Chapter 13 Musculoskeletal Abnormalities
LAMENESS AND STIFFNESS
Lameness, is the term used to describe a condition in which an animal is incapable of normal locomotion. Generally lameness is characterized by an inability to maintain a normal gait, manifested by asymmetry in movement, apparent incoordination or weakness, and inefficient or ineffective motion of the limbs. Lameness usually can be assessed only when the animal is moving under its own power, although lameness severe enough to cause an inability to bear weight can be assumed at a standstill. The onset of lameness can be acute (e.g., fracture), chronic (e.g., degenerative joint disease), or acute on chronic (e.g., catastrophic fracture secondary to stress fractures).
Mechanisms of Lameness and Stiffness
The ultimate effects of any cause of lameness are restricted movement of the limbs or body, reduced performance, and abnormal gait. Causes of lameness are generally associated with conditions of the musculoskeletal system or nervous system. Most causes of lameness have both a musculoskeletal component (e.g., atrophy of the supraspinatus and infraspinatus muscles) and a neurologic component (e.g., suprascapular neurapraxia). Some causes of lameness have only a musculoskeletal component (e.g., upward fixation of the patella) and are not principally associated with either afferent nerve signs (i.e., pain) or efferent nerve signs (i.e., motor dysfunction). Similarly, other causes of lameness are solely related to a motor nerve deficit (e.g., radial neurapraxia).
Unlike the usual definition of lameness, “stiffness” refers to a generalized restriction in freedom of movement in a limb, the neck, or back. Stiffness is manifested by a limited range of motion by a joint, reduced length of stride, or decreased flexibility during bending or turning. For example, cellulitis and soft-tissue swelling in the area of the tarsocrural joint can cause restricted freedom of movement of the hindlimb and an apparent lameness, yet there may be no specific musculoskeletal or neurologic cause. Stiffness may have either congenital or acquired causes, and the clinical signs may be mild and transient or severe and persistent. Stiffness may or may not be associated with pain.
Approach to Diagnosis of Lameness and Stiffness in Horses
The lameness examination is the most commonly performed assessment of the musculoskeletal system in the horse. The examination should be well planned, consistent, and thorough. Knowledge of all diseases capable of causing lameness is not required, as long as the examiner maintains an open mind and objectivity during the examination (Box 13-1). The goals of the lameness examination are to determine which limbs are affected, differentiate between supporting limb and swinging limb lameness, and to establish the musculoskeletal and/or neurologic components producing the lameness.
Onset (e.g., When was the last time the horse was seen sound? Was the lameness acute in onset, or did it have a slow, insidious onset?) Characteristics of the lameness (e.g., Is the lameness seen more in hand, at the lunge, or under saddle?) Responsiveness to treatment (e.g., Has the horse received any type of treatment, and if so what was the response?)In addition, the signalment and the activity that the horse undertakes (e.g., jumping vs. racing) should be ascertained and may be a guide in determining potential causes of the lameness (e.g., stress fractures are more common in racing thoroughbreds, and osteochondrosis is more commonly diagnosed in young animals).
Conformation. A number of conformational abnormalities have been associated with lameness (e.g., upright pastern conformation predisposes to pastern disease and foot lameness; offset or bench knees predispose to carpal disease; and straight through the hocks or postlegged conformation predisposes to upward fixation of the patella, suspensory desmitis, and fetlock disease). Poor conformation can affect the young horse when it is put into training or can cause a slow insidious onset of lameness. Recognizing these conformational abnormalities at the time of examination can be helpful in diagnosing potential causes of lameness. When a horse is evaluated for purchase, recognition of poor conformation should be noted and discussed as a source of future lameness problems. Topographic symmetry of the front limbs, from the dorsal region of each scapula to the hoof
From the rear, the height and mass of the hip musculature and the symmetry between the hindlimbs should be assessed. From each side, abnormalities in stance (e.g., camped out in front) or load bearing (e.g., dropped elbow) and the position of the head and neck (e.g., hyperflexed poll) should be compared.
Thorough and useful systems for grading the severity of lameness are available. Most systems are designed to enable the practitioner to compare how lameness changes with time, assess the characteristic of lameness among horses, and accurately record information and communicate information to other veterinarians. Simple and consistent schemes that are easy to remember and modify can be developed (Table 13-1).
