Handbook of Veterinary Neurology, 5th Edition

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HANDBOOK OF VETERINARY NEUROLOGY ISBN: 978-1-4377-0651-2

Copyright © 2011, 2004, 1997, 1993, 1983 by Saunders, an imprint of Elsevier Inc.

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Notice

Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
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Practitioners and researchers must always rely on their own experience and knowledge in
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With respect to any drug or pharmaceutical products identified, readers are advised to check the
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Library of Congress Cataloging-in-Publication Data

Lorenz, Michael D.
Handbook of veterinary neurology / Michael D. Lorenz, Joan R. Coates, Marc Kent. — 5th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4377-0651-2 (hardcover : alk. paper) 1. Veterinary neurology—Handbooks, manuals,
etc. 2. Nervous system—Diseases—Diagnosis—Handbooks, manuals, etc. I. Coates, Joan R. II. Kent,
Marc. III. Title.
[DNLM: 1. Nervous System Diseases—veterinary—Handbooks. 2. Animal Diseases—diagnosis—
Handbooks. 3. Neurologic Examination—veterinary—Handbooks. SF 895]
SF895.O44 2012
636.089’680475—dc22 2010034818

Vice President and Publisher: Linda Duncan

Publisher: Penny Rudolph
Senior Developmental Editor: Shelly Stringer
Associate Developmental Editor: Brandi Graham
Publishing Services Manager: Catherine Jackson
Senior Project Manager: Rachel E. McMullen
Design Direction: Jessica Williams

Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1

 We dedicate this edition to our mentors who helped train and inspire each of us
in the discipline of clinical neurology. We are especially indebted to Alexander
deLahunta, John Oliver, Joe Kornegay, and Joe Mayhew who have paved our way
for the fifth edition of the Handbook of Veterinary Neurology. We are sincerely
grateful to our current and past colleagues who have continued to foster our knowledge
of veterinary neurology and neurosurgery and who have mentored us during our career
endeavors. We dedicate this book to our students, past, present, and future, whose
curiosity and questions have inspired us to develop better methods of teaching. And,
we dedicate this book to our families for their support and understanding that enabled
us to spend the extra time required to complete this edition.
 PREFACE

T
he fifth edition of Handbook of Veterinary Neurology has has been substantially updated to include new diseases
been substantially updated, providing students and reported since the fourth edition was published. It contains
practitioners with up-to-date information on small more than 1000 references.
and large animal neurology. The new edition is in full color,
enhancing the learning experience and providing a stronger Veterinary Neurology Cases
knowledge of neuroanatomy. We have continued to use the veterinaryneurologycases.com
problem-oriented format from previous editions. The empha-
sis remains on lesion localization because one cannot diagnose The fifth edition has an accompanying website that can be
what is wrong if one does not know where the lesion(s) is (are) found at www.veterinaryneurologycases.com. The website
located. includes 20 video case studies that correlate to all of the cases
Handbook of Veterinary Neurology is simple and easy to presented in Chapters 2 and 15 of the book. Each case study
use by veterinary students and practitioners. Numerous algo- on the website is presented as a narrated PowerPoint presenta-
rithms are included that diagram the logic necessary to local- tion with videos highlighting important aspects of each case,
ize lesions and to formulate diagnostic plans. Each chapter has such as symptoms, lesion localization, and diagnosis.
been extensively reviewed, updated, and heavily referenced.
A unique feature of our book is the Appendix. The Michael D. Lorenz
Appendix lists breed-associated, breed-specific, or inherited Joan R. Coates
neuromuscular diseases in domestic animals. The Appendix Marc Kent

vii
 ACKNOWLEDGMENTS

We are grateful for the assistance of the Elsevier team, Shelly Stringer, Brandi Graham,
Penny Rudolph, and Rachel McMullen. We acknowledge the College of Veterinary Medicine
at Cornell University for permitting use of neurologic images posted to their website.

We would like to especially acknowledge Philip J. Johnson, G. Diane Shelton, and

William F. Fales, who have assisted us with their areas of expertise in preparation of this book.

Finally, we thank all of you, our colleagues, for making the fifth edition necessary.

ix
 C HAPTER 1

Neurologic History, Neuroanatomy,

and Neurologic Examination

T
he objectives in the management of an animal with a Because chemistry panels are usually available at less cost
problem that may be related to the nervous system are than individual tests, selection of tests is usually not necessary.
to (1) confirm that the problem is caused by a lesion Otherwise, the selection of chemistry profiles should be based
in the nervous system, (2) localize the lesion in the nervous on the problems presented. Additions to the database are rec-
system, (3) estimate the severity and extent of the lesion in ommended for specific problems.
the nervous system, (4) determine the cause or the pathologic
process or both, and (5) estimate the prognosis with no treat-
ment or with various alternative methods of treatment. PROBLEM LIST
Many diseases may be accompanied by a complex combi-
nation of clinical signs and laboratory data. Diagnosis of these A problem list is formulated from information obtained from
diseases may seem impossible. Weed demonstrated the value the minimum database. For each problem, a diagnostic plan
of starting the diagnostic process by independently listing and is formulated. A diagnostic plan for a neurologic problem
analyzing all the patient’s problems.1 A minimum set of data includes the following steps:
(minimum database) is necessary to solve any medical prob- 1. The level of the lesion is localized with a neurologic
lem. The minimum database may be modified because of risk, examination. Confirmation of the lesion may require
cost, or accessibility as balanced against the severity of the dis- diagnostic imaging.
ease. Priorities should be established for collecting data that 2. The extent of the lesion is estimated both longitudinally
evaluate the most probable causes of a problem. Tests for rare and transversely (e.g., L4-6 spinal cord segments, left
diseases and those that are dangerous are reserved until last.
Weed’s problem-oriented system is eminently suited for
neurologic diagnosis. The steps necessary for the management BOX 1-1
of a neurologic problem are listed in Box 1-1.
Plan for Neurologic Diagnosis
MINIMUM DATABASE
Collect minimum database
The initial evaluation of a patient, including a history and a Identify problems
physical examination, usually provides evidence that a neuro- Identify one or more problems related to nervous system
logic problem is present (Table 1-1). Localize level of lesion
Some problems are difficult to classify, for example, syn- Estimate extent of lesion within that level
cope versus epileptic seizures, or weakness (loss of muscle List most probable causes (rule-outs or differential diagnosis)
strength) versus paresis (loss of motor control). The initial Construct diagnostic plan to determine cause or pathologic
physical examination of every patient should include a screen- injury
ing neurologic examination designed to detect the presence Determine prognosis with and without therapy
of any neurologic abnormality. The screening examination is
described later in the section on neurologic examination. Modified from Oliver JE Jr: Localization of lesions in the nervous
The minimum database recommended for an animal with system. In Hoerlein BF, editor: Canine neurology, ed 3, Philadelphia,
a neurologic problem is listed in Box 1-2. 1978, WB Saunders.

