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CANINE INTERNAL MEDICINE SECRETS ISBN-13: 978-1-56053-629-1

ISBN-10: 1-56053-629-2

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Notice

Knowledge and best practice in this field are constantly changing. As new research and experience

broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or

appropriate. Readers are advised to check the most current information provided (i) on procedures

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or formula, the method and duration of administration, and contraindications. It is the responsibility of

the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to

determine dosages and the best treatment for each individual patient, and to take all appropriate safety

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The Publisher

Library of Congress Cataloging-in-Publication Data

Canine internal medicine secrets/[edited by] Stanley I Rubin, Anthony P. Carr

p. cm.

Includes index.

ISBN: 1-56053-629-2 (sc)

1. Dogs—Diseases—Miscellanea. I. Rubin, Stanley I. (Stanley Ian), 1954- II. Carr, Anthony, P., 1960-

SF991.C236 2006

636.7¢0896—dc22

2006047245

Publishing Director: Linda L. Duncan

Publisher: Penny Rudolph

Managing Editor: Teri Merchant

Publishing Services Manager: Patricia Tannian

Project Manager: Claire Kramer

Designer: Jyotika Shroff

Printed in the United States of America

Last digit is the print number: 987654321

Contributors

Jonathan A. Abbott, DVM, Diplomate ACVIM (Cardiology)

Associate Professor

Department of Small Animal Clinical Sciences

Virginia Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

Charles W. Brockus, DVM, PhD

Assistant Professor

Department of Veterinary Pathology

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Clay A. Calvert, DVM, Diplomate ACVIM

Professor

Department of Small Animal Medicine

College of Veterinary Medicine

University of Georgia, Athens, Georgia

Anthony P. Carr, Dr. med. vet., Diplomate ACVIM

Associate Professor

Department of Small Animal Clinical Sciences

Western College of Veterinary Medicine

University of Saskatchewan

Saskatoon, Saskatchewan, Canada

John Crandell, DVM

Internist

Akron Veterinary Referral and Emergency Center

Akron, Ohio

Mala Erickson, DVM, MVSc

Monterey Peninsula Veterinary Emergency & Specialty Center

Monterey, California

Leslie E. Fox, DVM, MS

Associate Professor

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

v

David Clark Grant, DVM, MS, Diplomate ACVIM

(Internal Medicine)

Assistant Professor

Department of Small Animal Clinical Sciences

Virginia Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

Karen Dyer Inzana, DVM, PhD, Diplomate ACVIM

(Neurology)

Professor, Section Chief

Department of Small Animal Clinical Sciences

Virginia Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

Catherine Kasai, DVM

Internal Medicine Resident

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Robert R. King, DVM, PhD

Senior Clinician

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Dawn D. Kingsbury, DVM

Internal Medicine Resident

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Jo Ann Morrison, DVM

Clinician

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Astrid Nielssen, DVM, Diplomate ACVIM

Canada West Veterinary Specialists and Critical Care Hospital

Vancouver, British Columbia, Canada

David L. Panciera, DVM, MS, Diplomate ACVIM

(Internal Medicine)

Professor

Department of Small Animal Clinical Sciences

Virginia-Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

vi Contributors

Erin M. Portillo, DVM

Internal Medicine Resident

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Klaas Post, DVM, MVetSc

Professor and Head

Department of Small Animal Clinical Sciences

Veterinary Teaching Hospital

Western College of Veterinary Medicine

Saskatoon, Saskatchewan, Canada

Michelle A. Pressel, DVM, Diplomate ACVIM

Mid Coast Veterinary Internal Medicine

Arroyo Grande, California

Laura Gaye Ridge, DVM, MS, Diplomate ACVIM

Internist, Upstate Veterinary Specialists

Greenville, South Carolina

John H. Rossmeisl, Jr., DVM, MS, Diplomate ACVIM

(Internal Medicine and Neurology)

