Available via license: CC BY 4.0
Content may be subject to copyright.
95
Mac Vet Rev 2014; 37 (1): 95-105
Available online at
www.macvetrev.mk
Clinical Review
INTRODUCTION
Veterinary medicine has been developing very
rapidly over the last decades and the owners of
pets are more demanding for veterinary care. The
veterinarians are therefore facing more challenging
conditions in companion animals and are expected
to make the correct diagnosis, give the correct
prognosis to the owners and eventually to suggest
the most appropriate treatment or recommendation.
Neurological conditions are not more common than
in the past but are more recognised and investigated
because of this higher demand. The knowledge
about the neurological condition in small animals
NEUROLOGICAL EXAMINATION IN SMALL ANIMALS
Viktor Paluš
Dick White Referrals, Veterinary Specialist Centre,
Six Mile Bottom, Cambridgeshire, CB8 0UH
Received 19 December 2013; Accepted 16 January 2014
Corresponding author: Viktor Paluš, MRCVS, Diplomate ECVN
Hon. Assoc. Professor of Veterinary Neurology, University of Nottingham
E-mail address: viktorpalus@gmail.com
Present address: Dick White Referrals, Station Farm, London Road,
Six Mile Bottom, Suffolk CB8 0UH, UK
Tel: +44 01638 502012
Copyright: © 2014 Paluš V. This is an open-access article published
under the terms of the Creative Commons Attribution License which
permits unrestricted use, distribution, and reproduction in any medium,
provided the original author and source are credited.
Competing Interests: The authors have declared that no competing
interests exist.
Available Online First: 17 February 2014
http://dx.doi.org/10.14432/j.macvetrev.2014.02.011
This clinical review about the neurological examination in small animals describes the basics about the fi rst steps of
investigation when dealing with neurological patients. The knowledge of how to perform the neurological examination is
important, however more important is how to correctly interpret these performed tests. A step-by-step approach is mandatory
and examiners should master the order and the style of performing these tests. Neurological conditions can be sometimes very
distressing for owners and for pets that might not be the most cooperating. The role of a veterinary surgeon, as a professional,
is therefore to collect the most relevant history, to examine a patient in a professional manner and to give owners ad educated
opinion about the further treatment and prognosis. However neurological examinations might look challenging for many. But
it is only the clinical application of neuroanatomy and neurophysiology to an every-day situation for practicing veterinarians
and it does not require any specifi c in-depth knowledge. This clinical review is aimed not only to provide the information on
how to perform the neurological examination but it is also aimed to appeal on veterinarians to challenge their daily routine and
to start practicing on neurologically normal patients. This is the best and only way to differentiate between the normal and
abnormal in a real situation.
Key words: neurological examination, dogs, cats, hands off examination, hands on examination
is rapidly evolving and it is therefore expected that
veterinarians keep up-to-date with this, generally
considered “tough” field of veterinary medicine.
One would think that to make the correct
diagnosis and to recommend the appropriate
treatment for neurological conditions is not
possible without sophisticated tools like Computed
Tomography (CT) or Magnetic Resonance (MR).
But this is not always true and to have a thorough
knowledge about basic neurology is often necessary
in order to make an educated judgment about the
most likely diagnosis, severity of the condition and
the prognosis.
The aims of the neurological examination is to
answer the following questions:
1. Are we dealing with the primary neurological
condition or not? So is this the neurological
condition, or the condition affecting the function of
the nervous system, or is this a completely different
condition (orthopaedic, cardiovascular etc.)?
2. Can we localise the lesion within the nervous
system?
3. What are the most common differential
diagnoses?
4. How severe is the condition?
ABSTRACT
96
Paluš V.
The fi rst two questions are usually answered by
the neurological examination. The third question
is answered by combining the neurological
examination, neurolocalisation and history. And
the last question can help the clinician to advise
owners about the prognosis and further diagnostic
work-up(1-3).
