Brainstem Structure and Function

The brainstem can be subdivided anatomically into the diencephalon (thalamus, hypothalamus), mesencephalon (midbrain), ventral metencephalon (pons), and myelencephalon (medulla). Functionally, the diencephalon is more similar to the telencephalon (cerebral hemispheres) than to the rest of the brainstem, and it should be considered part of the forebrain (prosencephalon). Therefore in this chapter brainstem is used generally to refer to the midbrain, pons, and medulla. The brainstem has several different functions, including generation and control of locomotion (via upper motor neuron and proprioceptive tracts), motor and sensory control of the head (via cranial nerves), and maintenance of consciousness (via the ascending reticular activating system). Additionally, the brainstem is responsible for basic functions such as control of cardiac function, respiratory function, sleep, hunger, and thirst. Cranial nerves (CNs) are associated with each part of the brainstem: the optic nerve (CN 2) with the thalamus; the oculomotor (CN 3) and trochlear (CN 4) nerves with the midbrain; the trigeminal nerve (CN 5) with the pons; and the abducent (CN 6), facial (CN 7), vestibulocochlear (CN 8), glossopharyngeal (CN 9), vagus (CN 10), spinal accessory (CN 11), and hypoglossal (CN 12) nerves with the medulla.

Clinical Signs of Brainstem Disease

Recognition of brainstem disease is imperative for formulating an appropriate differential diagnoses list as well as for deriving an accurate prognosis. Diseases that affect brainstem function frequently carry a worse prognosis than diseases that affect cranial nerves peripherally or that affect the spinal cord.

The three main indicators of brainstem disease are changes in the horse’s mental status, cranial nerve deficits, and ataxia. In the author’s experience, it is uncommon to see changes in basic functions, such as cardiac or respiratory control, potentially because these derangements most often accompany severe disease that frequently leads to death of the animal before a veterinarian is able to undertake a neurologic assessment. Signs of brainstem disease should become apparent upon complete neurologic examination, which should be performed on any horse showing neurologic signs.

The horse’s attitude and behavior should be carefully evaluated because damage to the ascending reticular activating system (ARAS) may cause changes in mental status, ranging from dullness to coma. Most horses with brainstem disease are dull or obtunded. Careful consideration of the expected behavior for the patient is necessary; an unusually quiet demeanor may be the only indication that an ataxic Thoroughbred colt has brainstem rather than cervical spinal cord disease.

Complete cranial nerve examination should be performed. There are many different ways to perform a cranial nerve examination, and the following description is based on a regional approach. Begin with the eyes: perform a menace response (CNs 2 and 7), evaluate pupil size and check pupillary light reflexes (CNs 2 and 3), assess eye position (strabismus may indicate problems with extraocular muscles innervated by CNs 3, 4, and 6 or a vestibular problem—CN 8), look for normal physiologic nystagmus (CN 8 as well as extraocular muscles and CNs 3 and 6), and ensure that there is no abnormal nystagmus (CN 8 or central vestibular components). Assess the palpebral fissure for size and symmetry (CNs 3, 7, and sympathetic nerves) and evaluate the palpebral reflex (CNs 5 and 7). Look at the prominence of the third eyelid (sympathetic nerves). Evaluate the horse for normal facial expression and ability to move the ears, blink, and wiggle the muzzle or lips (CN 7). Assess the size of the muscles of mastication and evaluate facial sensation by touching all regions of the head (CN 5). Open the horse’s mouth to assess jaw tone (CN 5), and remove the tongue to assess the horse’s tongue strength and tongue muscle symmetry (CN 12). Observe the horse eating and drinking to assess ability to swallow (CNs 9 and 10). Endoscopy allows direct observation of the pharynx, larynx, and swallowing ability and may be useful if dysfunction is suspected. CN 1 (olfactory) is rarely specifically tested, but most horses with interest in food have normal olfaction. CN 11, which innervates cervical muscles, is also not usually specifically tested. Facial paralysis, vestibular disease, and dysphagia are particularly common signs of brainstem disease.

Two types of ataxia can be observed with brainstem disease: vestibular and general proprioceptive. A horse with vestibular disease usually has a head tilt and loss of balance with a tendency to lean or fall to one side. Recumbent horses often have a strong preference to lie on the affected side. In the acute stage of vestibular disease (first 12 to 24 hours), horses often develop abnormal nystagmus, which may then disappear. A horse with general proprioceptive ataxia shows proprioceptive deficits (toe scuffing or dragging, delayed protraction, knuckling, crossing over, stepping on itself, pivoting or circumduction when circling, and uneven or irregular stride length). General proprioceptive ataxia is almost always accompanied by upper motor neuron (UMN) paresis, which causes an elongated stride with similar characteristics to general proprioceptive ataxia (e.g., toe scuffing or dragging or delayed protraction). In general, horses with brainstem disease have spastic paresis and ataxia in all four limbs (bilateral disease) or in the two limbs ipsilateral to the lesion (unilateral disease). Severe disease may cause spastic tetraplegia. Exceptions occur with disease limited to the more rostral mesencephalon, which may cause contralateral gait deficits, or with diseases that spare the UMN and general proprioceptive tracts.

Practitioners must differentiate peripheral vestibular disease, which generally carries a better prognosis, from central vestibular disease. Ambulatory horses with peripheral vestibular disease tend to have a wide-based stance and are hesitant to walk but show no proprioceptive deficits. These horses are mentally alert despite even severe vestibular ataxia. Facial nerve deficits may be evident on the ipsilateral side, but no other cranial nerve deficits are present. Ambulatory horses with central vestibular disease often show marked proprioceptive deficits, an obtunded mental state (because of interference with the ARAS), and multiple cranial nerve deficits (e.g., facial nerve deficits and dysphagia). Involvement of the ARAS or UMN-general proprioception tracts confirms brainstem disease.