Large Animal Neurology E-Book

Joe Mayhew

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1914

Veröffentlichungsjahr: 2022

Beschreibung

A comprehensive and authoritative guide to neurologic disease in large domestic animals, world-wide. The newly revised Third Edition of Large Animal Neurology delivers a practical and complete reference for veterinarians, veterinary trainees and scientists dealing with large animal neurology. The book is vividly illustrated in full colour and contains many clinical photographs and detailed line drawings to highlight the concepts discussed within. Organised into three parts, Large Animal Neurology offers practitioners and students straightforward guides on how to perform neurologic examinations for domestic large animal species, including neonates. It also discusses the presenting clinical syndromes caused by common nervous system diseases, as well as giving details of the specific neurologic diseases of large domestic animals. The book includes: * A thorough introduction to the evaluation of large animal neurologic patients, including discussions of neuroanatomy, neurologic evaluation, ancillary diagnostic aids, and the important pathologic responses of the nervous system * Comprehensive exploration of 26 presenting clinical problems, including behaviour disorders, seizures, epilepsy, sleep disorders, blindness, strabismus, monoplegia, wobblers, tetraplegia, pruritus and cauda equina syndrome * Detailed coverage of the specific diseases, including those of genetic, infectious, nutritional, toxic and metabolic cause, and the many diseases with multifactorial and with unknown cause Perfect for all equine and farm animal veterinarians, veterinary neurologists, as well as trainees in the field, Large Animal Neurology, Third Edition is also an ideal resource for undergraduate veterinary students, animal pathologists, and neuroscience researchers.

Leseprobe

Large Animal Neurology

Third edition

I. G. Joe Mayhew

Massey University

Palmerston North, NZ

Robert J. MacKay

University of Florida

Gainesville, Florida, USA

This edition first published 2022© 2022 John Wiley & Sons Ltd

Edition HistoryJohn Wiley & Sons Ltd (2e, 2008), Lea & Febiger (1e, 1989)

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The right of I G Mayhew and Rob MacKay to be identified as the authors of this work has been asserted in accordance with law.

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Library of Congress Cataloging‐in‐Publication Data applied for[HB ISBN: 9781119477037]

Cover Design: WileyCover Images: Courtesy of Quentin Roper, Courtesy of Joe Mayhew

Preface to third edition

For this third edition of Large Animal Neurology, we have enlisted Rob MacKay as coauthor to help us keep up with current trends and to maintain a reasonably worldwide—albeit somewhat Anglosphere—perspective.

As with previous editions, the general structure of the book consists of three parts. Part I (Chapters 1–4) covers the background disciplines required for the evaluation of neurologic cases; Part II (Chapters 5–30) provides concise overviews of the commonly encountered, major clinical presenting scenarios; and Part III (Chapters 31–38) offers an extensively resourced discourse of most neurologic diseases of domestic large animals following an etiologic category. Readers thus can approach the text with a view to updating their evaluation of suspected clinical neurologic patients (Part I), with a specific clinical syndrome in mind (Part II), or to delve into details on most of the specific neurologic diseases of large domestic animals (Part III).

Since the second edition of 2008, genetics and modern imaging techniques, in particular, have had a major impact on large animal neurology. Despite their profound utility, these diagnostic tests are not perfect. Thus, even dramatic and clearly defined changes seen on an MR or a CT image of a patient with a neurologic syndrome does not always indicate cause and effect. Likewise, as our genetic modeling of many diseases unravels, particularly of those with complex genetic characteristics, identifying a genetic association with a particular disorder does not mean that the patient’s signs are due solely to that inborn—or even acquired—genetic fingerprint. Therefore, as with all diagnostic ancillary aids we use, the results must be taken in conjunction with the results of repeated examinations to help formulate the most appropriate diagnostic and therapeutic plans. It also must be considered before undertaking any test, whether the results, considering their margin of error, will inform clinical management to a degree that benefit outweighs risk and cost. Otherwise, we might be better off not undertaking them.

