.
Wasp sting © 2010 Elsevier B.V. All rights reserved.
Hymenoptera order
Stroke
Thrombosis

1. Introduction
Wasp sting commonly produce local reactions like immediate
pain, wheal and flare reaction. Multiple stings can lead to systemic
involvement like rabdomyolysis, intravascular thrombolysis, renal
failure and dyspnoea [1]. Although neurologic involvement is rare,
varied spectrum of neurologic manifestations are reported in
literature. There are few case reports of stroke as a complication
of wasp sting [1–4]. We report a case of both arterial and venous
involvement in the form of cerebral infarction and cavernous sinus
thrombosis after wasp sting, a rare combination.
2. Case report
A boy aged 8 years presented with a history of wasp sting on right
eyebrow and nasal bridge 15 days prior to presentation. On the next
day of bite patient had painful swelling of the right eye with inability
to open the right eyelid. Also his right eyeball became fixed, although
he could see things on manually lifting the right eyelid. Eight days
after the bite patient developed acute onset left hemiplegia with
altered sensorium. One day later patient also was unable to move the
right upper and lower limbs. On examination patient was drowsy, had
right sided proptosis (Fig. 1), complete right ophthalmoplegia
depicted by complete ptosis, dilated and fixed pupil along with total
absence of eye movements in all directions. Left eye examination
showed corneal ulcer, partial ptosis reduced range of eye movements
particularly in outward direction and sluggish papillary reaction.
He had left upper motor neuron type facial nerve palsy, at least
MRC grade 1 power in all four limbs with hyperreflexia with bilateral
extensor plantars. There was no carotid or orbital bruit or cardiac
murmur. The rest of the systemic examination was normal.
Investigations revealed hemoglobin of 6.3 g/dl, TLC of 4380/cmm
with DLC showing 50% polymorphs, 45% lymphocytes, 5% monocytes.
Platelets were 4 lacs/cmm. Random blood sugar was 118 mg/dl. Renal
and liver function tests were normal. Prothrombin time and activated
partial thromboplastin time were 16 s and 24 s respectively. Serologic
tests for HIV, VDRL and antinuclear antibody were negative. ECG,
chest X-ray and echocardiography were normal. Head CT revealed
nonhemorrhagic infarcts in left frontoparietal and bilateral subcortical
regions. MRI T1W, T2W, T2 FLAIR and diffusion weighted images
showed infarcts in the left frontoparietal cortex, posterior limb of the
left internal capsule and right subcortical region(Fig. 2 a–c). CT
contrast study was suggestive of bilateral cavernous sinus thromboses.
CT angiography revealed normal flow in bilateral internal carotid
and vertebral arteries (Fig. 3). The patient was treated with systemic
antibiotics, anticoagulants, topical antibiotic, anti-inflammatory eye
drops. Fifteen days after the treatment patient had regained
consciousness, started moving the left upper and lower limbs, eye
swelling and proptosis had reduced but patient still had right sided
complete ophthalmoplegia.
3. Discussion

⁎ Corresponding author. Tel.: +91 9235159269(mobile); fax: +91 5222258805. Wasps are included in Hymenoptera order along with bees and
E-mail address: drmukundvidhate@yahoo.co.in (M.R. Vidhate). ants [5]. Wasp stings are common worldwide. In India paper wasp

0022-510X/$ – see front matter © 2010 Elsevier B.V. All rights reserved.
doi:10.1016/j.jns.2010.10.020
 M.R. Vidhate et al. / Journal of the Neurological Sciences 301 (2011) 104–106 105

Fig. 1. Photograph of patient showing bilateral ptosis, right sided proptosis after wasp
sting.

