Forebrain Diseases

Chapter 88

Forebrain Diseases

Caroline Hahn

The forebrain comprises the two cerebral hemispheres (cerebrum/telencephalon) and the thalamus (diencephalon). Most of the gray matter is located superficially, forming the cerebral cortex, but gray matter is also located deep within the hemispheres in regions such as the hippocampus, basal nuclei, and septal nuclei. The hemispheres are divided into lobes named mainly for the overlying bone, and these lobes are loosely associated with different functions. The cerebral cortex contributes to several critical functions, including consciousness, complex behavior, fine motor activities, processing of sensory information, and vision. Portions of the temporal and frontal lobes are included in the limbic system, which is responsible for many emotions and innate survival behaviors, such as the protective maternal response. The principal structure of the diencephalon is the thalamus, which acts as a gateway to the cerebrum, and all incoming information (except olfaction) passes through the thalamus. In addition, neuronal pathways of the ascending reticular activating system, which helps maintain the level of consciousness, project from the midbrain through the thalamus and from there to the cerebral cortex.

Clinical Signs of Forebrain Disease

Focal and diffuse forebrain lesions can result in seizures, abnormal behavior and mentation, compulsive circling, abnormal head and neck postures, central blindness, contralateral hypalgesia, and occasionally, slight facial, tongue, and pharyngeal paresis. Horses with even profound forebrain lesions have a normal gait when walking in a straight line.

The nature and severity of clinical signs seen with forebrain disease is influenced by the location and extent of the disorder, and the resulting clinical signs may be subtle. In most instances, signs manifest as a decrease in alertness that ranges in severity from mild dullness and depression to obtundation, stupor, and coma. Lesions that involve the ascending reticular activating system tend to cause particularly severe depression of consciousness, such as stupor or coma. Rather than decreased alertness, certain forebrain lesions result in increased responsiveness to external stimuli, such as anxiety, mania, or aggression. Lesions of the limbic system are especially prone to cause these behavioral changes. Clinicians faced with a manic horse may consider administering detomidine (80 µg/kg), morphine (0.3 mg/kg), and acepromazine (0.1 mg/kg), mixed together in the same syringe and injected intramuscularly. Butorphanol (0.05 mg/kg) should be used if morphine is unavailable.

Evaluation of forebrain function is difficult in any non­human animal. Subtle behavior changes are best assessed by the owner or trainer who might know if the quiet 2-year-old colt, for example, is very well behaved or is in fact showing depressed mentation. A complete neurologic examination should be performed (see the sixth edition of Current Therapy in Equine Medicine, Chapter 130), and if a forebrain lesion is suspected, particular care should be taken in examination of the head. The examiner should be satisfied that the menace response is symmetrical because, if pupillary light reflexes are normal, a unilateral decrease in menace response could be caused by involvement of the occipital lobe and a degree of central blindness. Does the horse object equally to touching of the nasal septum on both sides? Lack of response is a sensitive test for depressed parietal lobe function.

Because horses have no effective corticospinal tract, their gait remains normal with motor cortex lesions. In rare cases, horses with a motor cortex lesion have contralateral paresis of the facial musculature and may fail to retract the tongue when it is pulled from the mouth: this is a result of disruption of corticonuclear tracts, which connect the motor cortex directly to brainstem somatic lower motor neurons. Hypertonicity and hyperreflexia of the facial muscles manifesting as facial grimacing can occasionally be seen when horses have focal thalamic and cerebral lesions. This is exemplified by horses with basal nuclei necrosis secondary to ingestion of yellow star thistle (western United States) or Russian knapweed (Australia).

Seizures are another sign of cerebral disease (see Chapter 87) and are commonly seen in conjunction with other neurologic abnormalities. Seizures are the physical mani­festations of paroxysmal changes in cerebral cortex elec­trical activity that start abruptly, end suddenly, and have a tendency to recur. In horses, seizures are recognized by the involuntary motor activities they cause and are often associated with a loss of consciousness. However, horses have a high seizure threshold, compared with humans and small animals, and idiopathic epilepsy (i.e., acute-onset, generalized seizures that persist into adulthood, which are most common in purebred animals) is not recognized in equids. When they do occur, seizures are presumed to be acquired or reactive, and may be partial, generalized, or partial with secondary generalization. Generalized seizures are associated with a loss of consciousness, collapse, and variable degrees of tonic-clonic motor activity. Partial seizures, on the other hand, involve a small number of neurons, resulting in localized involuntary movements with or without obvious alterations in consciousness. Common signs of abnormal motor activity associated with partial seizures include muscle twitching in the face or one limb, grimacing, and head turning. Some partial seizures will generalize as the activity spreads from a focal site throughout the cerebral cortex.

The time period subsequent to the seizure, the postictal phase, is also characterized by behavioral changes such as lethargy, restlessness, and anxiety. Some horses may have temporary blindness. Generally, the postictal phase lasts for minutes to hours, but occasionally it lasts for several days. In some cases, the seizure is never observed and is only suspected on the basis of postictal behavioral changes or the presence of repeated physical injuries.

Treating a horse with anticonvulsants is not a trivial decision because a horse is not safe to ride until it is clear that the anticonvulsants are preventing a devastating seizure. Details of anticonvulsant therapy and monitoring are summarized (Table 88-1). In an emergency, diazepam (50 mg, IV) should be administered, and can be repeated. If diazepam is unavailable, standard doses of α2-agonist drugs can be used.

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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Forebrain Diseases

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