A C6-T2 involvement will cause proprioceptive ataxia and upper motor neuron paraparesis along with lower motor neuron paresis
in the thoracic limbs because of gray matter involvement of the cervicothoracic intumescence. This results in a characteristic
"two-engine gait" with short, stiff steps in the forelimbs and slower, large, ataxic and spastic steps in the hindlimbs. A
C6-T2 lesion can also cause an ipsilateral Horner syndrome because of involvement of the sympathetic fibers coming from T1-T3,
the loss of the ipsilateral cutaneous trunci reflex, or both, since the innervation of the cutaneous trunci muscle (lateral
thoracic nerve) comes from the spinal segments C8-T1. If only the white matter is affected, signs similar to a C1-C5 involvement
will be seen.
Signs of T3-L3 involvement are usually well recognized, consisting of proprioceptive ataxia and upper motor neuron paraparesis
or paraplegia with normal function in the thoracic limbs.
With L4-S3 involvement, lower motor neuron paraparesis or paraplegia and proprioceptive ataxia occur. The ataxia might be
difficult to appreciate at this level.
As a rule, the prognosis for spinal cord disease depends mainly on the lesion's location (gray vs. white matter), severity,
etiology (treatable or not), and chronicity.7 Although the prognosis depends partly on the lesion's severity, the same type of lesion in two different spinal cord segments
does not necessarily carry the same prognosis. For example, since L5 is the most important segment for the femoral nerve,
a lesion affecting the gray matter at L5 will cause a femoral deficit. This would result in a loss of patellar reflex and,
most important, an inability to support weight in that pelvic limb.
The neuromuscular system
The neuromuscular system transmits information from the nuclei of the lower motor neuron to the effector muscle, resulting
in a muscle contraction. The main clinical sign of neuromuscular system involvement is weakness (lower motor neuron paresis).
As a general rule, lesions of the neuromuscular system will not cause ataxia, although a marked gait abnormality might be
noticed. For example, in a dog with a bilateral sciatic paresis, the gait may be characterized by reduced hock flexion during
protraction that is sometimes associated with excessive hip flexion (from the femoral nerve as a compensation). Because of
the reduced hock flexion and possibly a loss of proprioception (the afferent pathway being mainly the sciatic nerve for the
pelvic limb), the dog may also drag its toes (i.e. exhibit paresis). Despite the fact that the pet drags its toes, incoordination (i.e. ataxia) isn't present, and the gait is regularly abnormal because the same movement always occurs and you can predict where
the animal will place its feet on the floor. Neuromuscular system involvement can be focal (e.g. unilateral facial paralysis) or diffuse (e.g. generalized weakness associated with botulism). Keep in mind that the cauda equina is part of the peripheral nervous system
since it consists of spinal nerves and not spinal cord segments.
Suspect involvement of the neuromuscular system in patients with weakness and paresis without ataxia, in patients with cranial
nerve deficits without a change in mental status, and in patients with generalized weakness.
NEUROANATOMICAL DIAGNOSIS AND DIFFERENTIALS
After obtaining a patient's history and performing physical and neurologic examinations, create a list of neurologic abnormalities.
With this list in mind, determine which part of the nervous system is affected (e.g. spinal cord segment T3-L3, diffuse lower motor neuron). This is the neuroanatomical diagnosis. If possible, all the clinical
signs should be explained with a single anatomical location. For example, a dog with seizures and a conscious proprioception
deficit in the left thoracic and pelvic limbs most likely has a lesion in the right thalamocortical region rather than both
a cortical and a spinal cord lesion. When the clinical signs cannot be explained with a single neuroanatomical location, multifocal
involvement is likely. Once you've determined the neuroanatomical diagnosis, you can compile an accurate list of differential
diagnoses, taking into consideration the patient's signalment and the history (onset, progression) (Table 1).
Table 1. Examples of Common Differential Diagnoses by Neuroanatomical Localization