Equine protozoal myeloencephalitis—Presentation and progression

Summary Equine protozoal myeloencephalitis (EPM) remains one of the most frequently diagnosed neurological disorders of horses in North America, caused primarily by Sarcocystis neurona and less commonly Neospora hughesi . The clinical presentation is highly variable due to multifocal involvement of both grey and white matter, with asymmetric ataxia and weakness being most common. Cranial nerve deficits, though less frequent, can be severe, leading to dysphagia, facial asymmetry, tongue atrophy, or laryngeal dysfunction. This commentary discusses an unusual case of bilateral laryngeal paralysis occurring late in recovery from general anaesthesia in a Standardbred gelding with suspected EPM. The timing and nature of the respiratory compromise highlight the importance of considering neuropathic causes, including protozoal infection, in addition to mechanical or inflammatory factors following anaesthesia. Diagnostic confirmation of EPM remains challenging; paired serum and cerebrospinal fluid analysis is most reliable, while PCR lacks sensitivity. Despite this, empirical therapy is often pursued when owners decline testing, although clinical improvement alone cannot confirm the diagnosis. Treatment with approved antiprotozoal agents frequently leads to improvement, but complete resolution is uncommon and relapse may occur. Prognosis is guarded, particularly in cases with cranial nerve involvement, where outcomes are less favorable than for spinal cord deficits. This case underscores three key points: airway obstruction in the post‐anaesthetic period may arise from neurological injury as well as traditional causes; diagnostic confirmation is critical to guide appropriate therapy; and vigilant postoperative monitoring is essential, even after an apparently uneventful recovery.