Assistant Professor

Department of Small Animal Clinical Sciences

Virginia-Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

Stanley I. Rubin, DVM, MS, Diplomate ACVIM

Director, Veterinary Teaching Hospital

Western College of Veterinary Medicine

University of Saskatchewan

Saskatoon, Saskatchewan, Canada

Elizabeth Streeter, DVM

Clinician

Department of Veterinary Clinical Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Gregory C. Troy, DVM, MS, Diplomate ACVIM

(Internal Medicine)

Professor

Department of Small Animal Clinical Sciences

Virginia-Maryland Regional College of Veterinary Medicine

Virginia Tech, Blacksburg, Virginia

Contributors vii

Michelle Wall, DVM, Diplomate ACVIM

Upstate Veterinary Specialists

Small Animal Oncology Service

Greenville, South Carolina

Wendy A. Ware, DVM, MS, Diplomate ACVIM

(Cardiology)

Professor

Departments of Veterinary Clinical Sciences and Biomedical

Sciences

College of Veterinary Medicine

Iowa State University, Ames, Iowa

Staff Cardiologist

Veterinary Teaching Hospital

Iowa State University, Ames, Iowa

viii Contributors

Preface

Why write another reference text on internal medicine? Simply, we wanted

to provide the reader with a quick reference to find the essentials of canine

internal medicine. These are the same topics and facts that are discussed

during rounds and that appear on examinations, including board

examinations.

This book, which we hope is a useful learning tool for students, will also

be a vital reference for the practicing clinician. The book contains a great

deal of clinical information that can be applied on a daily basis. It is not

meant to replace the detail provided in reference textbooks. Our authors have

worked to distill the essence of what the clinician is looking for into

something that is user friendly.

We believe that the question-and-answer approach used in the Secrets

Series is a logical and efficient way to tackle clinical problems. This com￾plements a problem-based approach to medicine.

Small animal internal medicine has been blessed with an abundance of

high-quality textbooks. These, along with current journals, monographs, and

proceedings, serve to provide the clinician with a large amount of

information. Where does one start? Canine Internal Medicine Secrets is

different in that it relies on experienced authors to begin with a question that

may be asked on an examination or in clinical rounds and is followed with a

response that is based on the author’s experience and factual knowledge. The

book is not meant to be comprehensive; there are many standard textbooks

that can serve this role. The goal of this book is to provide readers with an

efficient means to find key information that will give them direction in the

management of their cases. Just as in veterinary school, we encourage

readers to continue reading other texts to further gain a better understanding

of their canine internal medicine problem.

We are proud to have authors who are not only well credentialed but also

highly experienced in their chosen fields. Their sections are interesting, up to

date, and concise. We would like to acknowledge our colleagues’ efforts in

completing this text; their contributions are greatly appreciated.

We are also indebted to Teri Merchant, Managing Editor, at Elsevier.

Without her, this project would not have happened.

We thank our wives, Diane and Suzette, and our children, Olivia, Kyle,

Luke, Sophie, Clara, and Joe. We could not have done this without their

support.

Stanley I. Rubin, DVM, MS, DACVIM

Anthony Carr, Dr. med. vet., DACVIM

ix

Section I

Neurology and Neuromuscular Diseases

Section Editor: Karen Dyer Inzana

1. Neurologic Examination and Lesion

Localization

Karen Dyer Inzana

1. Where do I start when performing a neurologic examination?

Always start by looking at the animal across the room. Look for abnormal body postures (i.e.,

head tilt or turn), abnormal movements (circling, head tremors), or behaviors that you would not

expect from an animal in the hospital environment (dementia, excessive solumnence or extreme

agitation). If any of these things are observed, then the problem must involve the brain lesion

(above the foramen magnum).