Table 13-1 A Five-Grade Lameness Scheme
| Grade | Description |
|---|---|
| 1 | An inconsistently observable lameness visible under special circumstances (in a circle, flexion tests, hard surface, etc.) |
| 2 | A consistently observable lameness visible only under special circumstances (in a circle, flexion test, hard surface, etc.) |
| 3 | A consistently observable lameness at a trot in a straight line |
| 4 | A consistently observable lameness at a walk |
| 5 | A non—weight-bearing lameness; horse is unable to use the leg |
Modified from the American Association of Equine Practitioners Newsletter, March:12, 1983.
Once the initial standing and mobile examinations are completed and the affected limb is identified and the lameness graded, isolating the specific region of the limb is the next goal of the lameness examination. Manipulative tests or stressing of articulations and associated soft-tissue structures can provide additional information as to the location of the source of lameness. Flexion and extension tests are designed to stress selective regions of the limb and observe the effects of the manipulation on the lameness. These tests are also commonly performed on the sound horse to reveal potential areas of concern particularly during prepurchase examinations. Flexion and extension manipulations also enable an assessment of range of motion. Interpretation of these tests should be approached with caution. They are seldom specific for one particular joint. For example, the fetlock flexion test not only stresses the fetlock joint but also places stress on the proximal and distal interphalangeal joints; the hock flexion test also flexes and stresses the stifle joint because of the presence of the stay apparatus. If a flexion tests results in a positive response, the horse should be walked out of the response and observed before additional manipulations. Occasionally exacerbation of the lameness will persist for an extended period of time, which changes the baseline lameness and clouds the interpretation of additional manipulations.
It is common for horses to be presented with multiple lamenesses. Secondary lameness or compensatory lameness is the result of increased stress or overloading of the other limbs in response to the primary lameness. This most commonly occurs in the contralateral limb but can also occur between front limbs and hindlimbs. The secondary lameness can also be the result of shifts in body mass that produce an apparent or phantom lameness. Phantom lameness is less severe than the primary lameness. The following guidelines can be used to aid in the differentiation between a real or compensatory and an apparent or phantom lameness.
Horses with primary hindlimb lameness and apparent or phantom contralateral frontlimb lameness. Each lameness should be considered as real. Horses with a primary forelimb lameness and apparent or phantom ipsilateral hindlimb lameness. Each lameness should be considered as real. Primary forelimb lameness may produce asymmetric pelvic movement causing the perception of a contralateral hindlimb lameness. Example: left foreleg lameness (head elevation) causing apparent or phantom right hindleg lameness (hip drop). Horses with a primary forelimb lameness and apparent contralateral hindlimb lameness. Block out frontlimb lameness first. Primary hindlimb lameness (≥3 to 5/5) can mimic ipsilateral forelimb lameness. Example: A horse shows a cranial load shift during the stance phase of lame limb that causes the head and neck to shift forward and nod down, giving the perception of ipsilateral lameness—“down on sound.” Horses with a primary hindlimb lameness and apparent ipsilateral forelimb lameness. Block out the hindlimb lameness first.Assumptions as to the cause of a horse’s lameness based solely on the physical examination and visual inspection should be avoided unless obvious signs, for example severe swelling or crepitus, are present. After the physical and visual examination, evaluation of the horse with diagnostic analgesia is mandatory for the accurate isolation and diagnosis of equine lameness. A thorough knowledge of anatomy and the structures desensitized by blockade of the appropriate peripheral nerves or synovial structures is essential (Table 13-2). When performing perineural analgesia it is important to remember to block from distal to proximal., An improvement in gait indicates a favorable response to a nerve or joint block; complete elimination of gait asymmetry is unusual and generally should not be expected after intraarticular or peripheral nerve analgesia. If necessary, improvement in gait can be confirmed by repeating the successful block the next day. By that time residual effects from multiple blocks performed previously should be absent.
Table 13-2 Structures Desensitized by Commonly Performed Nerve Blocks
| Nerve Block | Nerve(s) Affected | Structures Desensitized* |
|---|---|---|
| Palmar (plantar) digital | Palmar (plantar) digital | Heel bulbs; frog; bars; navicular bone and bursa; palmar regions of the third phalanx, distal interphalangeal joint, sole, and soft tissues |
| Abaxial sesamoid | Palmar (plantar) | Coronary band, interphalangeal joints, lamellar and solar corium |
| Low palmar (volar) | Palmar, palmar metacarpal† | Skin of medial and lateral pastern, metacarpophalangeal joint, proximal sesamoids, flexor tendons, tendon sheath |
| High palmar (volar) | Palmar, palmar metacarpal† | Skin and deep structures of palmar cannon region (flexor tendons, suspensory ligament except origin, interosseous ligaments of splint bones) |
| High two-point | Lateral palmar, medial palmar | Origin of suspensory ligament |
* Includes all structures listed up to and including the particular block; first structure listed in each block is also the area that can be tested with point pressure to evaluate the effectiveness of the block.
