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THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
The Healthy Spinal Cord
I. G. Joe Mayhew, BVSc, PhD, Dipl ACVIM, FRCVS, Dipl ECVN
Author’s address: Department of Veterinary Clinical Studies, Royal (Dick) School of Veterinary
Studies, and Large Animal Hospital, Easter Bush Veterinary Centre, University of Edinburgh,
Edinburgh, Scotland r 1999 AAEP.
1.
Introduction
2.
This first paper aims to review our current understanding of the structure and function of the normal
equine spinal cord and its associated vertebral column, beginning with the latter. Because of their
intimate relationship, an understanding of these two
structures is vital for localising signs of spinal cord
disease particularly as many spinal cord disorders
involve changes in the vertebral column. Clinically
relevant aspects of vertebral and spinal structure
and function that are important to the neurological
examination will be highlighted.
A plea is made here to use correct anatomical
terminology1 as detailed in Nomina Anatomica Veterinaria.2 Importantly, ‘‘backbone’’ and ‘‘spine’’ are human terms and are not used; ‘‘vertebrae’’ and
‘‘vertebral column’’ are appropriate animal terms
and are used. Also, the terms ‘‘dorsiflexion’’ and
‘‘ventroflexion’’ are hackneyed and incorrect. The
correct terms to be used are ‘‘extension’’ (or ‘‘lordosis’’) and ‘‘flexion’’ (or ‘‘kyphosis’’) of vertebrae.
Finally, little will be said of ancillary aids, because
these will be covered within the specific disorders
presented in part II.
The Vertebral Column
The generally accepted vertebral formula for the
domesticated horse3 is
C ⫽ 7, T ⫽ 18, L ⫽ 6, S ⫽ 5, Ca ⫽ 15–21,
and that for the donkey4 is
C ⫽ 7, T ⫽ 18, L ⫽ 5, S ⫽ 5, Ca ⫽ 15–17,
where C is cervical, T is thoracic, L is lumbar, S is
sacral, and Ca is caudal (coccygeal).
However, many variations exist for all equids. In
studies involving more than 250 equids, 7 cervical
vertebrae was the rule.5 Of almost 100 domestic
horses in these studies, 17 T vertebrae were found in
10%, 19 in 6%, and 181⁄2 (the 1⁄2 indicating a transitional vertebra) in 1%. In 3% of horses there were
only 5 L vertebrae and in 1% there were 51⁄2. The
sacrum varied more, with 5% having 4 vertebrae, 1%
having 41⁄2, 1% having 51⁄2, and 7% having 1 or 2
fused Ca vertebral bodies forming the sacral plate.
Variations in the remaining vertebrae need to be
interpreted somewhat cautiously, depending on
NOTES
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THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
one’s definition of ‘‘thoracic,’’ ‘‘lumbar,’’ and ‘‘sacral’’
vertebrae.5,6
In a recent study of 36 Thoroughbred racehorses,6
the proportions of L and S vertebrae in various
combinations were as follows: 5 L, 5 S: 3%; 5 L, 6
S: 28%; 6 L, 5 S: 61%; and 6 L, 6 S: 8%.
The T-L vertebral column is a relatively rigid
structure7 with little movement in all 3 axes at most
intervertebral complexes. The greatest degree of
flexion and extension appears to occur at L6–S1,
with some at T1–2 and most axial rotation and
lateral bending at T2–T16. Townsend and Leach8
related differences in the intervertebral articulations (size, angulation, etc.) with differences in mobility of the 4 regions of the back, viz. T1–2, T2–16,
T16–L6 and L6–S1. Recently,9 an in vivo study of
mobility of the back was reported for 10 horses
(average 16 hands high at withers). Average total
dorsoventral movement at the middle of the back
(T16) was 13 cm and average total left-right bending
movement was 15 cm.