2. How will changes in gait help localize lesions?

After observing the animal across the room, next watch the animal walk, preferably on a

nonslippery surface. Look again for abnormal head postures or movements, but then concentrate

on gait. Is there one side that appears weaker than the other? Is there a similar amount of

coordination in the front and rear limbs? If the front limbs are abnormal, are they more or less

abnormal than the rear limbs? Because the brachial intumescence in most dogs is located between

C6 to T2 spinal cord segments, normal to near normal gait in the front limbs with poor

coordination in the rear limbs suggests a lesion caudal to the second thoracic spinal cord segment

(T2). If the front limbs are as weak or weaker than the pelvic limbs, then the problem likely

resides within the cervical intumescence. If the front limbs are abnormal, but appear stronger than

the pelvic limbs, this usually indicates a lesion rostral to C6. If one side (thoracic and pelvic

limbs) appears weaker than the other (hemiparesis), the same rules apply as previously described,

but one side of the spinal cord or brain is more severely affected than the other.

3. How can you be sure that an abnormal gait is caused by neurologic disease rather

than an orthopedic condition?

Sometimes it can be difficult to differentiate between neurologic and orthopedic diseases. The

best way to do this is with a series of tests referred to as postural reactions. Postural reactions are

a series of maneuvers that place the animal’s feet in an abnormal position to bear weight. The

animal must first recognize that the foot is in an abnormal position (sensory systems) and then

have the strength to replace the foot in a more normal position (motor systems). Animals with

orthopedic disease can accomplish most postural reactions. Occasionally animals with orthopedic

disease will resist the postural reactions that require a lot of movement on the weight-bearing

limb (e.g., hemiwalking, hopping, wheelbarrowing). However, it is extremely rare that all

postural reactions are abnormal in an animal with only orthopedic disease. The following are the

more common postural reactions.

● Conscious proprioception: Gently support the animal’s weight and turn one foot onto its

dorsal surface. I place a hand under the pelvis when evaluating the pelvic limbs, and under

the chest when examining the thoracic limbs. All four limbs should be examined. A normal

1

2 Neurologic Examination and Lesion Localization

response is to immediately flip the paw over onto the normal weight-bearing surface.

Abnormal responses include leaving the foot in the abnormal position, repositioning it

slowly or repositioning it incompletely (i.e., leaving one or more toes turned over).

● Wheelbarrowing: Support the animal’s pelvic limb with all of the weight on the thoracic

limbs. Push the animal forward so it must take several steps with the thoracic limbs to

maintain balance. This is often accomplished first with the head and neck in a normal

position, then repeated with the head and neck elevated. Abnormal responses include

delayed positioning of one or both thoracic limbs or exaggerated placement. Exaggerated

placement may suggest an abnormality in the cerebellum or caudal brain stem.

● Extensor postural thrust: Lift the animal off the floor and gently lower it onto the pelvic

limbs. A normal animal will often extend the limbs in anticipation of contact and then take

several steps backwards to position the limbs correctly. An alternative technique for dogs

that are too big to be picked up is to lift the front legs and push them backwards. I have

rarely found this alternative helpful.

● Hemistanding and hemiwalking: Lift both front and rear limbs on one side so that one

side supports all of the animal’s weight. Most normal animals can then accomplish lateral

hopping movements with the supporting limbs.

● Hopping: This reaction is similar to hemiwalking, but all of the animal’s weight is

concentrated on one limb. Again, normal animals can make lateral hopping movements in

the one supporting limb.

● Visual and tactile placing: For small animals that are easily supported, bring the animal

close to a tabletop while the examiner supports most of its weight. A normal response is for

the animal to see the table and reach for it with the closest limb. A similar tactile response

can be elicited by covering the animal’s eyes and advancing the animal so one limb brushes

the side of the table. Again, a normal animal will attempt to place the limb in a position to

bear weight.

4. When do you test spinal reflexes?

After completing the postural reactions, I have a good idea if the gait abnormality is

orthopedic or neurologic in origin. If it is neurologic, I use the same information regarding

localization of gait abnormalities that I described previously. Spinal reflexes help determine if the

problem involves the intumescence (either cervical or pelvic) or is “upstream” of the

intumescence. As previously mentioned, the cervical intumescence resides within spinal cord

segments C6-T2, whereas the pelvic intumescence resides within spinal cord segments L4-S3.

