Posture, gait and reflexes in small animals

Cranial nerves III, IV and VI – oculomotor, trochlear and abducens nerves

The oculomotor, trochlear and abducens nerves are motor nerves responsible for the innervation of eye movements.

The abducens nerve controls globe retraction. The oculo-motor nerve also mediates pupillary constriction in the pupillary light reflex. Therefore, mydriasis (pupil dilation) may indicate occulomotor nerve damage.

Abnormalities of the occulomotor, trochlear and abducens nerves are seen primarily as strabismus (abnormal eye position). This can be assessed by ensuring the animal is able to position its eyes appropriately when its head is raised and lowered and moved from side to side.

Cranial nerve V – trigeminal nerve

The trigeminal nerve provides sensory innervation to the face and motor innervation to muscles of mastication. The temporalis and masseter muscles are palpated for asymmetry and atrophy. Bilateral weakness of masticatory muscles may result in an inability to close the mouth.

There are three sensory branches of the trigeminal nerve:

ophthalmic, maxillary and mandibular, that can be inde-pendently assessed:

1. Palpebral reflex elicits a blink reflex, which is mediated by the ophthalmic branch of trigeminal nerve.

2. Touching or pinching the upper lip lateral to the canine tooth in small animals results in wrinkling of face and blinking which is mediated by the maxillary branch of the trigeminal.

3. Touching or pinching the lower lip lateral to the canine tooth in small animals results in wrinkling of the face and blinking which is mediated by the mandibular branch of the trigeminal nerve.

To elicit the same response as (2) and (3) in horses, closed haemostats may be used to tap the face to produce a twitch response, often accompanied by a head nod. It is also important in cases where forebrain disease is suspected to determine that an appropriate behavioural response accompanies the local twitch response. To elicit more of a behavioural response the haemostats can be used to probe the sensitive nasal septum bilaterally.

Cranial nerve VII – facial nerve

The facial nerve provides motor innervation to the muscles of facial expression and also parasympathetic innervation of the salivary and lacrimal glands. The facial nerve is assessed by examining for facial asymmetry such as lago-phthalmus, flaccid facial features and/or lips and/or abnormal ear carriage.

In the horse, motor control of the face is assessed at the nostrils where any asymmetry will be most evident and may be the only area affected in distal lesions. The eyelids or strength of eyelid closure may be palpated when trying to determine if the eyes are also involved in more proximally

located lesions. Lesions that occur close to the exit of the facial nerve from the cranium will involve the auricular branch and the affected side will show an ear droop.

Cranial nerve VIII – vestibulocochlear nerve

The vestibulocochlear nerve provides sensory innervation for hearing and vestibular function. Hearing can be tested by evaluating the response to loud noise; however, this does not differentiate between unilateral hearing loss and normal hearing. Vestibular dysfunction includes head tilt, abnormal nystagmus (abnormal rhythmical eye move-ments) and an ataxic, broad-based stance.

In horses, the vestibular part of this nerve may be assessed using either a blindfold (Figure 7.3a & b) or moving the horse from the light into a darkened area (e.g. stable), which will accentuate any head tilt (as well as nystagmus and ataxia).

Cranial nerves IX and X – glossopharyngeal and vagus nerves

The glossopharyngeal and vagus nerves provide sensory and motor innervation to the pharynx. The vagus nerve also controls laryngeal function. The gag reflex is elicited by touching left and right sides of the caudal pharyngeal wall in small animals, and observing elevation of soft palate and contraction of pharyngeal muscles. An asymmetric response is more significant than bilateral loss of gag reflex.

Dysphagia, regurgitation, voice change and inspiratory stridor are other signs of nerve dysfunction.

Cranial nerve XI – accessory nerve

The accessory nerve provides motor innervation to the trapezius muscle. Muscle atrophy will be evident in acces-sory nerve lesions, although this may be difficult to assess.

Cranial nerve XII – hypoglossal nerve

The hypoglossal nerve provides motor innervation to the muscles of the tongue. The tongue is inspected for atrophy, asymmetry or deviation. Animals will usually lick their nose after finishing the gag reflex if the hypoglossal nerve is intact. Unilateral loss of innervation may result in the inability to lick one side of the nose or face.

In the horse, assessing the gag reflex is not possible with-out an endoscope. To assess pharyngeal function (as well as tongue tone and symmetry) a hand is placed into the horse’s mouth at the diastema, the tongue palpated, then gently retracted out of the side of the mouth, then released.

Normal horses should replace their tongue quickly and most swallow on replacing their tongue.

Specific tests of neurological function include:

Posture

Posture should initially be assessed while the animal is free to move in the consulting room. Abnormalities that may be noted include head tilt, abnormal truncal posture, improper limb positioning (conscious proprioception), and decreased or increased muscle tone.

Gait

Gait should be assessed on a firm, non-slippery surface, observe the animal walking from the side, behind and moving away and toward the examiner.

Conscious proprioception

Indication of deficits include knuckling, foot misplacement and scuffing of toenails while walking as well as an inability to right the foot when placed over on the knuckles (Figure 7.4).

