Читать книгу Large Animal Neurology - Joe Mayhew - Страница 117

Оглавление

12 Dropped mandible and masticatory muscle atrophy


With denervation of the muscles of mastication, the masseter, temporalis, medial and lateral pterygoid, and distal belly of the digastricus muscles on the affected side atrophy rapidly within 1–2 weeks. Unilateral neurogenic muscle atrophy is initially not associated with any major difficulty in chewing food. With time however there is deviation of the mandible toward the normal side (Figure 12.1).Many normal horses appear to have asymmetric appearance to the origins of the temporal muscles without having asymmetric supraorbital fossae, thus having equal tissue mass behind the eyeballs (Figure 12.2). On the other hand, some asymmetry of the temporalis and other masticatory muscles occurs quite frequently that is assumed to be associated with dental pain, as it can resolve with adequate dental care. Bilateral atrophy can result in a horse showing ponderous eating habits and dropping food from its mouth. Total mandibular paralysis in all large animals causes the jaw to hang down with food and saliva present in the mouth, and usually the tongue hangs out over the lower incisor teeth.


Figure 12.1 This horse suffered total left trigeminal nerve trauma from direct penetrating trauma to the dorsal guttural pouch several months previously. Atrophy of the left muscles of mastication resulted in pronounced sinking of the left supraorbital fossa (A) and the mandible became drawn to the right side with the tongue passively falling from the left side of the mouth (B). The cheek teeth arcades also required dental care.


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 cattle9,10 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).


Figure 12.6 Asymmetric temporalis (and masseter and pterygoid) muscle atrophy (A) can be associated with severe dental problems as seen in this teenaged Thoroughbred with a deep supraorbital fossa on the right side (yellow arrow) compared with that on the left side (white arrow). Long fibers of chewed forage were present in the feces (B) associated with the oral dysphagia displayed by the horse. All signs were resolved with appropriate dental care.

References

1 1 Pearson EG, Snyder SP and Saulez MN. Masseter myodegeneration as a cause of trismus or dysphagia in adult horses. Vet Rec 2005; 156(20): 642–646.

2 2 Conwell R. Hyperlipaemia in a pregnant mare with suspected masseter myodegeneration. Vet Rec 2010; 166(4): 116–117.

3 3 Step DL, Divers TJ, Cooper B, et al. Severe masseter myonecrosis in a horse. J Am Vet Med Assoc 1991; 198(1): 117–119.

4 4 Aharonson‐Raz K, Milgram J, Chai O and Sutton GA. Fibrosis of the masseter leading to trismus and dysphagia in a mare. Vet Rec 2009; 164(19): 597–608.

5 5 Schweizer G, Ehrensperger F, Torgerson PR and Braun U. Clinical findings and treatment of 94 cattle presumptively diagnosed with listeriosis. Vet Rec 2006; 158(17): 588–592.

6 6 Braun U, Stehle C and Ehrensperger F. Clinical findings and treatment of listeriosis in 67 sheep and goats. Vet Rec 2002; 150(2): 38–42.

7 7 Rebhun WC and deLahunta A. Diagnosis and treatment of bovine listeriosis. J Am Vet Med Assoc 1982; 180(4): 395–408.

8 8 Barlow RM and McGorum B. Ovine listerial encephalitis: analysis, hypothesis and synthesis. Vet Rec 1985; 116(9): 233–236.

9 9 Divers TJ and Peek SF. Rebhun's Diseases of Dairy Cattle. Saunders Elsevier, Philadelphia, PA. 2008.

10 10 Rebhun WC. Diseases of the bovine orbit and globe. J Am Vet Med Assoc 1979; 175(2): 171–175.

Large Animal Neurology

Подняться наверх