Temporohyoid osteoarthropathy and unilateral facial nerve paralysis in a horse

Abstract

A 13-year-old broodmare was referred for weight loss and left facial nerve paralysis. Bilateral temporohyoid osteoarthropathy was diagnosed based on proliferation of the temporohyoid joints and stylohyoid bones on radiographs and guttural pouch endoscopy. The left side was more severely affected. Treatment resulted in little or no improvement.

A pregnant, 13-year-old quarter horse broodmare was referred to the Western College of Veterinary Medicine (WCVM) Teaching Hospital to determine the cause of a 3-week history of depression, weight loss, left-sided ptosis, left ear droop, feed impaction between the left dental arcade and the cheek, and drooping of the left side of the lower lip.

The referring veterinarian had examined the mare approximately 3 wk previously for an acute onset of the above neurological signs and had treated the mare with ampicillin and sulbactam (Synergistin; Pfizer Canada, London, Ontario), 6.6 mg/kg bodyweight (BW) and 3.3 mg/kg BW, respectively, IM, q24h for 4 d. No improve ment was noted and the treatment was changed to ceftiofur (Excenel; Pharmacia & Upjohn, Orangeville, Ontario), 2 mg/kg BW, IM, q24h for 3 d and phenylbutazone (Butequine; Vetrepharm Canada, London, Ontario) 1 g, PO, q12h. The horse did not appear to respond to treatment and was referred to the WCVM for further evaluation.

On physical examination, the mare exhibited left-sided ptosis, left ear droop, feed impaction between the left dental arcade and the cheek, tongue protrusion out the left side of the mouth, drooping of the left side of her lower lip, and a slight deviation of the muzzle to the right. These signs suggested involvement of the left facial nerve. Palpation of the head region and an otoscopic examination of both external auditory canals revealed no obvious abnormalities. No other neurologic or physical abnormalities were detected. The mare was confirmed pregnant by ultrasonography; the fetal age was estimated to be 5 mo.

Blood samples were collected for a complete blood cell (CBC) count and an enzyme linked immunosorbent assay (ELISA) to test for antibodies to West Nile virus. Lateral skull radiographs of the middle ear and guttural pouch area were taken and then endoscopy of the guttural pouches was performed. The CBC count revealed a moderate neutrophilia (16.7 × 10⁹/L, reference 1.8 to 7.2 × 10⁹/L). Absence of a left shift and normal values for total solids, absolute fibrinogen concentration, and protein:fibrinogen ratio suggested that there was no marked inflammatory response. However, the neutrophilia was greater than is normally seen with a stress leukogram alone and suggested that a mild inflammatory response might be present. No detectable levels of immuno globulin (Ig)M or IgG antibodies to West Nile virus were observed on the ELISA.

Lateral skull radiographs of the middle ear and guttural pouch area revealed bony proliferation and sclerosis of the stylohyoid bones. The normally smooth contour of the stylohyoid bones was roughened and enlarged. Due to superimposition of the stylohyoid bones, temporohyoid joints, and the overlapping vertical rami of the mandible on the straight lateral view, the degree to which each individual temporohyoid joint was affected could not be determined. So, endoscopy was performed to allow complete examination of the guttural pouches. The right stylohyoid bone had a small area of enlargement near the temporohyoid joint, but it still retained its smooth contour. A similar amount of bony proliferation was seen at the left temporohyoid joint, and the left stylohyoid bone was also diffusely enlarged (Figure 1). The soft tissues within both guttural pouches appeared normal.

Figure 1. Endoscopic view of the left proximal stylohyoid bone and temporohyoid joint in the guttural pouch. Enlargement of the stylohyoid bone and minor bony proliferation of the temporohyoid joint is seen.

The most likely differential diagnoses included a guttural pouch infection; temporohyoid osteoarthropathy, with or without otitis media, otitis interna, or both; and peripheral facial nerve trauma. A diagnosis of bilateral temporohyoid osteoarthropathy was made, based on the radiographic and endoscopic evidence of bony proliferation in the region of the temporohyoid joint and stylohyoid bones.

The horse was treated with a 5-week course of ceftiofur (Excenel; Pharmacia & Upjohn) 2 mg/kg, IM, q24h. Four months after examination at the WCVM, the owner reported the mare was eating well, gaining weight, and apparently still pregnant. The left ptosis, left ear droop, and lower lip droop had shown only slight improvement. Nevertheless, the mare was compensating well for these neurological deficits. Feed material was no longer becoming impacted between the left dental arcade and cheek, and no other complications had been observed.

Temporohyoid osteoarthropathy involves bony proliferation of the tympanic bulla, proximal stylohyoid, and petrous temporal bones, which usually leads to fusion of the temporohyoid joint (1,2,3,4,5,6,7,8). The proposed pathogenesis is that otitis media causes an osteitis that extends ventrally to the tympanic bullae, temporal bones, and the proximal part of the stylohyoid bones (1,2,3,4,5,6,8,10). Alternatively, it has been suggested that the condition could be due to degenerative joint disease in the temporohyoid joint(s) alone (1,9).

Two clinical syndromes have been described in cases of temporohyoid osteoarthropathy. The first consists of abnormal behavior, such as head tossing, head shaking, ear rubbing, pain on manipulation of the ears, or avoidance of the bit (1,2,3,4,6,8,9). Pain due to arthritis in the temporohyoid joint(s) likely causes the behavior changes (1). Unfortunately, these signs are vague and may be overlooked or attributed to simple behavior problems by horse owners and veterinarians. The underlying otitis media, otitis interna, or both, often continue undiagnosed in these cases. The second consists of facial paralysis, vestibular signs, or both, usually with a sudden onset (1,3,4,10). In one retrospective study of 33 cases, facial nerve deficits were present in 87.9% and vestibulococh lear nerve deficits in 69.7% of cases (9). Another study of 35 cases suggested that vestibular signs are seen in all cases and may be present several days before facial nerve deficits (1). The glossopharyngeal, vagus (1,8,10), and hypoglossal (8) nerves may also be affected occasionally.

