Diagnosing and Treating Avian Neurologic Disease

Key Points

  • Understand avian anatomic variations in cranial and spinal nerve anatomy. The avian spinal cord extends the entire length of the vertebral column, and there is no cauda equina. The number of spinal nerves in the bird depends on the number of vertebrae.
  • Although the avian neurologic examination varies little from that of the mammal, assessment can be challenging.
  • Serial neurologic assessment aids in establishing diagnosis and prognosis.
  • Neurologic patients require rapid intervention, frequent assessment, and often intensive care.
  • Seizures are a common neurologic problem that may arise from many etiologies. Important differential diagnoses include renal disease or renal failure, hypocalcemia, hypoglycemia, hyperlipemic syndrome, proventricular dilatation disease, psittacosis, atherosclerosis, and lead toxicity. It is unclear whether hepatic encephalopathy truly occurs in birds since nitrogenous waste is not the end product of hepatic metabolism.

Anatomic variations

Peripheral nervous system

Birds have 12 cranial nerves similar to those of mammals. The number of spinal nerves depends on the number of vertebrae. Chickens have 15 pairs of cervical nerves, 6 pairs of thoracic nerves, and 14 pairs of lumbosacral nerves. Avian spinal nerves exit the cord laterally and supply nearby muscles and viscera, while in mammals spinal nerves travel caudally 1-3 vertebrae. The avian spinal cord also extends the entire length of the vertebral column, and there is no cauda equina.

The brachial plexus consists of the ventral branch of cervical and thoracic spinal nerves. It innervates muscles and skin of the forelimb and shoulder. Nerves of the wing arise from the brachial plexus; these nerves include:

Nerve Action
Axillary Elevation of the humerus
Medianoulnar Flexor muscles of the wing
Pectoral Downstroke of the wing
Radial Extensor muscles
Supracoracoid Upstroke

The lumbosacral plexus innervates the muscles and skin of the pelvic limb and pelvis. The roots of the plexus are in contact with or embedded within the kidney. Within the plexus is the rhomboid sinus, the caudal aspect of the neural tube, which contains a gelatinous structure or glycogen body.

Nerves of the leg Innervates
Femoral Dorsal pelvis, wing of the ilium, cranial thigh, motor to extensors of the knee (femorotibialis, iliotibialis)
Ischiatic (supplies the tibial nerve) Extensors of the hock (gastrocnemius), medial aspect of hock, metatarsus, deep digital flexors
Lateral femoral cutaneous Lateral knee, lateral proximal leg, skin of the thigh
Medial femoral cutaneous Iliofemoralis, medial knee, medial proximal leg, cranial leg
Obturator Medial and lateral obturators, ischiofemoralis muscles

Central nervous system

Grey and white matter are arranged in essentially the same manner in birds and mammals. Some structure of the avian telencephalon and diencephalon are completely different from that seen in mammals, however the function of regions like the telencephalon is similar.

Avian neurologic examination

Mentation

Is the patient aware? What is the level of consciousness?

Term Definition
Alert Normal awareness of surroundings
Lethargic Aware but slightly sluggish
Depressed Decreased response to environmental stimuli; sleeping when undisturbed
Obtunded Decreased response to stimuli; sleeping even in strange surroundings, but easily roused
Stuporous Noxious stimuli is required to rouse
Comatose No awareness of surroundings, no voluntary responses

What is the content of consciousness?

Term Definition
Confusion Disorientation
Dementia Little awareness of surroundings (fly into walls, etc.)
Delirium Hyperresponsive to stimuli

Cranial nerves

The cranial nerve exam differs little from that of mammals, however there are differences in innervation. As in mammals, menace and pupillary light response (PLR) require use of cranial nerves II (optic) and III (oculomotor), however menace is difficult to interpret in birds. Also, PLR may be overridden in birds due to the presence of striated iridal muscle. Evaluate PLR early in the exam using a sudden, bright light directed toward the medial canthus. Consensual PLR is absent due to complete decussation at the optic chiasm.

