Proceedings of the 11th International Congress of the ...

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Proceedings of the 11th International
Congress of the World

Equine Veterinary Association

24 – 27 September 2009

Guarujá, SP, Brazil

Next Meeting :
Nov. 2 -6, 2011 - Hyderabad, India

Reprinted in IVIS with the Permission of the Meeting Organizers

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Equine Neurologic Examination - What Do I Really Look For?
Joe Mayhew

Massey University
NEW ZEALAND
[email protected]

A description of all the manipulations that can be performed, and observations that can be made, when
undertaking a neurologic examination often doesn’t give the sense of efficiency and flow that is necessary to
effectively perform such examinations in practice. This presentation aims to assist the practitioner to develop
a flow to the equine neurologic examination without detracting from the clinical dictum that “it is easy to
look, but harder to see”; one has to know what one is looking for.

A. OVERVIEW
Traditionally, a detailed neurologic examination follows the collection of information on a patient’s

signalment and history, an evaluation of the environment, and a complete physical examination 1-10.
However, during evaluation of a horse suspected of having a neurologic disorder, most busy practitioners
include several components of a neurologic examination during the general physical examination. These
should include observation of behavior, mental status, head posture, vision, pupillary light reflexes,
structures of the eye, and inspection for facial symmetry, and inspection of the oral cavity. A laryngeal
adductor response or slap-test should be performed and evaluation of posture and gait while walking,
trotting, and turning quickly ought to be included. Inspection and palpation for muscle mass, bony integrity,
and patches of sweating over the body and limbs (horse) are also easily incorporated into this examination.
Tail and anal tone and reflexes can be evaluated when the rectal temperature is recorded.

Usually, this examination [Table 1] allows the practitioner to decide whether a more detailed
neurologic examination, as outlined below, is required.

Sometimes enough evidence is available from this examination alone to make a fairly accurate
anatomic diagnosis. Thus, a differential diagnosis and initial plan can be developed. If this cannot be
done, especially if a thorough case work-up is indicated, then a complete neurologic examination
should be undertaken, which will probably uncover further neurologic findings helpful to case work-up.

B. SIGNALMENT
The age, breed, gender, use, and value of a patient all are important considerations in the diagnosis and

prognosis of many neurologic conditions. Several diseases are age-dependent. Certain diseases are
associated with particular breeds. Only a few neurologic diseases depend upon gender. Certain uses to which
animals are put can be associated with certain diseases, and this impacts considerably on the prognosis that
accompanies the diagnosis. The value of the patient must always be kept in mind with respect to the depth of
evaluation, cost of therapy, and future performance and productivity; the survival of herd mates must also be
considered.

C. HISTORY
In addition to taking a general history of the patient, questioning of the client should focus on the

primary complaint. Information concerning the precise circumstances of the environment, other animal
contacts, and the nature of the first signs observed ought to be sought first. Further questioning is aimed at
defining a relationship between the severity of the syndrome and the passage of time.

Most congenital and familial diseases begin early in life and signs usually progress relentlessly.
Syndromes resulting from physical causes, particularly external injury, have a sudden onset and then often
stabilize or improve. Signs caused by infectious agents can be acute or chronic, and frequently fluctuate in
severity. Immune-mediated diseases often result in fulminant signs that can improve dramatically,

Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil

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particularly with therapy. Progression of metabolic, toxic, and nutritional disorders is variable. Finally, signs
due to neoplastic involvement of the nervous system may begin abruptly, but most often are progressive.

Historical data can give clues as to how widespread or focal the disease process is in the nervous
system, whether there was evidence of asymmetry, and how severe the signs have been. These aspects of
pathogenesis of diseases can also be helpful in the etiologic diagnosis.