The cranial nerve deficits observed in many cases of temporohyoid osteoarthropathy have several potential causes. Local extension of otitis media, otitis interna, or both, to involve peripheral nerves has been described. The facial nerve is vulnerable in cases of otitis media, as only the mucous membrane and a small amount of connective tissue separate a portion of the nerve from the tympanic bulla (middle ear) (11). Often the infection extends to the inner ear, when the vestibulocochlear nerve is also affected (11). In addition, osseous proliferation may impinge on the facial nerve where it runs inside, or where it emerges from, the skull (5,9). Cranial nerve deficits have also been attributed to skull fractures. Fusion of the temporohyoid joint due to excessive bone production occurs frequently. This predisposes the horse to fractures of the petrous temporal (most common) or stylohyoid bone (1,4,6,8,9), which may then result from normal movements, such as swallowing or exercise, that place tension on the hyoid apparatus (3,4,5,6,8). Fractures in initially asymptommatic horses with temporohyoid osteoarthropathy have also been described following nasogastric intubation for unrelated health problems (9).

As in the case discussed above, horses displaying unilateral clinical signs may have bilateral disease (1). Sixteen of 26 cases (4) and 7 of 33 cases (9) showed bilateral involvement on endoscopy, radiography, or both; although one side is almost always more severely affected (4). Ipsilateral corneal ulceration has been reported as a common sequela to facial nerve paralysis, due to an inability to close the eyelids and reduced tear production (3,4,9,10). If the petrous temporal bone fractures, infection occasionally extends into the central nervous system, leading to septic meningitis, encephalitis, or both (3,4,9).

In horses, possible routes of entry for middle or inner ear infections are extension of infection from otitis externa, ascending infection from the guttural pouch, or hematogenous spread (1). Unlike other species (2,10), equine cases of otitis media or interna have a low frequency of concurrent otitis externa. Evidence of otitis externa was detected in only 1 of 35 cases of otitis media or interna at one referral center (1) and 1 of 26 cases at another institution (4). No horses examined in these 2 studies showed evidence of guttural pouch infection (1,4). The case presented here supports previous findings that temporohyoid osteoarthropathy is not commonly associated with guttural pouch infection. As in most cases of temporohyoid osteoarthropathy, the source of infection in this mare was most likely hematogenous spread.

Radiographs of the temporohyoid joint area provide reasonably reliable diagnosis for temporohyoid osteoarthropathy. Radiographs resulted in the diagnosis being made in 23 of 26 cases in 1 study (4). However, recent studies suggest that endoscopy of the guttural pouches may be more sensitive than skull radiography for diagnosing temporohyoid osteoarthropathy (1,5,7,9). Endoscopy allows direct visualization of the entire guttural pouch, proximal stylohyoid bone, temporohyoid joint, and tympanic bullae. The procedure is relatively noninvasive and easy to perform. Endoscopy also provides a safer diagnostic test (especially in ataxic horses) than procedures requiring general anesthesia, such as tympanocentesis or ventrodorsal skull radiographs (1,5).

Current treatment recommendations for temporohyoid osteoarthropathy consist of a 30-day course of broad-spectrum antibiotics (1,3,7,9), such as potentiated sulfonamides, 2nd or 3rd generation cephalosporins, ampicillin, or aminoglycosides (1,4). If tympanocentesis is performed and pathogens are cultured, appropriate antibiotic therapy can be chosen based on sensitivity results (1). A nonsteroidal antiinflammatory drug should also be administered for a short period after diagnosis to reduce inflammation and discomfort (1). Some authors have suggested the short-term use of steroids and dimethyl sulfoxide in cases exhibiting acute neurological signs (4). If present, corneal ulceration secondary to facial nerve paralysis should be treated appropriately and monitored for recurrence. Prophylactic unilateral ostectomy of the stylohyoid bone has been proposed to prevent fracture of the petrous temporal bone and subsequent nerve damage in cases where the temporohyoid joint has fused (6). However, a limited amount of published data is available on this technique and further evaluation is needed.

The prognosis in most cases of temporohyoid osteoarthropathy is fair to good, with many horses returning to their previous activities (4,9). Head shaking, if it occurs, may cease once the temporohyoid joint fuses, but the horse is then at an increased risk of temporal bone fracture (1). Improvement in neurological function was observed in 22 of 26 cases following aggressive, long-term antibiotic and antiinflammatory treatment (4). Unfortunately, there is no way to reverse the bony proliferation present in these cases, and neurological deficits may remain (1). The most common residual deficits involve the facial nerve (9). Many horses compensate visually for unilateral vestibulocochlear nerve dysfunction, and vestibular signs are noted only after blindfolding these animals (1). Recovery is slow, and maximal improvement in neurologic deficits may take months to years (7,9).

Clients must be advised that any horse with vestibular deficits could pose a risk to owners or handlers, especially if the horse is ridden (9). In confirmed cases of temporohyoid osteoarthropathy without concurrent neurologic deficits, there is still a risk of a pathological fracture of the stylohyoid or petrous temporal bone occurring in the future. Such fractures may lead to vestibular deficits that would jeopardize the safety of the horse and rider.