with night blindness. Particularly at the onset of a fast gait, many normal horses will hold the head and neck deviated from the median plane: perhaps more related to a reaction to a mouth bit than to speed. Painful conditions such as dental disease, forelimb and hindlimb14 lameness, and caudal cervical arthritis, and asymmetric visual acuity, can also result in abnormal head, neck and trunk positioning during exercise or at rest.
The cerebellum modulates movement of the head and limbs so that cerebellar lesions usually result in alterations in the force, speed, and range of movement of body parts including the head and neck.15 With cerebellar disease, fine control of head positioning is often lost, resulting in awkward, jerky movements. Even at rest, the lack of control is often seen as bobbing movements of the head, which can be exaggerated by increased voluntary effort. The resulting fine jerky movements of the head are called intention tremor. Such animals will overshoot when positioning their head, when moving to eat, for example. Newborn foals normally hold their head flexed slightly on the neck and move it in a jerky manner, especially in response to visual or tactile stimuli, rather resembling cerebellar dysfunction.
Animals with neck pain may hold their neck in an abnormal fixed position and be reluctant to move the head and neck. Also, diseases causing neck weakness may result in an animal carrying its head lower to the ground. Examples of this include diffuse neuromuscular weakness seen with botulism and with equine motor neuron disease. This is also but rarely seen with extensive cervical spinal cord, final motor neuron lesions involving ventral gray matter, and for example with extensive cervical myeloencephalitis. Finally, an extended head and neck posture, referred to as a star‐gazing attitude, may indicate a severe forebrain disorder such as polioencephalomalacia of ruminants and basilar empyema, and is also present with diseases causing increased extensor muscle tone, such as equine tetanus and bovine myotonia.
Cranial nerves
In practice, it is convenient to evaluate separate parts of the head and face as described in the neurologic examination outline and forms (Tables 2.2 and 2.3; Figure 2.1). Thus, the evaluation moves from the eyes, face, jaws, and mouth to the pharynx and larynx. When the examination is completed, deficiencies ultimately need to be related to specific cranial nerves. Thus, the following section covers the interpretation of neurologic examination findings relative to individual cranial nerves.
Olfactory nerve—CN I
Normal function is usually equated with the patient’s ability to smell the hand of the examiner or its feed. However, because such stimuli almost certainly irritate the nasal mucosa, this test evaluates the sensory branch of the trigeminal nerve, probably as much as CN I.
Optic nerve—CN II
An owner may report that a patient appears to be acting blind. However, a moribund, somnolent or inattentive patient, or one with marked weakness or with loss of balance due to vestibular disease, may stumble over objects without being blind.
The visual pathway is tested by the menace response, whereby a mildly‐threatening gesture of the hand toward the eye elicits immediate closure of the eyelids (Figure 2.2). In large animals, 80–90% crossing of optic nerve fibers occurs at the chiasm (Figure 2.6).16 However, for initial, practical purposes, vision in one eye can be regarded as being perceived in the visual cortex of the opposite or contralateral cerebral hemisphere. The incoming, afferent pathway for the menace response is the ipsilateral eye and optic nerve, the optic chiasm, the contralateral optic tract, lateral geniculate nucleus in the thalamus, optic radiation, and visual cortex that is mostly in the occipital lobe (Figures 2.6 and 2.9). The outgoing, efferent pathway of the menace response is from this contralateral visual cortex to the ipsilateral facial nucleus effecting closure of the eyelids. With an intact efferent pathway resulting in blinking, it is assumed that the visual input reached the visual cortex. Some stoic, moribund, somnolent, and even excited animals may not respond to a hand menace with closure of the eyelids, or they may keep the eyelids closed. A true visual deficiency may be detected while the animal moves about its environment, when objects are placed in front of it—a visual maze test—or when nonaromatic objects are dropped noiselessly in its visual field. Partial, unilateral blindness can be difficult to detect and it may take repeated efforts, such as blindfolding each eye in turn, to determine this. Total unilateral blindness with absence of a menace response in only one eye is usually quite easy to detect. However, repeated testing is usually necessary to confirm an asymmetric but bilaterally present menace response, and the above assessments are very useful to detect such lesions.
Figure 2.6 Visual pathway.
As indicated, the true menace response is a blink that immediately follows a visually threatening gesture, without necessarily being accompanied by withdrawal of the head (Figure 2.2). The latter visual avoidance response may well not require an intact visual (occipital) cortex but most probably involves central pathways just within the brainstem and certainly without input from the ipsilateral cerebellar cortex as is the case with the menace response. If there is an absent menace response, then we use a more powerful threat, after tapping the forehead several more times, to try to detect eyeball retraction or head withdrawal that will at least confirm a partial afferent visual pathway input to the brainstem but not necessarily to the visual cortex. However, this can be somewhat problematic except in the most obliging patients. With little or no menace response but some visual avoidance response obviously present, then facial musculature and cerebellar function requires further evaluation. Should these be without problems, then a visual maze test may be required to better scrutinize visual acuity. Interpretation of artificial maze tests can be rather uncertain, and a decision on visual acuity often concludes with general observations of the patient’s response in its environment to nonauditory, nonaromatic, visual clues, such as a brightly lit open doorway or gate.
When a visual deficit is suspected, a visual field deficit may be determined in large animals having unilateral or prominently asymmetric cerebral or thalamic lesions. In describing these subtle field deficits, it is necessary to be clear about two things. First, the eye not being tested should be covered to avoid nonspecific crossover from visual stimuli. Second, the left visual field is detected predominantly via the nasal (medial) retina of the left eye and partly (~10–20%) via the temporal (lateral) retina of the right eye; the latter region of the retina containing most of the neurons whose axons do not cross at the optic chiasm (Figure 2.6). Likewise, the right visual field is perceived predominantly via the nasal retina of the right eye and partly via the temporal retina of the left eye. Thus, with a prominent lesion in the right dorsal thalamus, right occipital radiation, or right occipital cortex, a patient will appear to be blind in the left eye with normal pupillary responses bilaterally. The left visual field deficit may be detected as a poor or absent menace response in the nasal retina of the left eye when using the threatening stimulus directed from the lateral aspect of the left eye and by a poor response to a visual threat directed to the temporal retina of the right eye with the stimulus directed from the medial aspect of the right eye. The nontested eye should always be covered during these visual field tests.
Lesions of the eye and optic nerve result in ipsilateral blindness. Lesions of the optic tracts and lateral geniculate nucleus cause contralateral