2
 CHAPTER 1 Neurologic History, Neuroanatomy, and Neurologic Examination 3

TABLE 1-1 BOX 1-2

Clinical Problems in the Nervous System Minimum Database: Neurologic Problem
Problem Localization
History
Usually of CNS Origin Physical examination
1. Epileptic seizures Cerebrum, diencephalon Neurologic examination
2. Altered mental status Cerebrum, limbic system, Clinical pathology:
diencephalon Complete blood count
a. Stupor or coma Brainstem reticular activating Urinalysis
formation Chemistry profile
b. Abnormal behavior Limbic system Creatine kinase activity
3. Paresis, paralysis, See Tables 2-2 to 2-4
proprioceptive deficit Modified from Oliver JE Jr: Localization of lesions in the nervous
4. Ataxia system. In Hoerlein BF, editor: Canine neurology, ed 3, Philadelphia,
1978, WB Saunders.
a. Head tilt, nystagmus Vestibular system
b. Intention tremor, Cerebellum
dysmetria This chapter describes the fundamentals for making a cor-
rect neurologic diagnosis. It includes the neurologic history,
c. General proprioceptive Spinal cord
construction of a sign-time graph, neuroanatomy and organi-
deficits, no brain signs
zation of the nervous system, and the neurologic examination.
5. Hypesthesia, anesthesia See Figures 1-36,1-38, and Lesion localization is discussed in Chapter 2.
1-39; CN V
Possibly of CNS Origin
1. Syncope Usually cardiovascular, meta-
THE HISTORY
bolic
Traditionally, the history is taken by the veterinarian. Para-
2. Weakness See Figure 2-1 and Table 2-2; professional personnel (e.g., registered veterinary technician,
metabolic or muscular veterinary assistant, nurse) assist the process by obtaining a
3. Lameness Orthopedic: see Table 1-5 defined database that is used in conjunction with a problem-
4. Pain, hyperesthesia oriented medical record system.1 If one establishes a minimum
a. Generalized Thalamus, meningitis, lesions base of necessary information about every patient or about
affecting multiple joints every patient with a certain problem, then one can obtain that
muscles, bones information in a number of ways.
b. Localized See Figures 1-37 to 1-40; CN V
5. Blindness
Owner-Supplied History
A basic history can be obtained by use of a well-designed ques-
a. Pupils normal Diencephalon or occipital lobe
tionnaire. The receptionist gives the questionnaire to the cli-
of cerebrum (contralateral) ent, who completes it in the reception area. A paraprofessional
b. Pupils abnormal Retina, optic nerve, optic can assist the client in answering difficult questions. The gen-
chiasma eral medical history is available for review by the veterinarian,
6. Hearing deficit who notes important items that may need further clarification.
a. No vestibular signs Cochlear labyrinth Problem-specific owner histories can be used to supplement
b. Vestibular signs CN VIII, vestibular labyrinth, the general history.
rostral medulla
7. Anosmia Nasal passages, CN I Role of the Veterinarian
8. Urinary incontinence Pudendal/pelvic nerves,
The veterinarian should review most of the important parts of
the history with the client. Misinterpretation of terminology,
spinal cord, brainstem (see
a course of events, or clinical signs occurs frequently. The vet-
Chapter 3) erinarian may need to rephrase questions several times before
receiving a meaningful answer. The manner in which a question
Modified from Oliver JE Jr: Localization of lesions in the nervous is phrased is important. Questions that imply negligence or igno-
system. In Hoerlein BF, editor: Canine neurology, ed 3, Philadelphia, rance on the part of the client may lead to defensive answers.
1978, WB Saunders.
Questions that suggest a correct answer may lead the client to
interpret events incorrectly. All questions should be framed so
side). The neurologic examination provides most of this that the answer “I don’t know” is an acceptable alternative; oth-
information, but ancillary diagnostic procedures may be erwise the client may hypothesize rather than relate facts.2
of assistance.
3. The cause of the pathologic process is determined. The Neurologic History
history is most useful for establishing the class of disease Signalment
(neoplasia, infectious disease, trauma, and so forth). The species, breed, age, and sex of the patient may provide impor-
Laboratory, diagnostic imaging, or electrophysiologic tant clues to the diagnosis. Although few diagnoses can be posi-
tests are usually required to substantiate the diagno- tively ruled in or out on the basis of the signalment, many diseases
sis. From this information, the clinician can establish a are more or less likely to occur among certain groups of animals.
prognosis with and without appropriate therapy, based The prevalence of some diseases varies greatly among spe-
on information available about the disease. cies and breeds. Many infectious diseases are species specific,
4 PART 1 Fundamentals

