Last week we discussed a case of flaccid paralysis that was localized to the neuromuscular system, specifically either neuromuscular junction or peripheral nerve. This week, we'll talk briefly about pursuit of diagnostic testing and treatment for these cases.
Diagnostic Testing
This group of diseases is a diagnostic challenge. In academic, or specialty clinics, electrodiagnostic testing may be recommended to look for hallmark changes amongst these group of diseases. Aside from not being readily available, electrodiagnostic testing is also imprecise when attempting to differentiate between this group of diseases. So what do we do? We attempt to differentiate based on history and physical exam findings. For example, animals with polyradiculoneuritis (Coonhound paralysis) are often hyperesthetic with normal bladder function and may, or may not have a history of contact with wildlife (Racoon). By contrast, those with botulism often have urinary retention, reduced mentation and mydriasis. Dogs with tick paralysis rarely have cranial nerve deficits and may have the mildest signs of the group. Coral snake bite results in rapid death (and is only found in the southern states). Organophosphate toxicity is frequently discovered when reviewing the history. Signs of SLUD (see below) or a history of exposure to organophosphate containing products can help guide this diagnosis. Blood cholinesterase levels can be measured (I've never done it) but they aren't reliable once the neurologic signs are apparent.
Treatment Options
Clinical suspicion can only get us so far. At some point we start treatment for the most likely cause. I will often recommend application of a tick product (example: frontline), even if a "tick check" is negative for the patient. Tick paralysis typically begins to improve within 24 hours after application of the product, further increasing your suspicion of the cause.
Polyradiculoneuropathy can progress to respiratory failure so referral for ventilator support is critical for dogs exhibiting reduced cutaneous trunci reflexes. Evaluation of CO2 levels can help you detect if the animal is not ventilating appropriately. No specific treatment is available for polyradiculoneuropathy. Supportive care with assistance to eat, drink and nursing care to maintain cleanliness are critical during the recovery period. These animals can void voluntarily, however they cannot move away from soiled bedding therefore bedsores are a high risk for this patient population. Physical rehabilitation is helpful for recovery so please get these dogs to PT as soon as you can! Recovery may take 4 to 6 months in dogs with severe disease, or 1-3 months in dogs with mild cases.
Botulism is diagnosed with detection of the toxin in serum, feces or gastric contents. This is extremely hard to do, and rarely is a confirmed diagnosis made. Supportive care with fluid support, urinary bladder catheterization, and management of secondary infections may help reduce the risk of death however Botulism is commonly fatal. An older report (Bruchim Y, The Vet Record 2006) describes the rare successful treatment of a mixed breed dog with botulism utilizing supportive care measures.
My experience with coral snake envenomation is limited to only a few cases during my residency at the University of Florida. Each case had a fatal outcome so I don't have a lot of treatment recommendations or supportive care ideas. If you live in the southern US - reach out to your local neurologist for additional help if you encounter a case.
Organophosphate toxicity results in paralysis from blockade of the acetylcholinesterase in the body, thus causing prolonged exposure to AcH at the receptor. This results in acute SLUD (salivation, lacrimation, urination, and defecation) followed by muscle weakness. No specific treatment is available. Atropine does not help once the SLUD has passed and the dog has progressed into the neuromuscular weakness signs. Supportive care, again, is the way to go. This may include ventilator support, along with nursing care and nutritional support. Signs may improve within 7 days after onset, but death is common. (Hopper, K, et al. JVECC 2002)
Whew! These cases are tough! Sometimes we "treat for the treatable" causes because that is all we can do. Keep up the good work and thanks for including me in your case management. I love working with you on the "easy" and the "hard" stuff!
Flaccid Paralysis in the Midwest
It's Tuesday afternoon and you have an emergency case coming that is reported to be unable to walk. Your staff tells you that you will be seeing a 5 year old Labrador that was found unable to walk in the back legs today. You square your shoulders and remind yourself of the common neuroanatomic lesion localizations for the spinal cord, and enter the room. After performing a thorough neurologic exam (self high five!) you conclude the following findings:
Mentation: BAR
Cranial nerves: reduced blink reflex bilaterally with normal corneal reflex, menace response, PLR, physiologic nystagmus and gag reflex.
Gait: Non-ambulatory tetraparesis
Reflexes: absent withdrawal reflex in both pelvic limbs, absent patellar reflexes bilaterally, absent panniculus reflex bilaterally, and reduced withdrawal reflexes more right thoracic limb than left, but both affected.
Postural reactions: When supported, paw replacement is absent in all four limbs
Palpation: non-painful, normal cervical range of motion
You make a hasty exit from the room and search for the number to your closest neurologist. Just kidding! You take a deep breath and realize that due to the multiple reduced reflexes in multiple limbs and cranial nerves, this must be neuromuscular, not spinal and not brain. Great job! What does neuromuscular actually mean?
Neuromuscular Neuroanatomic Lesion Localization:
Neuropathy - reflexes are reduced to absent, paresis without ataxia.
Junctionopathy - reflexes are typically absent however Myasthenia gravis is a junctionopathy and reflexes can be normal for this disease. Again, paresis or plegia without ataxia.
Myopathy - reflexes are normal, dogs are just paretic and are not ataxia
This dog could be a neuropathy or a junctionopathy.
What are my top 5 differentials for a dog with acute, progressive, junctionopathy?
1. Tick paralysis
2. Polyradiculoneuritis (Coonhound paralysis)
3. Botulism
4. Coral snake envenomation (not common in the Midwest)
5. Organophosphate/carbamate intoxication
Stay tuned for next week's TidBit Tuesday to discuss how we might diagnose and manage these unique cases!
Thanks for reading - have a great week and stay safe.