History
It is very important to take a thorough history
as this can give many clues in making the most
likely differential diagnoses. It is important to
know species, breed, sex and age of animals before
taking the history. The signalment may infl uence
the primary differential diagnosis. The veterinarian
needs to carefully question owners about the main
complaint. It is relatively easy to lose track from
the important information and then to make the
wrong judgement. The onset, evolution and course
of the illness are most important for making the
most likely differential diagnoses. The onset of the
neurological signs should be defi ned as:
1. Acute (onset over minutes to hours)
2. Subacute (onset over days)
3. Chronic (onset over several days, weeks or
months)
4. Episodic (the patient returns to normal between
the episodes)
The evolution is described as progressive, static,
improving or waxing and waning.
Physical examination
Complete physical examination needs to be
performed before the neurological examination. It is
of upmost importance to do so as many conditions
that are not primarily neurological can be discovered
here and the diagnostic work-up can take a different
direction or can alter the final prognosis. An
example would be a dog with paroxysmal episodes
or suspected seizures in which a significant cardiac
arrhythmia is found and the episodes might be
a cardiac syncope. It is also important in the case
with traumatic injuries, where the multiple injuries
(e.g. diaphragmatic hernia, ruptured viscera, ruptured
urinary bladder, multiple pelvis fractures etc.) can
be discovered and this can alter the final prognosis
and the primary goal for stabilising these patients in
the emergency situation.
Neurological examination
The neurological examination should be
performed in animals that are not sedated, have
not received any analgesia or are recovering from
seizures or general anaesthesia.
Hands off examination
This part of the neurological examination can be
performed while collecting the history. The patient
should be left to explore the examination room. The
clinician can observe the awareness, behaviour,
posture and gait in an undisturbed manner.
Consciousness, awareness, behaviour
State of consciousness is classifi ed in order
of severity as lethargy, depression, obtundation,
stupor (semicoma) and coma. Generally if there is
an altered state of consciousness then the lesion is
affecting either diffusely both cerebral hemispheres
or focally the ascending reticular activating system
(ARAS) of the brainstem.
Changes in the patient’s level of awareness
and behaviour include disorientation, delirium,
aggression, compulsive walking, loss of learned
behaviour (e.g. in-house urination, defecation
etc.), vocalising and head pressing (Fig. 1).
Hemi-neglect or hemi-inattention syndrome is
the abnormal behaviour in animals with forebrain
lesions. The lesion in the forebrain is contralateral to
the apparently “ignored” side by the animal (Fig. 2).
Figure 1. Head pressing in a 4-year-old female
neutered Cocker Spaniel with meningoencephalitis
of unknown aetiology, immune-mediated hemolytic
anaemia and immune-mediated thrombocytopenia. She
was diagnosed with systemic lupus erythematosus.
97
Neurological examination in small animals
It should be remembered that extracranial
diseases can infl uence the forebrain function,
altering the behaviour and consciousness level (e.g.
hepatic encephalopathy due to portosystemic shunt,
hypoglycaemia, hypokalemia, hypernatremia etc.)
Posture and body position
Observation of the posture and body position at
rest can reveal mild asymmetry and can also assess
the balance at the stance. Common abnormalities
are:
Head tilt - abnormal posture of the head when
one ear is lower compared to the other one. A
head tilt indicates a vestibular disorder (central or
peripheral) (Fig. 3).
Figure 2. Hemi-inattention syndrome in a 2-year-old
female West Highland White Terrier with granulomatous
meningoencephalitis. Please note that she is completely
oblivious to food in the left side of the bowl. There must
be a lesion affecting predominantly the right forebrain.
Figure 3. Right side head tilt and also ventro-lateral
strabismus more appreciated in the left eye in a 2-year-old
female neutered French Bulldog with granulomatous
meningoencephalitis.
Figure 4. The same dog as in fi gure 2. Please note the
head turn to the right side that confi rms that the lesion is
predominantly affecting the right forebrain.
Ventrofl exion of the head - commonly
associated with a neuromuscular disorder or spinal
cord grey matter lesion.
Spinal curvature
a) Scolisosis (lateral deviation of the spine)
b) Lordosis (ventral curvature of the spine)
c) Kyphosis (dorsal curvature of the spine)
d) Torticollis (twisting of the neck)
Decerebrate rigidity - a posture when the
patient is recumbent and has extension of all limbs
and opithotonus (extension of the neck and head).
