Spinal cord diseases are frequent in the dog. To review the basic principles of lesion localization as it relates to the spinal cord, intervertebral disc disease has been used as model. In IVDD, there is spinal cord compression without instability. The spinal cord is composed of an outer layer of white matter and a core of gray matter. The white matter is made of axons while the gray matter is composed of cell bodies. Clinically, lesions that are limited to the gray matter behave similarly to lesions of the peripheral nervous system. It is the involvement of the white matter that leads to clinical signs of spinal cord disease.
Anatomical considerations (spinal cord white matter)
Ascending sensory fibers:
A. Reflex proprioceptive pathways:
Hind limbs: Dorsal and ventral spinocerebellar
Fore limbs: Rostral spinocerebellar
B. Conscious proprioceptive pathways:
Hind limbs: Fasciculus gracilis
Fore limbs: Fasciculus cuneatus
Nociception (pain perception) fibers
Descending motor fibers (Upper Motor Neurons):
Clinical signs associated with involvement of the spinal cord ascending sensory pathways:
a. Proprioceptive ataxia
b. Loss of pain perception
a. In spinal cord diseases, the proprioceptive fibers are the first to be affected by reason of their superficial location and their size, larger fibers being more vulnerable than the smaller fibers. Damage to these fibers results in proprioceptive ataxia. Proprioceptive ataxia is the salient feature of spinal cord disease. It is the first sign to appear and the most important to localize the disease to the spinal cord. The interpretation of the proprioceptive positioning (knuckling) must be done in the light of the entire neurological examination. In spinal cord disease, proprioceptive ataxia appears first and as the proprioceptive deficits worsen, knuckling occurs. Although proprioceptive positioning is a test that evaluates proprioception, its absence does not necessarily indicate proprioceptive loss. Generalized weakness, orthopedic problems and the animal’s personality may all affect this test.
b. The pain pathways are the last to be affected. The fibers are small and situated deep in the parenchyma.
Clinical signs associated with involvement of the spinal cord descending motor pathways or upper motor neurons (UMN)s:
a. Paresis / Paralysis
b. Normal to exaggerated reflexes (hyper-reflexia)
c. Normal to exaggerated tone (hypertonia)
d. Disuse atrophy
Assuming there is ataxia and paresis, the nature of the reflex plays a crucial role in the localization of the lesion. The decreased or absent reflex is of great localization value. If the reflex is diminished or absent, the lesion is at the level of the spinal gray matter. If the reflex is normal or increased, the lesion is somewhere cranial to the nerve(s) being examined.
Basic principles associated with spinal cord (white matter) compression
The examination of the gait must be done with attention to, and prior to, the evaluation of the reflexes. The clinician must define if the gait is normal, which limb(s) is/are affected, if there is ataxia, and if so of which type, cerebellar, vestibular or proprioceptive. If the animal is paralyzed, the gait cannot be examined. In such cases, the reflexes become the most important tool for lesion localization. The following applies to white matter lesions and not to the peripheral nervous system.
Order in which clinical signs appear
Proprioceptive ataxia with very mild weakness/paresis
Marked ataxia with marked weakness/paresis
Loss of pain perception
The return to function is in the reverse order.
Based on the presence of two pairs of limbs, the spinal cord has been divided for localization purposes in the following segments: C1 to C5, C6 to T2, T3 to L3, and L4 to the end of the cord.
1. Clinical signs associated with a spinal cord lesion between C1 and C5:
Proprioceptive ataxia all limbs.
Tetraparesis all limbs.
Normal to hyper-reflexia all limbs.
Normal to hypertonia all limbs.
If the disease is extradural, the hind limbs are more affected than the front limbs. If the lesion is within the spinal cord, the front limbs are more severely affected than the hind limbs.
2. Clinical signs associated with a spinal cord lesion between C6 and C8 affecting only the white matter (as in some cases of cervical instability of the Doberman):
Proprioceptive ataxia all limbs but milder in the front limbs.
Tetraparesis with some spasticity in the front limbs.
Normal to hyper-reflexia all limbs.
Normal to hypertonia all limbs.
The nature of the gait in the front limbs is not only milder but also different than in the hind limbs.
3. Clinical signs associated with a spinal cord lesion between C6 and T2 affecting white and gray matter:
Proprioceptive ataxia in all limbs.
Hyporeflexia and hypotonia in the front limbs.
Normal to hyper-reflexia and normal to hypertonia in the hind limbs.
Neurogenic atrophy in the front limbs.
4. Clinical signs associated with a spinal cord lesion between T3 and L3:
Deficits limited to the hind limbs. Proprioceptive ataxia associated with paraparesis
Normal to hyper-reflexia.
Normal to hypertonia.
5. Clinical signs associated with a spinal cord lesion between L4 and the end of the spinal cord (white and/or gray matter:
Mild proprioceptive ataxia in the hind limbs.
Paraparesis more pronounced than the ataxia.
Hypo- or areflexia.
Hypo- or atonia.
Since only nerve roots are located within the vertebral canal at L6-L7 and L7-S1, the clinical signs observed at those sites are similar to peripheral nerve lesion and not spinal cord lesion.
Asymmetry of the clinical signs
Space-occupying lesions usually lead to fairly symmetrical signs although there can be mild asymmetry. Only vascular accidents and inflammatory diseases cause profound asymmetry in the clinical signs.
Acute diseases have a better prognosis than chronic diseases
With chronic (over 10 days) spinal cord compression, 50% of the spinal cord diameter is affected prior to the apparition of clinical signs. There is axonal degeneration. The damage is most often irreversible. With an acute lesion, there is spinal cord damage with edema and hemorrhage that if treated aggressively and early may be reversible.
The prognosis for return to function depends on the:
a. Neurological status
b. Time of onset of the neurological deficits
Assuming the animal is paralyzed but has pain perception (even if decreased) and a treatable disease is present, the prognosis is favorable to regain capability to walk if the deficits have been present for less than 5 days. With a history of deficits for 5 to 10 days, recovery can go either way. With deficits present for more than 10 days, the animal likely will remain with neurological deficits and may never walk again if paralyzed.
In cases of fracture/luxation, return to function depends also of the stability of the injured site and to some extent on the animal’s size.