Diagnosis of Neurologic Disease by Presenting Signs

It is unusual for a goat to show a single, isolated sign of neurologic disease, and multiple signs may be exhibited serially or simultaneously during the course of disease. Therefore, in the following discussion of diagnosis of neu­rologic disease by presenting sign, the same disease may show up repeatedly under different headings as a possible cause of clinical signs.

Signs of Altered Mental State or Behavior

Excitability, Mania

Signs of excitation or mania include behaviors such as excessive bleating, resistance or overreaction to touch or handling, hyperesthesia, obvious fear or aggression, frenzy, aimless running, compulsive walking, head pressing, con­stant chewing, teeth grinding, or fluttering of the eyelids.

Infectious causes include rabies, pseudorabies, Borna disease, cowdriosis, scrapie, and bacterial meningoen­cephalitis. Thermal meningoencephalitis secondary to hot iron horn bud removal can also occur.

Possible parasitic causes include coenurosis (gid), aber­rant Oestrus ovis larval migration into the brain (false gid), trypanosomosis, and Strongyloides papillosus.

Metabolic causes include PEM, pregnancy toxemia, and hypomagnesemic tetany. Hepatoencephalopathy second­ary to liver disease can produce hyperesthesia or head pressing.

Toxic agents that can cause excitation in goats include organophosphates, chlorinated hydrocarbons, cyanide, nitrates, urea, nitrofurans, and the coyotillo plant (Karwinskia humboldtiana).

Levamisole or ivermectin given parenterally at therapeu­tic doses by injection may result in a transient excitatory reaction in some goats.

Coma

Infectious causes include meningoencephalitis, pseudora­bies, and enterotoxemia.

Metabolic causes include PEM, pregnancy toxemia, and milk fever. Hepatoencephalopathy secondary to liver dis­ease may result in coma, as can uremia.

Toxic causes include milkweed (Asclepias) poisoning; oxa­late poisoning; salt poisoning; and organophosphate, carba­mate, or chlorinated hydrocarbon insecticide toxicities.

Head trauma with subdural hemorrhage can result in coma. It is the nature of goats to frequently butt heads, but this does not preclude the possibility of occasional seri­ous injury.

Signs of Cranial Nerve Deficits

See Table 5.2.

Ocular Abnormalities

The differential diagnoses for abnormalities of pupillary function, blindness, ocular position, lid function, and sen­sation associated with the cranial nerves are discussed in Chapter 6.

Facial Nerve Paralysis

Characteristic signs include ear droop, eyelid droop, slack facial muscles with accumulation of feed in the buccal space, collapsed nostril, and drooling.

Infectious causes include CAE, listeriosis, brain abscess, otitis media, or otitis interna. Rupture of the tympanic membrane secondary to ear mite infection with Psoroptes cuniculi has resulted in facial nerve paralysis and signs of vestibular disease (Wilson and Brewer 1984).

Trauma to the facial nerve, which is superficial along much of its course, can also occur.

Dysphagia

Potential neurologic causes of difficult swallowing include rabies, CAE, bacterial meningoencephalitis, and listeriosis. The numerous non-neurologic causes of dysphagia are discussed in Chapter 10. Gloves and mask should be worn when examining a goat that presents with difficulty in swallowing, due to the risk of rabies.

Head Tilt

Persistent tilting of the head (one ear higher than the other) indicates vestibular dysfunction. Infectious causes of head tilt in goats include CAE, listeriosis, brain abscess, otitis media, and otitis interna.

Parasitic causes include cerebral nematodiasis caused by Parelaphostrongylus tenuis, Elaphostrongylus spp. or Setaria digitata, coenurosis (gid), or rupture of the tympanic mem­brane secondary to ear mite infection (Wilson and Brewer 1984).

Lymphosarcoma infiltrating the pituitary gland and pro­ducing a head tilt has been reported in agoat. Lymphosarcoma is discussed in Chapter 3. A choroid plexus carcinoma in a goat also produced a head tilt (Klopfleisch et al. 2006).

Deafness

On clinical examination, evaluation of deafness is difficult and interpretation subjective. However, deafness has been identified in neonatal kids with congenital beta mannosi- dosis. Otitis can also lead to deafness.