Another ongoing revolution of tools is in modern IT equipment and apps, not least, in a specialty so dependent on visual observation and pattern recognition, as a means of instantly sharing images and videos of cases to better indicate clinical findings. Thus, it made sense to develop a library of still and motion images of clinical material to share with readers in this edition of Large Animal Neurology. The video library is not only a compilation of a wide variety of cases we have been fortunate enough to see but, more importantly, provides examples of actions, movements, postures and syndromes, and particularly visual examples to assist in the definition of clinical signs and syndromes such as bizarre behavior, the ataxias, sleep attacks, tetany, and tremor.

As with most clinicians and neurologists, we have likely reviewed thousands of videos and images of clinical cases over the years. Very often, new aspects of a case come to light after multiple viewings at both normal and slow speeds. Similarly, and particularly with cases that are enigmatic or show fluctuating signs, by returning to study the patient or the video, subtle and interesting—and sometimes profound—signs that had not previously been noted become apparent. Typical examples of this include a change in eyelash angle seen in Horner syndrome; brief, repeated, minor facial grimaces of a foal with focal epilepsy; movement of lice toward areas of skin with sympathetic denervation; and reversion from pacing gait at birth, then four‐beat walk at 2 weeks of age, back to a pacing gait before the onset of overt ataxia in a young foal with progressive signs of spinal and other forms of ataxia. One can then approach new cases with this information so that when such “new” signs are present, one will look for them and thus see them. It is worth iterating:

More mistakes are made from not looking than not knowing, and further mistakes are made from not seeing rather than not looking

(Radostits et al., 2000).

Simply informing a student, at whichever stage of their career, of one’s expert opinion on a case is rarely helpful. As a clinical teacher, one should be prepared to “think aloud” and share the thought processes as to how one is synthesizing the facts of a case to arrive at a particular differential diagnosis and course of action, namely, the diagnostic reasoning used. We have also found two other maxims useful in teaching over the years. First, we should not take ourselves too seriously, we all make mistakes. Second, we need to remember that the next generation in our profession will be better equipped than us; if we can be fortunate enough to contribute to that advancement then so much the better.

Following on from the influence of our learned mentors, we have tended to remain critical of misuse of terminology, particularly regarding anatomic terms. We thus continue to strive to follow both the Oxford English Dictionary (OED, 2009), and particularly the Nomina Anatomica Veterinaria (NAV, 2017).

We humbly acknowledge the instruction, friendship, and encouragement that we have been fortunate to receive and share with colleagues at Massey University (NZ), Guelph University (Canada), the University of California at Davis (USA), the University of Florida (USA), Cornell University (USA), Cambridge University (UK), and the University of Edinburgh (UK). It’s been fun. Quentin Roper again deserves special thanks for his painstaking electronic draftsmanship in preparing many of the drawings in the second edition and again in this edition. Most especially, we are indebted to the many patients that, through their misfortune, taught us neurology.

Our families remain as our sustainers for which we are eternally grateful.

Joe Mayhew

Rob MacKay

Massey University

University of Florida

New Zealand

USA

NAV. Nomina Anatomica Veterinaria, International Committee on Veterinary Gross Anatomical Nomenclature (ICVGAN). 2017

OED.

Oxford English Dictionary

. Oxford University Press, Oxford. 2009

Radostits OM, Mayhew IG, and Houston DM .

Veterinary Clinical Examination and Diagnosis

. WB Saunders, London. 2000

About the companion website

Don’t forget to visit the companion website for this book:

www.wiley.com/go/mayhew/neurology

There you will find valuable materials, including:

Video clips presenting a wide variety of diseases that show actions, movements, postures, and syndrome characteristics of the disorders

Figures from the book as downloadable PowerPoint slides

Scan this QR code to visit the companion website

Part IEvaluation of Large Animal Neurologic Patients

Chapter 1

Practical neuroanatomy

Chapter 2

Neurologic evaluation

Chapter 3

Ancillary diagnostic aids

Chapter 4

Pathologic responses of the nervous system

1Practical neuroanatomy

Disease

Basic descriptive terminology

Functional neuroanatomy

References

Some of the most rewarding aspects of clinical neurology involve being able to associate observed signs and syndromes with neuroanatomic sites of the lesions. This may, for example, be experienced when recognizing a syndrome of ataxia in a purebred patient and associating it with a familial cerebellar disorder for a client. Alternatively, one may be able to explain to a producer how a certain lesion, detected by an astute neurologic examination of one representative animal and confirmed at postmortem examination is the cause of the clinical syndrome observed in the herd. The basic requirement for achieving this degree of diagnostic acumen is an understanding of applied neuroanatomy.