† For hindlimbs, additional anesthetic (i.e., ring block) is needed at the level of the particular perineural block to achieve the desired effect.
Common local anesthetics used in horses include 2% solutions of lidocaine, mepivacaine, and bupivacaine. These solutions all share a common mechanism of action, specifically the ability to block or inhibit nociceptive nerve conduction by preventing the increase in membrane permeability to sodium ions. Lidocaine and mepivacaine are considered to be fast acting and have a duration of action of 1½ to 3 hours and 2 to 3 hours, respectively. Bupivacaine on the other hand is intermediate in onset and has a much longer duration of action of 3 to 6 hours. Mepivacaine is reportedly less irritating to tissues than lidocaine.
Intrasynovial analgesia can be used to more specifically isolate a lameness to a joint, tendon sheath, or bursa. It can be used in combination with perineural analgesia or alone depending on the suspected source of the lameness. Proper patient restraint and strict aseptic technique including aseptic preparation of the skin, wearing sterile gloves, and use of a new bottle of anesthetic are imperative to avoid iatrogenic synovial sepsis. Lameness may be erroneously associated with a joint if intraarticular analgesia of several joints is performed within a short period of time; ample time (30 to 60 minutes) must be allowed between joint blocks to allow for adequate articular desensitization.
When performing intrasynovial analgesia it is not necessary to follow the distal to proximal rule. If intraarticular analgesia of a proximal joint results in no improvement in the lameness, immediate follow-up with distal limb perineural blocks is still possible. Exceptions to this rule exist with intrasynovial analgesia to the foot. When performing intrasynovial analgesia of the distal interphalangeal joint (DIPJ) or navicular bursa, it is important to take into consideration the volume of anesthetic used and the timing at which the lameness is reevaluated. The recommended volume of anesthetic for the DIPJ is 4 to 5 mL, and for the navicular bursa 3 to 4 mL. Once injections into these structures have been performed, the horse should be evaluated at 5-minute intervals to help with the interpretation of the response to the block.
Significant improvement in experimentally induced lameness to the navicular bursa can be seen at 5 minutes after intraarticular anesthesia of the DIPJ with 5 mL of 2% mepivacaine hydrochloride. Amelioration of bursal lameness is mostly likely caused by diffusion of the anesthetic into the bursa via an indirect or functional communication, or by diffusion of anesthetic into the periarticular tissues. The proximal palmar pouch of the DIPJ lies in close proximity to the palmar digital (PD) neurovascular bundles as they course along the medial aspects of the collateral cartilages, making it possible for anesthetic diffusion to block nerve conduction at that level.
Experimentally induced solar toe pain can also be ameliorated by intraarticular blockade of the DIPJ with 10 mL of mepivacaine hydrochloride. The structures innervated by the deep branch of the PD nerves include the DIPJ, navicular bursa, distal navicular ligament, laminar corium, and corium of the sole. The DIPJ capsule contacts the PD neurovascular bundle, and a local anesthetic injected into the DIPJ likely desensitizes the PD nerves below the level of the coronary band, and the structures innervated by them.
Variable responses are also seen with blockade of the DIPJ when different volumes of anesthetic are used. Blocking the DIPJ with 6 mL of mepivacaine (Carbocaine) results in significant improvement in lameness originating from the dorsal margin of the sole; however, lameness originating from the palmar sole shows no improvement. Using 10 mL of Carbocaine reduces lameness originating from the dorsal margin of the sole, as well as the palmar heel regions of the sole, but only after 30 minutes. The difference in response to analgesia of the DIPJ in attenuating pain at the dorsal margin of the sole versus the angles of the sole may be because these regions are innervated by different branches of the PD nerve. This may help distinguish between pain arising from the DIPJ or the navicular apparatus and palmar solar pain.
In contrast to the responses seen with blocking the DIPJ in the presence of navicular bursa disease, blocking the navicular bursa with 3.5 mL of mepivacaine hydrochloride in the presence of experimentally induced DIPJ lameness results in a significant improvement in lameness but only after 30 minutes. Experimentally induced lameness from the dorsal sole is improved by blockade of the navicular bursa; lameness originating from the palmar sole does not show significant improvement.