The intumescences contain the cell bodies for the lower motor neurons that innervate the thoracic

or pelvic limbs, respectively. Injury to the lower motor neurons will cause spinal reflexes to be

decreased or absent. Because the predominate clinical feature is caused by injury to the lower

motor neuron, paresis or paralysis with decreased or absent spinal reflexes is frequently referred

to as lower motor neuron clinical signs. Alternatively, if the lower motor neuron is intact but the

problem resides in one or more neurons upstream or closer to the motor center in the brain, then

spinal reflexes will still be intact and may be exaggerated even though the animal has lost some

or all voluntary motor ability in that limb. Paresis or paralysis with normal to increased spinal

reflexes if often referred to as upper motor neuron clinical signs that reflect that the injury is

upstream from the lower motor neurons.

5. Do spinal reflexes help distinguish between neurologic and nonneurologic diseases?

Rarely. Postural reactions do a better job of answering the question, Is the problem neurologic

or nonneurologic in origin? Spinal reflexes are strongly influenced by the temperament and

anxiety level of the animal. If the animal is anxious, then the muscles are tense, and spinal

reflexes often will appear exaggerated in an otherwise normal animal. If reflexes are abnormal, I

will repeat postural reactions. It would be most unusual for neuronal injury severe enough to

cause abnormal spinal reflexes to not also affect postural reactions.

6. Is it correct that spinal reflexes primarily distinguish between upper motor neuron

and lower motor neuron injury?

Yes, this is the primary value of spinal reflexes in a neurologic examination.

7. How do you perform spinal reflexes and what should they look like?

Thoracic limb reflexes include the following:

• Flexor reflex, withdrawal reflex, pedal reflex: Pinching the toe (or other noxious stimuli)

causes prompt flexion or withdrawal of the limb. The afferent branch varies with the area

pinched; the efferent nerves are those that mediate flexion of the limb (axillary,

musculocutaneous, median, and ulnar).

• Biceps reflex: This reflex is initiated by percussion of the biceps tendon (near its insertion on

the craniomedial aspect of the forearm) and both afferent and efferent axons are carried in the

musculocutaneous nerve (spinal cord segments C6-C8). The appropriate response is flexion of

the elbow. However, this is often hard to see when holding the limb, so often you only see a

visible contraction of the biceps muscle.

• Triceps reflex: This reflex is initiated by percussion of the triceps tendon near the olecranon.

Both afferent and efferent axons are carried in the radial nerve (spinal cord segments C7-T2)

and the appropriate response is extension of the elbow. This is the most difficult reflex to see

in the front leg.

• Extensor carpi radialis response: Percussion directly over the belly of the extensor carpi

radialis elicits extension of the carpus. Whereas they are both direct effects on the skeletal

muscle and stimulation of stretch receptors (and associated myotatic reflex), a normal response

requires an intact radial nerve. The appropriate response is extension of the carpus.

8. Pelvic limb reflexes include the following:

• Flexor reflex: This reflex is initiated by noxious stimulation of the limb. Afferents are carried

in either the femoral nerve (if the medial surface of the limb is stimulated) or sciatic nerve. The

efferent axons are carried in the sciatic nerve (L6-S1). The appropriate response is flexion of

the limb.

• Patellar reflex: Percussion of the patellar tendon elicits a brisk extension of the stifle. The

peripheral nerve controlling this reflex is the femoral nerve (spinal cord segments L4-L6).

• Perineal reflex: Noxious stimulation of the perineum results in constriction of the anal

sphincter and flexion of the tail (spinal cord segments S2-S3).

• Gastrocnemius reflex: Percussion of the Achilles tendon causes contraction of the

gastrocnemius muscle and extension of the hock. It requires an intact tibial branch of the

sciatic nerve (spinal cord segments L6-L7, S1).

• Cranial tibial response: Percussion directly over the cranial tibial muscle causes flexion of the

hock. Again this response is mediated by a combination of direct muscle contraction and a

myotatic stretch reflex. A normal response requires an intact peroneal branch of the sciatic

nerve (spinal cord segments L6-L7, S1).