such as canine distemper, feline infectious peritonitis, and disease may have been observed to stumble or to have diffi-
equine protozoal encephalomyelitis. Known inherited diseases culty with stairs for some time before clear manifestations of
must be considered, especially in cases involving multiple off- paresis were evident.
spring of the same litter or lineage. The Appendix lists many The course of the disease as revealed by the sign-time graph
of the diseases with a species or breed predilection. Infectious provides important information about the cause of the disease
diseases are discussed in Chapter 15. (see Figure 1-1). Slowly progressive diseases with an unrelent-
Young animals are more likely to have congenital and inher- ing course are immediately distinguished from acute diseases.
ited disorders and infectious diseases. Older animals are more The first step in making an etiologic diagnosis is classifying the
likely to have degenerative and neoplastic diseases. Although problem as acute or chronic and progressive or nonprogres-
these criteria are not absolute, the probability is much greater sive. With this information, the problem logically falls into a
that a 8-year-old brachycephalic dog experiencing seizures group of diseases (Figures 1-1 and 1-2 and Table 1-2).
will have a neoplasm of the central nervous system (CNS) The neurologic examination can further narrow the choice
rather than a congenital anomaly. In the preliminary assess- of diseases by indicating whether the problem is focal or dif-
ment, and sometimes in the final assessment, a diagnosis is an fuse (see Figure 1-2). After a general etiologic or pathologic
ordering of probabilities. diagnosis is considered, the diagnostic plan can be established
so that one can investigate each probable cause (see discussion
Sign-Time Graph of diagnostic methods in Chapter 4).
Construction of a sign-time graph is useful for evaluating the
course of a disease (Figure 1-1). Prognosis
The sign-time graph plots the severity of clinical signs (on Providing the owner with a reasonably accurate prognosis is
the vertical axis) against time (on the horizontal axis). A com- an essential part of clinical neurology. The prognosis is influ-
plete history allows the clinician to construct a graph that has enced by many variables. The major variables are the location,
no major gaps.3 The sign-time graph is not usually drawn and extent, and cause of the lesion.
entered on the case record. Rather, it is a useful tool for the The clinical course provides significant insight into the
clinician to construct mentally. prognosis. Slowly progressive diseases such as neoplastic or
The time of onset of some problems may be exact (e.g., degenerative conditions have a much poorer prognosis than
an automobile accident), or it may be difficult to determine, those that have passed peak severity and are improving (see
as in the case of neoplastic disease. The first time the client Figure 1-1).
recognizes a problem must be taken as the starting point. Clinical signs are also valuable clues to prognosis. Spinal
Sometimes seemingly unrelated episodes may be the earliest cord compression produces signs that vary with increasing
signs and are recognized as such only as the complete history compression (Figure 1-3).
unfolds. For example, an animal with degenerative spinal cord The signs are not related to the location of the tracts in the
spinal cord but do correlate with the diameter of the fibers.
With spinal cord compression, large fibers lose function before
small fibers are affected. Functional recovery is possible until
pain perception is lost. An animal with no response to a pain-
Trauma or Vascular
ful stimulus for more than 48 hours has a low probability of
Anomaly recovery. Animals that do recover still may have severe motor
CLINICAL SIGNS

deficits.
The duration of the lesion is also a significant factor in
prognosis because nervous tissue tolerates injury for only a
sm short time. Spinal cord compression has been studied more
opla
n

Ne thoroughly than most CNS injuries. Spinal cord compression

tio

e
ativ
ec

ner severe enough to abolish voluntary motor function but not

ge
Inf

De severe enough to abolish the response to a noxious stimulus

is associated with a reasonably good prognosis for recovery if
decompression is achieved within 5 to 7 days. The longer the
duration of compression, the slower the recovery.
The location and character of the lesion are also important.
TIME An infarction of the spinal cord can range from mild to severe.
Figure 1-1 Sign-time graph of neurologic diseases. Progression of Equally severe lesions have different prognoses, depending on
metabolic, nutritional, and toxic diseases is variable, depending on the location. For example, an animal with an infarct primarily
the cause. affecting gray matter at the L1 segment, with intact sensation

Acute Chronic

Progressive Nonprogressive Progressive

Young Adult Young Adult Young Adult

(<1 year) (>1 year) (<1 year) (>1 year) (<1 year) (>1 year)

Focal Diffuse Focal Diffuse Focal Diffuse Focal Diffuse Focal Diffuse Focal Diffuse
Anomalous Inflammatory Neoplastic Inflammatory Anomalous Rare Traumatic Rare Inflammatory Degenerative Degenerative Degenerative
Neoplastic Degenerative Toxic Traumatic Vascular (Abscess) Metabolic (Disk Vertebral) Metabolic
Inflammatory Toxic Degenerative Vascular Nutritional Neoplastic Inflammatory
(Abscess) Nutritional (Abiotrophy) Toxic Inflammatory Nutritional
Immunologic (Abscess)
Figure 1-2 Classification of neurologic diseases in approximate order of frequency.
 CHAPTER 1 Neurologic History, Neuroanatomy, and Neurologic Examination 5

to the pelvic limbs, has a reasonably good prognosis. The same clinical neurology. Although considerable debate exists over
degree of injury at the L5 segment is likely to produce perma- the amount of neuroanatomy that must be learned, for prac-
nent dysfunction because of destruction of the lower motor titioners and students, it is much less than the total body of
neurons supplying the femoral nerve. information currently available. The following sections present
an overview of the organization and function of the nervous
system.
ANATOMIC AND FUNCTIONAL
ORGANIZATION OF THE NERVOUS Central Nervous System
SYSTEM—AN OVERVIEW The CNS consists of the brain and spinal cord. Embryologi-
cally, the CNS develops from ectoderm that forms the neural
Neurologic examination and lesion localization are depen- tube. The brain is divided into the cerebral hemispheres, brain-
dent on understanding basic concepts of neuroanatomy and stem, and cerebellum. The five major areas of the brain are
neurophysiology and the terminology commonly used in the telencephalon (cerebrum), diencephalon, mesencephalon,
metencephalon, and myelencephalon (Figure 1-4).