D. PROCEDURE FOR THE NEUROLOGIC EXAMINATION
The primary aim of a neurologic examination is to confirm whether or not a neurologic abnormality

exists. Because omission of parts is the most common mistake made during the neurologic examination, the
order in which the examination is performed becomes important. I give here a precise practical format that is
logical in sequence, easy to remember with practice, and emphasizes the need for an anatomic diagnosis
[Where is the lesion?] to be made before an etiologic diagnosis [What is the cause of the condition?] is
made. The rationale for the sequence of this examination is: firstly, it starts at the head and proceeds
caudally to the tail; secondly, it is used for patients of all sizes and whether the patient is ambulatory or
recumbent; thirdly, it considers the anatomic location of lesions as the examination proceeds. Even if parts
of the examination must be omitted because of the nature of the patient, suspicion of fracture, or financial
constraints, the sequence ought to be followed through mentally. Frequently, the presence of a neurologic
lesion[s] cannot be deduced until the end of a thorough neurologic examination.

An outline of the recommended format for neurologic examination of horses is given in Table 2 and an
example of a recording form to record the results of the neurologic examination is given in Figure 1. Some
comment as to differences important to recall when evaluating neonates also are indicated.

I encourage those readers who are not reasonably well practiced in performing neurologic
examinations, and in recording the variety of responses obtained with direct observations, reflex testing and
response induction in normal patients, to practice on a friendly, neighborhood, mid-sized dog. The approach
for such an examination will be used for young foals and miniature horses. Should the practice dog or such
patient be small enough, the close aspects of the procedure used are readily performed by sitting with the
patient on one’s knees or standing above and behind the patient for restraint and comfort.

Below is given an overview of the practicalities of performing an efficient neurologic examination.
This is then followed by interpreting the findings to determine the presence, site(s) and extent of any
neurologic lesion.

1. Head
For the routine equine examination, I evaluate what I can from a distance, preferably before the patient

is disturbed, for the first observations of behavior, mentation and head, neck, trunk and limbs. Head and
neck deviations need to be assessed closely by straightening the neck along the midline to determine what
asymmetry may be present. I allow the patient to smell my [often peppermint-tainted] hand for introduction
and observe the face, particularly eyes and associated structures, for an expressional response. Then I
examine the parts of the head and neck for evaluation of cranial nerve function [Table 3].

At this stage I will make sure I have the patient’s attention by tapping lightly once or twice above the
eye with my finger tips on a cupped hand to induce a combined visual and facial response of palpebral
closure, proceeding to a menace response [Figure 2] from nasal and temporal fields.

This is followed by observation of eye position and pupil size and symmetry using a bright pen torch
from 12-24 inches. Swinging the light quickly from the fundus of one eye to the other and pausing for about
3s at each pupillary aperture as the light source is brought closer in front of each eye, allows the immediate
pupillary response to be observed, unencumbered by blinking. Any asymmetry or suspected deficit means
that a dazzle response must be performed and the tests need to be reperformed in dim and bright light, but
not direct sunlight. With practice, the central fundus and optic disc can be directly inspected by looking
directly along the shaft of light from a pen torch; otherwise an ophthalmoscope should be used. Evidence of

Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil

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optic atrophy, peripapillary retinal lesions, globe position and trembling and ataxic eye movements and
nystagmus all can all be detected.

Eyeball position in the bony orbit, along with the size of the palpebral aperture and angle of the dorsal
eyelashes then can be determined and both ventral movement and induced, normal, horizontal nystagmus of
the globe then can be evaluated by first slowly raising the mandible to horizontal and then rotating the head
to both sides through an arc of 60-90 degrees. Facial symmetry, reflexes, movement and especially muscle
tone, all can then be observed as well as the bulk of the temporalis [Figure 3], masseter and pterygoid
muscles being compared. During facial reflex testing with a blunt pair of needle holders sensation in the
form of cerebral perception and resentment is evaluated from the nasal septum on each side. During this
testing, any increased temperature and presence of sweat at the base of an ear will be evident. Nasal, oral,
laryngeal, pharyngeal and hyoid region inspection and particularly palpation are performed and the
thoracolaryngeal responses felt for.