This chapter provides the basic information necessary to allow the clinician to appreciate the fundamentals of a neurologic examination and to interpret, accurately, the results of such an examination. As the clinician becomes adept at these tasks, further anatomic details may be sought. These can be found in the texts listed in the references.

At this point, a plea is made for a clear use of anatomic terms, based on Nomina Anatomica Veterinaria, Nomina Embryologica Veterinaria and Nomina Histologica,1 along with the clinically applied terms used in functional neuroanatomy,2–4 clinical neurology,5–7 and veterinary neuropathology.8–10

Basic descriptive terminology

The following is a review of basic descriptive terminology; note that the derivation, abbreviation, combining form, synonym, or explanation is given parenthetically.

The central nervous system (CNS) consists of the brain (encephalo) (Figure 1.1) and spinal cord (myelo). It contains collections of neuronal cell bodies or somata in layers (laminae), nuclei, and columns of gray matter (polio). Tracts, sheets, and pathways of dendritic (afferent) and particularly axonal (efferent) processes of these cell bodies make up the white matter (leuko). These processes make up most of the CNS along with their fatty, myelin (myelino) coats. In tall, large animals, some of these neuronal fibers extend 2–3 m, and many exit and enter the CNS via the cranial and spinal nerves of the peripheral nervous system (PNS).

Figure 1.1 Basic areas of the brain can be readily recognized on this diagram of a median section of a horse brain. The terminology used in this book is shown. Wherever possible the authors use the terminology of Nomona Anatomica Veterinaria;

however, some license is taken with respect to forebrain, which here refers to the prosencephalon plus diencephalon, as clinically, lesions in these collective regions generally present the same syndromes. It is important to recognize these various areas when sending brain sections for histopathologic examination.

Structurally, the forebrain (prosencephalon) is composed of the cerebral hemispheres (most of the telencephalon), thalamus and hypothalamus (diencephalon), hippocampus, basal nuclei, and the limbic system, all situated in the rostral fossa of the neurocranium. The middle fossa contains the midbrain (mesencephalon). Caudally, the hindbrain (rhombencephalon) is composed of the cerebellum and pons (together with the metencephalon) and the medulla oblongata (myelencephalon) that all reside in the caudal fossa. Both the cerebrum (cerebro) and cerebellum (cerebello) have their own outer (cortical) and inner (medullary) portions, composed particularly of gray matter (neuronal cell bodies) and white matter (neuronal fibers), respectively. The remainder of the brain comprising the midbrain, pons, and medulla oblongata makes up the brainstem. This contains white matter pathways passing to and from brain and spinal cord regions, and gray matter, mostly contained in nuclei as relay centers and sensory and motor nuclear areas for the body, including the cranial nerve nuclei.

The spinal cord is the conduit between the brain and the peripheral spinal (non‐cranial) nerves and their innervated structures of the body. Thus, it contains all the afferent and efferent neuronal fibers connecting to and from the brain as superficial white matter tracts. It has a cervicothoracic (brachial) enlargement (intumescence) and a lumbosacral (pelvic) enlargement at the levels of the thoracic and the pelvic limbs, respectively. These swellings are the result of a higher density of neuronal cell bodies at these sites, collected in the butterfly‐shaped, central gray matter and supplying the sensory and motor spinal nerves for the limbs.

To avoid some confusion, vertebral levels are labeled as C7, T3, L4, S5, Ca6 (caudalis as opposed to coccygeal), etc., and spinal cord segments are labeled as C8, T3, L4, S5, Ca6, etc.

Clinically, the autonomic nervous system functions independently and involuntarily from the rest of the nervous system, receiving afferent input from the environment via the basic and special senses to maintain the body’s internal milieu. The parasympathetic component has a brainstem and sacral outflow to the head and body, whereas the sympathetic component has a thoracolumbar outflow.

