Paresis and Weakness

Richard Andrew LeCouteur

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).

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 13.7). 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.

■ BOX 13.7

Causes of Paresis and Generalized Weakness in Horses and Ruminants

Anemia

Cardiovascular disease

Chronic inflammatory disease Drug-related conditions Electrolyte disorders

Endocrine or metabolic disorders Exhaustion

Fever or sepsis

Gastrointestinal disease

Motor unit disease

Neoplasia

Nervous system disease

Nutritional disorders

Respiratory system disease Trauma

Toxicities 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.

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, toxicoses, 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 and joints affecting one limb also may affect the contralateral limb through overuse or misuse, and weakness of the contralateral limb may result.

Primary neuromuscular diseases are usually classified on the basis of the anatomic component of the motor unit that is involved. Such diseases are broadly 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 neurons and 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 13.8).

1. Signalment. Breed, age, sex, and use of the horse.

2. History. Feeding program, vaccination and deworming schedules, course of complaint, response to treatment, and possibility of exposure to toxins or trauma.

■ BOX 13.8

Causes of Paresis and Weakness in Horses

Degenerative

Equine degenerative myeloencephalopathy

Anomalous or Congenital

Hydrocephalus

Vertebral and spinal cord malformations

Metabolic

Exertional rhabdomyolysis

Hyperkalemic periodic paralysis

Hypothyroidism

Hyperthermia

Hypocalcemia

Hypokalemia

Equine hepatic lipidosis

Vitamin A deficiency

Nutritional

Macronutrient malnutrition

Vitamin E (selenium) deficiency

Neoplastic

Brain or spinal cord tumor

Lymphosarcoma

Melanoma

Leukemia

Infectious or Inflammatory

Encephalitis, myelitis

Equine protozoal myeloencephalitis

Diskospondylitis

Botulism

Rabies

Ehrlichiosis

Tuberculosis

Rhinopneumonitis

Hepatoencephalopathy

Tick paralysis

Cerebrospinal nematodiasis

Equine protozoal myeloencephalitis

Toxic

Snakebite

Plant poisons (star thistle poisoning, oleander, moldy corn poisoning, white snakeroot, locoweed, larkspur, delphinium, onion, moldy sweet clover)

Vitamin D

Phosphorus

Heavy metals (lead, arsenic)

Traumatic

Vertebral fracture or luxation

Vascular

Postanesthetic hemorrhagic myelopathy

3. Physical examination. The clinician must rely on clinical signs of abnormal function to identify the location of the neurologic dysfunction. 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).

4. Minimum database. Complete blood count, serum biochem­istry panel (including electrolyte determinations), fecal analysis, and urinalysis may be considered. Measurement of muscle-specific serum enzymes such as creatine kinase (CK), as well as aspartate aminotransferase (AST) and lactic dehydrogenase (LDH), may be helpful in identifying neuromuscular disorders in which myonecrosis is a principal pathologic feature. Urine can be tested for the presence of myoglobin released from damaged skeletal or cardiac muscle.

5. Specific diagnostic tests: Electrodiagnostic testing. Elec­tromyography (EMG) involves the detection and charac­terization of electrical activity (potentials) recorded from a patient's muscles. A systematic study of individual muscles permits an accurate determination of the distribution of muscles affected by a pathologic process.

6. Nerve and muscle biopsy examination. This procedure evaluates the morphology of portions of the motor unit and may differentiate neuropathies, junctionopathies, and myopathies. In some instances, results of muscle biopsy analysis may provide a definitive diagnosis (e.g., polysac­charide storage myopathy of horses).

Approach to Diagnosis of Paresis and Weakness in Ruminants

Sarel R. Van Amstel • Jan K. Shearer

The approach to the diagnosis of disorders causing paresis and weakness in ruminants (Box 13.9) is essentially the same as that for horses. The following should be included:

Signalment

Age, sex, breed, use (pet, dairy, beef)

History

Feed composition and storage, calving difficulty, exposure to trauma or toxins, recent purchase of new animals or new introductions into an established social group, vaccinations, housing

Physical Examination

Observe the animal from a distance to evaluate posture, signs of weakness or neurologic signs such as stumbling, and ataxia.

Other Diagnostic Tests

A hematocrit and total protein will give an indication of the degree of anemia or dehydration. A complete blood count including fibrinogen may indicate the presence of inflammatory disease. A blood smear should be examined for the presence of blood parasites and type of anemia present. Blood chemistry including electrolytes and the animal's blood gas status should be evaluated. A neurologic examination should be carried out. Reduced lower jaw and tongue tone, as well as dysphagia, may be indicative of botulism, rabies, polioencephalomalacia, or listeria. Other common cranial signs may include ptosis, anisocoria, delayed or absent pupil light response, dropped ears, facial asymmetry, delayed or absent sensory response to

■ BOX 13.9

Causes of Paresis and Weakness in Ruminants

Anomalous or Congenital

Progressive degenerative myeloencephalopathy of Brown Swiss cattle

Progressive ataxia of Charolais cattle

Inherited progressive spinal myelinopathy of Murray Grey cattle Inherited myophosphorylase deficiency in Charolais cattle Heart disease

Hydrocephalus

Metabolic

Hypoglycemia

Hypocalcemia Hypokalemia

Hypomagnesemia

Rumen acidosis

Anemia

Hypothermia Hepatic encephalopathy

Infectious or Inflammatory

Infectious diarrhea; for example, Salmonella

Tick paralysis Botulism

Rabies

Parasitism

Pneumonia

Spinal abscess

Sepsis

Bovine spongiform encephalopathy

Severe mastitis Endotoxemia

Encephalomyelitis

Nutritional

Starvation

Vitamin E/selenium Polioencephalomalacia

Diarrhea

Water intoxication/salt poisoning Copper deficiency

Neoplastic

Spinal lymphoma

Traumatic

Vertebral fracture or luxation Calving paresis

Parasitic

Parelaphostrongylus tenuis

Toxic

Lead poisoning Ionophore toxicity

the face, head tremors, blindness, and star gazing. Intension tremors may indicate cerebellar disease, whereas head pressing may indicate problems with the cerebral cortex.

The degree of ataxia and weakness can be tested by walking the animal in a tight circle and observing the proprioceptive response or pulling the tail (laterally) while walking next to it. Spinal reflexes can be done if the animal is recumbent. Box 13.9 lists causes of paresis and weakness in ruminants. A spinal tap should be considered, particularly in small ruminants including camelids where an eosinophilic pleocytosis is suggestive of meningeal worm infestation.