Knowledge of the previously described responses to intrasynovial analgesia of the DIPJ and the navicular bursa is helpful in localizing and interpreting lameness commonly seen in the horse. The anatomy and close approximation of the associated nervous and synovial structures of the foot give rise to a diffusion gradient associated with perisynovial infiltration of local anesthetic to peripheral nerves and variable responses to intrasynovial analgesia. Similar responses can be encountered with intraarticular analgesia of the carpus and distal tarsal joints. Instillation of anesthetic into the middle carpal joint and the tarsometatarsal joints can result in desensitization of the proximal suspensory ligament, a common site for soft-tissue injury and lameness in the horse.
Once the lameness has been described and localized, a radiographic or ultrasonographic examination can be performed as the next step to confirm a clinical diagnosis. Radiography should be performed using proper technique, an ideal film/screen combination, and multiple views to construct a thorough study (Table 13-3). Comparing radiographs of affected and unaffected limbs can help confirm or refute a suspected abnormality, evaluate the severity of the disease, and identify possible bilateral limb involvement.
Table 13-3 Recommended Radiographic Views of Extremities
| Radiographic Series | Minimum Radiographic Views |
|---|---|
| Distal extremity (navicular) | 45 degrees DP, 65 degrees DP (2), LM, flexor tangential* |
| Pastern | 45 degrees DP, LO, MO, LM |
| Fetlock | 45 degrees DP, LO, MO, LM, flexed LM |
| Metacarpal or metatarsal | DP, LO, MO, LM |
| Carpus | DP, LO, MO, LM, flexed LM, flexed skylines (distal radius, proximal and distal rows of carpal bones) |
| Tarsus | 0 degrees DP, 10 degrees DP, LO, MO, LM |
| Radius-ulna or tibia-fibula | Cr-Cd, LO, MO, LM |
| Elbow | Cd-Cr, LO, LM, patellar (delete patellar) |
| Shoulder | ML |
| Stifle | Cd-Cr, LM, flexed LM, Cd 30° L-CMO, patellar skyline |
Cd-Cr, Caudocranial; Cd 30,° L-CMO, caudal 30-degree lateral-craniomedial oblique; Cr-Cd, craniocaudal; DP, dorsopalmar (dorsoplantar); LM, lateromedial; LO, lateral oblique; ML, mediolateral; MO, medial oblique.
* View to highlight the flexor cortical margin of the navicular bone (50 degrees proximal palmaropalmaro distal oblique).
Although standard radiographic techniques are well documented and described, ultrasound is becoming more and more popular and useful in musculoskeletal imaging. Indications for ultrasonographic evaluation of a lameness include diagnosis of soft-tissue injuries, including muscular, vascular, tendon, tendon sheath, ligament, joint capsule, or bursal defects; evaluation of articular surfaces (articular cartilage thickness, osteochondritis dissecans lesions); assessment of fluid accumulation (synovial effusions, seromas, or sepsis); evaluation of bony surfaces; monitoring of the progression of healing; and monitoring of the effects of training on soft-tissue injuries such as tendonitis or desmitis.
When radiographic or ultrasonographic techniques are nondiagnostic, other methods such as thermography, nuclear scintigraphy, treadmill evaluation, computerized videographic gait analysis, force plate evaluation, computed axial tomography (CAT), or magnetic resonance imaging (MRI) may be useful. University hospitals and major regional referral centers are often the only locations where these adjunctive procedures can be performed because the procedures are expensive and technically complex and they require specialized equipment and experienced personnel. However, even these techniques have limitations; for example, nuclear scintigraphy may not identify the origin of an insidious (e.g., osteochondrosis) or chronic lameness as successfully as an acute lameness.
Approach to Diagnosis of Lameness and Stiffness in Ruminants
The limb should also be palpated to detect swelling, heat, or soreness, which may indicate inflammation from infection or soft-tissue trauma. Crepitation found by manipulating the limb may indicate a fracture or dislocation. Stiffness or pain on joint flexion may indicate joint disease, either septic or degenerative.
Flexion tests and nerve blocks are not used for diagnosis as routinely in ruminants as they are in horses, but they may be useful in certain instances. The technique is similar to that described for horses, but the location of the nerves is different. Radiographs are not necessary in most cases, although they can identify bony or articular lesions that may not be readily apparent or palpable. Examination of synovial fluid obtained by arthrocentesis can be used to differentiate septic from traumatic arthritis.
