Acute canine polyradiculoneuritis (APN) is an acute and ascending lower motor neuron inflammatory polyneuropathy in dogs. This disorder was first recognized in hound dogs that were in contact with raccoon’s saliva and was originally termed “coonhound paralysis”. However, this disease has subsequently found in dogs and countries with no contact to racoons, although other precipitating causes, such as vaccination or infection, may be identified in these cases. The triggers of this disorder remain largely unknown, but there has been some evidence to suggest the involvement of clostridial organisms in the intestine as a source of antigen. These external antigens are apparently similar to proteins comprising part of the ventral nerve roots and motor nerves, and clinical signs are caused by an immune-mediated attack of these structures with the invasion of inflammatory cells

APN is an inflammatory disease that affects to motor root (ventral root) of peripheral nerves. This explains why typically these dogs are weak with reduced spinal reflexes but sometimes very painful or sensitive to noxious stimuli.

Clinical presentation:

Dog are presented with an acute, progressive, flaccid quadriparesis that often ascends from the pelvic limbs to the thoracic limbs over one to several day period. On rare occasions, the thoracic limbs are more involved than the pelvic limbs. Hyporeflexia or areflexia with hypotonicity is usually present in all four limbs. Some tail movement may be preserved. The palpebral reflex may be depressed or absent in both eyes due to involvement of the facial nerve (CN VII) and dysphagia may be present due to vagus nerve (CN X) dysfunction. However, megaesophagus is uncommon. Sensation remains intact, and some animals have generalized hyperesthesia. The speed and severity of these clinical signs is variable and this is the reason why dogs should be monitored closely until these signs stabilizes or they start to improve. Our main concern will be that if a paresis or paralysis of intercostal and diaphragmatic muscles occurs, abdominal respirations, hypoventilation and hypoxia might occur and the patient will need to be mechanically ventilated.

ON THIS VIDEO:

We can see a 2 years old staffy cross female neutered,  that was presented with a peracute inability to walk. There was no recent contact with racoons or vaccination.

On the video you can observe the lack of muscle tone straight away. She’s not able to support her weight but she has some movements. You can appreciate she’s wagging the tail and she’s trying to move particularly the hind limbs, but she can’t support her weight: She has a non ambulatory tetraparesis.

When we perform the proprioception, this is absent on the left side but she’s almost trying harder on the right side. Observe how we’re supporting her weight when performing the propioceptive response! It’s important to do this, otherwise with the severe weakness she has you won’t be able to see any movement.

On the second part of the video we proceed with the spinal reflexes. The patellar reflex (femoral nerve) is absent, there’s no extension of the knee. The withdrawal (sciatic nerve) is also absent, there’s no flexion of the limb. However, you can see she feels the manouvre, as she gets really agitated when we’re pinching the paw. The withdrawal on the thoracic limbs is a bit better: Still reduced but she’s trying: remember how this disease tends to be “ascending”.

The video performed on day 4 of the hospitalization (6 days after the clinical signs started) showed a much stronger dog. She’s ambulatory with minimal support. When we repeat the proprioception (still holding her weight) it’s so much improved! Do you see  the strengh of the withdrawal reflex? But take a look how she will collapse on the front limb as soon as we’re not holding her weight.

Diagnosis of APN:

The diagnosis of APN is based on clinical history and neurological findings. The most important and challenging aspect for diagnosing this disease is ruling out other neuromuscular joint disorders that cause acute lower motor neuron tetraparesis (e.g., tick paralysis, botulism, or acute fulminating myasthenia gravis). Electrodiagnosis testing ( EMG and motor nerve conduction) can be used to differentiate APN from other low motor neuron disorders. Electromyography (EMG) changes take about 9 days to become obvious, therefore in fast progressing cases electrodiagnosis interpretation might be challenging.  Lumbar cerebrospinal fluid (CSF) analysis in APN patients commonly reveals a normal cell count with increased CSF protein levels, especially at 7 days or more after the appearance of clinical symptoms. So the reality is that these are very challenging cases as even if they can have a very good prognosis is many times difficult to give a definitive diagnosis and prognosis. Recently it’s been proved that Anti-GM2 and anti-GalNAc-GD1a immunoglobulin G anti-glycolipid antibodies represent serum biomarkers for acute canine polyradiculoneuritis for clinically affected cases in a large geographically heterogenous cohort.

Nerve biopsy can be performed for a definitive diagnosis and this will reveal characteristics of lymphocytic radiculitis and demyelination. However, this is an invasive and pricey way to diagnose a disease that could have a good prognosis without any specific treatment. Therefore it tends to be difficult to justify.

Treatment and prognosis

Only supportive treatment is necessary on these cases. Steroids do not change the speed of recovery and they could complicate the clinical presentation due to side effects.  Severe generalized muscle atrophy may occur making physical therapy essential. Intense physiotherapy with other supportive treatment for non ambulatory dogs is the current treatment. The prognosis is usually good with adequate support and most dogs recover in 4–12 weeks.

Plasmapheresis and immunoglobulins have been suggested but are not current treatments in routine cases.