2. Body
a. Neck & Thoracic Limbs
Attention is immediately moved to the neck where bone and muscle symmetry is assessed by close

palpation and the local cervical and cervico-facial responses seen and felt. A solid blunt instrument such as
6-12 inch artery forceps or needle holders are best for performing this and other cutaneous testing although
on occasion, with a very frightened patient, the tip of a rigid index finger may have to suffice as being more
tolerated. A very firm vertical stimulus is required to be applied over sites at the level of and 10-15cm dorsal
to the articular processes of cervical vertebrae.

b. Trunk & Pelvic Limbs
Testing can continue caudally to transfer to the thorax testing the cutaneous trunci reflex over the mid
third of the lateral thorax, again with forceful stimuli. There is a variable region over the point of the
shoulder, about the C7-T3 dermatomal region, where neither responses are obtained and the cutaneous trunci
reflex usually fades in the caudal thoracic region. Flexion, extension and lateral bending of the
thoracolumbosacral vertebral column then is conveniently tested with the instrument used to firmly stroke
the lateral dorsum from the withers to the caudal gluteal region. Two-pinch technique is used to test dorsal
dermatomes and limb autonomous zones for areas of hypalgesia if there is any evidence whatsoever of a
reflex or lower motor neuron spinal cord lesion. Regional loss of muscle bulk, bony asymmetry and areas of
sweating also should invoke detailed scrutiny.

c. Rectum, Bladder, Anus, Tail
Coccygeal extension and flexion is evaluated during anal reflex and perineal sensory testing. A strong,
blunt-probe stimulus applied to the anal ring results in its brisk contraction and flexion [clamping] of the tail,
whereas a light stimulus results in an anal reflex and with a stroking stimulus results in tail extension.

3. Gait & Posture
The minimal components of evaluation of posture and gait consist of the following.
 Walking in straight line viewed from the side as well as from behind and in front.
 Pulling laterally on the tail with the patient standing still and while walking forward, assessing
stride length and trajectory and placement of all four limbs.
 Trotting away from and back toward the examiner.
 Watching the patient walking in circles and turning tightly in circles in both directions.
 Taking the patient oneself and by walking backwards lead the patient in a serpentine path to
observe limb placement and lead in a manner such that the direction of each forefoot in turn is
required to change direction during its swing phases.

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 Leading the patient to walk in circles and to turn tightly in circles in both directions, continuing
these maneuvers while pulling on the lead rope and the tail simultaneously assessing strength of
resistance.

 Releasing the tail abruptly and stopping turning tightly to observe for adoption of and standing
with abnormal limb positions. Manually placing the limbs in abnormal positions and placing them
with the dorsum of the hoof resting on the ground are not useful in detecting neurologic motor or
proprioceptive abnormalities.

 Hopping the patient on at least the thoracic limbs [Figure 4].

Defining the presence and severity of gait and postural abnormalities Table 4], along with an
interpretation of evidence of upper and lower motor neuron abnormal reflexes and function [Table 5] can
assist in determining the site(s) of lesions in the nervous system.

A patient that is or can be placed in recumbency can be tested for classical limb reflexes. In practical
terms these simply consist of the flexor reflexes in thoracic and pelvic limbs and the extensor or patellar
reflex in the pelvic limbs. A reflex is regarded as present or hyperactive in a limb if such a response is
detected in the recumbent while the limb is uppermost OR is dependent. All other reflex testing really does
not usefully contribute to a neuroanatomic diagnosis and results of such additional limb reflex testing should
not be used to alter a neuroanatomic diagnosis achieved by interpretation of the remainder of the
examination.

At the conclusion of the gait evaluation, any issue that is unclear can be returned to for further
evaluation and confirmation, and further testing can be considered as appropriate. This will frequently
include reassessing the menace and pupillary responses and nasal septal sensation, observing the patient for
facial weakness and head deviation while it is resting quietly and undisturbed, blindfolding and, for the
smaller patients, hemi-walking, hoping on pelvic limbs, wheel barrowing on thoracic limbs with head and
neck held extended.