Signs of Involuntary Activity

Muscle Tremors

Some goats naturally tremble or shiver due to fear during an examination. This must be differentiated from nervous dysfunction. Infectious causes of tremors include rabies, scrapie, CAE, border disease, Borna disease, and bacterial meningoencephalitis. Tremors may also be an early sign of tetanus. Metabolic and nutritional causes include hypogly­cemia, PEM, hypomagnesemic tetany, hepatoencephalopa- thy, and enzootic ataxia or swayback.

Toxicologic causes include plant poisoning with bitter­weed or rubberweed (Hymenoxys spp.), neem tree (Azadirachta indica), coyotillo (Karwinskia humboldtiana), tropical soda apple (Solanum viarum), Ipomoea carnea, and possibly Bermuda grass hay (Cynodon dactylon), as well as cyanide poisoning, nitrate poisoning, oxalate poisoning, salt poisoning, boron ingestion, organophosphate, carbamate or chlorinated hydrocarbon insecticide poisonings, urea poi­soning, levamisole overdose, and diesel fuel consumption.

A hereditary cause of muscle tremors is beta mannosido- sis, which occurs in newborn kids of the Nubian breed.

Convulsions (Seizures)

Infectious causes include pseudorabies, Borna disease, enterotoxemia, tetanus, bacterial meningoencephalitis, and cowdriosis (heartwater).

Parasitic causes can include coenurosis (gid) and aberrant Oestrus ovis migration into the brain (false gid). Metabolic causes include PEM, hypomagnesemic tetany, pregnancy toxemia, hypoglycemia, and hepatoencephalopathy.

Toxic causes include the poisonous plants bitterweed or rubberweed (Hymenoxys spp.) and milkweed (Asclepias spp). Non-phytogenic poisonings include organophos­phate, carbamate, and chlorinated hydrocarbon insecti­cides; levamisole overdose; dinitro herbicides; and pentachlorophenol wood preservatives. Lead and salt poi­sonings are potential causes of convulsions, but are poorly documented in goats.

Lidocaine in sheep produces convulsive signs at an approximate dose of 6 mg/kg IV and circulatory collapse at a dose of 37 mg/kg IV (Morishima et al. 1981). Overdosing is most likely to occur in small kids when lidocaine is used as a local anesthetic.

Partial epilepsy of unknown cause has been reported as a cause of convulsions in an adult Nubian doe (Olcott et al. 1987).

Nystagmus

Infectious causes include rabies, CAE, listeriosis, brain abscess, and otitis.

Parasitic causes include cerebrospinal nematodiasis with either Parelaphostrongylus tenuis, Elaphostrongylus spp., or Setaria digitata and coenurosis (gid). Metabolic causes include PEM.

Toxic causes include locoism caused by consumption of locoweeds (Astragalus spp.) and possibly salt poisoning.

Hereditary beta mannosidosis causes nystagmus in affected newborn kids.

Pruritus

Primary dermatologic diseases are the most common cause of itching in goats, as discussed in Chapter 2. Pruritus of neurogenic origin tends to be more severe and animals frequently itch to the point of self-mutilation. All the neurogenic causes of pruritus in goats are of infectious or parasitic origin and include rabies, pseudorabies, scra­pie, Parelaphostrongylus tenuis, and Elaphostrongylus spp.

Gait Abnormalities

Circling

Circling in goats may be cerebral or vestibular in origin. Animals with circling caused by cerebral disease usually have other abnormalities of behavior or mental status to suggest cerebral involvement. Signs associated with circling caused by vestibular lesions are usually more localized and may be lim­ited to head tilt, nystagmus, hemiparesis, and other specific cranial nerve deficits such as facial nerve paralysis.

Infectious causes of circling include rabies, CAE, Borna disease, listeriosis, brain abscess, otitis media or interna, and cowdriosis (heartwater), and possibly scrapie (Konold et al. 2007).

Parasitic causes can include cerebrospinal nematodiasis with either Parelaphostrongylus tenuis, Elaphostrongylus spp., or Setaria digitata; trypanosomosis; coenurosis (gid); and aberrant Oestrus ovis migration into the brain (false gid).

Metabolic and nutritional causes are limited to PEM.

There is a report of neoplasia as a cause of circling. This was in an adult goat with a glioma in the cerebrum (Marshall et al. 1995).

Toxic causes include plant poisonings with Burttia pru- noides, or selenium-accumulating Astragalus spp., as well as chlorinated hydrocarbon insecticide toxicity and nitro­furan overdose.

