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Basil's Neurology Case

Basil, a 3-year-old male neutered French Bulldog, was presented to the Neurology and Neurosurgery team with a 2-day history of acute onset, painful and rapidly progressive tetraplegia.

On admission, Basil showed severe respiratory depression with open-mouth breathing and absent inspiratory thoracic expansion. He was tetraplegic and his withdrawal reflexes were absent in the thoracic limbs. The muscle tone was symmetrically reduced in both thoracic limbs. A central cord syndrome localised to a C1-T2 myelopathy was suspected due to the absent reflexes in the thoracic limbs and the paresis of the phrenic nerve. The differential diagnosis considering his breed, age, clinical presentation and diagnostic investigations included an intervertebral disc extrusion as the most likely diagnosis. However, an inflammatory disorder (i.e. meningomyelitis) could not be excluded.

Emergency bloods showed respiratory acidosis and hypoxemia on EPOC analysis (arterial blood sample) compatible with hypoventilation showing a partial pressure of carbon dioxide (PCO2) of round 70-80 mmHg (range 34-40). Immediate oxygen supplementation by nasal canula was started but was not sufficient. The continuous severe respiratory distress and hypoventilation required eventually endotracheal intubation and general anaesthesia to ensure adequate oxygenation.

An emergency computed tomography (CT) scan of the cervical vertebral column was performed confirming an oval and large hyperattenuating lesion (mineral material) visible at the level of C3-C4 intervertebral disc space consistent with an intervertebral disc extrusion (Figure 1).


The material occupied the ventral and central portion of the vertebral canal and resulted in marked spinal cord compression. A decompressive C3-C4 ventral slot was performed immediately thereafter and a large amount of degenerated disc material was removed resulting in successful spinal cord decompression.

After surgery, Basil continued to require intensive care due to his ongoing respiratory compromise and he remained in the intensive care unit over the following week. Increased inspiratory effort was persistent due to a combination of his brachycephalic obstructive airway syndrome (BOAS) and his poor thoracic compliance/ventilation from the spinal cord injury (phrenic nerve impairment). He remained oxygendependent for the first week after the surgery. Only mild neurological improvement was initially noted characterised by the presence of mild voluntary movement in both pelvic limbs yet leaving him initially recumbent. Unfortunately, he additionally regurgited a large volume followed by a brief vagal syncope episode causing further concerns for his wellbeing and complications to the clinical management. A continuous rate infusion of metoclopramide was started but was insufficient. Further episodes of gulping and regurgitation were observed suggesting gastroesophageal reflux as a more pertinent problem. Therefore, metoclopramide was gradually discontinued and cisapride was started alongside sucralfate and omeprazole.

Unfortunately, Basil worsened further over the following couple of days. Basil’s inspiratory effort deteriorated and pulmonary auscultation revealed crackles bilaterally in the cranioventral aspect of the thorax.

Thoracic radiographs confirmed the clinical concern of aspiration pneumonia (Figure 2), and antibiotic therapy (marbofloxacin and cefalexin) was started. The respiratory compromise continued to be severe and challenging to manage. Therefore, the decision was taken to perform an emergency staphylectomy and temporary tracheostomy placement to improve Basil’s ventilation and respiratory pattern. The next day, Basil had periods of fever and hyperventilation most likely secondary to his aspiration pneumonia. During his entire post-operative period, the medical treatment was combined with intensive nursing care characterised by regular turning, nebulization/coupage, tracheostomy care, regular physiotherapy, postural feeding with the help of a peanut ball and an elevated bed of 15º to 30º to reduce the risk of further regurgitations.

Finally, Basil started showing a gradual improvement. The oxygen supplementation was stopped 5 days post-surgery and the tracheostomy tube was removed 6 days post-placement. His neurological status also improved slowly. He was able to put himself in sternal position, yet remaining non-ambulatory tetraparetic at the time of the discharge on day 13 after admission. He recovered his ability to ambulate one-month post-surgery. He was breathing normally and his quality of life was considered good. Remaining neurological deficits included mild intermittent spinal ataxia and paresis in the right thoracic limb.


This report describes severe respiratory complications caused by a cervical intervertebral disc extrusion in a brachycephalic dog, treated with dedicated intensive care resulting in functional recovery.

Central cord syndrome is a clinical syndrome that refers to a spinal cord injury where motor weakness is more severe in the thoracic limbs compared to the pelvic limbs. Segmental spinal reflexes and muscle tone are reduced in the thoracic limbs but not in the pelvic limbs. It is caused by a lesion in the centre of the cervical spinal cord involving the grey matter and the axons that are lying more centrally and projecting to the motor neurons of the thoracic limbs. This syndrome is commonly caused by a spinal cord injury and in Basil, this was triggered by the contusive damage from the rapidly herniated disc material.

Severe cervical spinal cord disorders might require ventilatory support to treat hypoventilation when the phrenic nerve is injured. The phrenic nerve arises from the C5-C7 spinal cord segments (found at the cervical vertebral bodies C4-C6) and provides exclusive motor control to the diaphragm, the primary muscle of respiration. Affected patients experience ventilatory failure associated with a physical inability to move a sufficient amount of air into the lungs secondary to paralysis or paresis of the respiratory musculature. There is a serious risk of death unless hypoventilation is aggressively treated. Important clinical signs to look out for are open-mouth breathing, weak/reduced thoracic inspiratory expansion and laboured respiration especially in non-ambulatory tetraparetic and tetraplegic cases. The severity of hypoventilation is determined by measuring PCO2 ideally in arterial blood samples or capnography when intubated. Severe cases may require prolonged positive-pressure mechanical ventilation, which was also considered for Basil. However, the rapid assessment and diagnosis followed by spinal cord decompression and temporary tracheostomy placement were eventually enough in Basil to achieve sufficient oxygenation and to combat respiratory impairment caused by the aspiration pneumonia and BOAS.

A further complication that made Basil’s treatment challenging was the gastroesophageal reflux that led to aspiration pneumonia. Gastroesophageal reflux is frequently seen in French Bulldogs, especially in recumbent dogs and after general anaesthesia. Recumbency is associated with a slower recovery as it results in atelectasis, which worsens the already compromised lung capacity and compliance. Thus, adequate medical management and intensive physical rehabilitation play an important role in the management of gastroesophageal reflux in recumbent patients. Essential care for managing these patients include postural feeding, elevated bed, regular turning, regular oral and stoma care associated with the tracheostomy tube placement to avoid accumulation of secretions, and intensive physiotherapy.


It was such a pleasure to see Basil’s fantastic improvement and his good quality of life after this severe spinal cord injury causing such severe respiratory complications. Basil showed us once more, that with dedication, severe neurological conditions can have a good outcome.


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