In concordance with the greater rigidity of the
T16–L6 vertebral column, symmetrical or asymmetrical intertransverse articulations were found for at
least one site in all of 36 racing Thoroughbreds and
ankylosis of transverse processes in 28% of horses.6
Physeal closure in these T-L vertebral bodies occurred between 5 and 7 years of age. Also, a
‘‘ventral crest’’ was referred to without further explanation as spanning 4–8 vertebral bodies from
T16–L4.6 These may well represent ventral projections of the cranial and caudal physeal plates seen on
T-L vertebrae in several breeds of equids that can
appear to fuse at gross post mortem examination,
but radiographically show incomplete fusion (Figs. 1
and 2). Other degenerative and probably traumatic
pathologic articular changes were found in these 36
active racehorses.10,11 Half the horses had stress
fractures of the laminae of the arches of the vertebral
canal. The severity of these fractures was positively related to the severity of osteoarthritis in
Fig. 1. Median section of an equine thoracolumbar vertebral
section showing ventral extension of the cranial and caudal
physes to almost fuse ventrally.
the articular processes in the same horses.10
Impingement of dorsal spines and transverse lumbar processes were present in more than 90% of
horses and degenerative changes (osteoarthritis)
was present in almost all T, L, and L-S articular
processes; some of these changes were severe.11
The intervertebral disks at T1–2, T2–3, and L6–S1
were found to be thicker by 215%, 124%, and 131%,
respectively, compared with the average thickness of
the other T-L disks.8 In the 96 T-L intervertebral
disks examined there were only 3 (T8–11) in one
horse that had a gelatinous center, possibly a nucleus
pulposis.
There are consistently 7 cervical vertebrae in
mammals, and very occasionally rudimentary cervical ribs a few centimeters in length are present.
I have seen 2 horses with 6 neck vertebrae cranial to
a complete set of first ribs (Figure 3). Because the
entire spinal cord and vertebral column were not
fully examined, it must remain likely that these
structures represent ‘cervical ribs’ with thoracicalization of the seventh cervical vertebra in both cases.
Considerable morphologic variation exists in cervical vertebrae even within breeds,12 and 3 of these
variations are notable. Asymmetrical variations in
the bony borders for the second cervical nerve root in
its neurovascular bundle at the cranial region of the
Fig. 2. Radiograph of the thoracolumbar vertebral section shown
in Fig. 1.
Fig. 3. Lateral cervical radiograph of a Thoroughbred foal with 6
cervical vertebrae cranial to the vertebra that has the first (full)
set of ribs. There is angular deformity and stenosis with spinal
cord compression at C3–4.
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arch of the axis should not be confused with bone
disease. There can be simply a notch, or partial
separation into a foramen or a complete foramen on
one or both sides; this being also recognised at the
T-L intervertebral sites.13 Likewise, the radiographically variable, serpentine, vascular channel in
the dorsal spine of the axis and the separate centers
of ossification at the caudal end of the ventral
laminae of C6 should not be mistaken for fractures.
The most common major variation in cervical vertebrae is transposition of one or both ventral laminae
of the transverse processes of C6 onto C5 or, most
often, onto C7. This was found in 2 of the last
20 sets of cervical radiographs taken at the University of Edinburgh, Easter Bush Veterinary Centre.
These reasonably frequent anomalies are very important to identify individual cervical vertebrae correctly on radiographs, at surgery and at necropsy
examination.
Finally, quantitative morphological variations
have been identified in C3 to C7 in 4–23-mo-old
Thoroughbreds.14
Regarding the kinematics of the adult equine head
and neck, at least in cadaver specimens, most dorsoventral and some axial movement occurs at the
atlantooccipital joint but most of the axial movement
occurs at the atlantoaxial joint.15 Excluding atlantooccipital (head) movement, more dorsoventral and
lateral movement occurs in the caudal than in the
cranial neck, especially at C6–7 (Figs. 4–6).
Neonatal foals have greater range of motion of joints
so it perhaps is not surprising that cadaver necks
from foals (⬍12 months) have approximately 20%
more motion around all 3 axes than horses older
than 2 years.16 Current work using image analysis
will help provide in vivo data for cervical kinematics
in adult horses (Licka T, 1999, pers. comm.).
Morphologically, physeal closure in cervical vertebrae is very delayed compared with limb longbones;
the cranial physes of C3–7 are closed by 3 years,
whereas the caudal physes of C2–7 are present and
discontinuous by 6–9 years but absent by 12 years of
Fig. 4. Mean ranges of maximal cervical dorsoventral movement
at each intervertebral site and at the atlantooccipital site (AO).
