The cerebellum is responsible for fine coordination and movement adjustment and for vestibular functions. It also plays a
role in the ipsilateral menace reaction and pupillary size. Cerebellar diseases can lead to a lack of menace reaction with
normal vision. Anisocoria may also be seen. Signs of cerebellar involvement may include vestibular dysfunction (head tilt,
loss of balance), intention tremors, dysmetria (mostly hypermetria), and opisthotonos if the damage is severe. Opisthotonos
is an abnormal posture characterized by marked hyperextension of the neck. The hypermetria may be seen when you evaluate the
gait (e.g. excessive flexion of the limbs, bouncing gait) or the postural reaction (e.g. excessive movement of the tested limb during placing or hopping). Intention tremors are present on initiation of movement.
They are usually best identified when the patient moves its head to try to eat or smell something. Strength is not affected
by cerebellar disease since there are no upper or lower motor neuron nuclei in the cerebellum. When the caudal cerebellar
peduncles (at the cerebellomedullary junction) or the flocculonodular lobe of the cerebellum is affected, signs of a paradoxical
vestibular disease can be seen.4,6 With paradoxical vestibular disease, the head is tilted away from the lesion and other localizing signs indicative of cerebellar
(e.g. hypermetria) or brainstem (e.g. conscious proprioception deficit) involvement are present. It is important to recognize a paradoxical vestibular disease
as it allows for accurate lesion localization. A neoplastic process, a granuloma, and a vascular problem are the primary rule-outs.
The spinal cord is divided into four segments for function and lesion localization: C1-C5 (or C1-C8 white matter), C6-T2,
T3-L3, and L4-S3. Remember that these spinal cord segments are not necessarily in the corresponding vertebrae since the spinal
cord ends around the sixth or seventh lumbar vertebra in most dogs (L7-S1 in cats and small dogs). The spinal cord carries
the descending tracts (upper motor neuron) from the brainstem nuclei and other higher centers to the lower motor neuron nuclei
located in the ventral horn of the gray matter. It also carries the ascending sensory tracts (e.g. proprioception, nociception) from the body and limbs toward the superior center. In spinal cord disease, the lesion's location
defines the type of clinical signs, whereas the lesion's extent defines the severity.
Clinical signs seen with spinal cord disease vary depending on the segment affected. They usually progress in a specific order,
based on the size of the nerve fiber and its location in the spinal cord. The larger myelinated, peripherally located proprioceptive
and motor tracts will usually be affected first, causing proprioceptive ataxia and ambulatory paresis followed by a nonambulatory
paresis. With a more severe involvement, paralysis will occur along with incontinence, then loss of superficial pain, and
finally loss of deep pain perception. The latter is an indication of a severe cord lesion associated with a guarded to poor
prognosis. As a reminder, when evaluating for deep pain perception, it is extremely important to look for a reaction from
the patient (e.g. it cries or turns its head) and not to conclude that deep pain perception is present because of limb flexion (spinal reflex
only). Lesions involving the spinal cord only should not cause a change in mental status or a cranial nerve deficit.
Involvement of the C1-C5 segment causes proprioceptive ataxia and upper motor neuron tetraparesis. Tetraplegia is unlikely
with this location since it would also cause paralysis of the respiratory muscles (the diaphragm by the phrenic nerve and