Equine Neurologic Examination
Equine Neurologic Examination
Equine Neurologic Examination
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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.
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.
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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.
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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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Cranial Nerves
Eyes LEFT RIGHT Vestibular/Ear LEFT RIGHT
Ophthalmic Exam Eye drop, normal/abnormal
Vision; II Nystagmus; normal vestibular
Menace; II-VII, cerebellum Abnormal
Pupils, PLR; II-III, Symp. Blindfold
Horners; Symp. Tongue
Strabismus; III, IV, VI, VIII Mass & use; XII, cerebrum
Face Pharynx, Larynx
Sensation; Vs, cerebrum Voice; IX, X
Muscle mass/jaw tone; Vm Swallow; IX, X, cerebrum
Ear, eye, nose, lip reflex; V-VII Endoscopy
Expression; VII, cerebrum T-L reflex
Sweating; Symp.
GAIT & POSTURE LEFT RIGHT
Thoracic limb / Pelvic Limb / Trunk 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
Thoracic limb / Neck
Pelvic Limb / Trunk
Tail, Anus, Bladder & Rectum
ASSESSMENT General [circle]: cerebrum brainstem peripheral CNs cerebellum
Site of lesion[s] spinal cord peripheral nerve muscle skeleton
Specific:
Cause of lesion[s]
PLAN Diagnostic
Therapeutic
Prognostic
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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
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TABLE 4: Gait and postural abnormalities present with neurologic lesion at different locations.
Cerebrum +++ O O O O
Brain Stem ++ ++ ++ ++ ++
Vestibular +++ O ++ ++ O
Cerebellum ++ O +++ + +++
Spinal Cord / UMN ++ ++ ++ ++ ++
Peripheral Nerve / LMN ++ +++ + (++)* (+++)*
Musculo-Skeletal + ++ 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.
Proceedings of the 11th International Congress of World Equine Veterinary Association, 2009 - Guarujá, SP, Brazil