Data are given as percentages of total head and neck movement
(lighter bars) and as a percentage of total neck movement alone,
excluding AO movement (full bars, except the AO bar). (Modified
from Clayton and Townsend.15)
58
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Fig. 5. Mean ranges of maximal cervical axial movement at each
intervertebral site and at the atlantooccipital site (AO). Data are
given as percentages of total head and neck movement (lighter
bars) and as a percentage of total neck movement alone, excluding
AO movement (full bars, except the AO bar). (Modified from
Clayton and Townsend.15)
age. Cervical intervertebral disks are composed of
fibrocartilage but do undergo ageing changes. In
addition, fibrocartilage can be seen to bulge into the
vertebral canal in normal horses.17 A more recent
extensive study of 103 cervical vertebral columns
from animals 42 weeks gestational age to 23 years of
age revealed considerable, age dependant, degenerative changes in cervical disks in the absence of
clinical signs.18 In some cases there was necrosis of
fibrocartilage that could be detected radiographically (Fig. 7).
3.
Spinal Cord Structure
A.
Gross
The spinal cord in a 500-kg horse is almost 2 m long.
This can be divided into 5 functional sections as
shown in Table 1.
The lengths of these spinal (and corresponding
vertebral) sections are important in explaining why
focal compressive spinal cord lesions in horses less
often result in evidence of gray matter damage such
as profound weakness, reflex loss and muscle atrophy, and sensory loss compared with evidence in
small animals. For example, a C7–T1 compressive
lesion 2 cm long would potentially damage 6% of the
Fig. 6. Mean ranges of maximal cervical lateral movement at
each intervertebral site and at the atlantooccipital site (AO).
Data are given as percentages of total head and neck movement
(lighter bars) and as a percentage of total neck movement alone,
excluding AO movement (full bars, except the AO bar). (Modified
from Clayton and Townsend.15)
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Fig. 7. Postmortem radiograph of a section through the C4–7
cervical vertebrae of an aged riding horse. Necrosis of the
central portion of the 3 intervertebral disks can be seen as lucent
areas.
gray matter in the brachial intumescence of a horse
and would be most unlikely to cause localizing signs
noted above. In a standard-sized dog with a 40-cmlong spinal cord, a compressive lesion of, say, 1 cm
would potentially damage 15% of the gray matter in
the brachial intumescence and most likely cause
such localizing signs.
Because the spinal cord ends at S2 in the horse,1
there is the well utilised opportunity to sample
cerebrospinal fluid (CSF) from the reasonably voluminous L-S cistern. However the S3–4 segments
potentially can be damaged during this procedure.
Rarely is this the case however and a complication of
bladder paresis due to sacral parenchymal hemorrhage must have occurred at no more than 1 in 1000
in the author’s experience. It is almost impossible
to penetrate free-floating S1–4 nerve roots at this
site unless there is violent movement of horse or
needle with the spinal needle bevel acting as a knife;
the author has not known for this to occur.
B.
Subgross
The sub-gross anatomy of the spinal cord has been
well-studied19 and a summary of the relationship of
cross sectional areas of spinal cord gray matter,
white matter and sub-dural (CSF) space is given in
Fig. 8. This gives an indication of how large the
vertebral canal must be to contain the spinal cord at
each variably-sized section. Although the absolute
values for cross sectional areas given by Braun17
(Fig. 8) are smaller than measurements taken from a
spinal cord from a 500-kg horse measured by the
author, the relative proportions do appear to be
Table 1.
Functional Sections of the Equire Spinal Cord
Section
Length (cm)
C1–5
C6–T2
T3–L3
L4–S4
S5–Ca⫹
Total
55
33
88
18
6
200
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Fig. 8. Diagram of relative cross-sectional areas (‘‘volumes’’) of
the spinal cord grey matter, white matter, and the subarachnoid
space (CSF). (Modified from Braun.19)
useful (Fig. 8). It is probably axiomatic that the
vertebral canal diameter will depend upon the size of
the dural compartment or sac (Fig. 8). Also, the
amount of sub-arachnoid/dural space (CSF) will
depend on the amount of dorsoventral and lateral
movement at each site (see above).
4.