The entire CNS is protected within the bony neurocranium of the head and in the vertebral canal within the vertebral column. It is covered by meninges consisting of the thick (pachy) dura mater and thin (lepto) arachnoid and pia mater. Between the latter two membranes, is cerebrospinal fluid (CSF), produced by the choroid plexuses of the lateral and fourth ventricles. This fluid also fills the cavities within the brain (ventricles) and spinal cord (spinal canal), which are lined by ciliated ependymal cells.

Because we refer to vertebral structures very often, it is worth reviewing the recommended correct nomenclature as in Nomina Anatomica Veterinariahttp://www.wava‐amav.org/wava‐documents.html

Columna Vertebralis

Corpus vertebrae

Extremitas cranialis (Caput vertebrae)

Extremitas caudalis (Fossa vertebrae)

Crista ventralis

Arcus vertebrae

Pediculus arcus vertebrae

Lamina arcus vertebrae

Foramen vertebrale

Canalis vertebralis

Spatium interarcuale

Foramen intervertebrale

Incisura vertebralis cranialis

Incisura vertebralis caudalis

Foramen vertebrale laterale

Sulcus n. spinalis

Processus spinosus

Processus transversus

Processus costalis

Processus articularis cranialis

Processus articularis caudalis

Processus accessorius

As well as meningeal cells, ependymal cells, neurons (somata and their axons and dendrites), and blood vessels, several other types of supporting, protective, and nutritive glial (glue) cells (neuroglia) make up a large part of the volume of the CNS. The largest of these glial cells are the astrocytes with their star‐shaped processes. These cells basically act to support the CNS, which has little cytoskeletal framework. They also act as pseudofibroblasts and can lay down collagen in response to injury to the CNS. Originally, the processes of other small glial cell types were thought to be few (oligo); these cells being named oligodendrocytes. We now know that their processes are extensive and extend to and maintain all the myelin sheaths covering CNS axons. The small microglial cells appear to be the tissue macrophages of the mononuclear phagocytic system within the CNS, responding along with migrating inflammatory cells from the circulation when there are inflammatory processes occurring in CNS tissues.

The neuronal processes in the peripheral nervous system (PNS) with their myelin sheaths are called nerve fibers and make up the nerve roots, nerve plexuses, and peripheral nerves. Some neurons, particularly those in the autonomic nervous system and the sensory neurons, have their cell bodies in aggregations known as ganglia. Also, several networks of interwoven nerves (plexuses) occur in the PNS, the largest of which are the brachial plexus supplying the thoracic limbs and the lumbosacral plexus for the pelvic limbs.

The cells that ensheathe PNS nerve fibers are Schwann cells. These assist in maintaining a framework for nerves, as well as producing the abutting layers of myelin that surround all the larger fibers, allowing quite rapid saltatory (leaping, jumping) conduction of electrical impulses. The PNS has a fibrous connective tissue cytoskeleton that consists of the epineurium that wraps around a whole nerve, the perineurium that surrounds a bundle or fascicle of fibers, and the endoneurium that separates the individual nerve fibers.

Functional neuroanatomy

Probably the most important structural and functional unit of the nervous system is the simple reflex pathway (Figure 1.2). A neurologic examination basically involves testing simple and complex reflex pathways and interpreting the effected reflex activity and complex responses (see Chapter 2, Neurologic Evaluation).

A simple spinal reflex pathway, depicted as a patellar tendon reflex in Figure 1.2, is composed of two neurons. Stimulation of a sensory stretch receptor in a tendon with its sensory neuronal cell body in the dorsal root ganglion stimulates an efferent motor neuron. These motor neurons are usually alpha motor neurons and are collectively referred to as final motor neurons, having their cell bodies in the ventral gray matter of the spinal cord (and in cranial nerve nuclei in the brainstem). Reflex motor responses to sensory stimuli will occur without any other afferent or efferent connections within the CNS; so long as these two (or more) neurons comprising the reflex arc, as well as the sensory nerve ending, the neuromuscular junction, and the effector muscle, all are intact. In contrast, lesions, due to any cause, that damage parts of the reflex pathway will suppress those reflexes. Indeed, if the damage is to the alpha motor neurons in the ventral gray matter of the spinal cord or the cranial nerve motor nuclei, or to their peripheral axons, there will be loss of reflexes and severe weakness and ultimate muscle atrophy, i.e., signs of a final motor neuron lesion.

