CHAPTER 130 Making a Neuroanatomic Diagnosis
Establishment of a neurologic diagnosis requires thorough and orderly completion of several procedures, beginning with obtaining a history and performing physical and neurologic examinations. The signalment, environment, and function of the horse, as well as the husbandry practices of the owner, can provide tremendous insight into predisposing disease factors.
The purpose of the neurologic examination is to identify and attempt to quantify neurologic dysfunction. Once neurologic abnormalities have been identified, the next step is to make a neuroanatomic diagnosis or determine the problem’s location within the nervous system. Successful neuroanatomic localization is crucial in the management of horses with neurologic disease, because the potential list of differential and etiologic diagnoses is best generated after consideration of diseases with a propensity to affect the given area of the nervous system. Neuroanatomic localization and differential diagnoses are used to guide the examiner in the selection and interpretation of the most appropriate ancillary diagnostic tests to be performed with the goal of establishing an etiologic diagnosis and therapeutic plan.
The nervous system is divided into functionally and anatomically related geographic regions. Abnormalities within these regions can often be determined by detection of characteristic clinical signs or deficits that are outwardly visible or evoked during the neurologic examination. After the examiner has identified the neurologic deficits, the next priority is to determine which geographic region of the neuraxis is affected: the intracranial region (e.g., the brain and associated cranial nerves), spinal cord, or neuromuscular system. Abnormalities detected during neurologic examination should be localized to the most discrete location possible within that region. When several clinical signs or neurologic abnormalities are detected that cannot be explained by a single focal lesion, it is deduced that the disease process is multifocal or diffuse or that the horse has multiple, possibly unrelated, concurrent neurologic diseases.
The three major regions of the nervous system are often further subdivided into more discrete neuroanatomic areas (Figure 130-1). Disease in each of these areas commonly manifests with a set of cardinal clinical signs that distinguish lesions in these regions and are reflective of dysfunction of the neurologic structures residing in each area. Individual animals may have one or more clinical signs referable to the affected region. The remainder of this chapter reviews the clinical features of disease affecting each of the regions of the neuraxis in horses.
Figure 130-1 Schematic representation of the major regions of the equine neuraxis. 1, Intracranial region; 2, cranial cervical region of the spinal cord (C1-C5); 3, cervical intumescence (C6-T2); 4, thoracolumbar region of the spinal cord (T3-L3); 5, lumbar intumescence (L4-S2); 6, sacrococcygeal region (S3-S5 and Cy1-Cy5);7, neuromuscular system, which includes the cell bodies of motor and sensory neurons, peripheral nerves, the neuromuscular junction, and skeletal muscle.
Localization of lesions to the intracranial region relies heavily on recognition of abnormalities in mentation, behavior, head or body position, and cranial nerve deficits. For clinical purposes, the intracranial region is subdivided into five areas: the telencephalon, which includes the cerebral cortex and subcortical (basal) nuclei; diencephalon (thalamus and hypothalamus); mesencephalon (midbrain); caudal portion of the brainstem (ventral aspect of the metencephalon [pons] and myelencephalon [medulla oblongata]); and dorsal aspect of the metencephalon (cerebellum).
Diseases of the telencephalon often result in unusual behaviors such as aggressiveness, head pressing, and aimless wandering, signs that are readily noticed and frequently form the primary complaint of horse owners. Telencephalic lesions may also cause various degrees of altered mentation ranging from delirium to coma. Other clinical signs of telencephalic disease include seizures, circling, head turns, and blindness. Horses with telencephalic lesions that circle do so toward the side of the lesion, and any associated head turn is also toward the side of the lesion. A head turn is characterized by lateral deviation of the head and neck from the sagittal plane without concurrent rotation about the poll. Blindness associated with a unilateral lesion of the occipital cerebral cortex, which contains the visual cortex, will cause a menace deficit contralateral to the lesion and will be associated with normal pupillary light reflexes. Although proprioceptive and postural reaction deficits can be detected in the limbs of horses with telencephalic lesions, they are often subtle and more pronounced in the limbs contralateral to the lesion and typically do not cause significant gait abnormalities. Deficits in olfaction (cranial nerve I or olfactory rhinencephalon) can also be present, although clinical detection of such an abnormality can be difficult in the absence of other signs. Relatively little cerebrocortical integrative function is needed to complete activities required for daily existence. Thus, telencephalic lesions can be clinically occult.
With a few exceptions, the clinical signs associated with diseases of the diencephalon appear identical to those seen with telencephalic lesions. Signs of endocrine or autonomic dysfunction, such as hirsutism, polyuria-polydipsia, appetite abnormalities including appetite loss and hyperphagia, bradycardia, or thermoregulatory abnormalities can be suggestive of a lesion in the diencephalon. Blindness caused by a lesion in the optic nerve (cranial nerve II) results in an ipsilateral menace response deficit, usually with some degree of mydriasis of the affected eye and an absent pupillary light reflex in either eye when the blind eye is stimulated. Blindness resulting from lesions affecting the other components of the afferent visual pathways intimately associated with the diencephalon, including the optic tract, lateral geniculate nucleus, or optic radiations, result in contralateral visual deficit and normal pupillary light reflexes.