POSTURAL DEFORMITIES
A postural deformity in horses or ruminants is an abnormal stance caused by neurologic deficit, pain, or a musculoskeletal problem. Postural deformities can range from subtle conformational faults such as broken forward foot axis to severe and unusual positions, such as when the animal is camped out in front. Inability to bear weight on a limb, asymmetric angles between joints, and lateral or medial deviations in the alignment of limbs are examples of postural deformities. Often the postural deformity itself is specific for certain diseases and conditions (Table 13-4).
Table 13-4 Examples of Postural Deformities and Possible Origins
| Postural Defect | Likely Site of Origin |
|---|---|
| Contracted heels | Foot; flexor tendons |
| Bucked knees | Suspensory ligament |
| Dropped elbow | Motor nerves to forelimb; olecranon |
| Tiptoe stance | Foot; flexor tendons; interphalangeal joints |
| Non—weight-bearing | Foot; any long bone; any limb articulation |
| Broken down (hyperextension) fetlock; dropped fetlock | Suspensory apparatus |
| Toe-out hindlimb and elevated hip | Coxofemoral joint; femoral neck |
| Basewide behind | Coxofemoral joint; femoral neck |
| Hyperextension of stifle and hock | Patella |
| Camped out in front | Bilateral forefeet |
| Carpal valgus | Distal metaphysis, physis, epiphysis, or carpal bones |
| Stiffly elevated head | Withers; cervical spine |
| Shifting weight between forefeet | |
| Recumbency | Any long bone; feet; spinal cord; myopathy |
Mechanisms of Postural Deformities
Postural deformities can be either congenital or acquired and result from maldevelopment, trauma, or disease (Box 13-4). Congenital deformities may be caused by tendon contracture or laxity, osseous malformation, and hypoplasia or aplasia of osseous structures or soft tissues. Acquired deformities are most often caused by trauma or disease. Disuse atrophy secondary to an unrelated musculoskeletal abnormality can result in abnormal posture. Occasionally diseases affecting proprioception and consciousness may cause an abnormal stance that appears as a postural deformity (e.g., head pressing) but is unrelated to neurologic pain or a musculoskeletal problem.
Approach to Diagnosis of Postural Deformities in Horses
A history can help the examiner determine if a postural deformity is congenital, as with arthrogryposis, or acquired. Because most postural deformities in horses arise from traumatic injuries or overuse, a complete lameness examination is essential. Occasionally a postural deformity does not cause lameness; in these instances the veterinarian must consider nontraumatic causes associated with abnormal development, improper nutrition, and seemingly unrelated disease such as carpal valgus deformity.
Diagnosis of the cause of a postural deformity begins with a detailed description of the deformity and assessment of the position and asymmetry of the anatomic structures involved. If the nature and severity of the deformity cannot be determined by direct observation, palpation and manipulation of the affected structure are required. Radiography and ultrasonography also can assist in the diagnosis and provide information on which to base treatment recommendations and prognosis.
Approach to Diagnosis of Postural Deformities in Ruminants
Because of the many differences in husbandry and management practices between ruminants and horses, most postural deformities in ruminants are congenital or arise from dietary nutritional imbalances or plant poisonings (Box 13-5). Traumatic injuries play a smaller role, except in dairy cattle, which commonly slip on concrete and injure themselves. History, visual inspection, manipulation, and palpation are important in the diagnosis of postural deformities in ruminants. In addition, other ruminants in the herd with similar abnormalities should be identified. Plant, feed, soil, and water samples should be taken to identify toxins that may have been ingested, resulting in the deformity. Often the signalment helps rule out certain breed- or species-specific genetic defects. Because goats jump off heights, they are subject to numerous fractures, sprains, and luxations, including unilateral or bilateral rupture of the gastrocnemius tendon.
SWELLINGS AND ENLARGEMENTS (SOFT AND HARD TISSUE)
Swellings and enlargements consist of soft tissue (e.g., tendon) or hard tissue (e.g., osseous) and can occur anywhere on an animal’s body. Generally, clinically significant swellings and enlargements associated with the musculoskeletal system occur on the limbs.
Swellings and enlargements can be further divided into two principal groups, depending on whether or not they are associated with a specific anatomic structure. For example, a soft fluctuant swelling in the region of the left carpus may be caused by an abnormality of the antebrachialcarpal joint (e.g., septic synovial effusion) or may not involve the joint at all (e.g., subcutaneous abscess). Although lameness can be associated with such a swelling, clearly it is important to determine the cause of the abnormality because the one involving the joint may require the more immediate treatment.
