Читать книгу Large Animal Neurology - Joe Mayhew - Страница 104

The location of lesions resulting in disorders of behavior essentially involves the forebrain, and such lesions can be focal, multifocal, and diffuse. Because normal behavior is extremely variable among species, breeds, individuals, and especially stages of reproductive cycles, if after a neurologic examination the only finding is a history of or evidence of a subtle change in expected behavior, the examiner must be cautious while assuming that a morbid lesion in the forebrain accounts for the signs.

Frantic behavior of a bull during the mating season, jerky collapsing in a white pig with sunburn in full sun, bizarre antics of a mare in diestrus, and violent kicking in a colt having a new bandage applied over the hock all attest to unusual behavior syndromes that can easily be mistaken for morbid brain disorders.

Subtle alterations in behavior resulting from organic brain disorders include the following: continual yawning—that can be prominent in hepatoencephalopathy; a tendency to drift to one side when walking—that is often present with asymmetric lesions; and a lack of recognition of familiar animals (Figure 5.1), people, and objects—that is often the earliest expression of cerebral disease in foals. More prominent signs are seizures (Chapter 6), compulsive walking and circling (Figure 5.2), pressing the head on objects, running around frantically, biting at animate (including self) (Figure 5.3) and inanimate (Figure 5.4) objects, leaving food in the mouth, and adopting bizarre postures of the head, neck, trunk and limbs. Such syndromes are usually referable to lesions in the frontal lobes, temporal lobes, internal capsule, limbic system, thalamus or basal nuclei, or due to diffuse brain disease.

Figure 5.1 A newborn Thoroughbred foal that is not distracted by the presence of people, does not attend to the dam, and postures with its head flagging alongside its flank is behaving very abnormally and is likely suffering from forebrain disease. With such a syndrome, this foal did have an undiagnosed, aseptic meningoencephalitis from which it survived.

Figure 5.2 A patient that is variably obtunded and spontaneously turns and walks toward one side will have an asymmetric lesion in the forebrain, usually worse on the side toward which it turns—right in this case. This lamb has a chronic suppurative and granulomatous ependymitis and ventriculitis on the right side. Additional signs of forebrain involvement were poor vision and poor menace response in the left eye (with normal pupils) and decreased sensation perceived from the left nasal septum compared with the right. Typical of many lesions associated with perilesional edema, and especially those involving forebrain, the signs would wax and wane in severity so that at times the lamb would walk, trot, and run quite well in both directions. The only consistent abnormality with gait and posture was a delay in protracting the left limbs, especially the left forelimb as shown here, while turning right and while attempting to hop on each left limb in turn. This likely represents abnormal conscious proprioceptive processing from the left side of the body and limbs.

Usually, localized and diffuse lesions affecting only the forebrain result in combinations of behavioral changes (including seizures), blindness, and lethargy. Although often sluggish in movement, little or no alteration in gait occurs, at least in the subacute to chronic stages. Central motor pathways to and sensory inputs from cranial nerves can be disrupted, and such syndromes are discussed under the individual cranial nerve disorders. Particularly with metabolic diseases such as hyperammonemia, and with those focal and diffuse disorders accompanied by inflammatory lesions or by perilesional edema, there can be dramatic fluctuations in the severity of behavioral signs displayed over periods ranging from minutes to weeks. This can even mean that there are no overt signs demonstrated at a point in time, and within a few hours there may be prominent behavioral changes and even an uncontrollable patient.

Nondomesticated and unhandled domestic large animals, particularly adult bulls, boars and horses, can become exceedingly defensive when incapacitated by all sorts of disorders and behave quite violently and aggressively. Additionally, Equidae routinely respond to visceral pain in surprisingly violent ways (Figure 5.5) such that colic always needs to be considered differentially when dealing with aberrant behavior in these species.

Figure 5.3 Self‐inflicted lesions caused by biting are quite unusual and can be spectacular with horses suffering from the self‐mutilation syndrome. In the Arabian stallion shown here, such signs were due to rabies virus infection, as was a proclivity to assault learned professors wearing white coats. Possibly associated with aggressive anti‐inflammatory therapy, these signs progressed slowly over many days, with the patient surprisingly surviving for well over a week after the onset of abnormal behavior. Self‐inflicted biting trauma can also be seen in horses with other encephalomyelitides and with metabolic encephalopathies.

