Large Animal Neurology. Joe Mayhew

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Large Animal Neurology - Joe Mayhew


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loud noises and prodding with a blunt instrument (Figure 8.1). Also, lesions involving the thalamus, internal capsule, or sensory parietal lobe of the cerebrum can be associated with decreased sensation on the contralateral side of the face, most prominent on the nasal septum. This exceeds degrees of nonresponsiveness that can be expected from any associated obtunded mental state.

      To witness a large animal suddenly collapse, or to be called urgently to evaluate a patient that has suffered one or more episodes of collapsing, can be confusing for the clinician and certainly distressing for the owner or caregiver. On most occasions, the situation resolves quickly to one of sudden death, recovery with recumbency, a gait abnormality, another neurologic syndrome, recovery with or without evidence of a non‐neurologic problem, or repetitive episodes of collapsing. Poorly informed clients and children must be reminded of their own safety and should be advised to keep clear of a collapsing large animal until the veterinarian arrives. An informed client may be directed to stop any massive bleeding or roll a heavy animal that might be cast. In the event that the animal arises, the client can guide it if it is ambulatory to soft ground, away from potentially harmful objects.

Photo depicts a neonatal Limousin cross calf suffering from bacterial meningitis demonstrated opisthotonus and was in a semicoma being nonresponsive to physiologic stimuli and inappropriately responsive to noxious stimuli.

      The presence of any compound or complicated fractures that may mean a hopeless prognosis (e.g., femur), that may be life‐threatening (e.g., ribs) or that may require splinting (e.g., metacarpus) must be identified, and appropriate measures should be taken.

      A thrashing patient may require sedation or even anticonvulsant therapy if it is deemed to be due to cerebral seizure. If shock or respiratory depression are not problems, and there is no good evidence of seizure activity, then an α‐2 agonist sedative drug, pentobarbitone, or even acepromazine can be instituted. Diazepam IV or midazolam IM or IV in 5–10 mg (foal) to 25–100 mg (horse) doses can be given to control seizures. A horse recumbent for any reason can become terribly violent in its frantic attempts to rise and in response to pain, and it may be impossible to distinguish this behavior from true seizures. With the latter, the horse is in a state of unconsciousness, and its attention cannot be attracted. Also, the face and jaw muscles usually show spasmodic or continuous contractions, the eyeballs move to abnormal positions, opisthotonus tends to occur, and sometimes urine and feces are voided.

      Important facts to be noted include the duration and repetition of the episode of collapse, any exposure to various environmental factors such as recent lightning/thunder storm, proximity to stray voltage sources, excessive heat, poisonous plants, exogenous chemicals, previous or prodromal illness, different feeds, and whether other herd mates have been affected.

      A brief physical examination can then be undertaken. The general aim at this stage is to determine which basic category of acute collapse best fits the particular case.1 These general categories include syncope and seizure (Chapter 6), sleep disorders (Chapter 7), coma, motor paralysis (Chapters 23 and 24), and generalized and metabolic disorders.1 Some of the characteristics of each of these are given here to assist in making an accurate diagnosis.

      A small number of animals that experience one or more episodes of acute collapse are suspected of having syncope or a fainting condition. This suspicion is usually because of the presence of a cardiac arrhythmia or a cardiac murmur. Definitive cardiac disease is confirmed in a proportion of these cases.2–4 Such documented disorders include atrial fibrillation, ruptured chordae tendineae, myocardial infarction, myocardial fibrosis, dissecting aortic aneurysm, aortic endocarditis, and pericarditis.

      With syncopal attacks, usually there is little or no premonitory warning of collapse; because of cerebral hypoxia, a temporary, quiet, comatose state ensues. Some struggling may occur during recovery, before the patient regains its footing, unless of course the patient has suffered severe head trauma on way to recumbency. Other overt signs of cardiac failure may become evident. Polycythemia5 and upper airway obstruction—including untoward effect of cribbing throat collar—rarely can also result in syncopal attacks.6

      A seizure , convulsion, or fit is the physical expression of bizarre but synchronous electrical neuronal discharges in all or part of the cerebrum and is introduced in Chapter 6. Often a preictal aura of a few seconds to minutes occurs, then the ictus or seizure lasts seconds to minutes with an accompanying variable period of coma or semicoma. This is followed by a postictal phase lasting several minutes to days. The initial aura may cause the animal to be distracted from its environment, to have a blank facial expression, and to occasionally become restless. If the seizure becomes generalized, the patient becomes recumbent and may lay rigid for a while before paddling or thrashing for several seconds to minutes. With status epilepticus, this phase is repeated continually and is fatal unless chemical, anticonvulsant restraint is used. A postictal animal usually regains its footing relatively easily then may pace, act blind, constantly drink or eat, and may not recognize herd mates, its handler, or its environment. Depending on the underlying cause, other neurologic signs may be evident. Anticonvulsant therapy may be required if more than one generalized seizure has occurred; although if familial juvenile epilepsy of Arabian foals is suspected, therapy can be started immediately.

      Coma is a state of recumbency with unconsciousness and total unresponsiveness. It is primarily associated with profound changes in the forebrain or midbrain. Head trauma, birth asphyxia, bacterial meningoencephalitis, thiamine‐responsive polioencephalomalacia, parasitic infarction/migration, spontaneous hemorrhage, moldy corn intoxication, liver disease, intracarotid injections, and many poisons are some


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