A Retrospective Study of Horner Syndrome in Australian Wild Birds, 2010-2016.
Key words: Horner syndrome, trauma, sympathetic nervous system, ptosis, bird, avian
Horner syndrome, or oculosympathetic paresis, results from any interruption of the 3-neuron pathway of the oculosympathetic tract from the brain to the eye and adjacent structures. (1,2) Clinical signs described in birds are ptosis and contralateral erection of facial feathers with or without miosis. (3)
Unilateral Horner syndrome has been reported in an African spotted eagle owl (Bubo africanus) with ptosis and mild miosis; an eastern screech owl (Megascops asio) with ptosis, facial feather asymmetry, and mild miosis; and a red-bellied parrot (Poicephalus rufiventris) with ptosis and facial feather asymmetry without miosis. (3-5) Central and peripherally induced Horner syndrome have also been induced experimentally in domestic fowl and the house finch (Carpodacus mexicanus), respectively. (6,7)
The oculosympathetic tract has been well described in birds. (3) Sympathetic supply originates at the hypothalamus and traverses the thoracolumbar spinal cord and cranial cervical ganglion to innervate the eye, vasculature, and feather follicles of the head and neck. (3,6) Facial asymmetry caused by unilateral ptosis and erection of facial feathers is induced by loss of adrenergic innervation of the smooth muscle of the eyelids and feathers. (6,8,9)
Based on the few published reports of Horner syndrome in birds, the condition is assumed rare or difficult to identify. (3) The purpose of this study was to report the occurrence, clinical history, and outcome of wild birds presenting with Horner syndrome.
Materials and Methods
The medical records from all avian admissions to the Currumbin Wildlife Hospital between August 10, 2010, and December 8, 2016, were retrospectively reviewed. The 30 777 cases were extracted into Microsoft Excel (Microsoft, Redmond, WA, USA) for analysis, and 25 cases were identified with a diagnosis of Horner syndrome and consistent clinical notes. Extracted case data included accession number, time of accession, history, admission notes, weight on arrival, age, species, duration of hospitalization, diagnosis, and treatment notes.
All affected birds were subject to distance observation and physical examination, followed by examination under general anaesthesia and complete body radiographs once each patient was deemed stable. Horner syndrome was defined in this study as ptosis and ipsilateral erection of facial feathers, with or without miosis.
A total of 25 birds were diagnosed with Horner syndrome during the 6-year period, yielding an admission rate of 1 case per 1231 admissions (Table 1). Clinical signs of ptosis and asymmetric erection of facial feathers were quite distinct on physical examination and were consistent across species (Figs 1 and 2). Time and month of admission were highly variable among cases with no clear seasonality or temporal pattern.
Species affected included rainbow lorikeet (Trichoglossus haematodus), scaly breasted lorikeet (Trichoglossus chlorolepidotus), tawny frogmouth (Podargus strigoides), southern boobook (Ninox novaeseelandiae), laughing kookaburra (Dacelo novaeguineae), crested tern (Thalasseus bergii), crested pigeon (Ocyphaps lophotes), Torresian crow (Corvus orru), and grey butcherbird (Cracticus torquatus) (Table 2). Birds were more likely to be adults (64%; n = 16) than subadults (36%; n = 9), and Horner syndrome was not observed in any juvenile birds. Affected rainbow lorikeets, the most commonly affected species, represented 0.2% (13 of 7069) of all rainbow lorikeets admitted to Currumbin Wildlife Hospital with a primary diagnosis of trauma during the study period.
The most common reasons for presentation were "found on ground" (40%; n = 10), "unable to fly" (20%; n = 5), "window strike" (12%; n = 3), and "vehicle impact" (8%; n = 2). The remainder included "cat attack," "found in swimming pool," and "unknown." Most cases were admitted for traumatic injuries (88%; n = 22); however, a single case (4%) was affected by psittacine beak and feather disease, and in 2 cases (8%), the primary cause was undetermined.
All cases of Horner syndrome were unilateral, reported as left (40%; n = 10), right (32%; n = 8), or not recorded (28%; n = 7). Concurrent traumatic injuries were reported in 10 cases (40%) and were ipsilateral to the Horner syndrome when restricted to one side. There were 14 cases (56%) that demonstrated altered demeanor, and 19 (76%) had concurrent neurologic deficits (Table 3).
