Difference between revisions of "Polyneuritis Equi"
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Also know as: '''''Neuritis of the Cauda Equina — Cauda Equina Syndrome — Cauda Equina Neuritis — PNE''''' | Also know as: '''''Neuritis of the Cauda Equina — Cauda Equina Syndrome — Cauda Equina Neuritis — PNE''''' | ||
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:Abberant parasite migration (e.g. [[:Category:Strongyloidea|''Strongylus spp.'']]) | :Abberant parasite migration (e.g. [[:Category:Strongyloidea|''Strongylus spp.'']]) | ||
:In endemic areas, such as the USA ''[[Sarcocystis|Sarcocystis neurona]]'' myelitis ([[Equine Protozoal Myeloencephalitis|equine protozoal myelitis]]) | :In endemic areas, such as the USA ''[[Sarcocystis|Sarcocystis neurona]]'' myelitis ([[Equine Protozoal Myeloencephalitis|equine protozoal myelitis]]) | ||
− | :[[Rabies]] and ''[[Rhodococcus equi]]'' | + | :[[Rabies]] and ''[[Rhodococcus equi]]'' myeloencepahlitis should also be considered. |
The definitive diagnosis is made on '''post-mortem examination'''. Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed. | The definitive diagnosis is made on '''post-mortem examination'''. Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed. | ||
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[[Category:Neurological Diseases - Horse]] | [[Category:Neurological Diseases - Horse]] |
Revision as of 17:55, 31 July 2012
Also know as: Neuritis of the Cauda Equina — Cauda Equina Syndrome — Cauda Equina Neuritis — PNE
Introduction
Polyneuritis equi is uncommon and caused by a progressive immune-mediated lymphocytic infiltration and demyelination of the sacrococcygeal and lumbosacral nerve roots of the cauda equina. Nerves outside the cauda equina, such as the cranial nerves, may also be affected.
The aetiology of the disease is unknown, but evidence suggests that it is an allergic-mediated polyneuropathy similar to Guillain-Barré syndrome in humans and experimental allergic neuritis (EAN) of laboratory rodents. Infection with Equine Herpesvirus-1 and Campylobacter have been proposed, but there has been no confirmation.
It is seen in adult horses of all breeds in North America and Europe.
Clinical Signs
Typically, there is a slow progressive paralysis of the tail, rectum, anus and bladder and hindlimb weakness and ataxia.
There will be urine scalding of the hindlimbs, hyperaesthesia and muscle fasciculations over the hindquarters.
Muscle atrophy is variably present.
Cranial nerve involvement, particularly CN V, VII and VIII, may also be present and is usually asymmetric. This will present as paralysis of the facial muscles, head tilt, nystagmus, tongue paralysis and difficulty swallowing.
Diagnosis
Currently there are no specific antemortem tests to detect the disease in horses.
The diagnosis is one of exclusion, supported by the clinical signs and history.
An ELISA can be performed to detect antibodies against P2-myelin protein, but the test is not available commercially and is not specific for the disease.
On routine haematology: evidence of chronic inflammation is usually detected.
Analysis of the CSF reveals: xanthochromia and a mildly increased protein and cell count.
Differential diagnoses that should be ruled out before a diagnosis of PNE is considered include:
- Equine herpesvirus-1 myeloencephalopathy
- Sacral/coccygeal trauma
- Equine motor neuron disease
- Abberant parasite migration (e.g. Strongylus spp.)
- In endemic areas, such as the USA Sarcocystis neurona myelitis (equine protozoal myelitis)
- Rabies and Rhodococcus equi myeloencepahlitis should also be considered.
The definitive diagnosis is made on post-mortem examination. Extradural and intradural nerve roots of the cauda equina are grossly thickened and are infiltrated with inflammatory cells. Demyelination and axonal degeneration are present. Similar changes in the cranial nerves may be observed.
Treatment
Treatment is palliative, including managmenent of urinary and faecal incontinence, managing cystitis and minimising urine scalding.
Horses with dysphagia may need tube feeding.
Treatment with corticosteroids has provided some palliative benefits but the effect is short-lived.
The condition is slowly progressive, but the prognosis is generally poor.
Polyneuritis Equi Learning Resources | |
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Flashcards Test your knowledge using flashcard type questions |
Equine Orthopaedics and Rheumatology Q&A 06 |
References
DeLahunta, A. (2008) Veterinary neuroanatomy Elsevier Health Sciences
Merck and Co (2008) Merck Veterinary Manual Merial
Taylor, F. (2009) Diagnostic techniques in equine medicine Saunders
Furr, M. (2008) Equine Neurology John Wiley and Sons
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
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