For documentation, further study and possible consultation purposes, taking a video of any possible
neurologic signs displayed by a patient is worth considering. It must be recalled however that a badly
produced video clip is likely to be worse than a verbal or written description. At best, video sequences of
neurologic movement abnormalities, particularly involving the gait, are less precise and accurate than in real
life.

E. FINAL INTERPRETATION; WHERE AND WHAT IS THE LESION?
Results of the neurologic examination should be documented and not left to memory [Figure 1].
After completion of the neurologic examination, the examiner may be able to decide if and where any

possible lesion exists. Sites include the basic areas of the:
1. Cerebrum
2. Brain stem
3. Peripheral cranial nerves
4. Cerebellum
5. Spinal cord
6. Peripheral spinal nerves
7. Neuromuscular junctions
8. Muscles
9. Autonomic nervous system
Often the exact location of a lesion or lesions within these divisions will be able to be defined more

precisely. If the location of a lesion is not clear, then it is often worthwhile returning to the patient and
performing an even more critical evaluation. Thus if facial weakness is suspected but not clearly seen the
examiner can return to observe the horse for facial asymmetry while it is standing quietly in its stall without any

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stimulation. Also, a blindfold may be applied to exaggerate evidence of vestibular disease. Finally, a very
fractious or a very excited horse suspected of having a degree of weakness in the limbs may be exercised before
a re-evaluation for evidence of weakness is made.

The presence of lameness can undoubtedly interfere with the interpretation of a horse’s gait and posture.
If this is suspected then appropriate regional analgesia or the use of short acting synthetic opioid drugs
(analgesics) may help to resolve the matter. With more chronic lameness cases, non steroidal anti-inflammatory
drugs may be given at relatively high doses for several days or weeks, the horse’s gait can then be re-evaluated
when any confounding lameness will have been reduced or eliminated.

At some time or other, all equine clinicians will come across cases that have some indication of a
morbid nervous system lesion but no definitive proof can be obtained. Often, such cases are suspected to be
suffering from conditions such as a painful musculoskeletal disorder, a peripheral neuromuscular movement
disorder, a behavioural problem such as belligerency or laziness or back disease. Such patients may show
one or more of the signs listed in Table 6. Examples of other forms of frantic behavior have been associated
with a strong suspicion of exposure to nettles or poison ants, but in these situations the signs usually abate
with time. A few of these unusual syndromes are discussed in latter sections.

F. INITIAL PLAN
Following consideration of anatomic and etiologic diagnoses, an initial plan must be devised. This will

include use of ancillary aids to help rule in and rule out certain disease processes, a therapeutic plan, and a
plan for client education, including economic advice, herd health management, and prognostic
considerations.

REFERENCES

1. de Lahunta A. Veterinary Neuroanatomy and Clinical Neurology. 2nd ed. W.B. Saunders Company. 1983.
2. Oliver JE, Hoerlein BF and Mayhew IG. Veterinary Neurology. WB Saunders. 1987; 7-56.
3. Palmer AC. Introduction to Animal Neurology. 2nd Ed ed. Blackwell Scientific Publications. 1976; 91-113.
4. Reed SM, Bayly WM and Sellon DC. Equine Internal Medicine. 2nd ed. W. B. Saunders. 2004; 1680.
5. Reed SM, Saville WJ and Schneider RK. Neurologic Disease: Current Topics In-Depth. 49th Ann Conv Amer Assoc Equine

Pract; 2003.
6. Ronéus M and Gustafsson K. Use of neurologic examination with focus on aetiologies in horses. 2000, SVA: Bålsta. 173-185.
7. Blythe LL and Engel HN. Back problems. Neuroanatomy and neurological examination. Vet Clin North Am Equine Pract

1999; 15:71-85, vi.
8. Adams R and Mayhew IG. Neurologic diseases. Vet Clin North Am Equine Pract 1985; 1:209-234.
9. Furr M and Reed SM. eds. Equine Neurology. 2008, Blackwell. 412
10. Mayhew IG. Large Animal Neurology. 2nd ed. Wiley-Blackwell. 2008.

