Nerve root compression
The dog had been yelping intermittently for 1 month. Left forelimb lameness commenced 1 week prior to the referral. Although the dog was described as active, there had been no history of trauma.
A weight-bearing left forelimb lameness and a resistance to lateral neck flexion were found. No neurological deficits were present.
Nerve roots to the left forelimb, within the vertebral canal to account for the neck pain.
MRI was chosen to investigate the causes of neck pain because of the potential for nerve root compression. A lateralized extrusion of disc material into the intervertebral foramen is difficult to outline with myelography as the subarachnoid space is not sufficiently compressed. Rotated views may help, but the lesion may not be outlined even then.
MRI showed ventral compression of the cord over the C5–6 IVD space (Fig. 51.1).
IVD extrusion was confirmed at surgery and the cord was decompressed. The lameness and neck pain resolved and the dog remained normal without pain relief.
Forelimb lameness may precede or occur simultaneously with the onset of neck pain caused by a lateralized disc extrusion. Signs may wax and wane and are generally of sudden onset. Progression to tetraparesis, or weakness of the forelimbs can occur.
Myelography shows the filling of the subarachnoid space with contrast agent. Dorsal and vertical nerve roots are enclosed by the subarachnoid space just to the level of formation of the spinal nerve. Lateral compression of the spinal nerve at the intervertebral foramen will go unnoticed by myelography. MRI is an ideal tool to detect this and other causes of neck pain. Transverse slices should be taken through each IVD space from C2–3 to C7–T1. Prognosis for relief from pain and restoration of strength is excellent after surgery.
One month’s duration of difficulty getting into the car, reduced activity, and non-weight-bearing on the left hind when standing. A bunny-hopping, synchronous hindlimb gait occurred when the dog tried to run. Atrophy of the hindlimbs had been noted. The dog was slow to squat when defecating and had stopped lifting a hindlimb to urinate.
The dog was alert and ambulatory with decreased weight-bearing on the left hind when standing and a shortened stride of the left hind. The hindlimb gait was not ataxic but the altered stride length did give it an irregular look when viewed front on and from the rear but when viewed from the side the left hind lameness and right hind compensation was easier to see.
Atrophy of the muscles of the left hind was noted. Hopping and proprioception were normal. The patellar reflex was 3+ bilaterally and the withdrawal reflex was normal in all limbs. The anal tone was normal. Pain could be elicited by pressure over the LSJ.
Applying firm pressure to the lumbosacral joint while elevating the pubis elicited pain. Hip pain was found by forced extension of the hips. To differentiate the source of pain, avoid hip extension when applying pressure to the LSJ.
Decreased tarsal flexion during limb withdrawal (flexor reflex) indicates sciatic involvement. A lack of antagonism from sciatic deficits creates pseudo-hyperreflexia of the patellar reflexes.