9. What would a lesion between L4 and S3 spinal cord segments look like?

The animal would have gait abnormalities in the pelvic limbs. Postural reactions should be

decreased in the pelvic limbs and normal in the thoracic limbs. Spinal reflexes should be

decreased to absent in the pelvic limbs. In addition, the limb would feel flaccid and muscle

atrophy would occur quickly.

10. What would a lesion between T2 and L4 spinal cord segments look like?

The animal would have gait abnormalities in the pelvic limbs. Postural reactions should be

decreased in the pelvic limbs and normal in the thoracic limbs. Spinal reflexes should be

increased in the pelvic limbs and, occasionally, you may see abnormal reflexes. The limb should

not feel flaccid; muscle atrophy occurs slowly from disuse.

Neurologic Examination and Lesion Localization 3

11. What do you mean by abnormal reflexes?

There are several reflexes that are typically masked and only become apparent when the upper

motor neuron has been injured. These include a crossed extensor reflex and Babinski’s reflex.

The crossed extensor reflex is seen with the animal in lateral recumbency and appears as an

involuntary extension of the opposite limb during the flexor reflex. This is a normal reflex when

the animal is standing, but inhibited by descending spinal pathways in a recumbent animal. The

presence of this reflex is reliable evidence that these descending pathways have been injured.

Babinski’s reflex is elicited by stroking the caudolateral surface of the hock, beginning at the

hock and continuing to the digits. An abnormal response is extension of the digits. This reflex is

also an indicator of injury to inhibitory descending spinal pathways.

12. Does the presence of abnormal reflexes indicate a worse prognosis?

Abnormal reflexes become more prominent over time. Therefore their presence is an

indication that the problem has existed for weeks to months. Obviously, a more chronic lesion

would have a worse prognosis. However, the ability to consciously recognize painful stimulation

to areas caudal to the lesion is the most reliable prognostic indicator. Animals without conscious

pain sensation caudal to the lesion have a much worse prognosis than those that can still feel their

limbs.

13. Can you localize a lesion between the T2 and L4 spinal cord segments more precisely

with a clinical examination?

It is difficult to be extremely accurate with localization in areas other than the intumescences.

However, the panniculus reflex may be helpful. The panniculus reflex is caused by contraction of

the cutaneous trunci muscle in response to a sensory stimulus of the skin. Dorsal cutaneous

afferent nerves are stimulated. The impulse is transmitted up the spinal cord in ascending

superficial pain pathways that synapse on the lateral thoracic nerve (located between the C8 and

T2 spinal segments). The response is blocked in segments caudal to the injury. For example, an

animal with injury at T13-L1 would have a normal response cranial to the level, but the response

would be absent caudal to this point. This can be helpful in narrowing the localization within the

spinal cord. However, this is not the most reliable response and may still be present in animals

with severe spinal injury and absent in some with mild injury.

A focal area of pain (hyperpathia) can be a more sensitive lesion localizer. For example, an

animal with a type I disk herniation at T13-L1 may or may not have a panniculus response that

corresponds to this lesion. However, deep palpation in this area will often appear to cause pain.

Focal hyperpathia is only useful for animals with lesions that cause meningeal or periosteal

irritation. The spinal cord does not have pain receptors and so lesions that are confined to neural

parenchyma alone are not painful.

14. How would a lesion between the C6 and T2 spinal cord segments appear clinically?

The animal would have upper motor neuron signs to the pelvic limbs that would be

indistinguishable from the previous case. However, the thoracic limbs would also be affected and

would show lower motor neuron clinical signs because this is in the area of the cervical

intumescence. Occasionally, injury between C8 and T2 will also damage the sympathetic

innervation to the head because the first efferent neuron in the sympathetic chain is located in this

area. Clinical signs would include miosis, ptosis, and enophthalmus of the ipsilateral eye.

15. How would a lesion between the C1 and C6 spinal cord segments appear clinically?

These animals would be weak in all four limbs and spinal reflexes should be normal to

increased. As previously mentioned, the animals generally appear worse in the pelvic limbs than

in the thoracic limbs. It is rare to see an animal completely paralyzed with a cervical spinal lesion

because severe injury will cause paralysis of the respiratory muscles and death.

