A 10-year-old, castrated Labrador retriever was presented for excessive salivation.
According to the owners, the dog’s onset of hypersalivation was recent and his regular veterinarian had prescribed maropitant citrate at 60 mg PO q24h for apparent nausea and topical mometasone furoate (small amount in ear q24h for 7 days) for confirmed otitis externa of the left ear. Follow-up 1 week later showed persistent salivation and otitis externa, along with apparent pain on neck palpation and weight-bearing lameness of the right thoracic and left pelvic limbs. The dog was referred for neurologic evaluation.
The dog was alert and responsive with normal hydration status. Physical and orthopedic examinations were unremarkable except for a finding of mild weight-bearing lameness of the right thoracic and left pelvic limbs. The previously reported hypersalivation and apparent cervical pain were not evident. During continuous walking, the dog’s gait became progressively short-strided in all limbs, until it collapsed and was unable to stand. The dog recovered after resting for a few minutes and was able to resume a gait similar to that seen before the exercise-induced collapse. Additional abnormalities were not detected on neurologic examination. Results of CBC, serum biochemical profile, and total T4 were unremarkable.
1. If the patient is neurologically abnormal, what is the neuroanatomic localization of signs?
2. What is the primary differential?
3. What is the MDB that should be obtained for this condition?
4. What screening test could increase the index of suspicion for the most likely neurologic cause of exercise-induced collapse, and how does it work?
5. Which laboratory test is most likely to confirm the diagnosis?
Diagnosis: Generalized neuromuscular disorder
Initial gait analysis suggested that the lameness resulted from an orthopedic condition, as the initial neurologic examination was normal (see Collapse: Neurologic or Not?). However, the patient developed a progressively short-strided gait in all 4 limbs while walking around the hospital. Short-strided gait can be caused by disease affecting the spinal intumescence of the affected limb(s), orthopedic conditions, or peripheral neuromuscular disease. Because all limbs were affected, both cervical and lumbar intumescence would have to be affected. This was unlikely because ataxia or apparent spinal pain was not present, and the postural reactions and segmental reflexes remained normal even as the patient became progressively weaker.
Collapse: Neurologic or Not?
Possible differentials for exercise-induced collapse in dogs include:
- Bone/joint disorders (eg, polyarthritis)
- Cardiovascular disorders (eg, subvalvular aortic stenosis)
- Respiratory disorders (eg, laryngeal paralysis, pulmonary parenchyma or pleural space abnormalities)
- Generalized neuromuscular disorders (eg, MG, polymyositis, metabolic myopathies, acquired peripheral polyneuropathies)
- Acquired spinal cord disease (eg, chronic intervertebral disk disease)
Orthopedic disease was considered less likely, as no orthopedic abnormalities (eg, joint pain or effusion) were detected. As a result, generalized neuromuscular disease was considered the likely localization. Myasthenia gravis (MG) was the primary
differential because it is the disease most frequently identified in dogs with exercise-induced collapse, laryngeal/pharyngeal weakness (eg, excessive salivation, gagging/retching), and generalized weakness. Other differentials included myopathies (eg, polymyositis, degenerative myopathies), polyneuropathies, and orthopedic diseases (eg, polyarthritis).