The mental status is often stuporous or comatous
and the lesion is commonly localised in the rostral
brainstem.
Figure 5. Decerebellate rigidity in a 6-month-old
female Border Collie with cystic lesion in the fourth
ventricle.
Head turn - characterised by the posture when
the nose and often whole body (pleurothotonus) are
turned to one side and ears are at the same median
plane. This is most commonly associated with an
ipsilateral forebrain lesion. (Fig. 4).
Decerebellate posture - a posture when the
patient is recumbent, has extended thoracic limbs
and opisthotonus but the pelvic limbs are usually
flexed. The mental status is normal and the lesion is
likely to occur in the cerebellum (Fig. 5).
98
Paluš V.
Schiff-Scherrington posture - observed in
animals with severe thoracic or cranial lumbar spinal
cord trauma. The animal has extended thoracic
limbs with the normal function but has paralysis of
the pelvic limbs. This sign is present only in acute
lesions and does not have any prognostic value.
Evaluation of gait
Abnormalities of the gait are one of the most
common reasons to seek veterinary advice. It is
therefore important to assess whether the animal is
uncoordinated (ataxia), has an abnormality in the
strength of voluntary movement (paresis) or is lame
(neurological or orthopaedic).
Ataxia means uncoordinated gait. Ataxia can
be a consequence of peripheral nerve or spinal
cord dysfunction (general proprioceptive ataxia),
vestibular system (vestibular ataxia) or cerebellum
(cerebellar ataxia).
Paresis is defined as a loss of ability to support
weight or to generate the gait. Plegia or paralysis
refers to the complete loss of a voluntary movement,
whereas paresis implies that the voluntary
movements are still present. The animal can be
tetraparetic (affected all four limbs), paraparetic
(affected pelvic limbs), monoparetic (affected one
limb) or hemiparetic (affected only one side of the
body). There are clinical differences if the lesion is
affecting the upper motor neuron (UMN) or lower
motor neuron (LMN). An UMN lesion causes a
delay in the onset of the protraction, which clinically
looks like a stride being longer than usual. Whereas
a LMN paresis causes diffi culties in weight bearing
which clinically looks like a short-strided and
choppy gait with inability to support weight.
Lameness presents as a short stride of the lame
limb and long stride in the contralateral limb. It
is more commonly associated with orthopaedic
diseases but diseases affecting the nerve root(s) can
cause the same presentation (nerve root signature)
(Fig. 6).
Hands on examination
Cranial nerve examination
Olfactory Nerve – (CN I)
It is generally difficult to asses the smell in small
animals and in a majority of cases it is the owners
who complain about the loss of smell (anosmia)
rather than the finding on neurological examination.
Letting the animal to sniff something aromatic while
blindfolded can test the smell. Irritating substances
should not be used as this can stimulate CNV.
Optic Nerve (CN II)
This is not a peripheral nerve by strict defi nition
but it is the extension of the brain. CNII is an
important central visual pathway and it is afferent
for menace response and pupillary light reflex
(PLR).
The visual pathway has three important
neurons(1).
1. The bipolar cell in the retina is the fi rst one
in the row. This cell receives the information from
neuroepithelial cells (i.e. rods and cones)
2. The ganglion cell in the retina is the second
one. The axons of these cells form the optic nerve
and the majority of them cross to the contralateral
site in the optic chiasm (66% decussation in cats and
75% in dogs)(4).
3. The neuron body in the lateral geniculate
body in the diencephalon is the last one in the row.
The axons project to the visual cortex (mostly the
occipital lobe – which is mostly contralateral to the
stimulated retina).
Menace response (Fig. 7) is learned and
cortically mediated blink produced by a threating
gesture in front of the visual area of the patient.
Puppies will not have this response prior to 10-12
weeks of age. The afferent part is the same as the
visual pathway and the efferent is very complex but
involves coordination of the visual cortex, motor
cortex, facial nerve nucleus, cerebellum and facial
nerve. The absent menace response can be a result
of any of the parts involved in this pathway and does
not always mean that the animal is blind.
