Posterior Paresis

Posterior paresis is synonymous with rear leg weakness. Generalized weakness in ferrets is often more pronounced in the rear legs and may be mistakenly attributed to primary neurologic disease. A ferret that is weak loses the normal upward arch in its back, so that the long axis of its body becomes parallel to the ground when it is standing or walking.

Ataxia

Ataxia is incoordination; it can be characterized as either cerebellar, vestibular, or proprioceptive. Cerebellar ataxia is caused by a disruption in transmission of sensory impulses from the vestibular system, cerebral cortex, and spinal cord via the cerebellum. Because the cerebellum does not initiate motor activity but rather coordinates it, affected patients will demonstrate abnormal rate, range, or force of movement with intact strength. Paresis is not present with cerebellar dysfunction. Vestibular ataxia occurs when damage or disease affects the vestibular system within the inner ear. Motor activity is not initiated but is refined and coordinated via the vestibular system by controlling muscles used to maintain head position, eye movement, and equilibrium. Dysfunction results in loss of balance; animals often list or fall to one side and may have head tilt. Proprioceptive ataxia is caused by spinal disease, which will result in proprioceptive deficits that can be localized to the affected region of the spinal column. Trauma, intervertebral disk disease, and tumors arising within or compressing the spinal cord or nerves should be considered.³⁵

Seizures

Seizures are a common neurologic presentation in middle-aged and older ferrets. As with paresis and ataxia, the most common cause of seizures is hypoglycemia secondary to insulinoma. Prolonged seizure activity can also result in hypoglycemia. Thus it is important to monitor blood glucose concentration long-term in patients that present with low blood glucose during or shortly after seizure activity. Other potential causes of seizures include toxin ingestion; CNS infection, inflammation, trauma, or neoplasia; and metabolic disturbances such as hepatic or renal failure. Idiopathic epilepsy has not been reported in ferrets.

Diagnosis of Posterior Paresis, Ataxia, and Seizures

Record the medical history and perform a complete physical examination, auscultating carefully for cardiac murmurs or arrhythmias. Ferrets may normally have a respiratory sinus arrhythmia. Palpate for peripheral pulses to evaluate the strength of cardiac contraction and to determine the presence of dropped or extra beats. Check mucous membranes for evidence of cyanosis. Palpate the abdomen carefully to detect discomfort, an abdominal mass, urinary calculi, or a distended urinary bladder. Include evaluation of the spine and neck for pain, fractures, and muscle asymmetry.

Evaluate results of a complete blood count (CBC) and plasma biochemical analysis in any ferret with neurologic signs to rule out a metabolic or infectious component. Check the blood glucose concentration immediately to minimize artifactual decreases caused by faulty sample shipment or failure to separate plasma or serum from red blood cells. Correct any underlying abnormalities and reassess the animal for changes in neurologic status. Perform whole-body radiography and, if you suspect cardiac disease, perform echocardiography.

If you suspect primary neurologic disease, perform a complete neurologic and orthopedic examination³⁵ (Fig. 10-1). Characterize the signs as diffuse or focal, acute or chronic, progressive or static; localize the lesion to areas of brain or spinal cord.²⁷ Evaluate reflexes and palpate for spinal cord pain or hyperesthesia. Keep in mind during examination that the ocular menace response in ferrets is normally diminished or absent.

Fig. 10-1 Neurologic examination checklist for ferrets.

For signs that can be localized to the CNS, perform computed tomography (CT) or magnetic resonance imaging (MRI) if available. Administer an intravenous contrast medium to enhance brain lesions. For CT scanning, use 2.2 mL/kg of 400 mg/mL iodinated contrast medium (iothalamate sodium, Conray 400; Mallinckrodt Inc., St. Louis, MO); for MRI, use 0.2 mL/kg of gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)⁴⁹ (Fig. 10-2).

Fig. 10-2 Magnetic resonance imaging of a ferret with a cervical chordoma of C2-3. The spinal cord is compressed ventrally by the mass (arrow), which also extends into the bones of the skull. A, T1 Saggital view. B, Coronal view. C, Transverse view.

If signs are localized to the spinal column, take spinal radiographs to look for possible fractures or bone abnormalities, such as proliferative or lytic lesions. Myelography is useful for localizing lesions of the spinal cord and determining a site for surgical approach if needed (see Fig. 10-3). If possible, perform a spinal tap to obtain a sample of cerebrospinal fluid (CSF) for analysis. Sites for CSF tap and myelography are the atlanto-occipital and the lumbar (L5-L6) regions. Use a 25-gauge spinal needle, as in canine and feline myelography; a suggested contrast medium is iohexol at 0.25 to 0.5 mL/kg⁵⁰ (Fig. 10-4). Reference values for CSF fluid analysis are total protein 28 to 68 μg/μL and nucleated cells 0 to 8/μL.³⁷ Some spinal lesions may be amenable to surgical resection or stabilization; many, however, carry a poor prognosis.