Spinal Cord Physiology and Biochemistry
Much of what is understood about the function of
tracts and regions of the equine spinal cord has been
assumed from work in other species and derived
from observed syndromes caused by naturally occurring equine neurological diseases. For the purpose
of this review, three findings will be mentioned here
as having clinical relevance.
Firstly, the pyramidal (cerebrospinal) tract in mammals is the direct motor pathway from the motor
cortex in the forebrain to motor nuclei of cranial
nerves in the brainstem and lower motor neurons in
the ventral gray columns of the spinal cord. In the
horse this tract certainly ends cranial to the brachial
intumescence and probably in the cranial cervical
segments.1 Major lesions in this pathway alone
(e.g. a motor cortex lesion) result in little or no
permanent gait abnormality.
An interesting involvement of spinal afferent fibers
in respiratory control has been shown in ponies.20
One month after dorsolateral spinal lesions at L2
were created (mainly sectioning the dorsal spinocerebellar tracts) there was attenuation of exercise
hypocapnea (PaO2 not measured) recorded at the
onset of treadmill exercise compared with pre-lesion
measurements. It is thus possible that minor spinal lesions may influence performance through effects on respiration.
An important role for proprioceptive afferent input
from the neck via the first 3 cervical dorsal nerve
roots21 appears to have been overlooked in equine
neurology. Local anesthetic block of these nerve
roots in 10 macaque monkeys and baboons consistently caused severe defects in balance, orientation
and coordination, mimicking the vestibular signs
recorded in monkeys with bilateral inner ear ablation (labyrinthectomy). Post mortem confirmation
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Table 2.
THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
Basic Tests That Can Be Included in a Physical Examination to
Assist in Detection of a Spinal Cord Disorder
Symmetry of neck, trunk, and limbs
External thoracolaryngeal (slap) reflex
Tail and anal tone
Anal reflex
Examination of rectum and bladder
Postures adopted at rest
Gait at walk and trot
Gait while turning
Faster gaits
of the site of deposition of the anesthetic solution was
confirmed in 4 animals. Bilateral neurectomies of
the C1– dorsal (sensory) roots in 2 monkeys produced the same syndrome that improved over 2
weeks. The same temporary clinical syndromes of
symmetrical vestibular signs has been produced in
more than 20 ponies by local anesthesia of the
cranial cervical dorsal nerve roots (C. Frigast, Denmark, 1999, pers. comm.). Correct deposition of the
anesthetic solution around the dorsal nerve roots
(and not around the spinal cord) was confirmed with
radiography and at post mortem dissection.
Finally, it is probably of some clinical importance
that, both biochemically22 and morphologically,23
foals’ spinal cords appear to mature before birth;
these findings are consistent with the strong gait
demonstrated by foals a few hours old compared with
other domestic species.
5.
Neurological Examination for Spinal Cord Disease
A.
Neurological Testing in the Physical Examination
The procedure for neurological examination of the
adult horse is based on information given in references 24–30. Frequently it will not be clear whether
a horse suspected of having a spinal cord disorder
indeed does in fact have one until neurological
evaluation has been made. This is particularly so
for mild gait abnormalities and following some injuries when orthopedic and neurological disease are
both possible and suspected.
The physical examination should incorporate several basic neurological tests to assist the practitioner
decide whether or not a neurological disorder exists.
Table 2 indicates some of the observations that can
easily be included within a routine physical examination that will help indicate if a neurological abnormality is present in the great majority of cases in which
the signs are not intermittent.
B.
Neurological Examination Procedure
After evaluation of the head for evidence of brain and
cranial nerve disorders, an evaluation of the neck,
forelimbs, trunk, hindlimbs, tail and anus is then
undertaken. Evidence of bony and muscular asymmetry, localized sweating, focal muscle atrophy, decreased pain perception and localized painful
responses should be searched for and documented.
Areas of sweating and decreased sensation (hypalge60
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sia), and depths and diameters of muscle masses
suspected as being atrophied should be measured
accurately. When marked abnormalities of gait are
evident it is relatively easy to determine which limbs
are affected. The degree of limb involvement and
the characteristic of any abnormality is recorded in
order to determine the site and extent of any neurological lesion (Table 3).
