The ataxic dog - is it neurological or orthopaedic? - part 2
Alejandro Artiles, DVM
How do I conduct a neurological examination?
The purpose of the neurologic examination is threefold:
• To determine whether or not a patient has a damaged nervous system.
• To neurolocalize - i.e. determine whereabouts the nervous system is altered. Is it central or peripheral? If central: encephalic or medullary? If encephalic: cerebellum or brain stem?
• To perform a differential diagnosis which may indicate which complimentary tests are justified.
The patient's mental state, posture, behaviour and gait should be observed first. The mental state may be normal, or the patient may be depressed, in a stupor or even a coma. Assess the posture of the animal. The most frequent changes are head tilt, neck flexion, or spinal abnormalities (lordosis, kyphosis). Note which limb(s) fail when walking and if the dog walks to one side or circles. An abnormal gait can include:
• Paresis (weakness of voluntary movement): this can affect one limb (monoparesis), front and hindlimbs on one side (hemiparesis), both hindlimbs (paraparesis) or all four (quadraparesis).
• Paralysis (inability to move voluntarily): this can present as mono, hemi, para or quadriplegia.
• Ataxia: this can be proprioceptive (sensory, vestibular or cerebellar:
- Proprioceptive ataxia affects spinal afferent pathways and will involve postural deficits. It often includes UMN signs.
- Vestibular ataxia may present as dizziness, imbalance, or lack of coordination, accompanied by head tilt and/or nystagmus. It may be peripheral or central. The latter is accompanied by proprioceptive deficits and/or involvement of other cranial nerves.
- Cerebellar ataxia presents as a spastic incoordination of gait which usually involves hypermetria without paresis. Other signs of cerebellar dysfunction are intention tremor, threat reflex deficit and abnormal nystagmus.
Alterations of motor pathways can be either UMN or LMN in origin. UMN signs include paresis, normal or hyperactive spinal reflexes, normal or increased muscular tone (Figure 3) and muscular atrophy. LMN signs can include lameness and/or weakness, but in contrast with an orthopaedic lameness, a LMN lesion will show depressed or absent spinal reflexes, loss of muscle tone, paresis or paralysis and neurogenic atrophy (5). Postural reactions and general proprioception should be assessed, as they may detect deficits not shown by gait examination. A proprioceptive deficiency indicates a neurological deficit, although it is a non-specific, non-localizing sign. Postural tests include:
• Proprioceptive test: this requires the patient to weight bear on a knuckled paw. The patient should quickly correct to a normal position.
• Trolley (wheelbarrow) test: this requires the patient to walk in a straight line on its forelimbs, with the hindlimbs lifted.
• Hop test: the patient is held so that body weight is on only one limb, forcing it to hop or walk on that limb.
• Tactile placement test: with the eyes shielded, lift the patient towards the edge of a table; as the back of the paws contact the table the patient should lift its legs to position them on the table.
• Visual placement test: identical to the tactile placement test but the patient is allowed to see the table edge, and should lift its legs as it approaches the table.
• Postural extensor test: raise the patient by the axillae and lower it towards the floor. As the patient approaches the floor, it should progressively extend the hindlimbs.
Not all tests have to be performed; the choice is governed by the neurological status of the patient. If there are no postural deficits and gait is normal, a patient will look neurologically normal (6).
The cranial nerves should also be assessed. Defects in one or more of these nerves will localize lesions to the brain. The clinician is recommended to consult appropriate texts for details of these tests, but special attention should be paid to menace and pupillary reflexes.
Evaluation of spinal reflexes is of vital importance when locating nerve damage. They provide not only information on the reflex arc, but evaluate UMN and LMN function and require only a reflex hammer and artery forceps. With the patient in lateral recumbence and as relaxed as possible the limb reflexes can be assessed. The most important tests are:
• Forelimb: flexor, extensor, carporadial and triceps reflexes.
• Hindlimb: patellar, flexor, cranial tibial and gastrocnemius reflexes.
The perineal and pannicular reflexes should also be assessed. Reflexes may be normal, increased, decreased or absent. Depending on the degree of involvement of these reflexes, we can determine if there is UMN or LMN dysfunction. Reflexes may obviously increase or be absent, but in some cases changes may be quite subtle. Note this examination is done after testing gait and postural reactions; it makes little sense to study reflexes if there is no evidence of proprioceptive, postural or gait deficit. Spinal reflex examination should allow neurolocalization of spinal cord injuries (in the absence of cranial nerve involvement) as follows:
• Ataxia/quadriparesis and UMN signs: C1-C5 lesion.
• Ataxia/quadriparesis, with anterior limb LMN signs and posterior limb UMN signs: C6-T2 lesion.
• Ataxia/paraparesis of posterior limbs with UMN signs: T3-L3 lesion.
• Ataxia/paraparesis of posterior limbs with LMN signs: L4-S1 lesion.
An additional test is also to assess the degree of limb sensitivity, by pressing toes or pads between finger and thumb; if the patient shows no sign of pain use artery forceps to increase pressure. Note that the patient may withdraw the limb without showing head movements, vocalization, pupil dilation or other obvious signs of discomfort; this may only be a reflex arc and does not necessarily indicate conscious sensation. Presence or absence of sensitivity is not a localizing sign, but may help to establish the prognosis (7).
Physical examination will show whether a patient with ataxia and incoordination is an orthopaedic or neurological case. Figure 4 shows how a careful neurological examination can assist localization of the problem. Complementary tests are required for final diagnosis, and may include urine and blood analysis, CSF analysis, radiology, myelography, MRI, CT, EMG, and muscle and nerve biopsies (8). MRI is now the gold standard to detect and characterize morphological and/or structural damage to CNS: cerebrovascular disease (9) (ischemia, stroke…), inflammatory disease (meningitis, encephalitis…), trauma, congenital malformations (hydrocephalus, hydromyelia...), neoplasms, compressive and degenerative disease of the spinal cord and nerve roots, and even neurodegenerative disease (lysosomal storage disease and other metabolic problems (10); the clinician should make an objective choice of diagnostic tests based on a thorough physical examination.
This article was kindly provided by Royal Canin, makers of Mobility diet for dogs and cats. For the full range please visit www.RoyalCanin.co.uk or speak to your Veterinary Business Manager:
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This article was first published in 2011