Spinal reflexes

Spinal nerves Assessment Comments
Brachial plexus Wing withdrawal Pinch digit → replacement of wing to normal position
Lumbar plexus (located in the cranial renal division) Patellar reflex
Gastrocnemius reflex
Sacral plexus (middle renal division) Leg withdrawal Lower motor neuron (LMN) damage → decreased/ absent withdrawal; Upper motor neuron (UMN) damage → crossed extensor reflex in contralateral leg
Pudendal plexus (caudal renal division) Vent sphincter reflex LMN → flaccid sphincter, cloaca; UMN → hypertonic vent

Cutaneous sensation

Due to the absence of a cutaneous trunci muscle, birds lack a panniculus response. Use feather follicles to assess feeling instead, although location of avian dermatomes has not been described.

Deep pain sensation

Pain fibers are located deepest within the spinal cord, therefore evaluate deep pain only when there are abnormalities of gait, reflexes, or proprioception. Remember that withdrawal alone merely indicates an intact reflex arc; there must be conscious awareness of pain.

Posture and gait

Lower motor neuron (LMN) deficits lead to paresis, reduced or absent spinal reflexes, or flaccidity. Upper motor neuron (UMN) lesions cause increased muscle tone or rigidity distal to the lesion (Fig 1). Generalized weakness or recumbency are non-specific signs that may involve neurologic or metabolic disease. An UMN lesion of the cerebellum or brainstem causes opisthotonus. Lesions of the rostral brainstem cause decerebrate rigidity or extension of all four limbs and trunk.

 

lovebird sternal

Figure 1. Evaluate the neurologic patient for evidence of upper motor or lower motor neuron deficits. Click image to enlarge.

 

Common signs of vestibular disease include head tilt or nystagmus. Loss of balance may manifest as falling, rolling, circling, leaning to one side, or a wide-based stance. Central vestibular disease may also cause abnormal mentation or proprioceptive deficits.

To assess gait, evaluate coordination and strength. Voluntary and involuntary movements require intact cerebral, cerebellar, vestibular, and proprioceptive pathways. Cerebral lesions may disrupt finely tuned movements. The bird may miss perches or be unable to move in certain directions. Cerebral lesions may also cause seizures or muscle tremors. Cerebellar lesions are associated with hypermetria, hypometria, or intention tremors.

Seizures

It is important to control seizure activity since prolonged convulsions may result in permanent deficits.

  1. Administer diazepam intravenously (IV – see Fluid Therapy) if possible at 0.5-1.0 mg/kg.
    1. IV administration is often a challenge, so diazepam may be given intramuscularly (IM) instead. Double the dose if necessary IM.
    2. Cloacal administration takes advantage of transmucosal absorption (double the dose).
    3. Repeat diazepam up to three times or begin constant rate infusion (CRI) IV or intraosseously (IO) at 1.0 mg/kg/hour. Once seizures have ceased for 12-24 hours, taper CRI slowly over another 12-24 hours.
  2. Check blood glucose. If necessary, administer dextrose slow bolus IV or IO.
  3. If cerebral edema is suspected, consider:
    1. Mannitol (0.5-1.0 g/kg IV over 20 minutes)
    2. Short acting corticosteroids
      1. Prednisolone sodium succinate or methylprednisolone sodium succinate (10 mg/kg IV) or
      2. Dexamethasone sodium phosphate (1-2 mg/kg IV)
      3. Do not administer steroids repeatedly as birds are highly susceptible to their immunosuppressive effects.
  4. If diazepam does not control seizures, begin bolus phenobarbital (4.5-6 mg/kg IV) or CRI (2-10 mg/kg/hour). Phenobarbital may be given in conjunction with diazepam.
  5. Monitor for respiratory depression.
  6. If the patient is non-responsive, add dextrose IV or IO. Some small, anorectic birds may become hypoglycemic, however this is relatively rare in adults.
  7. Once seizure activity is controlled:
    1. Determine the underlying cause of seizure activity if possible.
    2. Consider phenobarbital for long-term management. Check blood levels within 2-3 weeks of starting therapy.
    3. Potassium bromide can also be used, however it may take 60-90 days for drug levels to achieve a steady state in the dog. (This has not been confirmed in birds).
    4. Adjust dosages based on blood levels and clinical signs