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TABLE 1: Neurologic tests and criteria evaluated in a physical examination.

Mental attitude / awareness Symmetry of neck, trunk and limbs
Normal behavior patterns Tail and anal tone
Menace tests Anal reflex
Pupillary light reflexes Rectal examination
Funduscopic examination Postures adopted at rest
Symmetry of parts of the head Gait at walk and trot
Inspection of the tongue Gait while turning
Absence of nasal discharge Faster gaits
External thoracolaryngeal (slap) reflex

TABLE 2: Outline of recommended format for the neurologic examination.

Region Evaluation Division General Comment Neonate
Forebrain History important Adjustment over 2-7 days
Head Behavior Seizures; especially mild and focal
Thalamus Response to environment Adjustment - 24 hours
Mentation / Sensorium Cerebrum
Midbrain Head tilt verses head turn Flexed head posture
Head Posture & Movement Physical causes Jerky movements
Forebrain – turn Evaluate regions of head
Cranial Nerves Vestibular – tilt Subtle asymmetry in menace Menace deficit <7 days
Body Neck & Forelimbs Tremor – check eyeballs response & nasal sensation Eye posture
CN II - XII Particularly asymmetry
Trunk & Hindlimbs Brainstem Flexor reflex only All reflexes
Cervical sympathetic supply Hopping Hyperreflexia
Gait Rectum, Bladder, Anus, C1-T2 Particularly asymmetry Crossed extension
& Perineum Flexor & patellar reflexes only All reflexes
Tail T3-S2 Hyperreflexia
Posture ORTHOPEDIC L4 – femoral n. S1-2 is common fracture site Crossed extension
PROBLEMS! L5 – cranial gluteal n. Extensor thrust
Extension & flexion
Positional deficits S1-5 Shoulder & gluteal atrophy SEPSIS!
Extensor weakness common
Flexor weakness Co1- Possible analgesic trial Prematurity
Ataxia Placing feet non-contributory Dominant extensor strength
All CNS-PNS Especially LMN
Brain stem, spinal cord, PNS Normal to degree
Brain stem, spinal cord, PNS Irregular position & placement Wide based to degree
Spinal ataxia Hypermetria characteristic; F > H
Cerebellar ataxia Crouched posture
Vestibular gait Deliberate [predictable] stepping
Wide based, staggering gait

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FIGURE 1 NEUROLOGICAL EVALUATION

Massey University -- Veterinary Teaching Hospital – IVABS

Case No. ………………………………. HISTORY:
Owner's Name:…………………………..
Tel. No: ……………………......…………. PHYSICAL EXAMINATION:
Animal's Name…………………………… Head Posture [tilt, turn]
Species……………………………………
Breed……………………………………
Ref. Vet. ………………………………….
VTH Clinician…………………………….

*********Affix label here**********

NEUROLOGICAL EXAMINATION VIDEO?

HEAD Behaviour, seizures

Mental Status Head, Neck & Trunk Movement & Coordination

Cranial Nerves LEFT RIGHT Vestibular/Ear LEFT RIGHT

Eyes Eye drop, normal/abnormal
Nystagmus; normal vestibular
Ophthalmic Exam Abnormal
Vision; II Blindfold
Menace; II-VII, cerebellum Tongue
Pupils, PLR; II-III, Symp.
Horners; Symp. Mass & use; XII, cerebrum
Pharynx, Larynx
Strabismus; III, IV, VI, VIII
Face Voice; IX, X
Swallow; IX, X, cerebrum
Sensation; Vs, cerebrum Endoscopy
Muscle mass/jaw tone; Vm T-L reflex
Ear, eye, nose, lip reflex; V-VII
Expression; VII, cerebrum LEFT RIGHT
Sweating; Symp. Pelvic Limb / Trunk
GAIT & POSTURE

Thoracic limb / Thoracic limb / Neck Pelvic Limb / Trunk
Neck

Paresis
Ataxia
Hypometria
Hypermetria
Posture
Postural Responses [hop, hemi, knuckle]
Lameness