Hypermetria

A high-stepping gait with overflexion of joints has been reported in coenurosis (gid), coyotillo (Karwinskia hum- boldtiana) poisoning, and enzootic ataxia. The author (DMS) has observed pronounced hypermetria in an adult Saanen buck that, on necropsy, had a focal meningioma impinging on the anterior cervical spinal cord.

Ataxia (Incoordination)

Ataxia or incoordination in goats most frequently suggests spinal cord lesions, but cerebellar, vestibular, and occasion­ally cerebral lesions can produce ataxia. Signs include a stag­gering gait, swaying or weaving from side to side, difficulties with abduction or adduction of the limbs, crossing of legs when standing or walking, general unawareness of place­ment and position of feet, and pivoting on the inside limb when circled.

Infectious causes include rabies, scrapie, CAE, listerio­sis, bacterial (or thermal) meningoencephalitis, brain abscess, and cowdriosis (heartwater).

Parasitic causes include cerebrospinal nematodiasis with either Parelaphostrongylus tenuis, Elaphostrongylus spp., or Setaria digitata; coenurosis (gid); aberrant Oestrus ovis migration into the brain (false gid); tick paralysis; trypano- somosis; and possibly Strongyloides papillosus.

Metabolic and nutritional causes include milk fever, PEM, hypomagnesemic tetany, and enzootic ataxia. A sin­gle case of renal (uremic) encephalopathy confirmed at necropsy has been reported in a 2-year-old male Boer goat. The animal showed chronic weight loss, an inability to rise, and ataxia (Radi et al. 2005).

Toxic causes include plant poisonings resulting from ingestion of coyotillo (Karwinskia humboldtiana), locoweeds (Astragalus spp.), guajillo (Acacia berland- ieri), cycad palms (Cycas, Zamia, Microzamia, and Bowenia spp.), milkweed (Asclepias spp.), larkspur (Delphinium spp.), fool's parsley (Aethusa cynapium), tropical soda apple (Solanum viarum), Ipomoea carnea, maize contaminated with the fungus Diplodia maydis, and possibly rye grass and Bermuda grass hay (Cynodon dactylon). The incoordination occurring with Astragalus spp. consumption may be due to either locoism or sele - nium toxicosis.

In addition to plant toxicities, incoordination can be seen with bromide, lead, salt, oxalate, urea, cyanide, or nitrate poisonings; organophosphate, carbamate, or chlorinated hydrocarbon insecticide intoxications; diesel fuel con­sumption; and nitrofuran or levamisole overdosage.

Neoplastic causes of ataxia have been reported sporadi­cally. Lymphosarcoma associated with the brain or menin­ges has resulted in incoordination (Craig et al. 1986). A choroid plexus carcinoma in a goat also produced ataxia (Klopfleisch et al. 2006).

Congenital or hereditary causes include congenital ver­tebral or spinal abnormalities such as hemivertebra (Rowe 1979). There is a report of atlanto-axial malarticula- tion in two young Angora goats that led to spinal cord degeneration at the level of the atlantoaxial joint, resulting in ataxia (Robinson et al. 1982).

Diseases of unknown etiology that can produce incoordination include polyradiculoneuritis and caprine encephalomyelomalacia.

Postural Abnormalities

Opisthotonos

Opisthotonos is a backward arching of the head and neck caused by spasm of extensor muscles. It may be observed in standing or recumbent animals. The list below includes those diseases in goats for which observation of opisthoto­nos has been specifically reported. However, opisthotonos may be observed during convulsions and the list of causes of convulsions should be consulted when the two signs are seen together.

Infectious causes include rabies, CAE, enterotoxemia, tetanus, brain abscess, and bacterial (or thermal) meningoencephalitis.

Disseminated toxoplasmosis is rare in goats and only one report has identified clinical signs of encephalitis, includ­ing opisthotonos, torticollis, and paresis (Fatzer 1974). Nevertheless, evidence of brain involvement may be com­mon on necropsy of stillborn kids or fetuses (Nurse and Lenghaus 1986). Trypanosomosis is another potential pro­tozoal cause of opisthotonos.

Metabolic and nutritional causes include hypomagne- semic tetany and PEM. Toxic causes include plant poisonings by bitterweed or rubberweed (Hymenoxys spp.), locoweeds (Astragalus spp.), salt poisoning, and chlorin­ated hydrocarbon toxicity.