Of the 25 birds with Horner syndrome, 8 (32%) were released and 17 (68%) were euthanatized or died. The species most likely to be released were scaly breasted lorikeets (50%; 2 of 4), rainbow lorikeets (38%; 5 of 13), and tawny frogmouths (50%; 1 of 2), whereas all other species died or were euthanatized during treatment. Outcome was not affected by age, with a likelihood of release of 31% (5 of 16) and 33% (3 of 9) for adults and subadults, respectively. Survivors spent between 3 and 78 days in the hospital, with a median of 7 days and an average of 22 days.
All cases were treated with parenteral meloxicam during the initial assessment, followed by oral meloxicam twice daily until symptoms resolved. Meloxicam dose rates were split chronologically within the group, with cases 1-7 receiving 0.2 mg/ kg and cases 8-25 receiving 1 mg/kg because of a revision in hospital treatment protocols. Cases 1-7 had a 0% survival rate and a mean hospitalization time of 55 hours (range, 24-102 hours). Cases 8-25 had a survival rate of 44%, with a mean hospitalization time of 517 hours (range, 68-1867 hours) and 17.5 hours (range, 0-96 hours) for released and fatal cases, respectively.
This is the first retrospective study, to our knowledge, of Horner syndrome in birds and confirms ptosis and the asymmetric erection of feathers as consistent clinical signs. The few observed cases suggests that Horner syndrome is a rare condition, even among species such as rainbow lorikeets, which are frequently observed with traumatic injuries. This is consistent with the scarcity of published reports of Horner syndrome among birds. In comparison, a 40-year study of Horner syndrome in people younger than 19 years reported an incidence of 1.42 per 100 000 cases, which is significantly less common than the 81.23 per 100 000 cases reported in wild birds here. (1) Aalbers et al (10) reported that 68% of rats developed Horner syndrome after experimental carotid surgery; however, the incidence of Horner syndrome in other species and naturally occurring cases is unknown.
All cases in this study demonstrated very obvious facial asymmetry caused by ptosis and feather erection on physical examination. More subtle cases may have been overlooked, leading to an underestimate of Horner cases; however, our findings suggest that the condition has been underreported in the literature. Classic signs of Horner syndrome in mammals are miosis and ptosis, with or without concurrent anhidrosis, iris heterochromia, and pupillary dilation lag. (1) Ptosis and erection of facial feathers appear to be consistent clinical signs among captive and wild birds, whereas miosis is variable and anhidrosis is not a feature of birds. (3)
Horner syndrome has been reported in dogs, cats, birds, rats, horses, cows, pigs, sheep, goats, and people. (2,3,10-12) Common causes in mammalian species relate to trauma, inflammation, or impingement of the 3-neuron oculosympathetic pathway. Horner syndrome in cats was commonly associated with a diagnosis of focal trauma, infection or inflammation, neoplasia, or idiopathic. (13) Reported causes in dogs are otitis media and interna; neoplasia of the thorax, thyroid, brain, and vagal nerve; intrathoracic tube displacement; encephalitis; intervertebral disc disease; and trauma to the head, neck, thorax and brachial plexus, and trigeminal nerve. (14) Half of all reported canine and human cases are idiopathic, and 10% of nonidiopathic human cases are iatrogenic. (14-16) In adult humans, traumatic carotid or vertebral artery dissection, cervical adenopathy, neck and spinal surgery, congenital abnormalities, and infection are common causes. (1,17) In children, Horner syndrome is most commonly congenital, including birth trauma, vascular malformations, and neoplasia. (1) Although an anatomic diagnosis was not pursued for cases in the present study, further investigation by imaging or necropsy may provide additional information on the occurrence of arterial damage or the presence of tumors.