Pupillary light reflex (PLR) (Fig. 8) has some
parts in common with the afferent part of the visual
pathway. The axons involved in the vision pathway
reach the cortex via the lateral geniculate body,
however axons involved in PLR have the third
neuron in the pretecal nucleus. From there, most
Figure 6. Nerve root signature of the left thoracic
limb in a 9-year-old female neutered Lurcher with C7
vertebral body tumour impinging left C8 nerve root.
99
Neurological examination in small animals
of the axons cross again to the parasympathetic
nucleus of the oculomotor nerve (ipsilateral to
the stimulated retina). The oculomotor nerve
then constricts the pupil. This is a direct PLR.
Consensual PLR (constriction of non stimulated
eye) is explained by partial crossings along the PLR
pathway (optic nerves in optic chiasm and axons
from the pretecal nucleus in mesencephalon). PLR
should be performed in all blind animals, as it shares
only part of the pathway for vision.
Fundic examination should be also performed in
all animals to visualise the optic nerve
Oculomotor Nerve (CN III)
This nerve innervates ipsilateral dorsal, ventral
and medial recti muscles and ventral oblique
muscle. It also innervates the levator palpebrae
superioris muscle which is important for upper
eyelid movement. And fi nally the oculomotor
nerve plays an important role as an efferent arm
of PLR. It controls the pupillary constriction by its
parasympathetic component.
By observing the eyeball position and movement
of the eyeball by testing for physiological nystagmus
(see the vestibulocochlear nerve) this nerve can be
easily assessed. Another observation needs to be
done by assessing the normal position of the upper
eyelid. PLR of course must be assessed and if non
functional then thinking about the full PLR pathway
needs to be remembered in order to localise the
problem along this pathway.
An oculomotor nerve lesion results in ventrolateral
strabismus and an inability to rotate the eye
dorsally, ventrally and medially. It can also produce
unresponsive mydriasis and narrowing of the palpebral
fi ssure (ptosis of the upper eyelid). (Fig. 9)
Figure 7. The menace response is performed by
making the threating gesture at the eye. The contralateral
eye should be blinded. Care must be taken not to touch the
eyelashes or to create air current as this stimulates the CN
V and produces the palpebral or corneal reflex rather then
genuine menace response.
Figure 8. The pupillary light refl ex (PLR) is tested by
shining a direct light into the eye. The normal response is
the constriction of the ipsilateral pupil (direct PLR) and
also contralateral pupil (consensual PLR).
Trochlear nerve (CN IV)
This is assessed by observing the position of
the eyeball as well as by testing for physiological
nystagmus. This nerve innervates contralateral
dorsal oblique muscle. Dysfunction usually results
in dorsolateral strabismus of the contralateral eye.
Trigeminal nerve (CN V)
The trigeminal nerve provides sensory
innervation of the face as well as motor innervation
of the masticatory muscles. It has three major
branches:
1. Ophthalmic branch – innervates medial
canthus of the eye, nasal septum, cornea and dorsum
of the nose.
Figure 9. Ptosis of right upper eyelid and narrowing
of the palpebral fissure in a 10-year-old male neutered
Staffordshire Bull Terrier with right side CN III peripheral
nerve sheath tumour.
100
Paluš V.
2. Maxillary branch – innervates lateral canthus,
skin of cheeks, muzzle, palate and teeth of the upper
jaw.
3. Mandibular branch – innervates mandibular
area of the oral cavity.
The motor function is assessed by evaluating
the symmetry and size of the masticatory muscles
as well as by opening the jaw. The sensory function
is assessed by corneal reflex which is done by
touching the cornea with a sterile cotton bud. The
palpebral reflex tests ophthalmic and maxillary
branches (afferent arm of the reflex) by touching
medial or lateral canthuses, respectively. A normal
response for corneal and palpebral reflex is the
blink of the tested eye that is mediated by the facial
nerve (efferent arm of the reflex). Other tests that
can assess the trigeminal nerve are nasal stimulation
and pinching of the skin of the face that results in
the ipsilateral blink or twitch of the facial muscles.
Unilateral dysfunction of the motor part results
in unilateral masticatory muscle wastage, (Fig. 10)
whereas bilateral dysfunction results in the dropped
jaw and inability to close the jaw voluntarily.
Dysfunction of the sensory part results in facial
hypoesthesia or anaesthesia and can also result in
decreased tear production and neurotropic keratitis.