Paresis (Weakness)

Neurogenic impairment of motor function leading to weak­ness may result from lesions of the brain stem, spinal cord, peripheral nerves, or neuromuscular junctions. Tetraparesis, paraparesis, hemiparesis, or involvement of a single limb may occur. Signs can include difficulty in rising, dragging of one or more limbs, trembling when standing, difficulty in standing for long periods, and collapse or buckling of the limbs. When hemiparesis is present, leaning, falling, or roll­ing to one side may be noted. Careful observation and thor­ough neurologic examination are necessary to distinguish ataxia from paresis when both are present.

Infectious causes of paresis include rabies, CAE or visna, listeriosis, and botulism. Parasitic causes include cerebro­spinal nematodiasis with either Parelaphostrongylus tenuis, Elaphostrongylus spp., or Setaria digitata; coenurosis; and tick paralysis.

Metabolic and nutritional causes include milk fever, preg­nancy toxemia, and enzootic ataxia or swayback. Toxic causes include plant poisonings by coyotillo (Karwinskia humboldtiana), locoweeds (Astragalus spp.), carpetweed (Kallstroemia hirsutissima), milkweed (Asclepias spp.), tropi­cal soda apple (Solanum viarum), Ipomoea carnea, and maize contaminated with the fungus Diplodia maydis. Toxic causes other than plant poisoning include salt poisoning, bromide intoxication, boron toxicity, organophosphate and carbamate insecticide poisoning, and pentachlorophenol toxicity.

Neoplastic causes of paresis are uncommon, but reports include lymphosarcoma sporadically associated with the brain or meninges (Craig et al. 1986), a malignant mela­noma metastasized to the vertebral canal (Sockett et al. 1984), and a primary congenital intradural melanoma surrounding the spinal cord of a 9-day-old Saanen goat, where the tumor likely derived from melanocytes or mel­anocytic precursors within the meninges of the lumbosa­cral spinal cord (Sinnott et al. 2020).

Congenital or inherited causes include hydrocephalus and progressive paresis of Angora goats. Caprine encepha- lomyelomalacia, a disease of unknown etiology, can also produce paraparesis or tetraparesis.

Paralysis

Paralysis is the complete loss of motor function in any part of the body. Many of the conditions that cause paresis progress to paralysis. Regarding the limbs, tetraplegia, par­aplegia, or hemiplegia may be observed. Paralysis of the limbs may be flaccid or spastic depending on the location of the lesions. The former is associated with hyporeflexia and the latter with hyperreflexia.

Infectious causes include rabies, pseudorabies, CAE or visna, Borna disease, botulism, and brain abscess. Parasitic causes include cerebrospinal nematodiasis with either Parelaphostrongylus tenuis, Elaphostrongylus spp., or Setaria digitata, and tick paralysis.

Metabolic causes include milk fever and enzootic ataxia or swayback. Toxic causes include mycotoxicosis caused by consumption of maize contaminated with the fungus Diplodia maydis and organophosphate or carbamate insec­ticide toxicity.

Congenital or hereditary causes include hydrocephalus and congenital malformations of the vertebral canal or spi­nal cord, such as hemivertebra, and progressive paresis of Angora goats.

Trauma is the usual cause of peripheral nerve injuries leading to paralysis. While injury may occur to any of the peripheral nerves, the most common peripheral nerve dysfunction in goats is damage to the sciatic nerve from mechanical injury caused by poor IM injection technique or the introduction of irritating medications on or near the nerve. The problem may be aggravated by the secondary development of abscesses. Typical signs of sciatic nerve injury include flaccid carriage of the entire hindlimb, with the dorsum of the hoof dragging on the ground during walking and a loss of skin sensa­tion over most if not all of the limb. A case of hindlimb paralysis caused by a metastatic malignant melanoma of the sciatic nerve has also been reported (Sockett et al. 1984).

Radial nerve paralysis related to trauma occurs in goats. Signs include flaccid carriage of the forelimb, with a dropped elbow and an inability to extend the carpus and fetlock joints. The limb is dragged on ambulation. Skin sensation loss occurs on the anterior aspect of the pas­tern, fetlock, and digit. Restoration of limb use in a goat with radial paralysis by transplantation of the flexor carpi radialis tendon has been described (Batcher and Potkay 1976).

Trauma to the vertebral column can lead to paralysis by damage to the spinal cord. Vehicular injuries and fighting between goats are the most common causes of vertebral trauma, but fractures of the vertebrae may be predisposed to by the presence of abscesses or osteoporosis associated with rickets.

Caprine encephalomyelomalacia, a disease of unknown etiology, can also produce paraplegia or tetraplegia.