For the most part, neurological gait abnormalities
involve degrees of weakness and ataxia. Weakness
may predominantly involve flexor or extensor muscle
groups and ataxia can be characterized as having
components of decreased range of joint movement
(hypometria or spasticity), and increased range of
joint movement (hypermetria or high striding).
Extensor weakness in a limb is best evaluated by
observing for muscle trembling, buckling on a limb
when turning and the ease in which the patient can
be pulled to the side by the tail, both while standing
still and while moving (Fig. 9). Flexor weakness
may be more evident as dragging of a toe and a low
foot flight, particularly while turning. Subtle degrees of weakness in the thoracic limbs may be
accentuated by performing a hopping test wherein
one forelimb is held up and the horse made to hop
laterally away from the examiner on the other
forelimb (Fig. 10). A horse with extensor weakness
often will buckle on an affected limb. Pelvic limb
and/or thoracic limb weakness can be detected by
attempting to pull on the halter and tail at the same
time. This is particularly useful if there is asymmetry in the degree of weakness. Normal alert horses
resist such pulling whereas a weak animal is easy to
pull to the side.
Mild degrees of ataxia can be detected by performing additional postural maneuvers. Considerable
time usually is spent in performing serpentine maneuvers, circling wide and tight (Fig. 11), elevating
the head while walking the patient on a flat (Fig. 12)
and on a sloped (Fig. 13) surface, turning tightly
upon stopping abruptly from a trot and backing.
These maneuvers alter visual, gravitational, vestibu-
Table 3.
Prominent Gait and Postural Abnormalities Present with
Neurologic Lesions at Different Locations
Gait and Postural Abnormalities
Lesion Location
(tracts and sites)
Spinal cord—UMN
Vestibulospinal
Spinocerebellar
Spinal cord—LMN
Musculoskeletal
Postural
Hypo- HyperDeficits Paresis Ataxia metria metria
⫹⫹
⫹⫹⫹
⫹⫹
⫹⫹
⫹/⫹⫹
⫹⫹
䊊
䊊
⫹⫹⫹
⫹⫹
䊊
⫹⫹
⫹⫹
⫹⫹⫹
⫹⫹⫹
⫹⫹
䊊
(⫹⫹)*
䊊
0 (⫹⫹)†
⫹⫹
䊊
⫹⫹⫹
䊊
䊊
NOTE. Characteristics of many musculoskeletal disorders are
included for comparison.
UMN, upper motor neuron; LMN, lower motor neuron; 䊊, not
usually expected; ⫹, mild if present; ⫹⫹, usually present; ⫹⫹⫹,
quite characteristically present.
*Due to weakness.
†Mechanical.
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THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
Fig. 11. Turning in tight circles can often make hypermetric
ataxia more evident in a pelvic limb.
Fig. 9. Testing for extensor weakness by evenly (not jerkily)
pulling laterally on the tail while the horse walks forward.
Fig. 10. The forelimb hopping test is performed by lifting one
forelimb and forcing the horse to hop laterally by pushing on its
shoulder.
Fig. 12. Walking this horse on flat ground exaggerates hypometric ataxia in the thoracic limbs.
lar and proprioceptive input to the nervous system
such that any subtle sensory or motor deficit can
become more clearly expressed. The overall severity of any gait abnormality in each of the four limbs
can be graded 1 through 4, as subtle, mild, moderate
or severe.
With the neurological examination completed the
examiner may be able to decide if and where any
possible lesions exists. If this is not clear then it is
often worthwhile returning to the patient and performing an even more critical evaluation. With a
very fractious or a very excited horse suspected of
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THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
evidence from signs resulting from primary orthopedic disorders.
C.
Fig. 13. Walking this ataxic horse up an incline with the head
extended exaggerates the hypermetria in the thoracic limbs.
having a neurological abnormality involving the
limbs, exercise such as lunging or running on very
soft going for 20 minutes can be undertaken and
then a re-evaluation made.
When lameness is present or is suspected, possibly
interfering with interpretation of a horse’s gait and
posture, then appropriate regional analgesia or short
acting systemic analgesia (e.g. using synthetic opioids), may be used. In more chronic cases, nonsteroidal anti-inflammatory drugs may be given at a
relatively high dose for several days (or weeks) and
then the horse’s gait can be re-evaluated, when
lameness often will be reduced.