Abducent nerve (CN VI)
This nerve innervates the ipsilateral lateral
rectus and retractor bulbi muscles. The assessment
is therefore done by observation of the eye position,
testing the physiological nystagmus and by corneal
reflex (retracting of the eyeball). Dysfunction results
in ipsilateral convergent strabismus, inability of the
eye to cross the midline when testing physiological
nystagmus and inability to retract the eyeball.
Figure 10. Unilateral wastage of the masseter and
temporal muscles in an 8-year-old male neutered German
Wire Haired Pointer with left side CN V peripheral nerve
sheath tumour.
Facial nerve (CN VII)
This nerve provides motor function to the
muscles of the face and sensory function to the
rostral two thirds of the tongue and palate. The facial
nerve also carries the parasympathetic component
that innervates the lacrimal glands, and mandibular
and sublingual salivary glands. The motor function
is assessed by observation of the symmetry of the
face and spontaneous blink and movement of the
nostrils. The facial nerve provides the efferent arm
for palpebral reflex, corneal refl exes and menace
response and can be assessed by performing these
tests. The Schirmer tear test should be performed to
assess the parasympathetic part of this nerve (Fig.
11). Unilateral dysfunction produces the ipsilateral
Figure 11. Schirmer tear test is an important part of
neurological examination in dogs and cats.
drooping of the face, inability to move the ear
and nostril, widened palpebral fi ssure and absent
blinking response (Fig. 12). It can also produce
keratoconjunctivitis sicca by inability to produce
enough tears by loss of parasympathetic innervation
to the lacrimal glands.
Figure 12. Right side dropping of the lips and ear
in a 4-year-old female neutered Boxer with right side
idiopathic facial neuritis.
101
Neurological examination in small animals
Vestibulocochlear nerve (CN VIII)
This nerve is involved in hearing and vestibular
function. The vestibular system consists of the
peripheral part (special proprioceptors in the inner
ear and vestibular nerve) and central part (four
nuclei in the brainstem and part of cerebellum).
The hearing part involves the sensory receptors in
the cochlea (inner ear). The input from the cochlea
is then transmitted though the cochlear nerve,
brainstem and midbrain to the contralateral auditory
cortex, mainly in the temporal lobe.
Observation of the gait, body and head posture
can give a lot of information about the vestibular
function. Specifically physiological nystagmus can
test the functional integrity of the vestibular system.
This involves moving the head from side to side and
up and down. A normal response is the involuntary
“jerk” movement of both eyes to correct their
position in relation to the position of the head.
To assess the hearing part is difficult but
whistling or a handclap can be used to assess this.
Dysfunction of this nerve usually results in a
head tilt (Figure 3), falling to the side, leaning to
the side, rolling, circling, pathological (abnormal)
spontaneous or positional nystagmus, positional
strabismus (Fig. 13) or asymmetrical ataxia. The
clinical signs can be a result of dysfunction of
either the peripheral or central part. The presence
of pathological nystagmus indicates vestibular
dysfunction, however in some cases of bilateral
vestibular dysfunction this might not be present. In
this case wide based stance and symmetrical ataxia
with inability to elicit physiological nystagmus is
usually present.
Figure 13. Positional predominantly left side ventro-
lateral strabismus in a 9-month-old male neutered
Labrador Retriever with meningoencephalitis of unknown
aetiology.
Glossopharyngeal nerve (CN IX) and Vagus
nerve (CN X)
These two cranial nerves share the same
motor and sensory nuclei in the brainstem. The
glossopharyngeal nerve supplies the musculature
of the pharynx and palate and it provides sensory
innervation to the caudal third of the tongue and
pharyngeal mucosa.
Figure 14. Gag reflex can be elicited by applying
gentle pressure on the thyroid cartilage and hyoid bone.
The parasympathetic part innervates parotid
and zygomatic salivary glands. The Vagus nerve
supplies musculature of the larynx, pharynx and
oesophagus and it provides sensory innervation
of larynx, pharynx and thoracic and abdominal
viscera. The parasympathetic part of the nerve
supplies all thoracic and abdominal viscera, except
those of the pelvic region. The pharyngeal or gag
reflex can assess the function of both nerves. Gently
applying pressure to the thyroid cartilages provokes
swallowing in a normal animal (Fig. 14). Observing
a patient while eating or drinking can also provide
useful information about the function of both nerves.
