Communicating Hydrocephalus in a Mature Goffin's Cockatoo (Cacatua goffini).
is described in an adult Goffin's cockatoo (Cacatua goffini). Marked cerebral atrophy without evidence of inflammation was observed grossly and histologically in the bird in this report. The segmentally hypertrophied arachnoid membrane provides a cause for the hydrocephalus and corresponding cerebral atrophy. Metaplastic change in the leptomeninges leading to communicating hydrocephalus is characteristic of vitamin A deficiency in other species. Such a deficiency was supported in this case by characteristic changes in the integument and a history of an all-seed diet. Improved recognition of hydrocephalus in pet birds combined with an accurate dietary history is essential to establishing the prevalence of such changes and to confirm our proposed mechanism of neurologic disease.
Key words: communicating hydrocephalus, vitamin A, deficiency, avian, bird, cockatoo, Cacatua goffini
An 11-year-old Goffin's cockatoo (Cacatua goffini) was presented for hospitalization because of severe weakness, ataxia, and weight loss. The cockatoo was purchased at a bird fair 6 years previously and was estimated to be 5 years old at the time of purchase. The bird was fed a seed diet, of which it preferentially ate sunflower seeds. The cockatoo was housed separately in a room with a blue and gold macaw (Ara ararauna) and another Goffin's cockatoo. The owners reported that over the preceding 12 months the bird's condition had deteriorated from a decrease in daily activity and intermittent incoordination to the inability to stand without support. The owners also noted that the cockatoo had not regrown new plumes from the previous molt. The bird began feather picking and barbering 3 months before presentation.
Six months previously, the owners had taken the cockatoo to another veterinary hospital for evaluation. At that time, the bird tested negative for psittacine beak and feather disease by polymerase chain reaction assay (Research Associates, Milford, OH, USA), and results of serum biochemical profile and a complete blood cell count were unremarkable (Antech Diagnostics, New York, NY, USA). The owners declined further work up, and the bird was sent home with instructions to change the diet to pellets supplemented with fruits and vegetables. The owners were unable to convert the bird to the new foods and continued the seed diet. Because of the progressive inability of the bird to prehend seed, the owners supplemented the diet with water-soaked monkey chow.
On physical examination, the bird was emaciated, weighing only 228 g. Nearly all of the contour feathers were missing and the down was plucked from the entire body with no evidence of regrowth. All of the primary and secondary feathers were broken, barbered, and frayed to within several millimeters of the follicle. The wing tips were ulcerated from the bird's attempts to stabilize itself and ambulate. Three of the 8 toenails were missing, and the remaining nails were broken and flaking. The beak was covered with excess keratin and was pitted. The cockatoo was unable to perch and could not stand. If disturbed (sound or touch), the bird would thrash and roll uncontrollably until it came to rest on its back in exhaustion. When placed on a towel, the bird was able to stand with a wide-based stance and the head pressed forward, resting the dorsal aspect of beak on the towel for support. Results of fecal and choanal Gram's stains were 60% gram-negative bacteria. On initial blood tests, the estimated absolute white blood cell count was approximately 40 000 cells/[micro]l (reference range, 5 000-25 000 cells/[micro]l), hematocrit was 31% (reference range, 43%-55%), and the heterophils were mildly toxic. (1)
The owners declined additional diagnostic testing. The bird was treated with dexamethasone sodium phosphate (2 mg/kg IV once), lactated Ringers solution (8 ml SC q8h), B-complex vitamins (2 mg/ kg SC q24h), vitamins A, D, and E (0.1 ml/300 g IM), calcium lactate (10 mg/kg IM ql2h), and enrofloxacin (15 mg/kg IM ql2h; Baytril, 22.7%, Bayer Corporation, Shawnee Mission, KS, USA). The bird was placed in an avian isolette with dim light in a quiet room and ambient temperature of 31[degrees]C-32[degrees]C (88[degrees]F-90[degrees]F). One hour later, the ataxia appeared slightly less severe, and the bird was gavage fed a balanced avian hand-feeding diet. The next day, treatment was with enrofloxicin and sub cutaneous fluids, and gavage feeding was continued. The bird attempted to eat seed but was unable to because of its profound ataxia and incoordination. On the third day, the bird had a brief seizure. A grave prognosis was given to the owner, but they elected to continue treatment and declined further diagnostic testing. Calcium EDTA (20 mg/kg IM ql2h) therapy for possible heavy metal toxicosis and treatment with dexamethasone was repeated. Seizures continued and owners elected euthanasia on the fifth day.