LOCALISING SIGNS [reflexes, sensation etc] LEFT RIGHT

ASSESSMENT Thoracic limb / Neck cerebrum brainstem peripheral CNs cerebellum
Site of lesion[s] Pelvic Limb / Trunk spinal cord peripheral nerve muscle skeleton
Tail, Anus, Bladder & Rectum

General [circle]:

Specific:

Cause of lesion[s]

PLAN Diagnostic
Therapeutic
Prognostic
KEY: 0 = absent; 1+ = hyporeflexic; 2+ = normal; 3+ = hypereflexic; 4+ = hypereflexic & clonus

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TABLE 3: Assessment of cranial nerve function

CRANIAL NERVE MAJOR FUNCTION REFLEX/RESPONSE/ASSESSMENT
I Olfactory Sense of smell Challenge
II Optic Afferent pathway for vision and light Menace response
Pupillary light reflex
III Oculomotor Pupillary constriction Swinging light test
IV Trochlear Extra-ocular muscles Pupillary light reflex
V Trigeminal Sensory Extraocular muscle (dorsal oblique) Medial movement of globe
Sensory to head and face Ventrolateral rotation of globe
Motor Motor to muscles of mastication
VI Abducens Extra-ocular muscle (retractor oculi) Ear, eyelid and lip (facial) reflexes
VII Facial Extra-ocular muscle (lateral rectus) Pain perception: head, nasal septum
Motor to muscles of facial expression Chewing, jaw tone, muscle mass (temporalis,
VIII Vestibular masseter, pterygoid)
Afferent branch of vestibular system Eyeball retraction (corneal reflex)
Cochlear Lateral movement of globe
IX Glosso-pharyngeal Hearing Ear, eyelid and lip (facial) tone, reflexes, and
X Vagus Sensory / motor to pharynx movement
XI Accessory Sensory / motor to pharynx and larynx Facial symmetry
XII Hypoglossal Head posture
Motor to tongue Induced eyeball movement
Normal vestibular nystagmus
Normal gait
Blindfold test

Response to noise
Swallowing (observation and palpation)
Gag reflex (nasal tube)
Endoscopy

Tongue size and symmetry

FIGURE 2

Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil

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FIGURE 3

FIGURE 4

Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil

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TABLE 4: Gait and postural abnormalities present with neurologic lesion at different locations.

LESION GAIT AND POSTURAL ABNORMALITIES
LOCATION
POSTURAL PARESIS ATAXIA HYPOMETRIA HYPERMETRIA
DEFICITS

Cerebrum +++ O O O O
Brain Stem ++
Vestibular ++ ++ ++ ++ O
Cerebellum +++
Spinal Cord / UMN +++ O ++ ++ ++
Peripheral Nerve / LMN (+++)*
Musculo-Skeletal ++ O +++ + O

++ ++ ++ ++

++ +++ + (++)*

+ ++ O +

O = not usually expected
+ = mild if present
++ = usually present
+++ = quite characteristically present
* = usually only with selection sensory fiber involvement

TABLE 5: The common clinical features of Upper and Lower Motor Neuron Defects

FUNCTION DEFECT

UPPER MOTOR NEURON LOWER MOTOR NEURON

Paralysis Normo- to hypertonic Hypotonic to flaccid

Muscle atrophy None or disuse* Significant

Muscle fasciculations NOT present Present

Reflexes Normo- to hyperactive Hypoactive to absent

* becomes evident quickly in proximal muscles with lameness and disuse

TABLE 6: Syndromes in which neurologic lesions may be suspected but usually not proven.

 Prominent toe dragging  Prominent sinking with dorsal lumbar pressure
 Intermittent & unusual lameness  Throwing to the ground when saddle applied
 Shivering  Rearing violently when first ridden
 Stringhalt-like movements  Extreme difficulty in rising
 Hyperreflexic movements  Localized hypertonia & tremor

Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil