Sự khác biệt là bệnh nhân hiện diện với một tình trạng tê liệt giảm dần, bắt đầu với Ds Dozen của dây thần kinh sọ não tiến triển bệnh khô miệng, nhìn đôi, giãn nở đồng tử, mí mắt Droopy, sự nghiên mặt, gag phản xạ suy giảm, khó nuốt, dysarthria, dysphonia, người đứng đầu nâng khó khăn | CLINICAL CASES 333 food-borne but can also present with intravenous drug use surgery and wounds. The difference is that patients present with a descending paralysis beginning with the Dozen Ds of cranial nerve progression dry mouth double vision pupil dilation droopy eyelids facial droop diminished gag reflex dysphagia dysarthria dysphonia difficulty lifting head descending paralysis and diaphragmatic paralysis. Rapid administration of botulism antitoxin halts worsening although mechanical ventilation can still be required. Tick paralysis produces a rapidly ascending paralysis with areflexia ataxia and respiratory insufficiency much like Guillain-Barré syndrome particularly in children with a history of outdoor exposure. Removal of the discovered female tick can be curative by elimination of the source of the neurotoxin. Clinical Presentation The mean interval from onset of Guillain-Barré syndrome to the most severe degree of impairment is 12 days with 98 of patients reaching the end point of clinical worsening nadir by 4 weeks. The mean time to improvement starts at 28 days and clinical recovery usually occurs by 200 days. Eighty-five percent of patients recover completely although up to 15 have permanent deficits. Three to eight percent of patients die in spite of intensive care management. A major cause of mortality in elderly victims is arrhythmias. The history should be meticulous to identify corroborating symptomatology and triggers as discussed above and to rule out other causes of acute flaccid paralysis. The physical examination should focus on the vital signs reflexes and extent of weakness in the extremities diaphragm and cranial nerves. Fever and mental status changes are unusual and signal hypoxic respiratory failure or a different etiology. The principal laboratory test is the lumbar puncture showing rising protein levels up to 400 mg L with no associated increase in cell count albuminocytologic dissociation although protein elevation may not be seen
