Large Animal Neurology. Joe Mayhew

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Figure 12.2 Interpreting asymmetry of muscles of mastication can be problematic. This is especially so for temporalis muscles that often appear asymmetric in normal horses. Both these horses (A and B) have asymmetry to the shape of their parietotemporal regions associated with a difference in the appearance of origin of each pair of temporalis muscles at the temporal crests of the parietal bones (arrows). One good guideline as to whether or not there actually is an asymmetry of muscle bulk between the pairs of temporalis and masseter muscles is whether or not there is an asymmetry to the depth (or filling) of the supraorbital fossae (arrowheads). However, any asymmetry in the bulk of tissue in the bony orbit, to include the eyeballs, muscles, and fat, can result in a change in the appearance of the supraorbital fossae. In actual fact, the first horse (A) had neurogenic atrophy of the temporal muscle associated with S. neurona encephalitis involving the right motor nucleus of the trigeminal nerve. The muscle asymmetry present in the second horse (B) was incidental—very likely due to asymmetric chewing, perhaps resulting from dental disease.

Sudden onset of a dropped mandible in a large animal patient should prompt the clinician to suspect trauma to the temporomandibular joint or mandible, with or without fracture of the mandible (Figure 12.3). Neurologic diseases resulting in a dropped mandible with no other neurologic signs rarely occur in large animals. An immune‐associated masseter myositis and selective, immune‐associated, transient trigeminal (nongranulomatous) neuritis without systemic polyneuritis do not yet appear to have been documented in large animals. Bilateral myopathy of muscles of mastication occurring in horses, particularly those in poor condition, appears to be related to vitamin E and possibly selenium deficiency.¹ This should be differentiated from neurogenic and physical causes of loss of mandibular muscle function. The acute phase of this can result in swollen masseter muscles (palpation of which eliciting a pain response), exophthalmos, chemosis, and protrusion of the third eyelid,^2,3 whereas the chronic phase progresses to muscle atrophy, difficulty in eating, and degrees of trismus.^1,4

Figure 12.3 Large animals, especially cattle that develop a jaw that does not close, will have the tongue resting slightly out from the mouth (A). That this is not glossal weakness is evident by the patient being able to withdraw the tongue into the mouth with stimulation and by the patient being able to move the tongue to attempt to eat and to lick its nares (B). This calf was involved in a squeeze‐shute accident and lost the ability to close its jaws. No temporomandibular damage could be detected, and as mandibular function returned quite quickly within about a week it was believed that this was due to a motor mandibular nerve neurapraxia, perhaps associated with (sub)luxation of the temporomandibular joint, as the nerve and its branches pass by the joint.

Many encephalitides that may involve the pontomedullary region where the motor nucleus of the trigeminal nerve resides can effect the syndrome of mandibular muscle atrophy. Degrees of weakness, ataxia, obtundation, and other cranial nerve palsies are usually evident. On the American continents, a syndrome of unilateral and much less commonly bilateral atrophy of mandibular muscles is seen in horses suffering from S. neurona and other protozoal myeloencephalitides, sometimes with no other evidence of brainstem disease. Thus, this mimics peripheral CN Vm neuropathy (Figures 12.4 and 12.5). Ruminants suffering from listeriosis have also been seen with brainstem disease to include unilateral and sometimes bilateral mandibular muscle atrophy, some having a flaccid mandible with the latter.^5–8

Marked masseter, temporalis, and pterygoid muscle atrophy also results in slight degrees of enophthalmos and drooping of the upper eyelid, at least in cattle^9,10 and horses. This appears to be caused by the loss of muscle mass behind the globe, which is signaled by sinking of the retrobulbar tissues in the supraorbital fossa. Non‐neurologic causes of oral dysphagia, such as temporomandibular disorders and particularly dental problems, can be associated with atrophy of the muscles of mastication that at times can be very asymmetric (Figure 12.6).

Figure 12.4 In the absence of other neurologic abnormalities or other evidence of a lesion in the region of the rostral base of cranium, atrophy of the muscles of mastication on one side in a horse from the Americas is very likely to be caused by S. neurona encephalitis as was the case here. Neoplasia and trauma to the basilar region rostral to the guttural pouch also have produced such a syndrome of atrophy of the masseter, temporalis, pterygoid, and distal digastricus muscles innervated by the trigeminal nerve.

      To be differentiated from this problem is the trismus seen with tetanus and the dystonia of jaw and tongue muscles seen with equine nigropallidal encephalomalacia, among other orthopedic and neurologic disorders.

Figure 12.5 This horse was also suffering from S. neurona encephalitis partly involving left and right motor nuclei of the trigeminal nerves in the pontomedullary region. It had normal movement of the facial muscles, lips, and tongue but could not close the jaw (A). Drinking was achieved by lapping like a dog (B).

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