Mechanisms of Swellings and Enlargements
The mechanism by which swelling or enlargement develops depends on the tissue involved (Box 13-6). Soft-tissue swelling often is produced by trauma, inflammation, infection, or neoplasia; it can consist of interstitial fluid (e.g., edema), fluid within an open space (e.g., synovial hernia), or a localized accumulation of cells or fibrous tissue. Localized edematous swelling commonly is caused by inflammation and/or obstruction of venous blood or lymph flow. Generalized edema is usually the result of increased hydrostatic pressure caused by circulatory failure or an altered capillary-tissue osmotic gradient stemming from hypoalbuminemia. Fluctuant swellings such as hematoma, synovial effusion, a purulent abscess, or a plasma-filled cyst contain free fluid. Granulation tissue, fibrous scar tissue, and tumor cells are the most common constituents of firm soft-tissue swellings. Rupture of supporting or confining structures (e.g., prepubic tendon rupture) can result in unusual forms of soft-tissue swelling caused by herniation of internal organs.
Many factors influence new bone formation. Trauma and infections initiate bony enlargement (e.g., callus) by disrupting the periosteum, producing inflammation and eventually ossification. The extent of periosteal new bone formation depends on the cause of the stimulus and the size of the affected area. Remodeled bone may also arise from nontraumatic events, usually associated with altered metabolism or neoplasia. Bony enlargements associated with the metaphysis and physis in young, growing animals are usually secondary to a combination of nutritional and traumatic factors. For example, dietary calcium, phosphorus, and vitamin D imbalance can lead to abnormal bone growth. A bony swelling develops gradually and may become noticeable only after it enlarges, interferes with normal function, or becomes a source of lameness.
Approach to Diagnosis of Swellings and Enlargements in Horses
Palpation of a swelling can determine its consistency and association with anatomic structures. Osseous swelling indicates calcification, proliferation of bone, or fracture. Firm soft-tissue swelling indicates inflammation, abnormal proliferation of soft tissue (e.g., granulation, tumor), or herniation.
Warmth, redness, and pain associated with swelling indicate active inflammation. While new bone is forming, the swelling may be soft and sensitive to palpation. Cold and insensitivity to palpation suggest inadequate blood supply and possibly ischemia (e.g., gangrene).
Lameness caused by an injury or condition that results in a hard swelling or enlargement may be accentuated by performing a stress test, such as trotting the horse in hand after direct pressure on the swelling. Intraarticular anesthesia may substantially reduce a lameness caused by joint effusion associated with periarticular new bone.
Approach to Diagnosis of Swellings and Enlargements in Ruminants
PARESIS AND WEAKNESS
Paresis, may be defined as a deficit of voluntary movement. It may be monoparesis (paresis of a single limb), paraparesis (paresis of both pelvic limbs), tetraparesis (paresis of all four limbs), or hemiparesis (paresis of a thoracic and pelvic limb on the same side). Paresis results from disruption of the voluntary motor pathways that extend from the cerebral cortex, through the brainstem and spinal cord, to the motor unit (peripheral nerve, neuromuscular junctions, and muscle fibers). Complete loss of voluntary movement is referred to as paralysis (plegia)., Voluntary movements must be differentiated from reflex movements on the basis of neurologic examination findings and general observations.
Weakness, may be defined as impairment of strength and power. Most authors use the terms paresis, and weakness, synonymously; however, this may be confusing in some circumstances. For example, weakness may occur in the absence of paresis in some disorders of the nervous system, and weakness may result from many disease processes that do not primarily involve the nervous system (e.g., heart failure, respiratory insufficiency). The clinical signs of weakness may vary considerably and may include paresis, gait abnormalities, dysphagia, regurgitation, dyspnea, and dysphonia. Weakness may be present at rest or may occur after exercise. The distribution of involvement may be local, regional, or generalized. In addition, there may be gross deformities of muscle mass (e.g., atrophy, hypertrophy, skeletal deformities) associated with weakness.
This section focuses on paresis and weakness caused by conditions that affect the motor unit (Box 13-8). Diseases of other systems (e.g., respiratory and cardiovascular diseases or central nervous system disorders) that may result in paresis and weakness are discussed separately in other sections.