4 Neurologic Examination and Lesion Localization

16. Where would you localize the lesion in an animal with paralysis of all four limbs and

decreased spinal reflexes?

This would be the typical presentation of an animal with generalized peripheral nerve or

neuromuscular junction injury.

17. If an animal has a head tilt, where does this place the lesion?

An abnormal head posture is seen with injury rostral to the foramen magnum. Generally, the

head tilt is toward the side of the lesion. With careful observation, you will see that animals with

injury to the caudal portions of the brain have a typical head tilt that changes as you move

rostrally to a head turn. This is a subtle point and not always reliable, but it can be helpful at

times.

18. If all lesions in the brain cause a head deviation, then how can you localize lesions

within the brain?

Postural reactions are extremely helpful here. With focal lesions in the central nervous system

caudal to the midbrain, postural reactions will be abnormal on the same side as the lesion. With

focal lesions rostral to the midbrain, postural reactions will be abnormal on the side opposite the

lesion. It is easy to remember that this changes in the middle of the brain. Within the midbrain

itself, lesions in the caudal midbrain produce ipsilateral postural reaction deficits, whereas lesions

in the rostral midbrain, especially those rostral to the red nucleus, produce postural reaction

deficits on the side opposite the lesion. Because the head tilt is usually to the side of the lesion,

an animal with a right head tilt and postural reaction deficits on the right side has a lesion in the

midbrain or caudal. If an animal has a right head tilt and postural reaction deficits on the left side,

then the lesion is midbrain or rostral.

19. Can you localize lesions more precisely within the brain?

Cranial nerves can help localize lesions to very specific regions of the brain. Cranial nerves V

through XII are located in the metencephalon (pons) and myelencephalon (medulla); cranial

nerves III and IV are located in the mesencephalon (midbrain). Cranial nerve II is intimately

associated with the ventral diencephalon (thalamus, hypothalamus).

20. What do cranial nerves do?

Cranial nerve I is the olfactory nerve and mediates the sense of smell. It is difficult to

clinically evaluate this nerve.

Cranial nerve II is the optic nerve. You can often determine visual function from earlier parts

of the examination. By covering each eye of the animal and making a menacing gesture toward

each eye, you can evaluate vision in each eye. Unfortunately, other lesions such as facial nerve

paralysis or cerebellar disease may also alter the menace reaction. Pupillary light reactions are

also helpful in establishing optic nerve function. With injury to cranial nerve II, there will be no

direct pupillary light response on the abnormal side, and no consensual response in the other eye.

Cranial III carries parasympathetic innervation to the pupil. Injury to cranial nerve III will

cause the pupil on the same side to be dilated and not constrict with bright light. With a pure

cranial nerve III injury, the dog is still visual so menace reaction is still normal.

Cranial nerves III, IV, and VI (occulomotor, trochlear, and abducens nerves) innervate the

extraocular eye muscles. Injury to any one of these three will result in the eye being permanently

deviated to one side.

Cranial nerve V is the trigeminal nerve. It provides motor innervation to the muscles of

mastication and sensation to the entire face. Injury to this nerve often results in atrophy of the

ipsilateral temporalis muscle and analgesia to the ipsilateral side of the face.

Cranial nerve VII is the facial nerve. It controls the muscle of facial expression. Injury to this

nerve causes inability to blink or retract the lip. The nose may be deviated toward the normal side

Neurologic Examination and Lesion Localization 5

with early facial nerve injury and the nostril on the affected side will not flare with inhalation.

The facial nerve also carries the sensory fibers for taste, but this is rarely tested in practice.

Cranial nerve VIII is the vestibulocochlear nerve. It has two branches. The cochlear nerve

relays sensory impulses associated with sound. Bilateral injury results in deafness, but unilateral

injury can be difficult to detect without special electrophysiologic testing. The vestibular portion

of cranial nerve VIII mediates the sense of balance and orientation of the head and body with

respect to gravity. Deficits in this branch result in marked head tilt, and staggering or falling to

the side of the lesion. The vestibular nerve also plays an important role in coordinating eye

movement; therefore vestibular nerve injury often results in nystagmus and intermittent

strabismus.