Equine practitioners do find cases for which there
is some indication of spinal cord involvement but no
definitive proof. These cases usually are suspected
of suffering from a painful musculoskeletal disorder,
a peripheral neuromuscular spastic disorder, a behavioral problem (belligerency), laziness or back disease.
Such patients may show one or more of the signs
listed in Table 4. 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.
With horses that demonstrate a mild or unusual
gait or postural abnormality, emphasis often will be
on detecting evidence of spinal cord, peripheral
nerve and muscle disease and distinguishing such
Points to Emphasise in Cases of Spinal Cord Disease
i. The ‘‘Slap Test’’
The thoracolaryngeal response (‘‘slap test’’) is a
useful part of the complete neurological examination
of horses suspected to have involvement of the vagal
or recurrent laryngeal nerves or cervicothoracic spinal cord.31 The test can be performed in cooperative
horses by palpating the dorsal and lateral laryngeal
musculature while simultaneously slapping the contralateral dorsolateral thoracic (saddle) region, from
the cranial withers to near the last rib (Fig. 14).
The hand slap should be performed during expiration and examiners may find it easier to perform a
double slap, palpating for a double movement of the
laryngeal musculature and/or cartilages. If there is
difficulty in interpretation of this test, observing the
larynx via an endoscope while performing the test
may be necessary.
This response is not consistently absent in horses
with cervical vertebral malformation or other forms
of cervical spinal cord disease (wobblers) and may
inexplicably be absent in some apparently normal
horses. Depression or absence of the reflex on the
left side must be taken as strong evidence for the
presence of recurrent laryngeal neuropathy or prior
laryngeal surgery.32,33 Exercising the horse will be
necessary to confirm any clinical problem arising
from laryngeal paralysis. Bilateral absence of the
palpable response in the absence of other signs of
laryngeal or cervicomedullary disease must be interpreted cautiously particularly in excitable horses.
Table 4. Syndromes Wherein an Organic Spinal Cord or Vertebral
Column Lesion May Be Suspected but Usually Not Proved
Prominent toe dragging
Intermittent, unusual lameness
Prominent sinking with dorsal
lumbar pressure
Throwing to the ground when a
saddle is applied
Rearing violently when first
ridden
62
Shivering
Stringhalt-like movements
Other spastic movements
Extreme difficulty in getting up
Lying down a lot
Fig. 14. The thoracolaryngeal response (slap test) can be performed by slapping the cranial dorsolateral thorax while palpating the dorsolateral laryngeal musculature on the opposite side
for movement.
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ii. Cervical Reflexes
The local cervical and cervicofacial reflexes34 can be
useful to help confirm the presence and sometimes
the location of a cervical lesion. The former is the
contraction of the cutaneous coli (neck) muscle in
response to tapping the neck with a blunt probe.
The sensory input for this reflex is segmental but the
motor output from the CNS is not completely clear
but includes ventral spinal nerve roots, especially
C6. The second of these reflexes is twitching of all
facial muscles including the cutaneous facei (facial
sub-cuticular) muscle in response to the same cervical stimulus as for the first reflex. The same segmental cervical sensory input likely applies to this
reflex. However, both the sensory and motor pathways may be more complex as there is an anastomotic connection from the C2 nerve (and
subsequently the first 6 cervical nerves via the
transverse cervical nerve) and a cervical branch of
the facial (cranial nerve VII) nerve. The fact that
this anastomosis could contain sensory or motor or
both types of fibers makes accurate interpretation of
this reflex enigmatic.
Finding depressed and particularly asymmetrical
local cervical and cervicofacial reflexes can be useful
in localizing a cervical spinal cord lesion. Because
of the incomplete understanding of these reflexes
interpretation may need to be as imprecise as ‘‘consistent with a caudal cervical lesion’’ or ‘‘consistent with
a cranial cervical lesion.’’
iii. Cutaneous Trunci Reflex and
Cutaneous Sensation
The cutaneous trunci reflex (incorrectly referred to
as the panniculus reflex) is a robust reflex in horses.