Figure 1.2 Basic monosynaptic spinal reflex pathway (patellar reflex) showing the sensory neuron synapsing on the final motor neuron. In many other reflex pathways, there is at least one internuncial neuron within the CNS allowing further modulation of the reflex.

The various reflex pathways with their respective final motor neurons throughout the brainstem and spinal cord are controlled for voluntary movement by neurons in motor centers in the brain which are collectively referred to as central motor neurons. Figure 1.3 depicts generic central motor pathways. Corticospinal motor pathways with neuronal cell bodies in the cerebral cortex (A) are very important in primates but do not appear to be very important in initiating voluntary limb and body movement in domestic animals. Quite massive lesions destroying the cerebrocortical motor centers that would be devastating in higher species do not cause permanent demonstrable abnormality in the gait of large animals. After the acute effects of such large lesions in our veterinary species have resolved, there can be subtle deficits in motor functions such as jumping fences and hopping on the thoracic limb opposite the side of the lesion. In contrast, quite small lesions in the midbrain and medulla oblongata usually result in hemiparesis or tetraparesis because of damage to central motor centers and tracts such as the rubrospinal (Figure 1.3B), reticulospinal (Figure 1.3C), and vestibulospinal (Figure 1.3D) pathways. These central motor neuronal pathways tend to have a calming effect on reflexes, particularly those involved with supporting the body against gravity such as the patella reflex. Because of this, central motor pathway lesions do not suppress reflexes and can indeed result in hyperactive reflexes and responses. The major role of these central motor pathways however is to direct the various final motor neurons in (voluntary) movement such that central motor pathway lesions will result in poor or absent voluntary effort (paresis or paralysis) in the face of very active spinal (and cranial) reflexes.

Just as brain motor centers help control the final motor neurons within the reflex arcs, the sensory inputs to these arcs are relayed to brain centers to give feedback on position sense (proprioception) touch, and pain perception (nociception) (Figure 1.4). Sensory pathways travel to the thalamus, and probably to the somatosensory cerebral cortex, for the perception of pain. These pathways are multisynaptic and contain small fibers, both characteristics making them resistant to interruption. Proprioceptive pathways that are presumed to be consciously perceived (position sense at rest) travel to thalamic and thence to cerebral conscious proprioceptive centers. Other subconscious proprioceptive information (movement sense) is contained in spinocerebellar tracts that pass directly to the cerebellum.

Figure 1.3 Central motor neuronal pathways predominantly originate in the brainstem and synapse on final motor neurons to effect motor activity. Depicted here are A the cortico (rubro)spinal, B the rubrospinal, C the reticulospinal, and D the vestibulospinal neurons and tracts.

Figure 1.4 Sensory pathways convey somatic, proprioceptive, and visceral input to brain centers. Subconscious proprioceptive neurons A project to the cerebellum, whereas conscious proprioceptive neurons B and somatic and visceral afferent neurons C project to the thalamus and ultimately project to forebrain centers.

In summary, damage to the spinal cord at the level of a reflex arc at its final motor neuron will denervate the effector muscle, resulting in flaccid (loss of tone) paralysis with degrees of hypotonia and hyporeflexia at the level of the lesion. In contrast, a similar severe lesion cranial or rostral to a reflex arc will result in hypertonic (spastic) paralysis. The latter is characterized by loss of voluntary motor function as with a final motor neuron lesion, but the reflex is not diminished. Indeed, the reflex may be released from the calming influence of its controlling central motor pathways and be hyperactive with concomitant hypertonia (spasticity—sic.) or stiffness in body parts such as limbs. When a central motor pathway lesion causes a degree of spastic paralysis, the involvement of adjacent proprioceptive and nociceptive sensory pathways also results in ataxia and possibly hypalgesia, respectively.