Mechanisms of Paresis and Weakness
Voluntary movement is initiated by the cerebral cortex. Muscular activity occurs subconsciously after activation of successively lower levels of the nervous system: basal nuclei, midbrain, pons and medulla, cerebellum, brainstem, spinal cord, and motor unit. The function of these lower levels is vital, and without their input voluntary movements become impossible.
Monoparesis (or monoplegia) is a common problem in horses and ruminants. It may be caused by dysfunction of the lower motor neuron or neuromuscular junction. Monoparesis is commonly caused by trauma to a nerve or plexus, although neoplasia (e.g., lymphoma, neurofibroma) and inflammation or infection (e.g., early stages of rabies) of peripheral nerves have been reported to cause monoparesis.
Bilateral pelvic limb paresis, ataxia, or paralysis may occur as a result of a neurologic disorder localized to the spinal cord caudal to the T2 spinal cord segment. Various congenital vertebral and spinal cord malformations may result in pelvic limb paresis. Equine protozoal myeloencephalitis and equine degenerative myeloencephalopathy may result in lameness, weakness, and ataxia that may progress to tetraparesis. Musculoskeletal disorders resulting only in bilateral pelvic limb weakness and paresis are unusual. Possible causes include trauma (e.g., postcalving or postfoaling paralyses caused by lumbosacral nerve root compression or contusion), vascular disorders (e.g., thrombosis), and early stages of an infectious disorder that may progress to tetraparesis.
The causes of tetraparesis are numerous and include progression of many of the disorders mentioned previously. Outbreaks of intoxication with Clostridium botulinum, occur sporadically in horses and ruminants; the condition results in a flaccid paralysis that starts with the pelvic limbs and progresses cranially. Depending on the amount of toxin involved, large numbers of animals may be affected. Polyneuropathies (congenital and acquired) and polymyopathies (congenital, metabolic, infectious, and immune-mediated) are causes of tetraparesis.
Muscle weakness may result either from a primary neuromuscular disease or disorders that affect muscle secondarily. In the latter category, problems of horses and ruminants that commonly result in weakness include poor diet, underfeeding, toxicity, and anorexia. Systemic diseases and disorders such as dehydration, low circulating blood volume, anemia, and metabolic abnormalities (e.g., acidosis or alkalosis) also may result in weakness. Disorders of bones (e.g., fractures) and joints (e.g., septic arthritis) affecting one limb also may affect the contralateral limb through overuse or misuse, and weakness of the contralateral limb may result.
Primary neuromuscular diseases usually are classified on the basis of the anatomic component of the motor unit that is involved. Such diseases broadly are subdivided into neuropathies (disorders of the neuron, its cell body, axon, and/or Schwann cells [myelin]); junctionopathies (disorders of the neuromuscular junction); myopathies (disorders of muscle fibers); and neuromyopathies (disorders of both the neurons and the muscle fibers).
Dysfunction of the motor unit results in lower motor neuron signs, seen clinically as muscle weakness. The expression of this weakness may vary considerably, and the distribution of involvement may be local, regional, or generalized. Atrophy, hypertrophy, and skeletal deformities may accompany the muscle weakness. Any patient with some form of clinical weakness should be viewed as potentially having a motor unit disorder. That the patient is “weak merely because it is sick” should not be readily assumed without meticulous evaluation of the motor unit.
Approach to Diagnosis of Paresis and Weakness in Horses
Establishing a diagnosis requires an informed and coordinated approach to defining a problem list through associations and direct observations (i.e., a diagnostic plan) (Box 13-9).
The first step in locating a neurologic lesion is to determine the level of the abnormality along the longitudinal plane of the neuraxis (i.e., brain, spinal cord, or motor unit). The second step is to further localize the lesion within an anatomic region (e.g., motor unit should be further localized to peripheral nerve, neuromuscular junction, or muscle). The third step is to determine the location of the lesion in the transverse plane at the appropriate longitudinal level (e.g., left or right side).
Approach to Diagnosis of Paresis and Weakness in Ruminants
The approach to the diagnosis of disorders causing paresis and weakness in ruminants is essentially the same as that for horses (Box 13-10). Differences may be encountered as a result of the intended use of ruminants. Most ruminants live in a herd setting, and the level of human supervision and care of the herd will vary. In some cases animals will be monitored daily for signs of abnormal behavior, whereas in other cases animals may not be observed for varying periods of time. Infectious diseases, disorders arising from nutritional problems, parasites, or toxicity may progress to affect several individuals before a problem is noticed. Signalment, history, and a physical and neurologic examination are essential to determine first if the paresis and weakness are neurologic in origin and second to make a neuroanatomic diagnosis. These findings should be combined with a knowledge of diseases and disorders that produce this clinical picture in order to arrive at a diagnosis.