TABLE 1-2 Telencephalon (Cerebrum)

This large area includes the lobes of the cerebral hemispheres,
Checklist for Differential Diagnosis subcortical basal nuclei, olfactory bulbs (cranial nerve I
[CN I]), cerebral peduncles, and hippocampus. In general, dis-
Category of Disease Examples
tinct gross landmarks separating the various lobes are absent.
D = Degenerative Primary axonal degeneration From a clinical standpoint, lesions cannot be reliably localized
Storage disorders to a specific lobe of the cerebrum. The following are the lobes
of the cerebral cortex:
Myelin disorders
Frontal: This lobe includes the neurons responsible for
Neuronopathy voluntary motor functions, especially learned or skilled
Intervertebral disk disease responses. The major motor pathways are the cortico-
Spondylosis spinal tracts.
Spondylopathy Piriform: This lobe is the termination site for tracts that
A = Anomalous Congenital defects relay information for smell.
M = Metabolic Nervous system disorders secondary Parietal: This lobe largely functions for conscious per-
to an abnormality of other organ ception of touch, pressure, temperature, and noxious
systems (e.g., hypoglycemia, stimuli.
uremia, hypoxia, hepatic) Temporal: This lobe functions for conscious perception
of sound (hearing) and shares some functions with the
N = Neoplastic All tumors
parietal lobe.
Nutritional All nutritional disorders
Occipital: This lobe contains vision centers.
I = Idiopathic Epilepsy The following are the three types of axons (fibers) from
Facial nerve paralysis cortical neurons:
Vestibular dysfunction Association fibers: axons that communicate with other
Trigeminal nerve neurons in the same cerebral hemisphere.
Immune Myasthenia gravis (acquired) Projection fibers: axons that leave the cerebrum via the
Polyradiculoneuritis internal capsule to enter the brainstem (e.g., the cor-
Myositis ticospinal tracts). These fibers have important clinical
Inflammatory Infectious and noninfectious diseases application to lesion localization and will be described
further in the section on Motor Functions.
Immune mediated
Commissural fibers: axons that cross from one cerebral
T = Traumatic Physical injury
hemisphere to the other.
Toxic Exposure to all toxic agents (may
include tetanus and botulism) Diencephalon
V = Vascular Infarct The diencephalon includes the thalamus and hypothalamus.
Ischemia The rostral-ventral border is demarcated by the optic chiasm.
Hemorrhage The optic tracts lie on the lateral surfaces. The thalamus con-
tains nuclei that receive sensory information from many areas.

Figure 1-3 Progression of signs in spinal cord compression.

6 PART 1 Fundamentals

The ascending reticular activating system (ARAS) arises

in the pons and is responsible for consciousness. The pons
contains motor pathways from the cerebrum that synapse in
the cerebellum. The cerebellum composes the dorsal met-
encephalon. It coordinates motor activity and helps regulate
muscle tone.

Myelencephalon (Medulla Oblongata)

The myelencephalon contains the neurons of CN VI through
XII (Figure 1-5) and central components of the vestibular sys-
tem. Motor tracts (medullary reticulospinal) also arise from
within this area. The major centers for respiratory and vaso-
motor (cardiac) function lie mostly in the medulla.

Forebrain
The forebrain contains the telencephalon and diencephalon.
Lesions affecting these areas generally create contralateral
clinical signs and generally are similar. Forebrain signs include
blindness, depression, seizures, contralateral loss of postural
reactions, and contralateral sensory deficits.

Midbrain
The midbrain has been described already (see section on
Mesencephalon). Lesions in the midbrain produce abnor-
mal mentation, disorders of ocular movement (nystagmus
[oculocephalic reflex]) and position (strabismus), dilated
(parasympathetic dysfunction) or constricted (sympathetic
dysfunction) pupil(s), poor or absent pupillary light reflexes,
gait deficits, and contralateral or ipsilateral postural reaction
Figure 1-4 Segmental organization of the brain. Five major deficits.
regions are significant clinically: the cerebrum, including the
cerebral cortex, cerebral white matter, and the basal nuclei; the Hindbrain
diencephalon, including the thalamus and the hypothalamus; These three structures lie in the caudal cranial fossa (cau-
the brainstem, including the midbrain, the pons, and the medulla dal to the osseous tentorium) of the skull. The hindbrain
oblongata; the vestibular system, including the labyrinth (periph- includes the pons, medulla, and cerebellum. The pons and
eral) and the vestibular nuclei (central) in the rostral medulla; medulla also contain upper motor neurons responsible for
and the cerebellum. (From Hoerlein BF: Canine neurology, ed 3, the generation of gait. Lesions in the pons and medulla cause
Philadelphia, 1978, WB Saunders.) ipsilateral motor and sensory deficits, vestibular dysfunction,
deficits in cranial nerve function (CN V-XII), and abnormal
mentation. Clinical signs of cerebellar dysfunction include
It serves as the major relay center for afferent (sensory) fibers incoordination, cerebellar ataxia predominated by hyperme-
projecting to the cerebral cortex. The hypothalamus lies ven- tria in which there is overflexion of the joints of the limbs
tral to the thalamus and has neuroendocrine and autonomic during the swing phase of the gait. The overall impression
functions. It connects to the pituitary gland via the infundibu- is that the animal is overreaching as it advances the limb.
lar stalk. Additionally, intention tremors may be present. Because the
cerebellum has direct connections with the vestibular sys-
Mesencephalon (Midbrain) tem, cerebellar disorders also can cause signs of vestibular
The mesencephalon contains the neurons for CN III (oculo- dysfunction. Lesions in the cerebellum also can cause men-
motor) and CN IV (trochlear), which innervate extraocular ace deficits with normal vision; the pathway for this is still
muscles. The rostral and caudal colliculi, located in the tectum unknown.
(roof) or dorsal aspect of the midbrain, are associated with
visual and auditory reflexes, respectively, and relay informa- Brainstem
tion to the cerebellum. The centers for pupillary light reflexes Anatomically, the brainstem contains the diencephalon, mes-
(parasympathetic-pupillary constriction) (parasympathetic encephalon, metencephalon, and myelencephalon. Func-
motor nucleus of CN III) and motor to extraocular muscles tionally, it includes all structures except the diencephalon.
(oculomotor nuclei of CN III) also are located in the dor- Functionally, most clinicians restrict the brainstem to the pons
sal aspect of the midbrain. Beneath the tectum lies the teg- and medulla. Clinical signs are those previously described for
mentum, the origin of the tectotegmentospinal tract, which the midbrain and hindbrain. Moreover, clinical signs of dien-
provides the upper motor neurons (UMNs) pathway for the cephalic lesions can be indistinguishable from those involving
sympathetic innervations. Finally, centers (red nucleus) for the telencephalon.
motor control of gait are located here.
Anatomic Organization of the Spinal Cord
Metencephalon The spinal cord comprises peripheral white matter composed
The metencephalon contains the pons and cerebellum. The of nerve tracts. The tracts are organized into specific motor
pons contains neurons for CN V (trigeminal), whose axons (efferent) and sensory (afferent) pathways. Gray matter is
innervate the muscles of mastication. It also provides sensory located centrally and is composed of interneurons and motor
innervation to the face (maxillary and ophthalmic regions) neurons that innervate muscle. Specific structures are dis-
and mandible and is the location of the center for micturition. cussed in sections on functional organization of the CNS.
 CHAPTER 1 Neurologic History, Neuroanatomy, and Neurologic Examination 7