Acquired Horner syndrome was the most likely cause of neuropathy in each of the wild bird cases presented. Trauma is common among birds presented to the wildlife hospital, caused by window strikes, car accidents, predation, or other misadventure. In 2 cases, dull demeanor prevented a full neurologic assessment on admission, but demeanor improved rapidly when treated with meloxicam. The presence of additional neurologic deficits in most cases may be suggestive of central, or first-order, Horner syndrome, in which ataxia, postural-reaction deficits, altered mental status, and cranial nerve deficits are common. (17) Radiographs were obtained for all affected patients; however, further imaging such as computed tomography and magnetic resonance imaging are recommended to identify anatomic lesions, such as dissecting artery or neoplasia. (17,18)
Topical pharmacologic testing was not used in these cases but is recommended to confirm or localize Horner syndrome lesions. (12) Cocaine and hydroxyamphetamine are not readily available in Australia; however, phenylephrine has been used in birds and apraclonidine has been suggested as a more-accessible alternative. (5,19) Phenylephrine is a direct-acting sympathomimetic amine that allows localization of Horner syndrome lesions through denervation hypersensitivity. (20) Results can vary with the time delay from injury and the completeness of the lesion injury. (13) Future investigation would benefit from pharmacologic testing, especially when the time of injury is known, to better elucidate the underlying causes of Horner syndrome in wild birds.
A marked variation in outcome was observed between dosing regimens of meloxicam, with the dose of 1 mg/kg appearing more effective than 0.2 mg/kg for traumatic cases of Horner syndrome. The limited number of cases prevented statistical analysis but is warranted in future studies. It is clear, however, that Horner syndrome in wild birds confers a poor prognosis for recovery and is a significant finding of the neurologic exam. Resolution of clinical signs is variable and often prolonged in domestic mammals and birds. (3,21) Hospitalization times in wild birds were highly variable, and resolution was gradual. However, fatal cases treated with meloxicam at 1 mg/kg were more likely to decline rapidly in the first 4 days. Persistence of Horner syndrome beyond resolution of surrounding soft tissue trauma appears to be a common feature of Horner syndrome in birds and is consistent with previous reports. (5)
Further investigation of the underlying causes of Horner syndrome in birds and wider reporting of affected cases are necessary to provide prognostic guidelines and accurate recommendations for management and treatment.
Andrew G. Hill, BVSc, MVSc, MANZCVS (Avian)
From the Currumbin Wildlife Sanctuary. 28 Tomewin Street, Currumbin, QLD 4223, Australia.
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Caption: Figure 1. Acquired Horner syndrome in a rainbow lorikeet with concurrent beak trauma. Unilateral denervation causes a clear central demarcation of feather erection in frontal (a) and oblique right (b) views. Ptosis and feather erection on the affected left side (c), creating asymmetry compared with unaffected right side (d).
Caption: Figure 2. Right-sided feather erection (open arrowhead) and right ptosis (black arrowhead) in an Australian magpie with Horner syndrome.
Table 1. Summary of clinical findings from 25 wild birds with unilateral ptosis and facial feather erection admitted to Currumbin Wildlife Hospital between 2010 and 2016. Case No. Spccies Age History 1 Rainbow lorikeet Subadult Unable to fly 2 Crested pigeon Adult Ground find 3 Torresian crow Adult Unknown 4 Laughing kookaburra Adult Vehicle impact 5 Crested tern Subadult Ground find 6 Rainbow lorikeet Adult Ground find 7 Southern boobook Adult Referred by caregiver 8 Rainbow lorikeet Adult Swimming pool incident 9 Rainbow lorikeet Subadult Unable to fly 10 Rainbow lorikeet Adult Unable to fly 11 Rainbow lorikeet Adult Vehicle impact 12 Scaly breasted Adult Ground find lorikeet 13 Rainbow lorikeet Subadult Window hit 14 Rainbow lorikeet Adult Window hit 