It consists of contraction of the cutaneous trunci
muscle in response to tapping the lateral trunk with
a blunt probe. The sensory input is segmental
through dorsal thoracic nerve roots passing cranially
through the spinal cord to reach the motor neurons
in the cranial thoracic gray matter to reach the
cutaneous trunci muscle via the lateral thoracic
nerve. This reflex can be useful in delineating the
cranial extent of a thoracic spinal cord lesion particularly when such a lesion is asymmetrical.
Rarely, a degree of hypalgesia can be detected
caudal to the cranial extent of a region of cutaneous
trunci hyporeflexia. This is seen only with severe
thoracic spinal cord disease.
Evaluating for hypalgesia over the trunk, as elsewhere, should be performed with a two-pinch test.
This is performed by pinching the skin into a fold,
inserting the fold into the jaws of a strong hemostat
or needle holder and after the patient has settled to
this, a brief, sharp squeeze is applied to elicit a
behavioral response.
iv. Neck pain
It is difficult to interpret an apparent reluctance of a
patient to move the neck passively or actively in any
direction as indicating neck pain or stiffness. On
the other hand, a horse that will not lower its head to
eat usually is quite evidently compromised, usually
because of mechanical or painful disruption to flexion of the caudal cervical vertebrae (Fig. 15) or
extension of the atlanto-occipital and/or the atlantoaxial joints.
v. Sweating
Identifying the presence of well-delineated regions of
cervical and thoracic sweating can be useful in
localizing a spinal cord lesion. Such areas can
represent focal sympathetic denervation (decentralization) of the vasculature in the skin, resulting in
increased circulating epinephrin stimulating sweat
glands. However, care must be taken in interpreting patchy sweating that is not well delineated.
Very asymmetrical patchy sweating can occur in
horses that are excited or distressed, particularly
when in a draughty trailer or stall, without a sympathetic lesion being present.
vi. Gait and Posture
As noted above, when spinal cord disease is suspected, considerable time should be spent in evaluating gait and posture of the patient (Table 3). Rather
than manually placing limbs in abnormal positions
to evaluate conscious proprioception, it appears more
reliable to maneuver the horse rapidly (say in a
circle) and stop the maneuver abruptly. This often
results in an initial awkward placement of a limb
and then the examiner can determine how long the
horse leaves the limb in such an abnormal posture to
determine the presence or not of a conscious proprioceptive deficit.
To determine the presence of weakness in the
limbs of a horse suffering from spinal cord disease
the three most useful tests are the tail pull (Fig. 9),
the tail and halter pull and thoracic limb hopping
(Fig. 10). Pulling the tail while the patient remains
static initiates an extensor (patellar or quadriceps)
reflex. This reflex is poor with lower motor neuron
disease at the level of L3–4 and the patient will
demonstrate weakness while standing still (hypotonia) as well as voluntary extensor weakness while
moving. In contrast, a horse with an upper motor
neuron lesion (wobbler) will have good resting muscle
tone and be difficult to pull to the side in a singular
movement while standing still. However, such a
patient will be easily pulled to the side while walking
(Fig. 9). This demonstrates voluntary extensor
weakness but the presence of intact or even hyperactive extensor reflexes in the pelvic limb.
Pulling on a lead rope and the tail simultaneously
while circling the horse around the examiner is a
postural reaction that also evaluates voluntary extensor strength and in addition can exaggerate a patient’s tendency to pivot on a hindlimb and to
maneuver limbs in an ataxic fashion. Flexor weakness leads to the patient not flexing the affected limb
well and thus dragging the toe on the ground. A
worn toe will result. Some neurologically normal
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THE EQUINE SPINAL CORD IN HEALTH AND DISEASE
single insult of cervical spinal cord compression a
year before examination may have an unusual,
perhaps hypermetric, mild ataxia in the pelvic limbs
with no evidence of weakness. There may be no
signs in the thoracic limbs save for a questionable
response to hopping.
D.
Fig. 15. Refusing to eat from the ground, or consistently adopting a very abnormal posture (as shown) can be quite good evidence
of neck pain. This horse had osteomyelitis of C6–7.
horses will ‘‘toe-drag’’; many of these will have
orthopedic disease.
A horse that has extensor weakness in a thoracic
limb often will tend to tremble on the limb while the
opposite thoracic limb is held up on initiation of the
hopping test. It also will have difficulty in hopping
to the side when pushed with the examiner’s shoulder (Fig. 10).