A period of calm or of induced sedation may be taken as an opportunity to search for localizing signs of brain disease that are often overshadowed by any accompanying wildly aberrant behavior. These will include subtle signs such as asymmetric menace responses, anisocoria, asymmetric nasal sensation, head tilt, head turn, facial hypotonia, and drifting to one side walking undirected with blindfold applied.

Faced with an animal showing aggressive or violent behavior, for safety reasons the clinician must consider sedating the patient. Most times diazepam will not be at hand but expedient IM or IV administration of moderate to high doses of a readily available α‐2 agonist drug combined with a synthetic opioid drug is perfectly satisfactory in most circumstances. Obviously, with a patient from a rabies‐endemic area, this diagnosis must be considered of paramount importance. Some diseases that result in such a fulminant syndrome of wildly abnormal behavior can have a positive outcome, and therefore euthanasia must be given careful consideration while sedation takes effect. Examples of those diseases with a more favorable prognosis include thiamine‐responsive polioencephalomalacia, hypoadrenocorticism,¹ neonatal hypoxic and ischemic encephalopathy, salt poisoning, hypomagnesemia, hypocalcemia, hypoglycemia, hepatic, exogenous and intestinal ammonia intoxication, ketosis, metaldehyde toxicosis, macrocyclic lactone overdose, and immediate post‐head trauma delirium.

Figure 5.4 This milking Friesian cow likely was suffering from ketosis with episodes of bizarre behavior characterized by vigorously attacking animate and especially inanimate objects such as the metal bars of her pen as shown; she recovered fully with treatment. Such extremes of abnormal behavior in cattle can also be seen with many morbid and functional encephalopathies including rabies, hepatoencephalopathy, ammonia intoxication, and lead poisoning.

Asymmetric forebrain lesions frequently cause an animal to hold its head and neck turned to one side, usually toward the same side as the lesion. This can be difficult to distinguish from a vestibular head tilt where there is rotation of the poll around the muzzle. In a more prominent form, a head turn due to vestibular or cerebral disease may involve bending of the whole neck and head toward the flank. The presence or absence of a vestibular head tilt is best evaluated after the nose and neck have been held back into a midline position. In some animals with forebrain lesions, the eyes are also deviated and the whole body spins in circles in the direction of the head turn. Such episodes may be precipitated by any stimulus to either side of the animal, when such a response can be regarded as an adversive movement. This sign of cerebral disease is mostly seen with prominently asymmetric lesions, such as lateral ventricle cholinisteric granuloma, forebrain abscess, parasitic thromboembolism or verminous migrations, and with head trauma.

Figure 5.5 Painful processes, perhaps especially abdominal pain, frequently cause unexpected and abnormal behavior in large animals frequently, and such actions need to be distinguished from those caused by morbid neurologic diseases. This racehorse would unexpectedly rear uncontrollably while being walked. There were no other signs of brain abnormalities, and the only lesions detected clinically were focal, suppurative pleuritis and pneumonia from which he recovered with appropriate treatment.

Figure 5.6 The Thoroughbred racehorse shown here (A) is a tongue sucker and demonstrated this stereotypic behavior frequently. The horse appeared to appreciate having its tongue grasped and manipulated, and such a maneuver would set off an episode of the tongue‐sucking behavior shown. The mare (B) also demonstrates this behavior. Her healthy newborn foal accompanied her into the hospital and within days was seen to demonstrate the same repetitive and nonproductive behavior (inset).

Figure 5.7 Horses diagnosed as headshakers usually have little else in the way of physical and neurologic signs. They usually display the syndrome best during some form of movement or exercise such as this Clydesdale gelding (A) and gray Thoroughbred mare (B) while being lunged. In addition to the dorsoventral and sometimes lateral flicking movements of the head on the neck, some will repeatedly snort and attempt to rub their nasal region on the ground (B) or forelimbs while moving to cover their distal face with dirt (inset). The syndrome is aptly explained by the adage “acting as if it has a bee up its nose.” Riding becomes dangerous or impossible with severe cases. After demonstrating the signs, some horses will rub their muzzle and face on objects.

Figure 5.8 Radiographs of the atlantooccipital region of a horse demonstrating headshaking. There is marked modeling of the caudal aspect of the occipital protuberance (arrows). This riding horse would only perform persistent dorsoventral head movements while fully tacked‐up with a bridle for ridden work. Local anesthetic solution 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.