Figure 1-5 The origin and distribution of the cranial nerves in the dog. N, Nerve; OPHTH,
ophthalmic nerve; MAX, maxillary nerve; MAN, mandibular nerve. (From Hoerlein BF: Canine
neurology, ed 3, Philadelphia, 1978, WB Saunders.)

Peripheral Nervous System neuronal cell body, its axon, junction between the axon and
The peripheral nervous system contains the axons of the spi- muscle (neuromuscular junction), and muscle are known as the
nal and cranial nerves and their receptors and effector organs. lower motor neuron unit (LMN unit). The anatomic distribu-
It includes both general and autonomic components. Peripheral tion and function of spinal nerves are discussed later (see section
nerves may contain fibers that are motor, sensory, or both. The on lower motor neurons, or LMNs) and in Chapters 3 and 5.
motor neuron cell body is typically located in the CNS. The Cranial nerves are further discussed in Chapters 8, 9, and 11.
8 PART 1 Fundamentals

Autonomic Nervous System Special Visceral Efferent System

The autonomic nervous system contains sympathetic and Neurons in the special visceral efferent (SVE) innervate stri-
parasympathetic divisions. It is a multineuron system. Cen- ated muscle derived from brachial arch mesoderm. They are
tral neurons are located in the hypothalamus, midbrain, pons, found in CN V, VII, IX, X, and XI.
and medulla. The hypothalamus is the primary center for inte-
grating autonomic functions. Axons traverse the brainstem to General Somatic Afferent System
affect autonomic LMNs, referred to as preganglionic neurons, The general somatic afferent (GSA) system includes sensory
located in the brainstem and spinal cord. Autonomic LMNs neurons that have receptors in the surface of the head, body,
innervate the smooth muscle of blood vessels and visceral and limbs. The neurons are located in CN V and all spinal
structures, glands, and cardiac muscle. Sensory fibers from nerves. It detects touch, temperature, and noxious stimuli.
body viscera are included in the peripheral component.
The LMNs of the sympathetic nervous system are distrib- Special Somatic Afferent System (SSA)
uted in the thoracolumbar spinal cord segments and generally This system includes vision and hearing, and neurons are asso-
use the spinal nerves for distribution to muscle and skin. Spe- ciated with CN II and VIII.
cific nerves control visceral function. The cranial sympathetic
nerve has considerable importance to clinical neurologists in General Visceral Afferent System (GVA)
lesion localization. For example, the LMNs of the sympathetic This system includes sensory neurons from visceral structures
nervous system destined to innervate the eye are located in of the head, body cavities, and blood vessels. Neurons are
spinal cord segments T1-3, and these axons leave the spinal located in CN VII, IX, and X, and in spinal nerves.
cord associated with roots of the brachial plexus. The cra-
nial sympathetic nerve traverses the thorax and the cervical Special Visceral Afferent (SVA)
region in association with the vagus nerve (vagosympathetic This is the system for taste and smell. Taste receptors are asso-
trunk). Axons synapse on neurons in the cranial cervical ciated with CN VII, IX, and X, and smell is associated with
ganglion. Axons from these neurons course near the middle CN I.
ear and are distributed to the head via the vasculature and
other cranial nerves. Of the numerous structures of the head General Proprioception (GP)
innervated by sympathetic fibers, clinical signs are typically Proprioception is detection of changes in position of the trunk,
appreciated because of the effect of the axons that innervate limbs, and head. General proprioception neurons are associ-
the dilator muscle of the pupil, which are carried to the eye ated with all spinal nerves and CN V.
along with fibers of CN V (ophthalmic branch).
The LMNs of the parasympathetic nervous system are Special Proprioception (SP)
located in the brainstem (CN III, VII, IX, and X) and sacral This is the vestibular system, and neurons are associated with
spinal cord segments. The pupillary light reflex is described in CN VIII.
following sections. The vagus nerve (CN X) is the major motor Over the years we have determined that this “classic”
nerve for innervation of the muscles of the larynx, esophagus, scheme is difficult for students and practitioners to remem-
and thoracic and abdominal viscera (see Chapter 9). The pel- ber. Therefore we use a scheme that describes function based
vic nerve innervates the detrusor muscle of the bladder (see on motor, GP, vestibular, general sensory (touch, temperature,
Chapter 3). pressure, and response to noxious stimuli), special sensory
(smell, taste, vision, and hearing), cerebellar, and cognitive
Functional Organization of the Central Nervous systems. These major systems are described in subsequent
System sections.
Functionally, the CNS can be classified in several ways, but a
simple scheme includes motor (efferent), sensory (afferent), Motor Systems
and autonomic systems (efferent and afferent). The term The motor system is composed of two divisions, the upper
efferent means conducting away from a center and usually and lower motor neurons. Lesions of the motor system pro-
indicates motor function. Afferent means conducting toward duce clinical signs called paresis or paralysis, depending on the
a center and usually indicates sensory function. Neuroanato- severity or completeness of lesions.
mists may divide the major functions according to a scheme
that relates function to embryologic development. That Upper Motor Neurons
scheme is presented because the terms are still used in clini- UMNs are responsible for initiating voluntary motor func-
cal literature.4 tions and modulating the activity of the LMN units. They are
located in the cerebral cortex and brainstem and are found
General Somatic Efferent System in both the somatic and autonomic systems. Their axons are
The general somatic efferent (GSE) system includes motor organized into specific tracts, and they synapse in spinal cord
neurons that innervate voluntary striated muscle of the head gray matter on interneurons or directly on LMNs. The UMN
and skeleton. These neurons are found in CN III, IV, VI, and system is divided into the pyramidal and extrapyramidal sys-
XII and all spinal nerves. tems (Figure 1-6).
The pyramidal system allows animals to perform finely
General Visceral Efferent System skilled movements but is not necessary for initiation of gait
The general visceral efferent (GVE) system includes motor in animals. Neurons are located in the frontal/parietal lobe
neurons of the autonomic nervous system. It includes neu- of the cerebral cortex (caudal cruciate gyrus) and the axons
rons in CN III, VII, IX, X, and (for parasympathetic division) are contained in the corticospinal tracts. Axons cross in the
XI and all spinal nerves. It includes sympathetic and para- pyramids located in the caudal medulla and descend on the
sympathetic divisions. The thoracic and lumbar spinal cord contralateral side. Axons synapse on LMNs in the spinal cord
regions contain preganglionic neurons for the sympathetic and cranial nerve LMNs in the brainstem. Lesions of the
division. The cranial (CN III, VII, IX, and X) and the sacral motor cortex or section of the pyramids produce little gait
regions contain preganglionic neurons for the parasympa- deficit but will cause postural reaction deficits in contralat-
thetic division. eral limbs.
 CHAPTER 1 Neurologic History, Neuroanatomy, and Neurologic Examination 9