Evaluation of horses while being walked across
kerbs has not proven to be a useful test of proprioceptive dysfunction. Normal horses, particularly if distracted, often will stumble and those that are quite
weak and ataxic but moving cautiously often can
maneuver such obstacles. In the author’s experience blindfolding a horse suspected of suffering from
spinal cord disease usually has not added anything
substantial to the neurological evaluation. Normal
horses react in different ways, from extremes of
excitement to calmness and the subsequent movements they make depends on this behavioral response.
In contrast, signs of dysmetric ataxia and loss of
balance will be markedly exacerbated when a blindfold is applied to a horse suffering from vestibular or
occasionally from spinocerebellar disease.
After the precise type of gait abnormality present
has been determined (Table 3), the most likely site of
an acute spinal cord lesion and the pathways involved frequently can be accurately defined, with
some exceptions. With peracute lesions, particularly those of an inflammatory nature and those with
soft tissues compressing the spinal cord (such as
with caudal cervical synovial cyst formation), resulting signs can wax and wane quite dramatically over
periods of hours to days. Such signs usually stabilize with subacute to chronic lesions.
On the other hand, a horse with chronic spinal
cord disease may show quite different neurological
signs. For example a horse that has suffered a
64
Neurological Examination of Foals
The neurological evaluation of foals is very similar to
that of adults but several developmental landmarks
should be borne in mind.23,26,35,36
The spinal reflexes are hyperactive in newborn
foals and the patellar reflex, cranial tibial and
gastrocnemius tendon reflexes are performed easily.
Up to one month of age there are normal, strong,
crossed extensor reflexes in the thoracic (Fig. 16) and
pelvic limbs. In addition, an extensor thrust reflex
is obtained, at least in very young foals, by rapidly
overextending the animal’s toe while the limb is
Fig. 16. Newborn foals have very active spinal reflexes for the
first few days to weeks of life. These can include a crossed
extensor reflex, as shown with flexion of the limb being tested, and
reflex extension of the other limb. The more active the foal, the
sooner these hyperactive reflexes return to normal (adult-like).
Fig. 17. Brainstem auditory-evoked responses are very robust
waveforms but do vary somewhat from horse to horse (left).
They are very repeatable in the same horse (right).
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already in extension. This results in forceful extension of the limb.
In addition to the evaluation of gait and reflexes in
nonrecumbent adults, other postural reactions can
be performed in foals and are of most benefit in
detecting subtle proprioceptive and motor pathway
lesions when the gait is normal. These include
wheelbarrowing the patient to make it walk on just
the thoracic limbs, hopping it laterally while supporting weight on just the left then the right thoracic
limb in turn and hemistanding and hemiwalking the
patient by making it stand and then move laterally
on both left, then both right limbs. Spinal cord
lesions cause postural reaction deficits on the same
side as the lesions. Lesions involving the proprioceptive and motor pathways to the limbs result in an
extremely slow or absent hopping response in that
limb.
E.
Objective Neurophysiologic Testing
Neurological examinations in horses have tended to
be primarily subjective however recent publications
addressing the use of objective electrodiagnostic
measurements in the horse are available. These
include the evaluation of the thoracolaryngeal reflex,37 recurrent laryngeal nerve conduction velocities38 and latencies,39 auditory brain stem evoked
potentials (Fig. 17),40,41 magnetic motor evoked potentials42 and sensory nerve conduction velocities.43
Needle electromyography can be a useful diagnostic
adjunct in defining the extent of any denervation
but probably should be delayed for 3–4 weeks
when repeatable denervation potentials will be
recordable.44
6.
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Conclusion
Variations in number and shape of vertebrae as well
as prominent performance-related and ageing
changes in vertebrae need to be understood to interpret disease states more accurately. More objective
measurement of vertebral canal and myelographic
diameters in different sized horses will definitely
improve identification of spinal cord compression.
The roll of cranial cervical afferent input to the
vestibular system and the clinical syndromes seen
with lesions to cranial cervical nerves need to be
better understood. Finally, critical documentation
of localizing signs such as hypalgesia, hyporeflexia
and sweating over the neck and trunk is often
difficult but can be extremely useful in localizing
spinal cord disease.
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