Cranial nerves IX, X, and XI (glossopharyngeal, vagus, and accessory nerves) provide motor

innervation to the pharynx, larynx, and palate. Injury to these nerves causes inability to swallow,

a poor gag reflex, and inspiratory stridor because of laryngeal paralysis. The accessory nerve also

provides motor innervation to the trapezius muscle and parts of the sternocephalicus and

brachiocephalicus muscles. Denervation atrophy in these muscles can be seen with careful

examination.

Cranial nerve XII (hypoglossal nerve) provides motor innervation to the muscles of the

tongue. Injury results in paralysis of the ipsilateral side of the tongue.

21. How do you evaluate cranial nerves?

Cranial nerve evaluation is simple. I look at the animal’s pupils for asymmetry and evaluate

pupillary light reflexes (cranial nerve II, parasympathetic and sympathetic innervation), then

elicit a menace reaction from each eye (cranial nerves II and VII).

I move the animal’s head from side to side to be sure it can move the eyes in all positions

(cranial nerves III, IV, and VI), then touch its face by the eye, nose, and lip to be sure it has normal

sensation (cranial nerve V) and movement of the face (cranial nerve VII).

I open the animal’s mouth to evaluate jaw tone (cranial nerve V) and stimulate the pharynx

with my hand to evaluate gag reaction (cranial nerve IX, X, and XII) and look at its tongue to be

sure it has normal motor (cranial nerve XII).

For cranial nerve VIII, I look for abnormal body postures during the earlier parts of my

examination and carefully examine the eyes to be sure that there is normal conjugate eye

movement. This is best done while you position the animal for evaluation of spinal reflexes.

22. How would a lesion in the pons and medulla appear?

The animal would have a head tilt toward the side of the lesion with ipsilateral postural

reaction deficits. You should also observe deficits in cranial nerves V through XII on the same

side of the lesion.

23. How would a lesion in the midbrain appear?

The animal would have a head tilt to the side of the lesion, postural reaction deficits may be

ipsilateral or contralateral, but deficits in cranial nerves III and IV should be on the same side of

the lesion. In my experience, focal midbrain injury is rare.

24. How would a lesion in the thalamus appear?

The animal would have a head tilt toward the side of the lesion, postural reaction deficits on

the side opposite the head tilt, and often it will have seizures. Complete loss of cranial nerve II

function will be present only if the lesion is in the ventral portions of the hypothalamus near the

optic chiasm. If the injury is in other areas of the thalamus, the pupils may appear asymmetrical,

but the deficits will not appear complete.

6 Neurologic Examination and Lesion Localization

25. How would a lesion in the cerebrum appear?

Lesions in the cerebrum are often indistinguishable from lesions in the thalamus. If the injury

affects the occipital lobes of the cerebrum, then the animal may not have a menace on the

opposite side, but pupillary light reactions will be normal. Because these areas often appear

clinically the same, the cerebrum and thalamus-hypothalamus are often collectively referred to as

the forebrain.

26. Do seizures occur only with injury to the thalamus-hypothalamus or cerebrum?

Yes, seizure activity is a sign of forebrain disease.

27. We left out the cerebellum. What do lesions in the cerebellum look like?

The cerebellum is a complex structure that coordinates movement throughout the body.

Portions of the cerebellum are involved with the vestibular apparatus, and selective lesions in this

region will appear similar to cranial nerve VIII deficits. Lesions in other areas will cause

movements to appear incoordinated. The animal’s limbs may appear hypermetric or hypometric

during movement. Often the animal’s head will tremor when it is concentrating on some activity

such as eating or drinking.

28. Does injury to the cerebellum cause postural reaction deficits?

A lesion that only affects the cerebellum (e.g., cerebellar hypoplasia) will not cause postural

reactions to be absent, but they may be performed poorly or with exaggerated movements.