Important differential diagnoses for seizure activity in the bird include:

  • METABOLIC disease:
    • Renal disease or renal failure may be caused by a variety of problems. Identify the underlying cause, if possible, and provide fluids, histamine blockers, and supportive care. Omega-3 fatty acids and anti-inflammatories may be helpful in chronic renal disease.
    • It is unclear whether or not hepatic encephalopathy truly occurs in birds. Unlike mammals, nitrogenous waste is not the end product of hepatic metabolism. Treat the underlying cause of hepatic disease, and provide fluids, vitamin B, lactulose, and antimicrobials if infectious disease is suspected. Also consider an alcohol-free formulation of milk thistle and/or S-adenosylmethionine.

    • Hypocalcemia is most commonly identified in African grey parrots (Psittacus erithacus), laying hens of any species, or pigeons and doves on a poor diet. In addition to seizures, signs may include muscle fasciculations, pathologic fractures, ataxia, and weakness. In hens, total calcium may be normal therefore ionized calcium levels are most useful. Treat with oral and injectable calcium, vitamin D, and supportive care including nutritional support. Prognosis is good if seizures can be controlled.
    • Hypoglycemia is most common in weaning juveniles, but otherwise rare unless lack of food approaches 24 hours. Blood glucose levels less than 150 mg/dl in a symptomatic bird warrant medical intervention. Give 50% dextrose slow bolus IV using an initial dose of 1 ml/kg, then repeated slowly after reevaluation. If necessary, follow with 5% dextrose CRI until normoglycemia can be maintained. Dextrose may also be gavaged in a 1:1 ratio with lactated Ringers or 0.9% saline. Provide adequate hydration since 50% dextrose is highly hypertonic. Treat the underlying cause of hypoglycemia and begin regular tube feeding of a highly digestible product.
    • Hyperlipemic syndrome is linked to hyperestrogenism in reproductively active hens. Cholesterol and/or triglycerides are consistently elevated. Excess lipid in the bloodstream causes vascular sludging and “lipid emboli”. The blood may become so saturated that it resembles a “strawberry milkshake” or “creamy tomato soup”. Use caution during venipuncture since these birds may have concurrent clotting disorders. Administer diuresis, cholesterol-lowering statin drugs (i.e. gemfibrozil [Lopid®, Pfizer], simvastatin [Zocor®, Merck], colestipol (Cholestipol), and dietary modification as needed. Niacin may be added as well. Leuprolide acetate (Depo Lupron®, TAP Pharmaceuticals) may reduce hormone levels in the acute stage. Treatment may be rewarding, but some deficits such as head tilt may persist.
  • INFLAMMATORY
    • Proventricular dilatation disease is most commonly associated with gastrointestinal (GI) disease, however central nervous system signs may be observed alone or in conjunction with GI disease. Diagnosis is often made post-mortem, and treatment is generally unrewarding, however cyclooxygenase (COX)-inhibitors such as celecoxib (Celebrex®, Pfizer) or meloxicam (Metacam®, Boehringer-Ingelheim) may be beneficial. (Editor’s note: Visit LafeberVet’s Avian Bornavirus Primer for more current information on PDD).
  • INFECTIOUS
    • Psittacosis (Chlamydophila psittaci) infection most commonly affects the liver and/or respiratory tract, however central nervous system disease can occur. Treat with doxycycline or azithromycin (Zithromax®, Pfizer ). Fluoroquinolones may have partial efficacy, but are much less likely to eliminate disease.
  • INFARCT:
    • Although the cause of atherosclerosis is not completely understood, predisposing factors include obesity and high-fat diets. Disease may exist in any species, however atherosclerosis is most common in Amazon parrots (Amazona spp.) and it is occasionally seen in macaws (Ara spp.) and African grey parrots. Cholesterol and triglyceride elevations may or may not be present, and diagnosis is usually made post-mortem. Clinical disease may include cyclical focal or grand mal seizures. Treatment is unrewarding. Seizure activity may appear to respond to therapy, but recur intermittently.
  • TOXIN:
    • Lead toxicity may be associated with seizure activity as well as hematuria in Amazon parrots and conures (Fig. 2), and clenched feet. Metal dense particles may be radiographically evident, but their absence does not rule out lead toxicity. Treatment includes fluids, supportive care, anticonvulsants, chelation with calcium EDTA, dimercaptosuccinic acid (DMSA), or D-penicillamine. Gavage with bulk feeding, peanut butter, and/or psyllium (Metamucil®, Procter & Gamble) to promote elimination of metal from the gastrointestinal tract. Use extreme caution if the patient is regurgitating or vomiting.
Hematuria

