deposited around the region of bone modeling almost stopped the syndrome occurring for about an hour, and infiltrating a repository glucocorticoid drug in the region attenuated the syndrome markedly for over a week. Ultimately, surgical exploration and removal of much of the new mineralized tissue was undertaken, and after healing of the surgical site the syndrome did not occur while the horse was ridden for several months before the case was lost to follow‐up. It is however worth recalling that horses without the problem of headshaking can have various radiographic changes present in this region (see Figure 3.9).
Quite bizarre syndromes can be seen as idiosyncratic reactions to intramuscular injections of depot forms of antipsychotic drugs including fluphenazine used for chronic sedation and sulpiride used for lactation induction protocol. Included in these can be episodes of unusual, monotonous movements of the limbs and of the head and neck with the thoracic limbs extended and the head touching the ground—even flexed between them in a “praying” posture.2 Episodes of bradykinesia or freezing can also occur. Such signs can be interrupted by unpredictable, violent events that render the situation dangerous although most cases have responded to anticholinergic therapy with diphenhydramine and/or benztropine.3 These syndromes can be compared to the extrapyramidal side effects seen in people with antipsychotic and antidopaminergic drugs including fluphenazine and metoclopramide, but they can also occur in animals suffering from brain injury and from meningitis.
With no other neurologic signs, it can be difficult to be sure whether subtle behavioral syndromes are learned repetitive behavioral traits—or simply actions perceived as being unacceptable responses to human‐induced management restrictions placed on domestic animals rather than being due to acquired morbid neurologic lesions. Examples of these include repetitive licking and sucking (Figure 5.6), head shaking (Figures 5.7 and 5.8), tail wringing, aggressiveness, self‐mutilation, and refusing to follow learned instructions such as taking jumps. Some of these syndromes are discussed in Chapter 28, although for a more detailed evaluation of equine behavioral aberrations, the reader is directed to further literature.4–15 Although tempting to speculate, there is not ample evidence that many forms of varied behavior, regarded as unacceptable in domesticated animals by humans, are genetic for the most part,16 and indeed many clinicians would rather suggest they are acquired, even when appearing in successive offspring.
Finally, the potential role of painful sensory inflammatory or degenerative lesions such as ganglioneuritis17 in causing unacceptable and dangerous behavior needs further ratification.
References
1 1 Couetil LL and Hoffman AM. Adrenal insufficiency in a neonatal foal. J Am Vet Med Assoc 1998; 212(10): 1594–1596.
2 2 McCrindle CM, Ebedes H and Swan GE. The use of long‐acting neuroleptics, perphenazine enanthate and pipothiazine palmitate in two horses. J S Afr Vet Assoc 1989; 60(4): 208–209.
3 3 Baird JD, Arroyo LG, Vengust M, et al. Adverse extrapyramidal effects in four horse given fluphenazine decanoate. J Am Vet Med Assoc 2006; 229(1): 104–110.
4 4 Crowell‐Davis SL and Houpt KA. Behavior. Vet Clin North Am Eq Pract 1986; 2: 465–671.
5 5 Hahn CN. Behavior and the Brain. In Equine Behavior: A Guide for Veterinarians and Equine Scientists, McGreevy P, Editor. Saunders, Philadelphia, PA. 2004.
6 6 Kiley‐Worthington M. Stereotypes in horses. Cause, function and prevention. Equine Pract 1983; 5(1): 33–40.
7 7 Kiley‐Worthington M, Wood‐Gush D. Stereotypic Behavior, in Current Therapy in Equine Medicine, Robinson NE, Editor. 2nd ed. Philadelphia. 1987; 131–134.
8 8 Beaver BV. Aggressive behavior problems. Vet Clin North Am Equine Pract. 1986; 2(3): 635–644.
9 9 Houpt KA. New perspectives on equine stereotypic behavior. Equine Vet Educ 1995; 27(2): 82–83.
10 10 Luescher UA. Porcine behavior problems. Comp Cont Edu Pract Vet 1998; 11: 515–518.
11 11 McGreevy P. Equine Behavior: A Guide for Veterinarians and Equine Scientists. Saunders, Philadelphia, PA. 2004; 369.
12 12 Price EO. Farm animal behavior. Vet Clin North Am Food Anim Pract 1987; 3: 217–481.
13 13 McGreevy PD, French NP and Nicol CJ. The prevalence of abnormal behaviours in dressage, eventing and endurance horses in relation to stabling. Vet Rec 1995; 137(2): 36–37.
14 14 McAfee LM, Mills DS and Cooper JJ. The use of mirrors for the control of stereotypic weaving behaviour in the stabled horse. Appl Anim Behav Sci 2002; 78(2–4): 159–173.
15 15 Houpt KA. Domestic Animal Behavior for Veterinarians and Animal Scientists. 6th ed. Wiley‐Blackwell, Hoboken, NJ. 2018; 448.
16 16 Hemmann K, Ahonen S, Raekallio M, Vainio O and Lohi H. Exploration of known stereotypic behaviour‐related candidate genes in equine crib‐biting. Animal 2014; 8(3): 347–353.
17 17 Story MR, Nout‐Lomas YS, Aboellail TA et al. Dangerous Behavior and Intractable Axial Skeletal Pain in Performance Horses: A Possible Role for Ganglioneuritis (14 Cases; 2014–2019). Front Vet Sci, 2021; 8: #734218.
6 Seizures and epilepsy
Seizures, abnormal sleep patterns, myotonic episodes, and syncopal episodes can be difficult to distinguish apart. The last of these, occurring in the absence of heart failure, is incredibly rare but the first two are quite distinguishable if observed or preferably captured on video. Particularly because they both more often occur at quiet periods when patients are not being observed, 24‐h video recording can be useful to capture suspected episodes of sleep disorders and epilepsy when they are not otherwise overt. Exposure to stray electric currents can be the cause of unusual repetitive recumbency akin to epilepsy.1 There are also many nonepileptic disorders imitating generalized idiopathic epilepsy that need to be considered when evaluating patients for repeated motor and hypotonic events. These include movement disorders classified as paroxysmal dyskinesia,2 benign myoclonus, hypotension, hyperekplexia, and many metabolic and toxic insults.3,4 Indeed, even severe Psoroptes ovis infestation (sheep scab) has been seen to induce convulsions in sheep5 and Otobius megnini (spinose ear tick) will cause fits in horses,5b and both of these syndromes resolve with antiparasitic therapy.
Acquired metabolic derangements including hypomagnesemia, hypocalcemia, hyponatremia, hypernatremia, hepatoencephalopathy, hyperammonemia, and uremia all can result in seizures, as also seen with terminal events in many toxicities.
Dyskinesias, although not apparently confirmed in large animals, do deserve mention here.2 These disorders are differentiated from epileptic seizures by there being no impairment to consciousness and no autonomic or postictal signs. Many of these phenotypic syndromes are yet to be specifically defined, but some involve genetic alterations to proteins involved in transmembrane conductance. Interestingly, the paroxysmal, familial ataxia in lambs (see Chapter 31) fits these criteria,6 but as with several inherited spinocerebellar ataxias in humans and dogs this disorder is likely a channelopathy.7 The onset of a myotonic episode in patients with myotonia (Chapter 31) can be exceedingly abrupt with whole body rigidity and recumbency that mimics a seizure, although again there is no loss of consciousness.
A seizure, fit, ictus,