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In the author’s practice, the two most common neurologic causes of dysphagia are botulism and EPM, with a less common cause being guttural pouch disease (particularly mycosis). Although neurologic Lyme disease (neuroborreliosis) is quite rare, the majority of cases seen by the author were dysphagic. Initial signs of botulism often mimic an episode of colic or esophageal obstruction. Affected horses might act lethargic, not finish their feedings, lie down frequently or for prolonged periods, have feed or water discharge from the nostrils, or have muscle tremors. Early recognition of botulism is imperative for treatment and survival, so practitioners in endemic areas should maintain a high degree of suspicion for this disease. Always consider botulism if a suspected choke case ‘resolves’ easily when nasogastric intubation is initially performed or if a “colic” case appears to want to eat or relaxes when recumbent. Two clinical tests Picture 3: The photo is an endoscopic image of the right guttural should be performed immediately: the tongue stress test, pouch demonstrating an enlarged stylohyoid bone, typical for during which the tongue is gently withdrawn from the temporohyoid osteoarthropathy. Note the clubby appearance of the proximal stylohyoid. mouth with the jaw closed and observed for appropriate retraction, and the grain test, during which the horse is fed eight ounces of grain in a feed pan and timed (normal are intimately associated with the guttural pouch; these horses finish the grain in less than two minutes).8 Addi- include the glossopharyngeal, vagus, and hypoglossal tional signs that might be present include mydriasis and nerves. Guttural pouch disease should be considered if slow pupillary light reflexes, weak eyelid tone, weak tail there is any history of purulent nasal discharge or epistaxis. tone, and weak anal tone. Endoscopy provides quick diagnosis of guttural pouch disBotulism diagnosis is primarily clinical. Confirmatory ease, allowing referral for definitive treatment such as laboratory tests include the mouse bioassay or PCR on sus- coil embolization for guttural pouch mycosis. Prognosis pect feed, gastrointestinal contents, or fecal samples. These depends on the amount of inflammation and subsequent samples can be collected and frozen for submission to a scarring around the cranial nerves, but can be favorable. In reference laboratory if desired. However, treatment should one retrospective study of transarterial coil embolization be initiated immediately without waiting for laboratory for treatment of guttural pouch mycosis, overall survival test results. was 84% (26/31), and 82% (9/11) horses with dysphagia Treatment of botulism is focused on specific anti-toxin recovered.10 However, another study showed only a 50% administration and general supportive care. Botulism anti- survival rate, with significant correlation between dysphatoxin can be obtained from Lake Immunogenics (Ontario, gia and non-survival.11 NY) or Plasvacc (Templeton, CA), and should be administered as soon as possible. Supportive care consists largely of maintaining adequate hydration and nutrition, generally via nasogastric intubation. Assuming appropriate treatVestibular signs include head tilt, nystagmus, and ment, prognosis is very good for horses that retain the abilloss of balance with a tendency to lean, drift, or fall to one ity to stand (95% survival), but poor (<20% survival) for side. Vestibular disease is categorized as peripheral or centhose that become totally recumbent.9 tral based on lesion location. Horses with peripheral vesDysphagia is the most common ‘brainstem’ sign seen by tibular disease generally have a head tilt towards the side the author in horses with EPM. Generally, the horse will of the lesion, horizontal or rotary nystagmus with the fast also be dull or obtunded and show proprioceptive (spinal) phase away from the side of the lesion, and normal mental ataxia. These clues should point the practitioner away from status. Although the vestibular ataxia can be so severe as botulism, as horses with botulism are generally alert and to cause recumbency, there is no evidence of proprioceprelatively coordinated, though they can show profound tive ataxia with peripheral disease. The peripheral course weakness. Treatment is as described in the “EPM” section, of the facial nerve is very close to that of the vestibular although clearly nasogastric administration of medication nerve, so facial paralysis might be seen in conjunction with is often required. Similar to EPM cases with altered behavperipheral vestibular disease. Horses with central vestibular ior, EPM cases with dysphagia have a reduced prognosis disease might have a head tilt towards or away from the and higher likelihood of relapse than EPM cases with just side of the lesion, any type of nystagmus, an altered mental spinal ataxia.5 status, proprioceptive deficits, and multiple cranial nerve Several cranial nerves that control eating and swallowing


Vestibular disease

20  The Practitioner  Issue 4 • 2017

Profile for FVMA

Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

Profile for fvma_faep