(Ropalidia marginata) is the commonly found species. Rural population

is particularly vulnerable to wasp sting as they encounter it during
field work. Wasp venom contains a wide array of amines, peptides and
enzymes that are responsible for local and systemic reactions. Low
molecular weight compounds like serotonin, histamine, acetylcholine
and various kinins mediate direct toxic effects. Enzymes in venom
include hyaluronidase which helps in the spread of venom and
phospholipase, a major venom allergen [5].
Vascular complications of bee and wasp stings are rare. There
have been only seven case reports of cerebral infarction after wasp
sting till date. The postulated mechanisms include vasoconstriction,
platelet aggregation, and retrograde stimulation of superior cervical
ganglion leading to occlusion of terminal internal carotid artery [4].
Wasp venom contains vasoactive, inflammatory, and thrombogenic
peptides and amines, including histamine, leucotrienes, and throm-
boxane [5].
Cerebral infarction can develop acutely as well as delayed ranging
from 30 s to 96 h [1]. Starr et al. first reported right hemiparesis
developed 30 s after multiple wasp stings in 37 year old man [3].
Crawley and Brown et al. described a 30 year lady presenting 48 h
after wasp sting with left occipital infarct [4]. Sachdev et al. [1]
reported a case of right ventral pontine and cerebellar infarction after
wasp sting. Riggs et al. [2] reported the occlusion of a cervical internal
carotid artery with cerebral infarction of the dominant hemisphere
2 days after multiple wasp stings. Bilateral sequential hemiparesis has
been reported previously in only one case report by Riggs et al. [2].
A 52 year old man had presented with left hemiparesis after acute
anaphylactic reaction to wasp sting and right hemiparesis three
weeks later. Our patient had developed orbital cellulitis after
wasp sting, followed by proptosis and total ophthalmoplegia, more
severe on right side after wasp sting. Cavernous sinus thrombosis was
demonstrated on CT by lack of contrast enhancement. Cavernous sinus
thrombosis might have been developed due to extension of acute local
inflammation caused by wasp venom. As previously mentioned wasp
venom contains various vasoactive and proinflammatory amines
leading to prominent local inflammatory reaction. Also probable
superadded bacterial infection from nearby sinuses in inflamed tissue
could have contributed to the development of cavernous sinus
thrombosis. We didn't find thrombosis of internal carotid arteries on
CT angiography. Riggs et al. had noted occlusion of both internal Fig. 2. a, b, and c: MRI T2 FLAIR and DWI showing infarcts in left frontoparietal
carotid arteries on cerebral angiography [2]. The angiographic findings region, right subcortical area (arrows) and posterior limb of left internal capsule
were attributed to stimulation of superior sympathetic ganglion (arrowhead).
106 M.R. Vidhate et al. / Journal of the Neurological Sciences 301 (2011) 104–106

arteries. Differential diagnoses of stroke in a child considered at 8 years

of age were congenital and acquired heart diseases; hematologic
disorders like sickle cell anemia, procoagulant states; vasculitis;
fibromuscular dysplasia; carotid artery dissection; moyamoya disease
etc. These potential causes of thrombosis at this age were ruled out by
appropriate investigations. Hence the symptoms were attributed to
wasp sting considering temporal profile of events.
Our patient had both venous involvement in the form of cavernous
sinus thrombosis and arterial involvement in the form of cerebral
infarction secondary to wasp sting. Also our patient had bilateral
involvement of neuroaxis which is of rare occurrence making the case
worth reporting.

References
[1] Sachdev A, Mahapatra M, D'Cruz S, Kumar A, Singh R, Lehl SS. Wasp sting induced
neurological manifestations. Neurology India Sept 2002;50(3):319–21.
[2] Riggs JE, Ketonen LM, Wymer JP, et al. Acute and delayed cerebral infarction after
wasp sting anaphylaxis. Clin Neuropharmacol 1994;17:384–8.
Fig. 3. CT angiography showing normal extra and intracranial vasculature.
[3] Starr JC, Brasher GW. Wasp sting anaphylaxis with cerebral infarction. Ann Allergy
1977;39:431–3.
[4] Crawley F, Brown M. Cerebral infarction: a rare complication of wasp sting. J Neurol
causing vasculopathy of distal internal carotid artery similar to Suzuki Neurosurg Psychiatry 1999;66:550–1.
[5] Maguire HJ, Spielman A, Pollack RJ. Ectoparasite infestations and arthropod bites
model of moyamoya syndrome. Bilateral cerebral infarcts with normal
and stings. Harrison's principles of internal medicineFauci et al (16th ed). New
cerebral angiography found in our patient could have been due to York: McGraw Hill Health Professions Division; 2005. 2600–2607.
transient vasospasm of the intracavernous portion of internal carotid