Large Animal Neurology. Joe Mayhew

it is important to determine if the animal has a history or evidence of trauma or of other premonitory neurologic signs. Immediately following head trauma, a temporary period of coma often ensues. Thus, the animal does not require euthanasia during the first 24 h, but at this time appropriate diagnostic and therapeutic approaches should be instituted. Access to specific toxic compounds should be sought in order to administer appropriate antidotes that can be lifesaving.^7,8 Future use of nanostructured biomaterials may well become generally available for unknown toxicities.⁹

      Collapse without loss of consciousness can be caused by loss of motor function. Motor pathways may be interrupted at the level of the brainstem, vestibular apparatus, spinal cord, peripheral nerve, neuromuscular junction, or muscle. A neurologic examination is needed to identify where the lesion is. Trauma is the most frequently occurring mechanism at the first three of these anatomic levels. Acute collapse without loss of consciousness is also caused by botulinum toxins including the shaker‐foal syndrome, postanesthetic myasthenic syndrome, postanesthetic neuromyopathy, exercise‐associated rhabdomyolysis, tick and elapid snake bite paralyses, and hyperkalemic periodic paralysis.

      Generalized and metabolic disorders resulting in acute collapse include hyperthermia, cardiovascular collapse, hypoglycemia, hypocalcemia, hyperkalemia, hypokalemia, endotoxemia, intestinal hyperammonemia, anaphylaxis, anaphylactoid reaction, acute exotoxemia, snake envenomation, and many terminal toxic states.^10–15 Usually, several body systems are found to be abnormal after a general physical examination and subsequent, appropriate detailed system examinations, and therapy can be undertaken.

References

      1 1 Fejerman N. Nonepileptic disorders imitating generalized idiopathic epilepsies. Epilepsia 2005; 46 Suppl 9: 80–83.

      2 2 Jesty SA and Reef VB. Evaluation of the horse with acute cardiac crisis. Clin Tech in Eq Pract 2006; 5(5): 93–103.

      3 3 Lyle CH, Turley G, Blissitt KJ, et al. Retrospective evaluation of episodic collapse in the horse in a referred population: 25 cases (1995‐2009). J Vet Intern Med 2010; 24(6): 1498–1502.

      4 4 Lyle CH and Keen JA. Episodic collapse in the horse. Equine Vet Educ 2010; 22(11): 576–586.

      5 5 Steiger R and Feige K. Case report: polycythemia in a horse. Schweiz Arch Tierheilkd 1995; 137(7): 306–311.

      6 6 Hay WP, Baskett A and Abdy MJ. Complete upper airway obstruction and syncope caused by a subepiglottic cyst in a horse. Equine Vet J 1997; 29(1): 75–76.

      7 7 Landolt GA. Management of equine poisoning and envenomation. Vet Clin North Am Equine Pract 2007; 23(1): 31–47.

      8 8 Khan SA, Kuster DA and Hansen SR. A review of moxidectin overdose cases in equines from 1998 through 2000. Vet Hum Toxicol 2002; 44(4): 232–235.

      9 9 Muhammad F, Nguyen TDT, Raza A, Akhtar B and Aryal S. A review on nanoparticle‐based technologies for biodetoxification. Drug Chem Toxicol 2017; 40(4): 489–497.

      10 10 Bandarra PM, Pavarini SP, Raymundo DL, et al. Trema micrantha toxicity in horses in Brazil. Equine Vet J 2010; 42(5): 456–459.

      11 11 Ozmen O, Sahinduran S, Haligur M and Sezer K. Clinicopathologic observations on Coenurus cerebralis in naturally infected sheep. Schweiz Arch Tierheilkd 2005; 147(3): 129–134.

      12 12 Giadinis ND, Psychas V, Polizopoulou Z, et al. Acute coenurosis of dairy sheep from 11 flocks in Greece. N Z Vet J 2012; 60(4): 247–253.

      13 13 Ozmen O and Mor F. Acute lead intoxication in cattle housed in an old battery factory. Vet Hum Toxicol 2004; 46(5): 255–256.

      14 14 Johnson PJ, Mrad DR, Schwartz AJ and Kellam L. Presumed moxidectin toxicosis in three foals. J Am Vet Med Assoc 1999; 214(5): 678–680.

      15 15 Brownlow MA, Dart AJ and Jeffcott LB. Exertional heat illness: a review of the syndrome affecting racing Thoroughbreds in hot and humid climates. Aust Vet J 2016; 94(7): 240–247.

9 Blindness

The visual and pupillary light pathways should be reviewed (Figure 2.9) as well as the discussion on testing for vision in the neurologic examination section in Chapter 2. Some cases of reduced vision with the associated pupillary changes are given here as examples of blindness in large animals (Figure 9.1).

Often animals suffering from forebrain lesions are blind with depressed menace responses in one or both eyes. A central blindness or amaurosis, with pupillary reflexes intact, occurs in an eye contralateral to a lesion involving an optic tract, dorsal thalamus (lateral geniculate nucleus), optic radiation part of the internal capsule, or the visual cortex predominantly in the occipital lobe of the cerebral hemisphere. These structures constitute the central visual pathways. Central to the chiasma, one optic tract receives circa >80% of all visual and light pathway fibers from the contralateral eye, and these functionally different fibers pass together in the first portion of the optic tract to the level of the caudal thalamus where the pupillary light fibers separate to synapse on the pretectal nucleus and thence to the parasympathetic oculomotor nucleus in the midbrain (Figure 2.7). Thus, one would expect that, as well as central contralateral blindness due to a lesion involving the (light and visual) afferent, immediate postchiasmal optic tract fibers, there should be (bilaterally) suppressed pupillary motor function evident when light is shone in the blind eye. However, clinically this is very difficult to discern. On the other hand, occasionally it is possible to detect visual field deficits with some selective and focal lesions involving these central visual pathways as discussed in the neurologic examination section in Chapter 2.

      A lesion in the eye or optic nerve on one side, with the other eye and its optic system normal, results in blindness and a suppressed menace response in that eye with slightly dilated pupils (mydriasis) and poor pupillary constriction in both eyes when light is shone in the blind eye. The degree of mydriasis evident will depend on the ambient light that the other normal eye is exposed to. A patient can be clinically blind with an absent menace response and a slightly dilated pupil in one eye due to an eye or optic nerve lesion, and can still have some pupillary constriction in response to a very bright strobe light shone in that eye. This discrepancy comes down to difficulties in determining when an animal is totally blind, and the fact that visual path fibers are probably damaged more readily with various eyeball and optic nerve lesions than are light pathway fibers destined for the oculomotor nuclei in the midbrain. With respect to visual perception, possibly the most sensitive test of crude visual pathway input is to place a blind patient having no menace responses in a dark enclosed area with a brightly lighted exit available to see if the patient can discern the escape route.

Figure 9.1 Following head trauma, bilateral blindness with dilated and nonresponsive pupils in a fully conscious horse as in top figure, is most likely due to bilateral optic nerve injury. In comparison, blindness with a normally responsive pupil, as in bottom figure, is more likely due to a contralateral, central, thalamic, or caudal cerebral lesion.

      The swinging light test can be useful to help sort out difficult visual deficits too, as performing and interpreting consensual or indirect pupillary light reflexes in large animals is problematic,