The extrapyramidal system allows animals to gait and to motor action and at the same time exerts inhibitory action
initiate voluntary movement. Neurons are located in nuclei in on other functions, such as spinal cord reflexes. Animals
all divisions of the brain. Some of the more clinically impor- with UMN lesions caudal to the midbrain may have exag-
tant motor pathways include the tectospinal, reticulospinal, gerated reflexes (hyperreflexia) and increased muscle tone
rubrospinal, and vestibulospinal tracts. Caudal to the mid- (hypertonia).
brain, lesions generally produce signs in ipsilateral limbs and
severe gait deficits. Lesions rostral to the midbrain produce Signs of Upper Motor Neuron Lesions
signs in contralateral limbs and less gait involvement. UMN lesions produce a characteristic set of clinical signs cau-
Upper motor neurons may stimulate or inhibit motor dal to the level of the injury. These signs are summarized in
actions. For instance, the UMN is necessary for voluntary Table 1-3 and are compared with signs of LMN lesions.
The primary sign of motor dysfunction is paresis. With dis-
ease of the UMN system, the paresis or paralysis is associated
with normal or increased extensor tone and normal or exag-
gerated reflexes. Abnormal reflexes (e.g., a crossed extensor
reflex) may be seen in some cases. Loss of descending inhi-
UMN bition on the LMN produces these findings. Disuse muscle
atrophy may occur and is slow to appear, is not complete, and
LMN includes the entirety of the affected limb(s) in most cases.
Because lesions at many different levels of the CNS may
produce UMN signs, localization of a lesion to a specific seg-
ment usually is not possible when only UMN signs are consid-
Cerebrum ered. Proper interpretation of UMN signs and other associated
signs, however, allows one to localize a lesion to a region. For
example, UMN paresis of the pelvic limbs indicates a lesion
cranial to L4 spinal cord segment. If the lesion were at L4-S2
Diencephalon spinal cord segments, LMN paresis of the pelvic limbs would
be present. If the thoracic limbs are normal, the lesion must
Red nucleus be caudal to T2 spinal cord segment. Therefore pelvic limb
Midbrain paresis (UMN) with normal thoracic limbs indicates a lesion
Decussation of between the T3 and L3 spinal cord segments.
rubrospinal tract
Pons
Pyramids
Lower Motor Neurons
Medulla oblongata The lower motor neurons (LMN) connect the CNS with mus-
Decussation cles and glands. All motor activity of the nervous system ulti-
of mately is expressed through LMNs. The LMNs are located in
corticospinal tract
all spinal cord segments in the intermediate and ventral horns
of the gray matter and in cranial nerve nuclei (CN III-VII, IX-
Interneurons XII) in the brainstem. The axons extending from these cells
LMN form the spinal (see Figure 1-6) and cranial nerves.
Peripheral nerves The nervous system is arranged in a segmental fashion.
A spinal cord segment is demarcated by a pair of spinal nerves.
Each spinal nerve has a dorsal (sensory) and a ventral (motor)
Figure 1-6 Neurons in the cerebral cortex and the brainstem root (Figure 1-7).
send axons to the lower motor neurons (LMNs) in the brainstem The muscle or group of muscles innervated by one spinal
and the spinal cord. The upper motor neurons (UMNs) provide nerve is called a myotome. Myotomes are arranged segmen-
voluntary control of movement. Two of the major voluntary tally in the paraspinal muscles but are more irregular in the
motor pathways, the corticospinal (pyramidal) pathway and the limbs. Dysfunction of a specific muscle is localizing to a spinal
corticorubrospinal pathway, are illustrated. nerve or a ventral root (Figures 1-8 and 1-9). The approximate

TABLE 1-3
Summary of Lower Motor Neuron (LMN) and Upper Motor Neuron (UMN) Signs
LMN: Segmental Signs UMN: Long-Tract Signs