Certainly, the concept of considering motor activity on the basis of “upper” and “lower” motor neuron function and lesions, even for quadrupeds, is entrenched in veterinary neurology, although not without some comment.3,5 Anatomically, upper and lower are not acceptable (with the exception of some cranial structures such as eyelids) as terms of direction in veterinary anatomy (Nomina Anatomica Veterinaria, 6th Edition),1 making the use of these descriptors confusing to say the least. Also, in contrast to “upper” and “lower” motor function generators and pathways, the concept of central pattern generators has its merits when considering gait and posture in humans and animals.11 In this model, there is a generator of highly developed skilled motor activity initiated, in primates, in the cerebrum. A further generator of motor function, most prominent in our large animals, resides in the midbrain and rostral medulla oblongata. Finally, there is a generator at the spinal level that can initiate reflex actions and indeed probably is responsible for primitive gait patterns (viz. “spinal walking”); the interested reader may find further reading on this concept quite intriguing.12–15 For several reasons, therefore, there is a strong argument in veterinary anatomy and neurology to dispense with upper motor neuron (UMN) and lower motor neuron (LMN) terminologies: a strategy we have accepted for this text. The CNS pathways involved with initiating motor function and maintaining appropriate muscle tone and hence body posture are referred to as central motor pathways that directly influence the final motor neurons innervating muscle to effect all motor functions. Many final motor neuron somata reside in the brainstem and spinal cord of the CNS with axons in the PNS, the exceptions being the presynaptic final motor neurons of the autonomic nervous system (ANS) which are wholly in the periphery.

The cerebellum is the major coordinating center for voluntary movement (Figure 1.5). It synthesizes impulses received from the cerebral cortex, the brainstem motor centers, and spinocerebellar and vestibular (special) proprioceptive pathways. It then provides feedback impulses to the motor centers to coordinate all motor functions.

Figure 1.5 Important cerebellar connections include subconscious general proprioceptive input from the body such as via spinocerebellar pathways shown as D (same as A in Figure 1.4). Other input is received from cerebrocortical A and brainstem B motor areas and vestibular centers C. All cerebellar efferent output is from cerebellar cortical (Purkinje) neurons connecting to brainstem B and cerebrocortical A motor areas.

Cranial nerves (CNs), numbering I through XII, leave the forebrain and brainstem (Figure 1.6). Some are involved with specialized modalities such as smell (CN I), sight (CN II), and balance and hearing (CN VIII). Some innervate eyeball muscles (CNs III, IV, and VI), muscles of facial expression (CN VII), pharynx and larynx (CNs IX and X), and tongue (CN XII). Others are involved with reflex functions such as facial reflexes (CNs V and VII) and the gag reflex (CNs IX and X). These cranial final motor neurons have central motor pathways controlling them. A final motor neuron lesion at the level of a CN or its nucleus can paralyze the motor function of the CN. Alternatively, a lesion affecting the efferent central motor pathways that influence the final motor neuron can curtail such CN motor function. As with spinal reflexes, in the latter case the structure (e.g., face) shows variable hypertonic, spastic paralysis (e.g., grimacing), with intact or hyperactive reflexes.

Figure 1.6 Some cranial nerves are involved with specialized modalities such as smell CN‐I, vision CN‐II, and balance and hearing CN‐VIII. Others innervate extraocular muscles CNs‐III, IV, and VI, pharynx and larynx CNs‐IX and X, and tongue CN‐XII, while some are involved with reflex function such as facial reflexes CNs V‐VII, similar to spinal reflex arcs.

Consciousness or mental awareness must be maintained within the forebrain (Figure 1.7A) for neurologic functions to occur. Numerous sensory inputs, including light, sound, touch, gravity, and metabolic and endocrine factors, interact, usually on an area of the brainstem known as the reticular activating system (Figure 1.7B). This system, by relaying impulses to the forebrain and brainstem, maintains the state of awareness and activity.

Figure 1.7 A state of alertness or consciousness is maintained by the forebrain A and particularly the reticular activating center B. These regions receive input from many other regions of the nervous system and are interconnected.

The final concept of clinical neuroanatomy important in interpreting large animal neurologic examinations is that of the specialized areas of relatively well‐developed functional centers that exist in the forebrain, but having brainstem connections, as introduced in Figure 1.8