Ataxia

Ataxia while walking is characteristic of neurological, but not necessarily spinal, disorders. There may be lack of co-ordination with or without spastic, paretic or involuntary movements.

Palpation

Palpation is important to assess the musculoskeletal system and integument. It is important to compare symmetry between sides.

7.4.1 Postural and proprioceptive assessment Proprioceptive positioning

If the dorsum of the paw is placed on the floor, the paw should be immediately returned to a normal position.

Delayed (>1 second) or absent conscious proprioception indicates neurological disease.

Figure 7.3 (a) A horse with a mild head tilt and facial nerve paralysis includ-ing an ear droop on the left side; (b) with the head tilt worsened by applyinclud-ing a towel as a blindfold.

Figure 7.4 A 6-year-old Alaskan Malamute with a right hind conscious proprioceptive deficit.

(a)

(b)

Movement

Determine if the animal is ambulatory, weakly ambulatory or non-ambulatory. Assistance may be required in weak animals. The absence of voluntary movement indicates severe but not irreversible disease.

Wheel-barrowing

When wheel-barrowing the animal is supported under the abdomen with weight bearing on the forelimbs. A normal animal will walk forward with coordinated forelimb move-ment. Slow initiation may indicate a lesion in the cervical spinal cord, brainstem or cerebral cortex. Exaggerated movement may indicate a lesion in the cervical spinal cord, lower brainstem or cerebellum.

Hopping

The animal is supported as per wheel-barrowing but weight bearing on one leg. The animal is moved lateral and medial.

Poor initiation of movement suggests a conscious pro-prioception deficit and poor movement suggests a motor deficit. Asymmetry may assist in lateralising the defect.

Extensor postural thrust

The animal is supported under the thorax and lowered to the floor. The pelvic limbs should move caudally with sym-metric walking movements. Slow initiation may indicate a lesion in the spinal cord, brainstem or cerebral cortex.

Exaggerated movement may indicate a lesion in the spinal cord, lower brainstem or cerebellum.

Hemistanding and hemiwalking

The front and rear limbs are elevated on one side and lateral walking movements assessed. Slow initiation may indicate a lesion in the spinal cord, brainstem or cerebral cortex.

Exaggerated movements may indicate a lesion in the spinal cord, lower brainstem or cerebellum.

Placing reactions

It is important to assess tactile placing and then visual placing.

With tactile placing the animal is supported under the thorax and eyes covered as limbs touch a table edge. A normal response is to immediately place the feet on the table for positional support. Visual placing is the same except the animal is allowed to visualise the table edge.

Visual placing requires visual pathways to the cerebral cortex, communication from the visual cortex to the motor cortex and motor pathways to the peripheral nerves of the forelimbs.

7.4.2 Spinal reflexes (or myotactic reflexes) Myotactic reflexes test the integrity of sensory and motor components of the reflex arc and the influence of the descending motor pathways on this arc.

There are three possible responses:

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Absent or depressed reflex due to complete or partial loss of either sensory or motor component of the reflex arc, this is described as a LMN response

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Normal reflex

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Exaggerated reflex due to an abnormality in the descend-ing pathway from brain to spinal cord, this is described as an UMN response

Forelimb reflexes Triceps reflex

The animal is placed in lateral recumbency with the upper-most leg supported under the elbow. The triceps tendon is struck with a reflex hammer just proximal to the olecranon.

A normal response is slight extension of the elbow. The triceps reflex is innervated by the radial nerve originating from spinal cord segments C7–T1. An absent or depressed response should not be interpreted as abnormal. Exagger-ated response indicates a lesion cranial to C7.

Biceps reflex

The animal is placed in lateral recumbency with the elbow slightly extended. A reflex hammer is struck on a finger placed over biceps tendon just proximal to the elbow.

A normal response is slight flexion of the elbow. The biceps reflex is innervated by the musculocutaneous nerve and spinal cord segments C6 – C8. Absent or depressed responses should not be interpreted as abnormal. An exag-gerated response indicates a lesion cranial to C6.

Thoracic limb withdrawal reflex

The animal is placed in lateral recumbency and mild noxious stimuli inflicted on the foot. A normal response is flexion of the entire limb. Thoracic limb withdrawal reflex primarily involves the spinal cord segments C6–T1.

Absent or depressed responses indicate a lesion of either spinal cord segments or peripheral nerves. An exaggerated response indicates a lesion cranial to C6.

Extensor carpi radialis reflex

The animal is placed in lateral recumbency with the elbow supported and flexed and carpus flexed. The proximal belly of the extensor carpi radialis muscle is tapped with the tendon hammer. A normal response is mild extension of the carpus. The extensor carpi radialis reflex innervated by the radial nerve and spinal cord segments C7–T1.

Hindlimb reflexes Patella reflex

The animal is placed in lateral recumbency with the affected leg uppermost and supported underneath the limb. The patella tendon is struck with a reflex hammer (Figure 7.5).

A normal response is a single, quick extension of the stifle. A unilateral loss suggests a peripheral nerve lesion (femoral

anal sphincter muscle. The sensory and motor innervation is via the pudendal nerve and spinal cord segments S1–S3.