Dysfunction results in dysphagia, absent gag
refl ex, inspiratory dyspnea (due to laryngeal
paralysis), voice change and regurgitation (due to
megaoesophagus).
Accessory nerve (CN XI)
This nerve supplies motor innervation to the
trapezius, sternocephalicus and brachiocephalicus
muscles and so the dysfunction results in atrophy of
these muscles and potential deviation of the neck.
However isolated lesions of this nerve are rare.
Hypoglossal nerve (CN XII)
This nerve innervates the muscles of the tongue.
Function of this nerve can be assessed by observing
102
for symmetry of the tongue and movement of the
tongue during the eating, or licking of food. Lesions
of this nerve result in problems with prehension
and mastication. Asymmetry of the tongue and
fasciculation of the musculature of the tongue can
also be seen.
Postural reactions
This part of the neurological examination is
important in distinguishing neurological disorders
from diseases of other body systems. Abnormality
of this group of tests indicates a neurological lesion,
however it does not localise the lesion within the
nervous system. Proprioreceptors are specific
receptors sensitive to detect the movements. They
are located in joints, tendons and muscles (general
proprioception) as well as in the inner ear (special
proprioception). The responses have a complex
pathway, but generally involve the afferent arc
(proprioreceptors, peripheral sensory nerve,
ascending spinal cord tracts and contralateral
somatic sensory cortex) and the efferent arc
(contralateral motor cortex, descending spinal
cord tracts, peripheral motor nerve and the skeletal
effector muscle).
Proprioceptive placing
This test is designed to evaluate the conscious
awareness of limb position and movement in
space. It is evaluated by flexing the patient’s paw
so that the dorsal surface contacts the fl oor. It is
important to support the patient with an arm under
the abdomen if the patient is too weak (Fig. 15).
A normal response is immediate correction to the
normal position. Another test involves putting the
patient’s paw on a piece of paper and sliding the
paper laterally. A normal patient will reposition its
leg when the limb reaches an abnormal position. An
abnormal reaction is delayed correction of the tested
paw.
Figure 15. Proprioceptive placing is tested by placing
the paw in the abnormal position, the patient’s body needs
to be sufficiently supported with the other arm.
Hopping reaction
Hopping reaction is performed by holding the
patient in a way so that the majority of its weight
is placed on one limb (Fig. 16). The animal is then
moved laterally (do not move medially as this may
cause an abnormal reaction even in a healthy animal)
and the normal response is to “hop” and correct
the centre of gravity when displaced laterally. An
abnormal reaction is a delayed “hop”, however
animals with severe orthopaedic disease will have
some difficulties if the body weight is not supported
sufficiently.
Placing response
Visual and tactile placing are other complex
postural reactions that can be used mainly if no
other abnormalities are identifi ed on previous
postural tests. Visual placing also assesses also the
vision whereas the tactile placing is tested with the
eyes covered. The animal with covered eyes is lifted
and then brought to the edge of the table so that the
distal parts of the limbs touch the table. The animal
should then place the limb onto the table. Visual
placing allows the animal to see the table so it can
reach and step before the limb touches the edge of
the table. An abnormal reaction is absence or delay
of this response.
Wheelbarrowing, Hemi-walking and Extensor
postural thrusting are other complex postural
reactions. I do not generally perform these tests
unless I cannot find any abnormalities of the above-
mentioned tests.
Spinal reflexes
Spinal reflexes evaluation needs to be done in
conjunction with assessment of gait and postural
reactions. The aim of the assessment of spinal
Figure 16. The hopping testing of the right thoracic
limb. The majority of the weight is put on the tested limb
and the animal is moved laterally.
Paluš V.
103
reflexes is to narrow down the problem within the
spinal cord segments or problems of the peripheral
nervous system. The spinal cord segmental in small
animals can be divided into four regions.
