an elderly woman with a history of high blood pressure and hypercholesterolemia was admitted to the emergency room for suspected stroke due to abruptly starting vertigo , blurred vision and difficulties in speech .
neurological examination within 3 h from the symptom onset revealed high blood pressure ( 206/130 mm hg ) , dysarthria and impaired right hand coordination .
twelve hours after symptoms onset , the patient could not speak or swallow but was able to move all extremities .
the patient was intubated because of breathing difficulties and co2 retention . at 24 h ,
the patient could not open her eyes , here pupils were dilated , and there were no spontaneous respiration or movements . yet
a brain mri revealed an old hemorrhage in the pons , and csf findings were normal .
nerve conduction study findings showed that motor amplitudes were negligible , but sensory responses were preserved . in electromyography of the finger
1 ) was observed , but no increment was found in repeated nerve stimulation ( rns ) .
serum , gastric fluid and stool samples were taken , and botulinum antitoxin was given 3 days after symptom onset . despite all treatment efforts , the patient died 13 days after admission to the hospital due to septic shock and multiorgan failure .
three days after the arrival of the first patient , a previously healthy 29-year - old woman was admitted to the emergency room for suspected stroke .
it was soon found that the patient was a relative of patient 1 , and that they had eaten the same food .
although she received the antitoxin treatment the same evening , her neurological symptoms deteriorated during the first 2 days .
she needed assisted ventilation for 3 weeks , although other symptoms were resolved within 1 week .
those olives were strongly positive for botulinum neurotoxin type b , and the gastric content and fecal samples of both patients tested by multiplex pcr were positive for clostridium botulinum type b. in addition , the serum of patient 1 was weakly positive for botulinum neurotoxin .
botulinum toxin binds irreversibly to presynaptic plates of the neuromuscular junction causing dysfunction of voluntary muscles , inner organs and the autonomic nervous system .
in addition , the toxin may modify the inhibition in the central nervous system , possibly due to altered afferent input from the muscle spindles .
botulinum antitoxin neutralizes only the circulating toxin and should thus be administrated as soon as possible before completing the laboratory tests .
the diagnosis must therefore be based on clinical findings ; bulbar palsy with descending paralysis is the most typical finding .
especially the combination of bilateral drooping of the eye lids , absent gag reflex and respiratory failure with relatively well preserved limb forces and a clear mental status are suggestive of botulism and , more uncommonly , of other possible diagnoses like brainstem ischemia or polyradiculitis .
botulism diagnosis is further supported by normal mri and csf findings . according to the literature , as a sign of presynaptic transmission defect , high - frequency rns shows often an incremental motor response in botulism patients .
however , no increment was observed in our two cases , possibly due to largely destroyed endplates .
neurological symptoms may develop acutely in food - borne botulism and may therefore be misinterpreted as brainstem ischemia .
 botulism is a muscle - paralyzing disease caused by neurotoxins ( types a  
 g ) produced by the bacteria clostridium botulinum . symptoms of food - borne botulism most commonly appear 1236 h after eating contaminated food , but the earliest neurological symptoms may in some cases start abruptly . here , we report the cases of two patients with food - borne botulism who were admitted to the neurological emergency room as candidates for intravenous thrombolysis for acute stroke . 
Case 1
Case 2
Discussion
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