Motor function Paresis to paralysis: flaccid muscles Paresis to paralysis: spastic muscles
Reflexes Hyporeflexia to areflexia Normal to hyperreflexia (especially myotatic
reflexes)
Muscle atrophy Early and severe: neurogenic; limb contracture Late and mild: disuse
Muscle tone Decreased Normal to increased
Electromyographic changes Abnormal potentials (fibrillation potentials, no posi- No changes
tive sharp waves) after 5 to 7 days
Associated sensory signs Anesthesia of innervated area (dermatomes); Decreased to absent proprioception,
paresthesia or hyperesthesia of adjacent areas; decreased perception of noxious stimulti
decreased to absent proprioception caudal to the lesion
10 PART 1 Fundamentals

relationship of spinal cord segments to vertebrae is illustrated paresis, but not paralysis, of the affected muscles. The reflexes
in Figure 1-8. may be depressed. Lesions of peripheral nerves are more likely
to cause severe loss of function, and all muscles innervated by
Signs of LMN Lesions the nerve are affected. The reflexes are usually absent in these
Lesions of the LMN, whether of the cell body, the axon, motor lesions (see Figure 1-9).
end plate, or muscle produce a characteristic group of clinical Differentiating UMN and LMN signs is extremely impor-
signs summarized in Table 1-3. Signs of LMN lesions are eas- tant for localizing lesions in the spinal cord and brainstem.
ily recognized on neurologic examination. Paresis or paralysis, UMN signs localize lesions to spinal cord regions, whereas
loss of muscle tone, and reduced or absence of reflexes occur LMN signs help localize lesions to specific nerves, nerve roots,
immediately after the LMN unit is damaged. Rapid muscle or spinal cord segments.
atrophy is detectable within 1 week and becomes severe. Atro-
phy is limited to denervated muscles. Proper interpretation of Sensory Systems
LMN signs allows the clinician to localize accurately lesions to In our organizational scheme, sensory systems are divided into
a specific segment of the CNS from which the affected LMN general proprioception, general sensory (segmental and long
unit arises. For example, LMN signs affecting the thoracic limb tract), and special sensory systems.
are localized to the C6-T2 spinal cord segments, peripheral
nerves, or muscles. Segmental Sensory Neurons
Most muscles are innervated by nerves that originate in Sensory neurons are located in the spinal ganglia within the
more than one spinal cord segment. For example, the quad- dorsal roots along the spinal cord (see Figure 1-7) and in the
riceps muscle is innervated by neurons originating in spinal ganglia of CN V. The receptors for temperature, pressure,
cord segments L4-6. Loss of one segment or one root causes touch, and noxious stimuli (nociception) are located on or
partial loss of the innervation of the muscle. The clinical sign is near body surfaces. Axons are located in peripheral nerves
and enter the spinal cord via the dorsal roots (see Figure 1-7).
After entering the spinal cord, axons synapse on interneurons
that stimulate limb flexion and inhibit limb extension in the
ipsilateral limb and facilitate extension and inhibit flexion in
the contralateral limb. This is the sensory component of with-
drawal and crossed extensor reflexes (Figure 1-10). Fibers are
also projected to the brain for conscious perception of sensory
information (Figure 1-11).
The area of skin innervated by one spinal nerve is called
a dermatome. Dermatomes also are arranged in regular seg-
mental fashion, except for some variation in the limbs (Figure
1-12). Alterations in the sensation of a dermatome can be used
to localize a lesion to a spinal nerve or a dorsal root. The area
of skin innervated by the sensory neurons of a named periph-
eral nerve has a different distribution (Figure 1-13), allowing
localization of lesions of peripheral nerves.
Cranial nerve V is the major nerve for facial sensation (see
Figure 1-7 Components of the spinal reflex. A, Muscle spindle. Figure 1-5). Sensory fibers project to the contralateral cerebral
B, Dorsal root ganglion. C, Ascending sensory pathway in the dor- cortex.
sal column. D, Ventral horn motor neuron (lower motor neuron).
E, Ventral (motor) root. F, Neuromuscular junction. G, Descend- Signs of Segmental Sensory Neuron Lesions
ing motor pathway in the lateral column (upper motor neuron). Lesions of the sensory neurons also produce characteristic
The dorsal and ventral roots join to form the peripheral nerve. clinical signs. Segmental sensory signs include (1) anesthesia
(From Oliver JE: Neurologic examination, Vet Med Small Anim (complete lesion), (2) hypesthesia (decreased perception of
Clin 68:151–154, 1973.) noxious stimuli, partial lesion), (3) hyperesthesia (increased

Figure 1-8 The spinal cord has a segmental arrangement; each segment has a pair of spinal nerves.
The approximate relationship of spinal cord segments and vertebrae in the dog is illustrated here.
Regions of the spinal cord that give rise to characteristic clinical signs when damaged are labeled. I,
C1-5, Upper motor neuron (UMN) to all limbs; II, C6-T2, lower motor neuron (LMN) to thoracic,
UMN to pelvic limbs; III, T3-L3, normal thoracic, UMN to pelvic limbs; IV, L4-S2, normal thoracic,
LMN to pelvic limbs; V, S1-3, partial LMN to pelvic limbs, absent perineal reflex, atonic bladder;
VI, caudal nerves, atonic tail.
 CHAPTER 1 Neurologic History, Neuroanatomy, and Neurologic Examination 11

sensitivity of nociception, irritative lesion), and (4) loss of General Proprioception

reflexes. Increased or decreased sensation of a dermatome can Proprioception means “sense of position.” The clinical sign
be mapped by pinching the skin. Mapping the distribution of of proprioception dysfunction is ataxia (incoordination). Gen-
sensory loss is accurate to within three spinal cord segments. eral proprioception describes the position of muscles, joints,
Similarly, the alteration of sensitivity in the distribution of a and tendons because proprioceptors are located in neuromus-
named peripheral nerve localizes the lesion accurately. cular spindles and Golgi tendon organs. Axons project within
peripheral nerves and enter the spinal cord via dorsal roots.
Long-Tract Sensory Pathways Neurons are located in the spinal ganglia. On entering the
Sensory pathways of clinical significance include those respon- spinal cord, axons may (1) synapse directly on alpha motor
sible for general proprioception (position sense) and general neurons for initiation of extensor reflexes such as the patellar
somatic afferent information (specifically, response to nox- or knee jerk reflex (monosynaptic reflex arc) (Figure 1-14),
ious stimuli). In animals, two types of fibers relaying informa- (2) synapse on interneurons to indirectly influence alpha
tion regarding noxious stimuli traverse the spinal cord. Based motor neurons, or (3) synapse on interneurons and then send
on the location of receptors, these are called superficial and afferent fibers via the spinal cord to the brainstem, cerebellum,
deep pathways. Superficial nociceptive pathways (for percep- and cerebrum (Figure 1-15).
tion of discrete noxious stimuli in the skin [e.g., a pinprick]) Proprioception is transmitted to the cerebellum via spino-
are located primarily in the ventrolateral (primate) or dor- cerebellar tracts. This information is used by the cerebellum
solateral (cat) portion of the spinal cord, with a relay in the to regulate muscle tone, posture, locomotion, and equilib-
thalamus. The pathway primarily projects to the contralateral rium. Lesions involving these tracts have a profound effect
cerebral cortex for conscious recognition of pain. The deep on gait and may create clinical signs similar to cerebellar dys-
nociceptive pathway (for perception of severe pain in the function (i.e., truncal swaying, hypermetria). Spinocerebellar
bones, the joints, or the viscera [e.g., a crushing pain]) is a tracts activate Purkinje neurons in the cerebellum that inhibit
bilateral, multisynaptic system that projects to the reticular protraction (flexion) of limbs. This facilitates limb extension
formation, the thalamus, and the cerebral cortex. In general, for weight bearing. Lesions in spinocerebellar tracts result in
damage must be bilateral and severe to block conscious per- overflexion of limbs, known as hypermetria. Clinical signs are
ception of noxious stimuli distal to lesions. ipsilateral to lesions.