15 Scaly breasted Adult Ground find lorikeet 16 Grey butcherbird Subadult Unknown 17 Tawny frogmouth Adult Ground find 18 Tawny frogmouth Adult Ground find 19 Rainbow lorikeet Subadult Ground find 20 Scaly breasted Subadult Window hit lorikeet 21 Rainbow lorikeet Subadult Unable to fly 22 Scaly breasted Subadult Unable to fly lorikeet 23 Rainbow lorikeet Adult Ground find 24 Rainbow lorikeet Adult Ground find 25 Rainbow lorikeet Adult Cat caught Case No. Spccies Demeanor Additional injuries 1 Rainbow lorikeet Quiet None 2 Crested pigeon Quiet Coracoid and clavicle fractures 3 Torresian crow Quiet None 4 Laughing kookaburra Normal Keel fracture. palate bruising 5 Crested tern Quiet None 6 Rainbow lorikeet Normal Left wing drop 7 Southern boobook Normal Corneal ulcer, pectin rupture 8 Rainbow lorikeet Normal Beak fracture 9 Rainbow lorikeet Normal None 10 Rainbow lorikeet Normal Beak fracture, superficial head trauma 11 Rainbow lorikeet Quiet Respiratory hemorrhage 12 Scaly breasted Quiet None lorikeet 13 Rainbow lorikeet Quiet Beak fracture 14 Rainbow lorikeet Normal None 15 Scaly breasted Normal None lorikeet 16 Grey butcherbird Normal None 17 Tawny frogmouth Quiet Corneal trauma 18 Tawny frogmouth Normal None 19 Rainbow lorikeet Quiet Beak trauma 20 Scaly breasted Quiet Beak trauma lorikeet 21 Rainbow lorikeet Quiet None 22 Scaly breasted Quiet PBFD feather loss lorikeet 23 Rainbow lorikeet Quiet None 24 Rainbow lorikeet Normal Beak injury, dyspnea 25 Rainbow lorikeet Quiet PBFD feather loss Abbreviation: PBFD indicates psittacine beak and feather disease. Table 1. Extended. Horner Other neurologic signs syndrome side Right Ataxia Left Loss of tail flick reflex Not recorded Ataxia Left Nystagmus and loss of corneal reflex Left None Right Ataxia Right None Right Loss of tail flick reflex Right None Left Hindlimb paralysis and loss of tail flick reflex Not recorded Hindlimb paralysis Left Hindlimb paralysis Left None Right Hindlimb paresis and loss of tail flick reflex Not recorded None Right Head tilt to right Left Left wing paresis Left Anisocoria and tongue deviation to left Not recorded Hindlimb paresis Not recorded Hindlimb paresis Not recorded Ataxia Not recorded None Left Loss of corneal reflex, hindlimb paralysis, and loss of tail flick reflex Left Hindlimb paralysis and loss of tail flick reflex Right Hindlimb paresis and voice change Horner Stay Outcome syndrome side length, hr Right 102 Died or euthanatized Left 24 Died or euthanatized Not recorded 42 Died or euthanatized Left 97 Died or euthanatized Left 39 Died or euthanatized Right 24 Died or euthanatized Right 54 Died or euthanatized Right 1557 Released Right 75 Released Left 161 Released Not recorded 25 Died or euthanatized Left 0 Died or euthanatized Left 167 Released Right 1867 Released Not recorded 166 Released Right 1 Died or euthanatized Left 3 Died or euthanatized Left 68 Released Not recorded 29 Died or euthanatized Not recorded 73 Not recorded 96 Died or euthanatized Not recorded 0 Died or euthanatized Left 16 Died or euthanatized Left 2 Died or euthanatized Right 3 Died or euthanatized Table 2. Species and survival of 25 wild birds presented to Currumbin Wildlife Hospital with Horner syndrome between 2010 and 2016. Affected, Survival. Species No. (%) No. (%) Rainbow lorikeet 13 (52) 5 (38) Scaly breasted lorikeet 4 (16) 2 (50) Tawny frogmouth 2 (8) 1 (50) Laughing kookaburra 1 (4) 0 (0) Southern boobook 1 (4) 0 (0) Crested pigeon 1 (4) 0 (0) Crested tern 1 (4) 0 (0) Grey butcherbird 1 (4) 0 (0) Torresian crow 1 (4) 0 (0) Table 3. Concurrent neurologic deficits observed in 25 wild birds with unilateral Horner syndrome. Birds affected. Neurologic deficit No. (%) Hindlimb paralysis/paresis 9 (36) Loss of tail flick reflex 6 (24) Ataxia 4 (16) Loss of corneal reflex 2 (8) Voice change 1 (4) Wing paresis 1 (4) Anisocoria 1 (4) Head tilt 1 (4) Nystagmus 1 (4) Asymmetry of tongue 1 (4)
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|Title Annotation:||Retrospective Study|
|Author:||Hill, Andrew G.|
|Publication:||Journal of Avian Medicine and Surgery|
|Date:||Jun 1, 2018|
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