1. Cranial cervical (C1-C5)
2. Cervicothoracic (C6-T2)
3. Thoracolumbar (T3-L3)
4. Lumbosacral (L4-S3)
If the lesion that causes spastic tetraparesis is
localised in the C1-C5 region then the spinal refl exes
usually will be increased or intact, the lesions of
C6-T2 that causes tetraparesis will usually produce
increased or intact reflexes in pelvic limbs but
decreased or absent in thoracic limbs. T3-L3 lesions
that cause spastic paraparesis will usually cause
increased or intact reflexes in pelvic limbs, whereas
the lesion of L4-S3 that cause paraparesis will
usually cause decreased to absent spinal reflexes
of pelvic limbs. I need to stress that these reflexes
must be evaluated in conjunction with evaluation of
the gait and postural reactions. The spinal reflexes
are decreased or absent if the lesion is affecting
peripheral nerve or generally the peripheral nervous
system. If the peripheral nervous system is affected
then the animals will suffer flaccid tetraparesis.
The most reliable spinal reflexes of the limbs that
are used in small animals are withdrawal reflexes of
thoracic and pelvic limbs and the patellar reflex (1, 4).
There are other spinal reflexes (extensor carpi
radialis reflex, biceps brachii and triceps reflex,
cranialis tibialis and gastrocnemius reflex) that can
be used but they are generally less reliable and I
do not perform them routinely unless specifically
indicated.
Withdrawal reflex in the pelvic limbs
This reflex evaluates the integrity of the L4-S2
spinal cord segment and sciatic and femoral nerves.
In order to perform this test the digit of the paw
needs to be pinched with the fingers (Fig. 17). The
Figure 17. Withdrawal reflex tested on the right
pelvic limb. Please note that all joints are sufficiently
flexed after the toe was pinched.
normal response results in the flexion of the hip
(femoral nerve), stifle and hock (sciatic nerve).
Patellar reflex
This is a monosynaptic reflex that evaluates
integrity of the L4-L6 spinal cord segment. The
animal needs to be placed in to lateral recumbency
with slight stifle flexion. The limb should be held
in a neutral position with the examiner’s hand
supporting the tested limb. The reflex hammer then
hits the patellar tendon and extension of the limb
should be observed (Fig. 18).
In some older dogs this reflex can be weak with
no clinical significance. In some excited animals
with no neurological dysfunction this reflex can
appear hyperreflexive and this is again of no clinical
significance.
Withdrawal reflex in the thoracic limbs
This reflex evaluates the integrity of the
C6-T2 spinal cord segment and brachial plexus and
peripheral nerves in the thoracic limb. Pinching of
the digits needs to be performed and the flexion of
all joints is considered to be a normal response.
Perineal reflex
This reflex is often overlooked and an important
part of the neurological examination. Stimulation
of the perineum with the haemostat should result in
the contraction of the anal sphincter and flexion of
the tail (Fig. 19). This reflex tests the integrity of
the S1-Cd5 spinal cord segment and the pudendal
nerve.
Figure 18. Patellar reflex is tested by hitting the
patellar tendon with the refl ex hammer. The tested limb is
supported by the other arm in a neutral position.
Neurological examination in small animals
104
Urinary bladder palpation
Palpation of the urinary bladder should not be
omitted during the neurological examination. The
innervation is very complex and involves normal
sympathetic, parasympathetic and somatic nerve
function. The normal function of the urinary bladder
is beyond the scope of this review. Flaccid urinary
bladder that is easily expressed is called lower
motor neuron bladder and suggests an S1-S3 spinal
cord segment lesion, whereas the full and turgid
urinary bladder that is not easy to express and has
overflow leakage of the urine indicates an upper
motor neuron disorder. The abnormal function
of the urinary bladder can as well be the result of
dysfunction of the autonomic nervous system.
Sensory evaluation
Sensory part of the nervous system can be tested
with postural reactions but also with the testing
for pain perception (nociception). Assessment of
the pain sensation requires a noxious stimulus and
appropriate response of the animal.