Spinal nerve Lumbosacral Peripheral nerve Muscle innervated

plexus
Iliopsoas
Femoral 4, 5, 6 Quadriceps
Sartorius

External obturator
Pectineus
Obturator (L4), 5, 6
Gracilis
Adductor
L4
Middle gluteal
Cranial gluteal L6, 7, S1 Deep gluteal
Tensor fascia lata
L5
Superficial gluteal
Caudal gluteal L7, (S1, 2) (Middle gluteal)
L6
Biceps femoris
Sciatic L6, 7, S1, (2) Semimembranosus
L7 Semitendinosus

S1 Peroneus longus
Lateral digital extensor
Common peroneal
Long digital extensor
S2 Cranial tibial
S3 Gastrocnemius
Popliteus
Tibial
Superficial digital flexor
Deep digital flexor

Pudendal S1, 2, 3

Caudal rectal External anal sphincter

Flexor reflex: sensory and motor: sciatic nerve

Patellar reflex: sensory and motor: femoral nerve
A Perineal reflex: sensory and motor: pudendal
Figure 1-9 A, Segmental innervation from cervical intumescence of thoracic limb muscles in the dog.
Continued
12 PART 1 Fundamentals

Spinal nerve Brachial Peripheral nerve Muscle innervated

plexus
Supraspinatus
Suprascapular (C5), 6, 7
Infraspinatus

Subscapular C6, 7 Subscapularis

C6 Biceps brachii
Musculocutaneous C6, 7, 8 Brachialis
Coracobrachialis

Deltoideus
C7 Teres major
Axillary (C6), 7, 8
Teres minor
(Subscapularis)

C8
Triceps brachii
Extensor carpi radialis
Radial C7, 8, T1, (2) Ulnaris lateralis
Common digital extensor
T1 Lateral digital extensor

T2
Flexor carpi radialis
Median C8, T1, (2) Superficial digital flexor
(Deep digital flexor)

Flexor carpi ulnaris

Ulnar C8, T1, (2)
Deep digital flexor

Flexor reflex: sensory: varies with area stimulated

motor: musculocutaneous, axillary, median, ulnar, radial
Biceps reflex: sensory and motor: musculocutaneous
B Triceps reflex: sensory and motor: radial
Figure 1-9—cont’d B, Segmental innervation from lumbosacral intumescence of pelvic limb
muscles in the dog. (From de Lahunta A: Veterinary neuroanatomy and clinical neurology, ed 3,
St Louis, 2009, Elsevier.)

Conscious proprioception is carried to the medulla via of a pinprick) and voluntary motor activity are often lost at
the dorsal columns (fasciculus gracilis [from pelvic limbs] the same time. Deep pain perception (perception of a strong
and cuneatus [from thoracic limbs]), whose fibers first pinch of a bone or a joint) is the last neurologic function to be
synapse in medullary nuclei (nuclei gracilis and cuneatus, lost during spinal cord compression. The level of a spinal cord
respectively). Axons from these nuclei cross to the opposite lesion can be determined if a level of hypesthesia or anesthesia
side via the deep arcuate fibers and then traverse the brain- can be detected (Figure 1-16).
stem in the medial lemniscus to the thalamus. Ultimately,
fibers are projected to the contralateral parietal lobe of the Special Sensory: Vision
cerebral cortex. The retina serves the function of a digital scanner. It contains
Lesions of these pathways are associated with general photosensitive cells (rods and cones), bipolar neurons, and
proprioceptive ataxia and delayed responses in the initiation ganglion cells. Axons from ganglion cells form the optic nerve.
of postural reactions (hopping, knuckling-paw placement). Just rostral to the ventral diencephalon, the optic nerves join
Lesions rostral and caudal to the midbrain create deficits in at the optic chiasm. In general, fibers from the medial (nasal)
contralateral and ipsilateral limbs, respectively. half of the retina cross at the optic chiasm, whereas fibers
from the lateral (temporal) half of the retina remain ipsi-
Signs of Long-Tract Sensory Lesions lateral. Post chiasm, fibers continue in bilateral optic tracts
The signs of sensory long-tract lesions are valuable for the for- located on the caudodorsolateral surface of the diencephalon.
mulation of a prognosis of CNS disorders and for localization. Most optic-tract fibers involved in vision synapse in the lat-
Spinal cord lesions frequently cause decreased sensation cau- eral geniculate nucleus of the thalamus; however, about 20%
dal to the level of the lesion. Proprioceptive deficits usually to 25% of fibers pass over the geniculate nucleus and termi-
are the first signs observed with compressive lesions of the spi- nate in the pretectal area of the midbrain and participate in
nal cord. Abnormal positioning of the feet and ataxia may be pupillary light reflexes. Visual fibers project from the lateral
present before any significant loss of voluntary motor activity geniculate nucleus to the contralateral occipital cortex, where
occurs. Superficial pain perception (the conscious perception the image is perceived.