LAUSR

A 47-year-old farmer was stung by a swarm of wasps and presented with swelling, pain, and itching on the skin of his head, face, neck, back, and both legs. Six hours later, he felt rightlimb weakness, accompanied by slurred speech. He was admitted to the emergency department 8 h after being stung. His Glasgow Coma Scale score was 8. His temperature was 37.2 C, pulse was 96 beats/min, respirations were 24 breaths/min, and blood pressure was 142/87mmHg. He was unresponsive to verbal stimulation. His pupils measured 3mm in diameter and were light-sensitive. Muscle tension in all extremities was slightly decreased. Orbital pressure induced left-limb avoidance. Head computed tomography was almost normal 8.5 h after the stinging occurred. We considered the diagnosis of cerebral infarction. He was treated with dexamethasone, edaravone, loratadine, and aspirin. His mental status gradually improved, and he was fully alert on the third day. He had motor aphasia and grade 3/5 right-limb weakness. Brain diffusion-weighted magnetic resonance imaging (Figure 1(A)) on day 3 after admission revealed a large and poorly-defined area of abnormal signal intensity in the left frontotemporal lobe and basal ganglia. Magnetic resonance angiography (MRA) (Figure 1(B)) showed occlusion of the left middle cerebral artery (MCA) and its branches and irregularities of the bilateral posterior cerebral arteries. One week later, he had 4þ/5 strength on his affected side. At a follow-up visit 2 months later, his speech had improved, he was able to express simple words, and his right-limb muscle strength had returned to normal. Transcranial Doppler (TCD) ultrasonography showed unobstructed blood flow in the left MCA. The transient coma may have been due to the venom’s direct toxic inhibition of the central nervous system. Follow-up imaging was inconsistent with prior studies [1,2]. The left MCA was unobstructed on TCD examination after 2 months, in contrast with the original MRA findings. We suspected arterial recanalization of the cerebrovascular occlusion. His strength had returned to 4þ/5 one week after admission, which is unlikely for a large cerebral infarction. Therefore, we presumed that recanalization occurred between the third and seventh day after admission, but the exact time was unclear. The temporal relationship between the onset of the neurological deficits and wasp-sting exposure suggested a causal role of the stings to the ischemic stroke. Researchers have suggested that cerebral infarction associated with wasp stings could be due to vasculitis, hypoperfusion, or retrograde stimulation of the superior cervical ganglion [1–3]. Transient coagulopathy in wasp venom anaphylaxis should also be considered [4]. Moreover, the bilateral posterior cerebral arteries appeared