Dr Zoran Loncar
Z.Loncar, DVM1
1Department of Orthopedic Surgery and Neurology, Veterinary Clinic Novak, Belgrade, Serbia
INTRODUCTION
A 3,5 years old mixed breed dog was presented at the clinic with finding of non ambulatory paraplegia. Dog was hited by a car 25 days prior to the presentation. Since then the dog has been treated conservatively without any improvement. Radiography study showed L7 fracture. MRI study showed T13-L1 compressive myelopathy caused by disc material, and lesion L2-3 and L3-L4 consisted with the findings of pseudomeningocoele in humans. The purpose of the article is to suggest that a lesion consisted with pseudomeningocoele in humans can be find in dogs in late MRI screening after nerve root trauma.
CASE HISTORY
Figure 1: Dorsal projection at T2 sequence shows multiple high intensity signal at the level of lumbal nerve roots L2-3, L3-4 to the right. Signal is homogenous, extradural consisted with pseudomeningocoele and CSF leakage
Figure 2. Sagital image of lumbal spinal cord segment in T2 sequence. Shows high signal intensity at the level of nerve root. Loss of signal intensity at the disc ventral to the lesion L3-4. L1-2 complete of signal intensity. Th13-L1 compressive myelopathy caused by disc extrusion.
A 18 kg BW, 3,5 years old mixed breed dog, without significant medical history was presented at the clinic with owners complain not to be able to walk on hind limbs. The owner had not noticed voluntary movements on hind limbs of dog since had been hited by a car 25 days prior to the presentation at the clinic. There was no other abnormalities on general exam except urinary bladder enlargement and overflow pattern of voiding. Neurology exam showed normal mental status. Non ambulatory paraplegia. Cranial nerves were in normal physiological limits. Segmental reflexes in front limbs were normal. Patellar reflex on left side was increased, on right side was decreased. Withdraw reflexes were decreased bilaterally. Perineal reflex was normal. Panniculus cut was at the level of L4 bilaterally. Deep pain was present. Hind limbs were spastic with mild muscle atrophy. The dog showed no pain during palpation of L7 fracture site and there was no crepitation during manipulation of the region. The dog reacted painfully during deep palpation at the level of first lumbal vertebras. The lesion was localized T3 to caudal because of mixture of UMN and LMN signs, slightly lateralized to right. Radiographs showed L7 fracture with complete dislocation of compartments. MRI findings showed :Fig 1 and 2
The dog was treated surgically right T13-L1 hemilaminectomy with disc fenestration. The owner refused to allow surgically treatment of L7 fracture. Postoperatively the dog was treated with antibiotics ( synulox 250mg BID 10 days), NSAID ( carprofen 25mg BID), and physical therapy. Dog was ambulatory 3 weeks after surgery. 1,5 month after the surgery there was no abnormalities at the neurological exam.
DISCUSSION
The case was analyzed for a probable etiology of L2-L3 and L3-L4 lesions visible at the MRI study considering case history, progression of signs, concurrent lesions, lesion distribution and pattern of appearance. It was also taken in count fast improvement of neurological condition immediate after decompression surgery at the level T13-L1. Most of the neurological findings were consisted with all three lesions find during MRI imaging. The lesions at the level of L2-3 and L3-4 were localized at the foramen, extradural, unilateral. Lesion were homogenous, there was no edema surrounding the lesions. Lesion showed T2 hyperintensity, T1 hypointensity. Vascular lesions at that time after the injury would show high intensity signal in both T1 and T2 sequences. Inflammatory or edema would show T2 hyper intensity and T1 hyper or iso intensity of the signal. Anomalous lesion would not be consistent with lesion pattern and neurological deficits connected to the localization without previous clinical signs. Neoplastic conditions would not fit with lesion distribution and progression of clinical signs, but would fit with signal intensity pattern. Taking all data in count lesion fits with the condition well described in human medicine as pseudomeningocoele caused by traction trauma to the nerve roots of lumbal intumescence. This hypothesis is limited by facts that MRI study is not complete. There is absence of FLAIR study wich would support theory that the T2 high signal is due to CSF accumulation. Contrast study would help to eliminate other possible lesions. One could ask question why just two nerve roots were traumatized. And the final limitation is that there is no follow up MRI study done after resolution of clinical signs. Pseudomeningocoele is condition of CSF accumulation due to dura tearing. Major causes are congenital, blunt trauma and traction trauma (1). The mechanism of traction trauma is not clear. It is suggested that can be caused by CSF pressure wave due to increased abdominal pressure (2), or flexion/abduction aggressive movement (3), or flexion/distraction movement (4). There is no correlation between severity of nerve root injury and pseudomeningocoele appearance (4). There is no definitive strategy for pseudomeningocoele treatment (4). Often nerve root injury is more distally than pseudomeningocoele site.
