The very thought of neuroanatomy can put a person into a cold sweat.  Many have less than fond memories of neuroanatomy class. We all had to learn the names of all the various nuclei in the brain and the origin and projection of tracts in the CNS. While it is important to have this understanding of neuroanatomy from a global veterinary perspective, being a good clinician does not require an in-depth knowledge of neuroanatomy. Do you really need to be able to recall from memory the foramen through which the oculomotor nerve exits or the origin and projection of the rubrospinal tract to be an excellent clinician? If you’re a neurologist or a neurology resident studying for boards, absolutely, but to be honest, it’s not as important in everyday general practice.

Clinical neurology requires an understanding of functional neuroanatomy. In other words, one must know the typical clinical signs that are observed when specific regions of the nervous system are affected. The minutiae of neuroanatomy are not required knowledge for the majority of general practitioners to be an excellent clinician. That being said, there are a few neuroanatomical pathways that are important to remember because they are frequently encountered in clinical practice. Examples include the visual pathway, sympathetic pathway leading to Horner Syndrome, and cutaneus trunci reflex. See the Neuro Exam pages for additional information.


Before discussing the clinical signs typically observed in the various regions of the nervous system, let’s review the concept of lower motor neurons (LMN) and upper motor neurons (UMN).

LMNs are the neurons that innervate peripheral structures, such as the skeletal muscles of the limbs. LMNs are excitatory to muscle, so dysfunction of LMNs results in decreased excitation of the target muscles and subsequent weakness. This is manifested clinically as reduced to absent muscle tone, spinal reflexes, and withdrawal reflexes depending on the severity of LMN dysfunction. Reduction in muscle stimulation or use leads to muscle atrophy. LMN dysfunction causes denervation atrophy where muscle atrophy occurs quickly and too a greater degree than with disuse. Remember that the motor fibers of cranial nerves (e.g., facial nerve) are also lower motor neurons.

UMNs are neurons originating in the brain that synapse on LMNs. These upper motor neurons are subdivided into the pyramidal and extrapyramidal systems. The pyramidal system is composed primarily of UMNs located in the motor cortex of the cerebrum and the tracts that are formed by their axons (e.g., corticospinal tract). The pyramidal system is very well developed and highly utilized in primates for conscious voluntary movement. The extrapyramidal system consists of UMNs located primarily in brainstem nuclei and their respective axonal tracts (e.g., rubrospinal tract). The extrapyramidal system is the primary motor system of non-primate animals, thus the gait in dogs and cats is generated primarily in the brainstem. This is why there is little weakness in dogs and cats with cerebral lesions, but sometimes profound weakness with brainstem disease.

Both excitatory and inhibitory UMNs exist, but dysfunction of inhibitory UMNs resulting in reduced inhibition of excitatory LMNs, is most apparent clinically. This is manifested as increased muscle tone, normal to exaggerated spinal and withdrawal reflexes, and disuse atrophy (late onset, slow, milder degree of muscle atrophy compared to denervation atrophy).


Both images at left present the same information from different perspectives. The bottom figure is adapted from Kirby R. Emergency management of spinal cord lesions. Clin Brief 2010; December:27-32.

*Significant lesions in the C6-T2 region typically cause LMN signs. However, the thoracic limbs may be normal, especially with compressive spinal cord lesions that affect the peripherally-located pelvic limb tracts while sparing the more centrally located LMNs in the gray matter. Patients with a severe T3-L4 spinal cord lesion may have increased tone in the thoracic limbs (Schiff-Sherrington).

After performing a complete neurologic exam, as well as a general physical exam and orthopedic exam (especially if any lameness or weakness), there are two questions that you should ask yourself:

  1. Does this patient have neurologic disease?
  2. If yes, where is the likely location of disease (neurolocalization)?

This may seem very simplistic, but they are important questions to ask yourself with every patient. Never assume that a patient that is weak or unable to walk is neurologic. Many non-neurologic conditions can mimic neurologic disease. For example, a dog that has bilateral cranial cruciate ligament tears or a cat with aortic thromboembolism may be unable to walk. The next step is to consider each of the individual neurologic abnormalities noted on exam and identify where the lesion could be located for each abnormality. Finally, determine whether one lesion location could account for all of the neurologic abnormalities.

Case example: You are presented with a cat that had a sudden onset of circling to the right. On neurologic exam, you discover an absent menace response in the left eye and postural reaction deficits in the left thoracic and pelvic limbs.  Now formulate a list of abnormalities and possible lesion locations.


Circling to right

Possible lesion location(s)

  • Right forebrain
  • Right (peripheral or central) vestibular

Absent menace OS

  • Left retina
  • Left optic nerve
  • Optic chiasm
  • Right forebrain (thalamus & occipital lobes for visual processing, somatosensory cortex for interpreting “threatening” gesture)
  • Left facial nerve
  • Left cerebellum

Left-sided postural reaction deficits

  • Left C6-T2
  • Left C1-C5
  • Left pons/medulla
  • Left (caudal) or right (cranial) midbrain
  • Right forebrain

Look back at your list to see if one lesion location is present in all of the abnormalities. For this patient, the only location listed for all 3 abnormalities is the right forebrain. Next, ask yourself if this makes sense to you. The patient is circling, which also can be seen with vestibular disease. Do you see any other clinical signs that would suggest vestibular dysfunction (e.g., head tilt, nystagmus, ataxia)? Always try to localize the lesion to one location, but never forget that multifocal disease is possible.

Neurologic syndromes

The nervous system can be divided into several anatomical regions, wherein dysfunction leads to a typical group of clinical signs referred to as neurologic syndromes. These functional regions include:

A great deal of day-to-day clinical neurology involves pattern recognition. As you become more experienced with the neurologic exam and neurolocalization, you will start to recognize these particular syndromes and be able to localize the lesion without having to physically formulate a list as described above.

The information presented in the localization pages on this website is adapted from the excellent veterinary neurology textbook, Clinical Syndromes in Veterinary Neurology by Kyle G. Braund, 2nd ed, which is no longer in print.