MUSCLE SPASMS AND MYOCLONUS
Muscle spasms are sudden, transient, and involuntary contractions of a single muscle or group of muscles, attended by pain and loss of function. Often all the muscles affected by a spasm are supplied by a single nerve. A painful, tonic, spasmodic muscular contraction is often referred to as a cramp.,
Myoclonus, may be defined as a disturbance of neuromuscular activity characterized by abrupt, brief, rapid, jerky, arrhythmic, asynergic, involuntary contractions involving portions of muscles, entire muscles, or groups of muscles, regardless of their functional association. The movements may be single or repetitive (10 to 50 per minute) and are similar to those that follow stimulation of a muscle. Myoclonus is seen primarily in muscles of the limbs, where involvement is often diffuse or widespread. Myoclonus also may be present in facial or masticatory muscles and muscles of the tongue, larynx, and pharynx. Myoclonus usually disappears during sleep.
This section describes muscle spasm and myoclonus as specific clinical signs associated with dysfunction of the musculoskeletal system.
Mechanisms of Muscle Spasms and Myoclonus
Spasms usually are of reflex origin and may result from irritation or stimulation at any level of the nervous system from the cerebral cortex to the muscle fibers. In most cases, however, spasms are caused by peripheral irritation affecting either muscles or nerves. Pain may cause either tonic or clonic spasms of muscles, especially should the painful stimulus be focal or discrete. Mechanical irritation may cause a localized spasm. There may be prolonged and characteristic muscle spasm associated with the hyperirritability of nerves and muscles in tetany or tetanus. Spasms may follow injury or irritation of peripheral nerves, particularly during the process of regeneration. Spasms may also result from irritation or diseases affecting cortical centers in the brain, motor nuclei in the brainstem, or descending motor pathways in the spinal cord.
There has been much discussion regarding the pathologic process underlying myoclonic movements. Whereas originally it was thought that the neural discharge that excites the muscular contraction of myoclonus was confined to the motor unit, it is now known that myoclonus also may result from dysfunction of the brain (cerebral cortex, brainstem, basal nuclei, thalamus, etc.), spinal cord, peripheral nerve, neuromuscular junction, or the muscle itself, alone or in combination. A variety of processes evidently lead to hyperexcitability of the cerebral cortex, subcortical structures, or even the lower motor neurons alone. Myoclonic movements or muscle spasms may occur in a variety of conditions. They have been observed in association with encephalitis, meningitis, toxic and postanoxic states, metabolic disorders, degenerative diseases, and vascular and neoplastic conditions. Myoclonus has also been reported in association with lesions of peripheral nerves, nerve roots, and spinal cord.
Specifically, disturbances in plasma electrolyte concentrations, certain drugs, toxins, and poisons may elicit involuntary muscle activity. In general, the mechanism that is common to all causes of spasm or myoclonus involves an inappropriate stimulation of a nerve or muscle cell, causing the cell to fire a series of action potentials, resulting in muscle contraction. For example, toxins may act directly on the muscle cell membrane to stimulate the release of calcium into the cell from the sarcoplasmic reticulum, thereby causing involuntary muscle contraction. Alternatively, some toxins may cause efferent neurons to release neurotransmitter across the neuromuscular junctions, thereby stimulating receptors on the muscle cell membrane.
Approach to Diagnosis of Muscle Spasms and Myoclonus in Horses
A broad spectrum of diseases may be associated with muscle spasms or myoclonus in horses (Box 13-11). A thorough investigation is needed to achieve an accurate diagnosis.
Approach to Diagnosis of Muscle Spasms and Myoclonus in Ruminants
The approach to diagnosis of muscle spasms and myoclonus in ruminants is essentially the same as that described for horses (Box 13-12). In ruminants a tetany panel (consisting of serum calcium, phosphorus, and magnesium determinations) should be completed in any animal exhibiting these signs. In lactating cattle on grass pasture, and in sheep transported long distances, hypomagnesemia and hypocalcemia, respectively, are highly suspected initially. Several infectious (e.g., rabies, pseudorabies), toxic, and inherited causes of muscle spasms and myoclonus should be suspected in ruminants. In postparturient animals and animals with wounds or bites, or animals recently castrated or tail docked, tetanus should be considered as a possible cause of muscle spasms and myoclonus.
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