Figure 2. Hematuria may be observed in Amazon parrots and conures with lead toxicity. Photograph provided by Dr. Isabelle Langlois. Click image to enlarge.

 

Drug dosages

Drug Dosage Comments
Azithromycin (Zithromax, Pfizer) 40 mg/kg PO q24h x 30 days Treatmentof psittacosis
Calcium EDTA 30-35 mg/kg IM q12h
Calcium glubionate 150 mg/kg PO q12h
Calcium gluconate 5-10 mg/kg SC, IM, slow bolus IV Dilute 1:1 with saline or sterile water
Celecoxib (Celebrex®, Pfizer) 10 mg/kg PO q24h May help to alleviate clinical signs with proventricular dilatation disease
Colestipol (Cholestipol)
D-penicillamine (Cuprimine®, Merck) 30 mg/kg PO q12h x 7 days
Diazepam 0.5-1.0 mg/kg IV
0.5-2.0 mg/kg IM, cloacally
1.0 mg/kg/hour CRI IV
Parenteral or cloacal doses may be repeated up to 3 times
Dextrose, 50% 1 ml/kg slow bolus IV 1:1 ratio with lactated ringers solution or 0.9% saline
Dexamethasone sodium phosphate 1-2 mg/kg IV
Dimercaptosuccinic acid (DMSA) 25-35 mg/kg PO q12h x 5 days per week Administer for 3-5 weeks
Doxycycline 25-50 mg/kg PO q12-24h
Gemfibrozil (Lopid®, Pfizer) 30 mg/kg PO q8h
Lactulose 200 mg/kg (0.3 ml/kg) PO q8-12h
Leuprolide acetate (Depo Lupron®, TAP Pharmaceuticals) 125-250 µg/kg IM q 2-3 weeks
Mannitol 0.5-1.0 g/kg IV Administer over 20 minutes if cerebral edema is suspected
Meloxicam (Metacam®, Boehringer-Ingelheim) 0.5 mg/kg PO, IM q12-24h May help to alleviate clinical signs with proventricular dilatation disease
Methylprednisolone sodium succinate 10 mg/kg IV
Milk thistle 100-150 mg/kg PO divided q8-12h
Niacin 50 mg/kg PO q8h
Omega-3 fatty acids 0.1-0.2 ml/kg PO or added to food Flaxseed oil mixed with corn oil at a ratio of 1:4 provides a ratio of omega-6:omega-3 fatty acids of 4-5:1
Penicillamine —– See D-penicillamine
Phenobarbital 4.5-6 mg/kg IV
2-10 mg/kg/h CRI
Potassium bromide 80 mg/kg PO q24h
Prednisolone sodium succinate 10 mg/kg IV
Psyllium (Metamucil, Proctor & Gamble) 0.5 tsp per 60 ml hand-feeding formula
Silymarin (see Milk thistle) —–
Simvastatin (Zocor®, Merck)
Vitamin B 2 mg/kg IM (thiamine) Dose for vitamin B complex is usually based on thiamine
Vitamin D3 3300 IU/kg q7d

References