Diagnosis of Neurologic Diseases
Signalment
The species, breed, age, and pedigree of an animal are important considerations in the differential diagnosis of neurologic disease.
■ TABLE 8.2
Dietary Deficiencies Associated With Neurologic Disorders of Livestock
| Dietary Deficiency | Disease Produced | Neurologic Sign |
| Copper Vitamin E Vitamin A Magnesium Potassium Calcium or phosphorus Vitamin E or selenium | Demyelination, pathologic vertebral fractures Demyelination Encephalopathy Grass tetany, transport tetany, milk tremors Weakness Milk fever, pathologic vertebral fractures, tetany Nutritional myodegeneration | Ataxia, recumbency Ataxia, recumbency Convulsions, blindness Convulsions, tremors, ataxia Postpartum recumbency Weakness, ataxia, recumbency, tetany Weakness, ataxia, recumbency, sudden death |
Many diseases are species specific, particularly in the case of infectious and genetic diseases.
Some diseases are not only species specific but also have higher incidence in certain breeds and ages of that species.1-13Some diseases are found in the neonate at birth. A large number of congenital disorders of the central nervous system (CNS) can affect domestic livestock. These diseases have a variable clinical course, depending on the nature of the disorder. Congenital disorders of myelin metabolism worsen with age, whereas other developmental conditions may remain stable throughout the animal's life.14-19 Examples of these disorders that have genetic tests available are listed in Chapter 52.
History
Many disorders of the CNS produce characteristic patterns of onset and progression. Some CNS diseases occur acutely, developing the full range of clinical signs within hours.
If the disease is not fatal, the signs either stabilize by 24 hours and remain constant thereafter or improve. Diseases that may display this clinical course include traumatic injuries and some types of toxic, infectious, and metabolic diseases. Diseases with degenerative, neoplastic, and certain viral causes may develop more slowly, requiring days to weeks for development of characteristic clinical signs.2,20,21Diet
The diet of patients with neurologic disease should be evaluated20-25 (Table 8.2). Equine motor neuron disease is seen mainly in horses that are housed without access to pasture and whose diet is deficient in vitamin E.26 Copper deficiency occurs in ruminants pastured in areas with shale or volcanic soils, which are either deficient in copper or contain high concentrations of molybdenum and sulfur; demyelination of the spinal cord in newborn small ruminants may result, as can vertebral fractures in calves. Overfeeding of protein and energy, as well as imbalance of certain trace minerals, has been linked to cervical vertebral stenotic myelopathy in horses (wobbler).27,28
Environment
Examination of the patient's environment may provide valuable information about the cause of CNS disease. Outbreaks of botulism and listeriosis have been associated with ingestion of rotting vegetation around haystacks, silos, and feed bunks.29,30 Plant poisonings are common in livestock, and identification of neurotoxic plants is important whenever multiple animals are affected simultaneously30-32 (Table 8.3). Nonplant neurotoxicants of livestock include lead, ethylene glycol, organic mercurials, chlorinated hydrocarbons, organophosphates, salt, sulfur, petroleum distillates, and many others. Dose of the neurotoxicant may be important, with different clinical signs appearing depending on the level of exposure. For example, ingestion of high concentrations of organophosphates or carbamates produces marked ataxia, coma, muscle tremors, salivation, and miotic pupils.
When low doses of organophosphates are ingested chronically, however, the result is an axonopathy of spinal cord and medullary neurons, resulting in pelvic limb paresis and ataxia, which may progress to tetraparesis and recumbency.33 Therapeutic and dietary interventions also may result in toxicoses when improperly administered. Overdosing of cattle with propylene glycol produces profound ataxia, depression, and coma.34 Ingestion of urea or ammoniated feedstuff produces hyperesthesia, excitability, coma, and convulsions. High concentrations of salt in drinking water or, more commonly, lack of fresh water or interruption of the water supply followed by unlimited access to water can result in laminar necrosis of the cerebral cortex or eosinophilic meningitis.33 The clinical signs are those of forebrain dysfunction, including blindness, dullness, seizures, coma, and death.35-37 Geographic area also may be important in the differential diagnosis of neurologic disease. Certain infectious diseases may be more common in particular areas of the country or even regions within a single state where the conditions for disease vectors are optimal.38 The travel history of the animal must be considered, as well as the animal's location at the time clinical signs appeared. Travel also may result in increased contact with other animals and greater risk of exposure to infectious diseases. Intermingling of horses from different premises is a potential risk for equine herpesvirus myeloencephalopathy (EHM).39Vaccination and Disease History
When a neurologic problem is evaluated, the vaccination history and previous herd or individual disease problems should be noted. Some vaccines are highly protective, such as those for rabies and tetanus. Neurologic disease may be a secondary complication of disease in another organ system. Foals and calves with severe diarrhea, for example, may convulse secondary to hypokalemia, hypernatremia, hyponatremia, or hypoglycemia.