A necropsy was performed and the bird was determined to be male. In addition to the integumentary lesions and poor body condition, an expanded subarachnoid space filled with CSF of normal consistency was found. The lateral ventricles of the brain were markedly dilated with associated cerebral atrophy. Atrophic changes were particularly pronounced in the occipital cortex, where only a thin ribbon of atrophic nervous tissue separated the ventricular lining from the overlying leptomeninges. There was also marked enlargement of the third ventricle and ventricle of the mesencephalic tectum (Fig 1).
[FIGURE 1 OMITTED]
Histologic evaluation of tissues showed no evidence of central nervous system (CNS) inflammation or neoplasia. Atrophic periventricular tissues exhibited marked astrogliosis. The arachnoid membranes exhibited moderate hyperplasia characterized by segmental proliferation of meningeal fibroblasts. The distribution of change was generalized (Fig 2). The tela choroidea of the choroid plexus showed fibromyxomatous hyperplasia with accumulation of lipid-laden macrophages. Overall, the changes in the brain were consistent with a communicating hydrocephalus with marked periventricular and submeningeal parenchymal atrophy with secondary ventriculomegaly and expansion of the subarachnoid space. Histologic evaluation of the skin exhibited a moderate orthokeratotic hyperkeratosis with marked follicular keratosis. No significant findings were observed in other organ systems.
[FIGURE 2 OMITTED]
This report describes the clinical course and pathologic findings in a Goffin's cockatoo with communicating hydrocephalus. The most likely cause of the hydrocephalus was vitamin A deficiency. In mammals, hydrocephalus most frequently results from decreased resorption of cerebral spinal fluid (CSF). Hydrocephalus secondary to increased CSF production is rare and generally poorly documented. (2) Anatomic descriptions of poultry and pigeons show the avian ventricular system is similar to mammals. CSF is produced within the ventricular system where it circulates between compartments to emerge on the surface of the brain and spinal cord? Here, CSF enters projections of the arachnoid membrane, the arachnoid villi. These villi, collectively referred to as granulations, act as one-way valves allowing outflow of CSF into the venous circulation. (4) Understanding of this resorption process is based on mammalian anatomy because a precise description of the avian counterpart has not been described.
Two forms of hydrocephalus occur: internal and communicating. Internal hydrocephalus is caused by an obstruction of CSF flow within the ventricular system, leading to brain atrophy and ventricular enlargement. Communicating hydrocephalus is caused by diminished resorption of CSF at the arachnoid granulations, leading to an expansion of both the ventricular system and the subarachnoid space. (2) Causes of hydrocephalus can be either developmental or acquired. Communicating hydrocephalus in this cockatoo was most likely the result of hyperplastic changes in the leptomeninges that, if generalized, would have interfered with the movement of CSF into the venous circulation. The subsequent rise in intracranial pressure would then induce tissue atrophy secondary to either transependymal edema with secondary periventricular demyelination or ischemia.
In mammals, leptomeningeal proliferative changes and integumentary hyperkeratosis are both manifestations of vitamin A deficiency. Increased CSF pressure has been documented in dogs, rabbits, swine, rats, chickens, sheep, and cattle with vitamin A deficiency. (5) A common sequella to increased CSF pressure is hydrocephalus. (2) Several studies have been published on the effects of hypovitaminosis A on the dura mater of calves. (6,7) These studies found a correlation between the degrees of thickening of the dura mater and the severity of vitamin A deficiency. With chronic vitamin A deficiency, arachnoid membranes become thickened and stiff. These changes were sufficient to inhibit the function of the arachnoid granulations, diminishing CSF resorption with a resulting communicating hydrocephalus. (6)
Reports of the effects of hypovitaminosis A on the skull and CNS in birds are generally restricted to gallinaceous species. Studies in Japanese quail and chickens fed diets deficient in vitamin A have shown development of neurologic signs associated with axonal swelling, neural tissue compression related to abnormal bony growth, and neuronal death. (8,9) Some of these quail also developed hydrocephalus. In these studies, the meninges of the quail were not evaluated. (9)
The history and physical and necropsy findings in this bird are consistent with a diagnosis of vitamin A deficiency. The Goffin's cockatoo only ate sunflower seeds. Seed diets have been associated with many nutritional deficiencies, including vitamin A deficiency, and this is particularly true for sunflower seeds. (10,11) Prolonged storage of seeds at room temperature and exposure to light or oxygen result in additional degradation of nutrients. Many estimates indicate that seeds packaged for sale are at least 1 year old. (11)
In addition to the hyperplastic meninges, hyperkeratotic lesions in the epidermis are also associated with vitamin A deficiency and were present in this bird. Retrospectively, liver vitamin A concentrations and histologic examination of other vitamin A-sensitive tissues, such as mucous glands of the oral cavity and the respiratory epithelium, would have been necessary to confirm vitamin A deficiency.