However, it is more common for the cerebellum to be injured along with the underlying pons and

medulla in which case postural reactions will be diminished or absent.

29. Can you have vestibular disease without postural reaction deficits?

Yes, if you injure any cranial nerve outside the calvaria, you will see loss of function of that

nerve, but the motor and sensory tracts in the brain stem will still be intact. Peripheral injury to

cranial nerve VIII commonly occurs with ear infections, some toxins, and idiopathic causes. In

this case, the animal will have a head tilt (to the side of injury) and a tendency to fall or roll to

that side. Sometimes they are so disorientated that postural reactions are difficult to evaluate.

However, if you are careful and persistent, you will find that postural reactions are still intact.

Another interesting feature of peripheral vestibular disease is that the nystagmus is always in the

same direction. It generally is horizontal with the fast phase away from the head tilt, although it

can be rotatory as well. What I mean by “always in the same direction” is you may not see

abnormal eye movements in all body positions, but when you do see it, the movement is always

the same. With injury to brain stem or cerebellar structures, the nystagmus often changes

direction when the animal is rolled in other body positions. We should note that both the facial

nerve and sympathetic innervation to the face pass through the inner ear and are also often injured

with inner ear infections. Cranial nerve VII is close to cranial nerve VIII in the brain stem and

these are often injured by a single lesion, but it is rare to see Horner’s syndrome with a lesion in

the central nervous system.

30. I feel comfortable with localizing lesions outside the brain, but I never seem to be

able to localize problems within the brain. Is this unusual?

Honestly, most of the intracranial diseases encountered in small animal practice are multifocal

or diffuse in nature. Things such as metabolic encephalopathies, toxic encephalopathies, or

infectious or inflammatory diseases typically affect more than one area of the brain and so they

are not readily localizable. Diseases that tend to be focal include tumors and infarcts; these can

be difficult to localize if they are large enough that they put pressure on large parts of the brain.

It is important to be able to localize lesions, though; otherwise you would not know that the

problem is multifocal or diffuse.

Neurologic Examination and Lesion Localization 7

2. Seizures

Karen Dyer Inzana

1. What is a seizure?

A seizure is a clinical sign of cerebral dysfunction. It results from a usually transient, hyper￾synchronous electrical activity of neurons. The outward manifestation of this electrical event

varies with the number and location of neurons involved. Partial seizures are a manifestation of

dysrhythmia occurring in only a limited number of neurons, whereas generalized seizures arise

from simultaneous activation of neurons in both cerebral hemispheres.

2. What causes a seizure?

Anything that lowers the brain’s ability to prevent hypersynchronous electrical activity will

cause a seizure. Many refer to this ability as the seizure threshold. Every animal is capable of

having a seizure, but there is a mechanism that prevents this from happening in a normal animal.

Exactly what constitutes this mechanism is not entirely clear, but most likely represents a balance

between excitatory and inhibitory influences (both ionic and neurotransmitter levels).

Below is a list of differentials for seizures and the age that they are most likely to occur

(Table 2-1). Note that a young dog (younger than 6 months of age) is more likely to have seizures

as a result of a congenital disorder (hydrocephalus, lissencephaly, portosystemic shunt),

intoxication, or infectious disease, whereas an older dog (older than 6 years of age) is more likely

to have neoplastic disease. Epilepsy is more likely to occur in middle-age animals.

8

Table 2-1 Common Causes of Seizures in Dogs by Age of First Seizure

CAUSE < 1 YEAR 1-5 YEARS > 5 YEARS

Degenerative

Storage disease X X X (uncommon)

Anomalous

Hydrocephalus X

Lissencephaly X

Primary epilepsy X

Metabolic

Portosystemic shunts X

Acquired liver disease X

Hypoglycemia X X

Hyperlipoproteinemia X X

Electrolyte imbalance X X X

Neoplastic (brain tumors) X

Infectious XXX

Inflammatory without infectious cause* X

Trauma (secondary epilepsy) XXX

Toxic XXX

*Granulomatous meningoencephalitis in dogs, nonsuppurative meningoencephalitis in cats.