Fig. 10-3 Normal lateral myelogram of a ferret. Contrast can be seen as two parallel lines along the spinal cord.

Fig.10-4 A, Cerebrospinal tap from the cisterna magna in a ferret. With the ferret in lateral recumbency at the edge of the table, the head is flexed so that the point of the nose is at 90 degrees to the long axis of the body. The wings of the atlas and the point of the occipital condyle are used as landmarks. B, Lumbar cerebrospinal fluid collection at L5-6. Only a few drops can be collected; to maximize the sample, the fluid can be collected directly into a microtainer (C) or hematocrit tube (D).

For clinical signs localized to peripheral nerves or muscular defects, consult with a veterinary neurologist to perform electromyelography (EMG) and nerve conduction velocity (NCV) studies. Although normal values for ferrets have not been published, comparison of values from the contralateral limb (in unilateral disease) or from another, unaffected ferret will aid in interpreting the results. Tensilon testing (edrophonium HCL) and physostigmine testing can be performed in ferrets at standard canine doses (0.1 mg/kg IV).^6,24,38,55 Obtain muscle biopsy samples in the same manner as in dogs and cats when indicated.

Treatment of Posterior Paresis, Ataxia, and Seizures

Treatment of posterior paresis, ataxia, and seizures in ferrets is tailored to the diagnosis. Follow the standard treatment regimens used for dogs and cats in managing a similar condition in a ferret.

In any seizing ferret, the initial treatment must be directed toward arresting seizure activity (Fig. 10-5). Check the blood glucose concentration immediately in any animal presenting with seizures, ataxia, or other neurologic signs. If the glucose level is lower than 60 mg/dL, give an intravenous bolus of 50% dextrose solution (diluted 1:1 in crystalloid fluid) at a dose of 2 to 5 mL/kg or titrate to effect.¹⁰ Begin a dextrose drip infusion adequate to maintain normoglycemia while further diagnostic testing is done. Some ferrets require as much as 10% dextrose added to intravenous fluids to achieve normoglycemia. Administer prednisone or prednisolone to hypoglycemic patients to enhance hepatic gluconeogenesis and inhibit glycogenolysis. If an insulinoma is suspected, initiate additional therapy as indicated (see Chapter 8).

Fig. 10-5 Treatment of seizures in ferrets. IV, Intravenous; CRI, continuous rate infusion.

If seizures persist and the blood glucose concentration is normal (or has been restored to normal), begin aggressive seizure management. Administer diazepam (0.5-1.0 mg/kg) intravenously^10,24,38; if venous access is not readily available, administer diazepam or midazolam intramuscularly, intranasally (for more rapid absorption), or rectally. Double the dose for rectal or nasal administration.²⁴ Repeat up to three times to arrest seizure activity. If grand mal or focal seizures persist, begin a constant-rate infusion of diazepam (0.1-1.0 mg/kg per hour added to IV fluids) or initiate phenobarbital (2-10 mg/kg per hour) as a constant rate infusion.³⁸ Phenobarbital can also be administered by bolus; use 3 mg/kg slow IV q30-60min up to a total dose of 18 to 24 mg/kg, then 3 to 5 mg/kg q12h.²⁴ Phenobarbital and diazepam can be administered concurrently.³⁸ Propofol can also be added; administer in aliquots of 2 mg/kg to effect, then 6 mg/kg per hour CRI to effect.²⁴ If cerebral edema is suspected, administer dexamethasone (0.2 mg/kg) or prednisone or prednisolone (1 mg/kg IV) and mannitol (0.5-1.0 g/kg IV over 20 minutes).^36,38 Once no seizures have occurred for 12 to 24 hours, taper the diazepam infusion slowly over the next 12 to 24 hours. Once seizures are controlled, use oral phenobarbital (1-2 mg/kg PO q8-12h) if necessary for long-term seizure management.³⁸ Potassium bromide can also be used for seizure control; administer orally at 70 to 80 mg/kg per day if used alone or at 22 to 30 mg/kg per day in combination with phenobarbital.³⁸ Check blood levels of phenobarbital within 2 to 3 weeks after starting therapy; potassium bromide levels may not reach a steady state for 60 to 90 days. Adjust dosages based on blood levels and clinical signs. The use of gabapetin, zonisamide, or levetiracetam has not been described in ferrets to date. Investigate any underlying disease stimulating the seizure activity after the patient is stable.

Physical therapy is an important but often overlooked adjunct treatment. For ferrets with paresis or paralysis and those debilitated or recumbent from seizures or metabolic disorders, begin passive range-of-motion exercises three to four times daily for affected limbs. This is essential to prevent contracture. Gently massage muscles to enhance blood flow. Implement active exercise as early as possible to preserve muscle tone and stimulate neural return.