The few cases of hydrocephalus reported in pet birds provide limited, if any, insight as to pathogenesis. Most of these cases appear to describe internal hydrocephalus. The first case of internal hydrocephalus in a psittacine bird was described in an African grey parrot (Psittacus erithacus timneh). The cause of hydrocephalus was not determined, however, and it was suggested to be secondary to a congenital lesion affecting CSF outflow. (12) A second case report described a 10-year-old African grey parrot with a 3-year history of seizures. The cause of the hydrocephalus was not identified in this bird. (13) Hydrocephalus was also described in a 5-year-old yellow-collared macaw (Ara auricollis) with a history of ataxia and falling. Microscopically, this bird had a mild nonsuppurative encephalitis. (13) The last cases were a conure (Aratinga species) and budgerigar (Melopsittacus undulatus), with hydrocephalus of unknown origin, and a budgerigar with internal hydrocephalus secondary to a choroid plexus tumor. (14)
Antemortem diagnosis of hydrocephalus in birds is challenging. The signs seen in this bird were similar to the signs reported in other birds and mammals with hydrocephalus, such as loss of coordination and fine motor skills, periods of dulled mentation, circling, paresis, and seizures. (2,5) These signs, however, are not specific and are also seen in animals with other diffuse CNS diseases. Differentials for progressive forebrain or vestibular signs in birds include thiamine, vitamin [B.sub.12], or vitamin E deficiency; proventricular dilatation disease; heavy metal toxicosis; neoplasia; aspergillosis; sarcocystosis; cerebellar atrophy; and several viral diseases, including those caused by paramyxovirus 1 and 3, avian polyomavirus, and adenovirus. (10,11,13) Determining CSF pressures, cellularity, and protein concentrations are critical data necessary for differentiating hydrocephalus from other diseases that might cause similar signs. Obtaining CSF in a bird is difficult, if not impossible, because of the synsacral fusion of vertebral bodies and venous sinus located at the level of the foramen-magnum. (15) Likewise, diagnostic imaging with nuclear magnetic imaging or computer tomography, which could provide a definitive diagnosis of hydrocephalus, has limited availability.
Had hydrocephalus been diagnosed in this bird while it was alive, the extent of hydrocephalus would have made recovery of this bird unlikely. Had the lesions been less severe, it is still unknown whether the problem could have been reversed. Mucosal and epidermal lesions resolve with vitamin A supplementation, but it is not known whether the changes in the arachnoid villi are reversible. The only treatment option currently available for mammals with hydrocephalus consists of placing an intraventricular shunt. This shunt allows the CSF fluid to exit the skull and drain into the peritoneal space. These shunts are difficult to maintain, and their use in birds has not been described. (2)
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(12.) Wack RF, Lindstrom JG, Graham DL. Internal hydrocephalus in an African grey parrot (Psittacus erithacus timneh). J Avian Med Surg. 1989;3:94-96.
(13.) Shivaprasad HL. Diseases of the nervous system in pet birds: a review and report of diseases rarely documented. Proc Annu Conf Assoc Avian Vet. 1993: 213-222.
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From Native Palm Animal Hospital, 10076 West Indiantown Road, Jupiter, FL 33478, USA (Johnston); Animal Clinic Northview, 34910 Center Ridge Road, North Ridgeville, OH 44039, USA (Lindstrom); and the Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA (Oglesbee).
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|Title Annotation:||Clinical Report|
|Author:||Johnston, Heather A.; Lindstrom, Jamie G.; Oglesbee, Michael|
|Publication:||Journal of Avian Medicine and Surgery|
|Article Type:||Clinical report|
|Date:||Sep 1, 2006|
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