Preexisting diseases in the population should be determined. For example, outbreaks of EHM are sometimes preceded by respiratory disease or abortions in herdmates.39 Historical evidence of limited colostral intake may be important in the diagnosis of bacterial meningitis of neonates. Bloody diarrhea often precedes the onset of nervous coccidiosis of calves.40Gestational Stage
Hypomagnesemia, eclampsia (hypocalcemia), hypokalemia, hypophosphatemia, and nervous ketosis are common causes of recumbency, convulsions, and tremors in adult livestock. These diseases usually occur between the beginning of the last trimester and the first 2 months after parturition.
Nervous System Examination
General Comments
A thorough physical examination should always precede or be performed concurrently with the neurologic examination. In some instances disease of organ systems other than the nervous system may take precedence for diagnosis and treatment. Such may be the case with animals that are in shock or suffering from other life-threatening cardiovascular or respiratory disturbances.
The neurologic examination should be carried out in a systematic fashion. The exact order of the examination is not
| ■ TABLE 8.3 | |
| Selected Poisonous Plants Producing Neurologic Signs (Also See Chapter 54) | |
| Plant Poisoning | Clinical Signs |
| Blue green algae (Aphanizomenon, Anabaena | Sudden death, tremors, salivation, miosis, bradycardia |
| flos-aquae) | |
| Bracken fern (Pteridium aquilinum) | Ataxia, weight loss, strip sweating (horses only) |
| Buckeye (Aesculus species) | Incoordination, twitching, sluggishness |
| Catsear (Hypochaeris radicata) | Hyperflexion of the hock during movement (stringhalt) |
| Cheesewood (Malva) | Tremors, worsened by forced exercise, hyperflexion of the hock during movement (stringhalt) |
| Creeping indigo (Indigofera spicata) and | Ataxia, obtundation, blepharospasm, corneal edema, lingual ulcers, seizures |
| Birdsville indigo (Indigofera linnaei) | |
| Dandelion (Taraxacum officinale) | Hyperflexion of the hock during movement (stringhalt) |
| Death camus (Zigadenus species) | Trembling, uncontrolled running, recumbency, opisthotonos, convulsions, vomiting, salivation |
| Dutchman's breeches (Dicentra) | Trembling, uncontrolled running, recumbency, opisthotonos |
| Fiddleneck (Amsinckia intermedia) | Ataxia, obtundation, somnolence, excitability, head pressing (hepatic encephalopathy) |
| Horse tail (Equisetum arvense) | Ataxia, weight loss, strip sweating (horses only) |
| Laburnum (Laburnum anagyroides) | Excitement, incoordination, convulsions, death |
| Larkspur (Delphinium) | Ataxia, collapse, recumbency, inability to lift head, tremors of face, flank, and hip; vomiting |
| Locoweed (Astragalus species) | Ataxia, weight loss, recumbency, hyperesthesia |
| Lupine (Lupinus) | Tremors, hyperexcitability, depression |
| Milkweed (Asclepias species) | Tremors, salivation, ataxia |
| Monkshood (Aconitum) | Restlessness, salivation, paresthesia, irregular heartbeat, recumbency, coma |
| Nightshades (Atropa species, Solanum species) | Tremors, ataxia, recumbency, convulsions |
| Poison hemlock (Conium maculatum) | Tremors, vomiting, ataxia, sudden death, abortions, pupillary dilation, bradycardia, coma |
| Rape (Brassica napus) | Blindness, ataxia, aggressiveness |
| Rattlebox (Crotalaria spectabilis) | Ataxia, obtundation, somnolence, excitability, head pressing (hepatic encephalopathy) |
| Rayless goldenrod (Haplopappus heterophyllus) | Lassitude, obtundation, arched back, stiff-legged gait, tremors, weakness, collapse |
| Russian knapweed (Rhaponticum repens, | Facial rigidity and dystonia, lack of prehension, ataxia, depression (horses only) |
| Acroptilon repens) | |
| Tansy ragwort (Senecio jacobaea) and common | Ataxia, obtundation, somnolence, excitability, head pressing (hepatic |
| groundsel (Senecio vulgaris) | encephalopathy) |
| Tobacco (Nicotiana species) | Tremors, salivation, ataxia, convulsions, birth defects |
| Water hemlock (Cicuta maculata) | Tremors, vomiting, ataxia, sudden death, convulsions, odontoprisis, pupillary dilation, abortions, bloat |
| White snakeroot (Eupatorium rugosum) | Tremors, salivation, convulsions |
| Yellow star thistle (Centaurea solstitialis) | Facial rigidity and dystonia, lack of prehension, ataxia, depression (horses only) |
important in itself, but procedures that may cause discomfort or pain, such as palpation of the spine, should be left until last.
A common system used by many neurologists is to start at the head and progress to the tail.41 Some clinicians prefer to examine the animal standing in the stall initially and then observe the gait. Because large animals are less amenable to handling than the typical cat or dog, another system for the neurologic examination is to begin with procedures that require minimal handling of the animal, such as observation of mental status, posture, and gait, and proceed to those that require greater manipulation.Neurologic examination alone rarely leads to definitive diagnosis but rather helps to answer the questions “Does the animal have neurologic disease?” and “What is the location of the neurologic lesion?” Once these questions are answered, a list of differential diagnoses can be made in light of other information such as the signalment of the animal and the history of the current problem. The diagnostic plan is based on the location of the lesion and the most likely differential diagnoses.