An absent or depressed response indicates a lesion in the sacral spinal cord or pudendal nerve.

Crossed extensor reflex

This reflex is observed during withdrawal reflexes of either the pelvic or thoracic limbs. Toe pinching of one limb results in flexion of that limb and extension of the contralateral limb. A crossed extensor reflex is caused by a lesion affecting descending inhibitory pathways UMN and is suggestive of severity or chronicity.

The Schiff–Sherrington phenomenon

This phenomenon is usually an indication of severe spinal cord injury. The Schiff–Sherrington reflex is caused by loss of ascending inhibition from pelvic limbs resulting in fore-limb and neck hypertonicity. The postural reactions and reflexes of the thoracic limb are otherwise normal.

7.4.3 Urinary bladder innervation

The bladder is innervated by both autonomic (hypogastric and pelvic) and somatic (pudendal) nerves. The pudendal nerve innervates the striated muscle of the urethra and maintains urinary continence. A lesion above S2–S3 will cause spasm of bladder outflow and difficulty in expression of the bladder UMN. A lesion below S2–S3 will cause lack of sphincter tone and an easily expressible bladder LMN. In general a LMN bladder carries a worse prognosis.

7.4.4 Pain perception

Pain perception provides important prognostic informa-tion and is the last test to be performed in a neurological examination. A painful stimulus is applied to each foot and the tail. Perception of pain is indicated by a significant behavioural response (i.e. turns and looks, vocalises or attempts to bite). Progressively stronger painful stimuli may be applied to assess presence of deep pain sensation.

Deep pain perception may be modified by temperament, drugs, pain threshold and experience. The absence of deep pain is a poor prognostic sign.

Hyperpathic level

Pressure is applied to the spinous processes and paraspinal muscles of the thoracic and lumbar region and transverse processes and paraspinal muscles of the cervical region. In-creased sensitivity may occur at the level of spinal cord disease.

7.4.5 Interpretation of gait posture and reflex abnormalities in small animals – spinal lesions (Table 7.3)

Spinal cord injury results in loss of function in the following order:

1. Conscious proprioception 2. Voluntary motor function nerve). Bilateral loss suggests a segmental spinal cord lesion

L4–L6. An exaggerated response suggests a lesion cranial to L4.

Pelvic withdrawal reflex

The animal is placed in lateral recumbency and mild nox-ious stimuli inflicted on the foot. A normal response is flexion of the entire limb. Spinal cord segment L6 – S1 and the sciatic nerve are in the withdrawal reflex arc. Unilateral loss suggests a peripheral nerve lesion (sciatic nerve).

Bilateral loss suggests a segmental spinal cord lesion L6–S1.

An exaggerated response suggests a lesion cranial to L6.

Sciatic reflex

The animal is placed in lateral recumbency with uppermost leg supported under the stifle and extended. A reflex ham-mer is tapped between greater trochanter and ischiatic notch.

A normal response is a flexion of the stifle and hock.

Gastrocnemius reflex

The animal is placed in lateral recumbency and the tendon of insertion of the gastrocnemius is struck dorsal to the hock. A normal response is extension of the hock. The gastrocnemius reflex is innervated by the tibial branch of the sciatic nerve and L7–S1 spinal cord segments.

Panniculus or cutaneous trunci reflex

A pinprick stimulus is applied to the skin of the back begin-ning from L5 and progressing cranially. Both left and right sides are assessed. A normal response is unilateral twitching of the cutaneous trunci muscle at the point of stimulation and cranial. An absence of response suggests a lesion 1–2 segments cranially. This reflex is not always reliable.

Perineal or anal sphincter reflex

Gentle stimulation is applied to the perineal area with a needle or forceps. A normal response is contraction of the

Figure 7.5 Patella (femoral nerve) reflex being assessed on a dog.

3. Superficial pain 4. Deep pain

Return of function following spinal cord injury is in the reverse order and, roughly, in a similar time frame to loss of function. That is, a Dachshund with Type I IVDD that loses voluntary motor function in 6 hours will, with decompres-sive surgery often be ambulatory in 24 hours, whereas a German Shepherd with chronic Type II IVDD that has 6 months of deterioration before becoming non-ambulatory may not walk again.

Aetiology of spinal cord lesions may be assessed on the basis of history of pain and paresis.

1. Acute and static:

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Vascular (e.g. fibrocartilaginous embolism (FCE) or infarction)

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Trauma (e.g. fracture–luxation)

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Degenerative (e.g. type I IVDD) 2. Acute and progressive:

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Degenerative (e.g. type I IVDD)

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Inflammatory (e.g. discospondylitis and vertebral osteomyelitis)

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Trauma (e.g. fracture–luxation)

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Anomalous (e.g. atlantoaxial subluxation) and tumour

3. Chronic and progressive:

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Degenerative (e.g. type I and II IVDD, cauda equina syndrome, caudal cervical spondylomyelopathy or degenerative myelopathy)

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Inflammatory (e.g. discospondylitis and vertebral osteomyelitis)

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Neoplasia of the meninges or spinal cord

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