Nociception testing
The sensory part of the peripheral nerve, the
spinal cord and the brainstem must be intact to
relay the nociception to the cerebral cortex. The
nociception pathways are located deep in the white
matter of the spinal cord and they also form multiple
synapses along the length of the spinal cord. It is
therefore an important test to do in the cases of
spinal cord diseases because it refl ects the severity
of damage to the spinal cord. The noxious impulse
(squeeze of the toe with the fingers or haemostat) is
applied to the tested area and the animal must show
a behavioural response (turning the head, trying to
bite, vocalisation) to say that the nociception is intact
(Fig. 20). The most common mistake is to confuse
Figure 19. Perineal reflex should not be omitted
during the neurological examination. It is done by gently
pinching the perineal area.
the withdrawal reflex (flexion of the limb) with
the conscious perception of the pain (behavioural
response). Many animals that have lost nociception
would still have intact withdrawal reflex and it is
therefore important to distinguish these two.
Cutaneous trunci reflex (panniculus)
This reflex is performed by pinching the skin of
the dorso-lateral aspect of the body between T2 and
L4-L5. The afferent arm tests the sensory nerves
of the skin and the efferent motor part is emerging
from the C8 nerve root and innervates the cutaneous
trunci muscle on the side of the body. A normal
reaction to the pinch of the skin is a twitch of the
skin (bilaterally, but more prominent on the tested
side) (Fig. 21).
Figure 20. ‘Nociception is tested by applying the
noxious stimulus to one of the digits in this patient. Please
note that the dog seems to be uncomfortable and aware
of the painful stimulus by looking and turning its head
towards it. (Please compare it to the withdrawal reflex in
fi gure 17., when the patient is completely oblivious to the
stimulus and only flexes the joints in the tested limb).
Figure 21. Cutaneous trunci reflex is tested by gentle
pinching of the skin on both sides of the patient’s back
with a hemostats.
Paluš V.
105
If this reflex is lost completely along the whole
spine then a lesion of C8 should be considered
(brachial plexus), however in the absence of other
neurological deficits this means very little as the
absence can sometimes be observed in normal
animals. With a presence of the spinal cord lesion
there might be a cut off of this reflex in the certain
area. In that case this reflex is sometimes absent
caudal to the lesion but present cranial to this lesion.
This is sometimes very useful to characterise better
the exact localisation of the lesion in the T3-L3
region of the spinal cord.
References and further recommended reading
1. Garosi, L., Lowrie, M. (2013). The neurological
examination. In: BSAVA Manual of Canine and Feline
Neurology. 4
th
edn. Ed Platt, S. & Olby, N. BSAVA,
Gloucester. pp 1-24.
2. Garosi, L. (2009). Neurological examination of the
cat: How to get started. Journal of Feline Medicine
and Surgery 11, 340-348.
3. Thomson, C., Hahn, C. (2012). The neurological
examination and lesion localization. In: Veterinary
Neuroanatomy a Clinical Approach. 1
st
edn. Ed
Thomson, C & Hahn, C., Saunders Elsevier, St. Louis.
pp 124-136.
4. de Lahunta, A., Glass E. (2009). The neurological
examination. In: Veterinary Neuroanatomy and
Clinical Neurology. 3
rd
edn. Ed de Lahunta, A. &
Glass, E. Saunders Elsevier, St. Louis. pp 487-501.
Figure 22. Palpation of spine and potentially painful
areas should be performed at the end of examination.
Please note that while the spinous processes are palpated
there is the other arm of the examiner under the abdomen.
When a spinal hyperaesthesia is present patients
sometimes respond by tensing up the abdominal
musculature.
Neurological examination in small animals
Please cite this article: Viktor Paluš. Neurological examination in small animals. Mac Vet Rev 2014; 37 (1): 95-105.
http://dx.doi.org/10.14432/j.macvetrev.2014.02.011
Palpation
Palpation and manipulation is important to
detect the muscle loss of the limbs and to detect
the painful areas. It is important to palpate the head
(assess the muscle mass, asymmetry, focus of pain
or persistence of fontanels), spine (pressure to the
spinous processes and then transverse processes can
detect spinal hyperaesthesia) (Fig. 22) and limbs
(joint swellings, contractures of the muscles or loss
of the muscle mass can be detected) to fi nalise the
neurological examination.
It is important to do this at the end of the
examination as this can be painful for the animal
and doing this earlier can discourage the animal to
cooperate.