CHAPTER 79 Dysphagia of Neurogenic Origin
The origin of the word dysphagia comes from the Greek words dys and phagein, which mean “difficult” and “to eat,” respectively. However, in human and veterinary medicine, some authors have defined dysphagia as the inability to swallow or difficulty eating and others only as difficulty eating. Difficulty eating includes problems in prehension, mastication, or swallowing. There are several nonneurogenic and neurogenic causes of dysphagia. This chapter focuses on neurogenic causes of difficulty in eating.
Ingestion of food begins with prehension by the lips, followed by cleaving of the feedstuff with the incisors. Prehension is a voluntary action controlled by the cerebral cortex and basal nuclei. The lips are innervated by the buccal branch (motor) of the facial nerve (cranial nerve [CN] VII) and by the maxillary and mandibular branches (sensory) of the trigeminal nerve (CN V).
Bolus formation is achieved through mastication and softening of the bolus with saliva. The masticatory muscles in the horse include the masseter, temporalis, pterygoideus lateralis, pterygoideus medialis, mylohyoideus, digastricus and occipitomandibularis muscles, all of which are innervated by the trigeminal nerve. The digastricus and occipitomandibularis muscles also receive innervation from the facial nerve. The buccinator muscle prevents feed retention between the teeth and buccal mucosa and is innervated by the buccal branch of the facial nerve.
The swallowing process consists of prepharyngeal (oral), pharyngeal, and postpharyngeal (esophageal) stages. The prepharyngeal stage is voluntary and involves passage of the food bolus to the oropharynx by tongue movements moving the bolus from side to side, a process that is assisted by the ridges of the hard palate. The presence of the bolus in the oropharynx triggers the involuntary pharyngeal stage. This stage consists of a series of movements that include elevation of the base of the tongue and soft palate to close the nasopharynx, contraction of hyoid muscles with subsequent rostral movement of the hyoid bone and larynx, closure of the rima glottis and epiglottis, and relaxation of the cricopharyngeal sphincter between the pharynx and esophagus. These movements result in propulsion of the bolus from the pharynx to the esophagus. This stage is coordinated by the glossopharyngeal (CN IX), vagus (CN X), and hypoglossal (CN XII) nerves; their nuclei in the caudal portion of the brainstem; and the reticular formation (the so-called swallowing center). The glossopharyngeal nerve is the primary afferent pathway in the swallowing reflex; therefore, its stimulation is sufficient to induce swallowing. However, in one study, no dysphagia developed in six healthy horses that underwent bilateral glossopharyngeal nerve anesthesia.
The esophageal stage of swallowing begins with closure of the cricopharyngeal sphincter immediately after passage of the bolus across the sphincter. This stage is followed by esophageal peristalsis, opening of the distal esophageal sphincter, and bolus propulsion into the stomach. Liquids do not require esophageal peristalsis to reach the distal esophageal sphincter. The esophagus is innervated by pharyngeal and esophageal branches of the vagus nerve.
Anatomically, dysphagia can be classified as prepharyngeal (abnormal prehension, mastication, or bolus propulsion to the oropharynx), pharyngeal (abnormal swallowing), and postpharyngeal (abnormal function of esophageal sphincters and peristalsis). Lesions involving both central and peripheral portions of the nervous system can result in dysphagia.
Clinical signs of dysphagia vary with cause and location of neurologic lesions. Signs associated with lesions affecting the prepharyngeal stage may include lack of prehension or attempts to prehend with the incisors, drooling, ptyalism, dropping of food (quidding) or water, lack of mastication, incoordinated or unsuccessful grinding movements, feed packing between cheek teeth and buccal mucosa, head tossing in attempts to move feed to the oropharynx, and submersion of the face to the level of the oropharynx in an attempt to drink.
Clinical signs associated with lesions affecting the pharyngeal stage include absent or decreased swallowing reflex, gagging, drooling, feed exiting the nose and mouth, cough, nasal discharge, extension of the neck during attempts to swallow, and restlessness. Signs associated with the esophageal stage are similar to those observed in the pharyngeal stage except that the swallowing reflex remains, depending on the lesion. Affected horses may stand with their necks extended, and retching may be seen. Regardless of the cause of dysphagia, horses may develop dehydration, aspiration pneumonia (the most common complication), and weight loss in chronic cases.
Viral encephalitis typically manifests as an acute onset of various central nervous signs, which may be preceded by fever. Vaccination history, season of the year, and presence of mosquitoes and other affected horses are important features to assess in investigation of viral encephalitis as a possible cause of disease. Residing in endemic areas for rabies and proximity to wildlife species in horses examined for acute and rapidly progressive neurologic signs should prompt consideration of rabies. Horses with rabies can have various clinical signs, including lameness, colic, muscle fasciculations including involvement of the muzzle, weakness, drowsiness, ataxia, fever, dysphagia, aggressive or “dumb” behavior, paralysis, and death.
Dysphagia is one of the most common signs of rabies and has been reported as affecting as many as 71% of affected horses. A history of vaccination does not rule out the possibility that a horse with signs of neurologic disease has rabies but it does make it less likely. Areas considered to be free of rabies are United Kingdom, Ireland, Scotland, Iceland, Nordic countries, New Zealand, Australia, and Caribbean and Pacific islands.
Verminous and equine protozoal myeloencephalitis also elicit a wide range of clinical signs, but progression of signs with this disease is usually chronic. The presence of natural definitive (opossum) and intermediate (raccoon or nine-banded armadillo) hosts in endemic areas (most of the American continent) for equine protozoal myeloencephalitis, together with diffuse or multifocal neurologic signs and asymmetric muscle atrophy, should alert the clinician to consider this disease.